The DOI matches its Crossref record; 156 of the 156 references it cites were found in a registry or an index; 79 of the 126 sources its claims cite were checked for support.
Current management of hypertrophic cardiomyopathy
Open accessAbstract
Hypertrophic cardiomyopathy is a common yet under-recognized genetic structural heart condition characterized by left ventricular hypertrophy. Patients may present with obstructive disease characterized by an elevated left ventricular outflow tract gradient or non-obstructive disease. Long established medical and surgical treatment options for patients with obstructive hypertrophic cardiomyopathy and refractory symptoms can be effective in eliminating outflow tract gradients and improving symptoms. Cardiac myosin inhibitors have emerged as a new class of evidence based medical therapy for patients with obstructive hypertrophic cardiomyopathy and an alternative to septal reduction therapies. However, effective treatments for patients with non-obstructive hypertrophic cardiomyopathy remain limited, with several clinical trials ongoing. Variants in cardiac sarcomeric genes are the primary genetic cause of hypertrophic cardiomyopathy and are being investigated as targets for gene based therapies. Stratification of the risk of sudden death is an important component of caring for patients with hypertrophic cardiomyopathy. Recommendations for implantable cardioverter-defibrillator implantation are based on well validated risk factors in combination with shared decision making. Atrial fibrillation is common in patients with hypertrophic cardiomyopathy, and anticoagulation is strongly recommended for stroke prevention. Rhythm control is essential for patients with symptomatic atrial fibrillation. Historically, vigorous exercise has been restricted; however, newer data suggest that the arrhythmic risk is less than previously thought and emphasize an individualized approach. Advanced heart failure is an uncommon but important cause of morbidity and mortality. Early identification is key to improving outcomes with advanced therapies including cardiac transplantation. The management of hypertrophic cardiomyopathy is rapidly evolving toward a more personalized approach, based on genotype and phenotype, to alter disease progression and improve patients’ outcomes.
Overview
AI snapshot
Written from the paper’s full text.
TL;DR
This BMJ review summarizes current management of hypertrophic cardiomyopathy, emphasizing cardiac myosin inhibitors as a new therapy for obstructive disease and persistent gaps in non-obstructive disease, arrhythmia, sudden-death risk, exercise, and advanced heart failure. It synthesizes guideline recommendations and trial data to argue that management is evolving toward genotype- and phenotype-based personalized care.
Key findings
- Hypertrophic cardiomyopathy has an estimated global prevalence of 1 in 500, has been described in at least 125 countries, and an estimated 80-90% of cases remain undiagnosed; 30-60% of patients harbor genetic variants, whereas no pathogenic variant is identified in around 40%.
- In obstructive disease, cardiac myosin inhibitors showed benefit: in EXPLORER-HCM the primary outcome occurred in 37% with mavacamten versus 17% with placebo (P=0.0005); in VALOR-HCM, 17.9% of mavacamten-treated patients versus 76.8% of placebo-treated patients met criteria for septal reduction therapy at 16 weeks (difference 58.9%, CI 44% to 73.9%), with 15.7% of the total study sample meeting the composite endpoint at 128 weeks; in SEQUOIA-HCM, aficamten improved peak oxygen uptake by 1.8 mL/kg/min versus 0.0 mL/kg/min with placebo (P<0.001).
- Exercise data challenge prior restriction: in RESET, moderate-intensity training improved peak VO2 versus usual activity (between-group difference 1.27, 95% CI 0.17 to 2.37; P=0.02), and in LIVE-HCM arrhythmic outcomes occurred in 4.7% of vigorous exercisers versus 4.6% of non-vigorous exercisers (adjusted hazard ratio 1.01, upper 95% one-sided CI 1.48).
- Atrial fibrillation is common, present in 5% at diagnosis and developing in another 10-22% during follow-up; thromboembolic risk occurs in up to 27% of those with atrial fibrillation, with a hazard ratio of 1.5 compared with patients with atrial fibrillation without hypertrophic cardiomyopathy.
Methods
- Narrative/critical review; source literature identified through PubMed and Medline searches using “hypertrophic cardiomyopathy” AND terms for medications, myectomy, septal reduction, sudden death, defibrillator, atrial fibrillation, and heart failure, with bibliographies scanned for further studies; no start time was set, and the most recent search was September 2024.
- Studies were prioritized by quality: randomized clinical trials were prioritized where available, and non-randomized or crossover studies were included when RCTs were not available; evidence was synthesized with guideline tables (2023 ESC, 2024 ACC/AHA) and trial tables.
- Patient involvement: a draft manuscript was shared with four patients living with hypertrophic cardiomyopathy, and their feedback was incorporated.
Limitations
- Stated: many recommendations lack randomized data, including management of acute hypotension, primary-prevention ICD use, and anticoagulation for subclinical atrial fibrillation; CMI trials enrolled patients with limited racial and ethnic diversity, so generalizability is unclear; cost and cost-effectiveness could limit adoption; and the ODYSSEY-HCM update was not peer reviewed or published.
- Stated: whether CMIs can be used as first-line therapy is unclear because trial participants were maintained on beta blockers, calcium channel blockers, and disopyramide; long-term surveillance is warranted for possible ejection fraction decline.
- Evident: as a narrative review, it does not use a systematic review or meta-analytic framework, and conclusions rely on selected literature, guideline comparison, and some observational or non-randomized evidence.
Model-written summary. Check it against the paper before relying on it.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
27 Supported · 27 Partly supported · 17 No full text of the sources · 8 Own interpretation · 7 Not checked yet · 6 Sources not found · 5 Supported so far · 4 No basis given · 1 Mixed support · 1 Couldn’t confirm · accuracy not yet measured
Every source the paper cites for this claim was checked and supports it.
In the paper
“On the basis of data from the phase 2 VANISH RCT, valsartan may attenuate adverse cardiac remodeling in younger patients (<45 years) with early stage disease and pathogenic or likely pathogenic sarcomeric variants and can be considered in this selected population.41”
§ Current management of hypertrophic cardiomyopathy > Management of acute hypotension
What the sources say
- Supportedcites [41] source
The Methods (Participants; page not available) specify that VANISH enrolled patients aged 8–45 with pathogenic or likely pathogenic sarcomeric variants. The Discussion (page not available) reports improved measures of cardiac remodeling with valsartan and says physicians and patients might consider individualized use, while noting that long-term clinical effects remain unknown. The paper’s upper age limit included 45-year-olds, a minor difference from the citing sentence’s “<45 years.” (LLM, conf=0.91)
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Use of mavacamten in obstructive hypertrophic cardiomyopathy is supported by the phase 3 RCT EXPLORER-HCM, 33 which evaluated the effect of mavacamten on peak exercise capacity and NYHA class.”
§ Current management of hypertrophic cardiomyopathy > Cardiac myosin inhibitors
What the sources say
- Supportedcites [33] source
The Summary (p. 1) identifies EXPLORER-HCM as a phase 3 randomized, placebo-controlled trial in patients with symptomatic obstructive hypertrophic cardiomyopathy. It specifies peak oxygen consumption and NYHA class as outcomes, and the Discussion (p. 9) reports that mavacamten was superior to placebo on the primary and secondary endpoints. (LLM, conf=0.94)
plaindirectn = 251- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Disopyramide has been shown in retrospective studies to be safe and associated with an improvement in both LVOT gradient and symptoms when used in combination with β blockers or non-dihydropyridine CCBs.”
§ Current management of hypertrophic cardiomyopathy > Sources and selection criteria
What the sources say
- Partly supportedcites [30] sourceExperimental — accuracy not yet measured
Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
- Supportedcites [31] source
Split into 2 atoms — 2 confirmed, 0 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“The primary outcome (≥1.5 mL/kg/min increase in pVO 2 with at least one NYHA class improvement or ≥3.0 mL/kg/min increase in pVO 2 with no worsening of NYHA class at 30 weeks) occurred in 37% of the mavacamten group compared with 17% of the placebo group (P=0.0005).”
§ Current management of hypertrophic cardiomyopathy > Cardiac myosin inhibitors
What the sources say
- Supportedcites [33] source
The Summary (p. 1) defines the primary endpoint using the stated pVO₂ and NYHA criteria over 30 weeks. Its Findings (p. 1) report that 45 of 123 patients (37%) on mavacamten and 22 of 128 (17%) on placebo met that endpoint (p=0.0005). (LLM, conf=0.95)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“the decrease in hypertrophic cardiomyopathy related mortality, from 3-6% a year in early cohorts to the current 0.5% year, 95 has been attributed in part to the increasing identification of patients with hypertrophic cardiomyopathy at risk for sudden death with subsequent ICD implantation.”
§ Current management of hypertrophic cardiomyopathy > Hypertrophic cardiomyopathy phenocopies
What the sources say
- Supportedcites [95] source
Split into 2 atoms — 2 confirmed, 0 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“In a long term multinational cohort of patients undergoing ASA, all cause mortality was independently associated with reduction in LVOT gradient.68”
§ Current management of hypertrophic cardiomyopathy > Obstructive disease
What the sources say
- Partly supportedcites [68] sourceExperimental — accuracy not yet measured
The Survival after alcohol septal ablation section reports that all-cause mortality was independently associated with the LV outflow tract gradient at the last clinical check-up. The Discussion distinguishes that residual gradient from the reduction in gradient, which it associates with NYHA class. The paper does not report an independent mortality association with the amount of gradient reduction. (LLM, conf=0.88)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“compared with 18% in relatives of probands with genotype positive hypertrophic cardiomyopathy”
§ Current management of hypertrophic cardiomyopathy > Gene elusive hypertrophic cardiomyopathy
What the sources say
- Supportedcites [87] source
The Results section reports that 88 of 491 relatives from genotype-positive families (18%) had HCM at baseline. The Discussion likewise states that 18% of screened relatives from genotype-positive families had phenotypic HCM at baseline. The figure is a baseline prevalence among screened relatives, not an estimate for all relatives. (LLM, conf=0.94)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“a lower rate of family history of hypertrophic cardiomyopathy”
§ Current management of hypertrophic cardiomyopathy > Gene elusive hypertrophic cardiomyopathy
What the sources say
- Not checked — no full text of the sourcecites [72] source
- Supportedcites [73] source
The Results section (“Effect of mutations in sarcomere genes”; page unavailable in our copy) reports that patients with a sarcomere variant had a higher frequency of family history of HCM than those without sarcomere variants. This supports the stated comparison between genotype-positive and gene-elusive patients. (LLM, conf=0.93)
- Could not verifycites [84] sourceExperimental — accuracy not yet measured
The Results (Clinical Characteristics) distinguish SARC+ from SARC− patients, and the Methods (Statistical Analysis) define a non-familial subgroup as SARC− patients without a family history of HCM. Neither passage compares the rate of family history between all SARC− and SARC+ patients; searches for family-history comparisons found no such result in our copy. (LLM, conf=0.74)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
The cited sources that could be checked couldn’t confirm or dispute this claim.
In the paper
“This is like the rate in SEQUOIA-HCM in which 3.5% of patients on aficamten versus 0.7% of patients on placebo had a transient drop in ejection fraction to <50%.36”
§ Current management of hypertrophic cardiomyopathy > Cardiac myosin inhibitors
What the sources say
- Could not verifycites [36] sourceExperimental — accuracy not yet measured
The available passage from the Abstract reports the treatment-group sizes and baseline ejection fraction, but not how many patients had a transient drop below 50%. Searches for 3.5%, 0.7%, and reductions in ejection fraction returned no passage establishing the claimed rates. (LLM, conf=0.72)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Could not verify
Every source the paper cites for this claim was checked and supports it.
In the paper
“Genome-wide association studies suggest a strong polygenic influence in hypertrophic cardiomyopathy, especially in sarcomeric negative disease.”
§ Current management of hypertrophic cardiomyopathy > Gene elusive hypertrophic cardiomyopathy
What the sources say
- Supportedcites [90] source
The paper reports a genome-wide association study and states that single-nucleotide polymorphism heritability indicates a strong polygenic influence, especially in sarcomere-negative HCM (Abstract). It also reports higher estimated heritability for sarcomere-negative than sarcomere-positive HCM (0.34 versus 0.16), supporting the claimed emphasis. (LLM, conf=0.95)
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Overall, the prevalence of hypertrophic cardiomyopathy in relatives of patients with gene elusive disease is less than in those with gene positive disease.”
§ Current management of hypertrophic cardiomyopathy > Gene elusive hypertrophic cardiomyopathy
What the sources say
- Supportedcites [70] source
The Discussion states that HCM affected 5% of relatives of genotype-negative index patients, a prevalence 6 to 10 times lower than among relatives of genotype-positive index patients. This directly supports the comparison in the claim. (LLM, conf=0.94)
- Supportedcites [87] source
The Discussion reports HCM at baseline in 12% of screened relatives from gene-elusive families versus 18% from genotype-positive families. It also reports a lower incidence during follow-up in the gene-elusive group, consistent with the claimed overall comparison. (LLM, conf=0.93)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“have milder disease”
§ Current management of hypertrophic cardiomyopathy > Gene elusive hypertrophic cardiomyopathy
What the sources say
- Not checked — no full text of the sourcecites [72] source
- Supportedcites [73] source
The Results section (‘Effect of mutations in sarcomere genes’; page not available) reports that sarcomere-positive patients had greater maximum left-ventricular wall thickness and a higher proportion of cardiovascular deaths than sarcomere-negative patients. This supports the comparison of milder disease in patients without an identified sarcomere variant. (LLM, conf=0.89)
- Supportedcites [84] source
The Discussion section, “Genotype Influences Outcome” (page unavailable), states that sarcomeric HCM has worse outcomes than HCM without sarcomere mutations. It reports a greater burden and earlier onset of complications in SARC+ patients, supporting the comparison with gene-elusive patients. (LLM, conf=0.93)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Recent studies report hypertrophic cardiomyopathy prevalences of 5% and 12% among living relatives within three generations of probands with gene elusive hypertrophic cardiomyopathy”
§ Current management of hypertrophic cardiomyopathy > Gene elusive hypertrophic cardiomyopathy
What the sources say
- Partly supportedcites [70] sourceExperimental — accuracy not yet measured
The Results report HCM in 5% of participating relatives of probands with normal genetic investigations. The Discussion says affected relatives appeared in 12% of families investigated—not that HCM prevalence was 12% among relatives. The claim conflates those two denominators. (LLM, conf=0.91)
- Supportedcites [87] source
The Discussion reports HCM at baseline in 5% of screened relatives from gene-elusive families in Nielsen et al. and 12% in this study. The Materials and Methods say a three-generation family pedigree was used to identify relatives for screening; this study’s estimates concern screened adult relatives. (LLM, conf=0.90)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“The phenotypic heterogeneity among patients with similar gene variants likely relates, in part, to the effect of functional “modifier” variants in other genes that influence the penetrance and phenotypic expression of the main pathogenic variants.83”
§ Current management of hypertrophic cardiomyopathy > Genotype positive hypertrophic cardiomyopathy
What the sources say
- Partly supportedcites [83] sourceExperimental — accuracy not yet measured
The Introduction and Discussion report that modifier loci contribute to variation in cardiac hypertrophy among family members sharing a causal HCM mutation. The paper studied phenotypic expression in one family; it did not establish effects on penetrance or identify functional modifier variants, which the claim also attributes to it. (LLM, conf=0.86)
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“The published CMI trials enrolled patients with limited racial and ethnic diversity, so how generalizable the benefits will be to patients who come from under-represented backgrounds is unclear.57”
§ Current management of hypertrophic cardiomyopathy > Cardiac myosin inhibitors
What the sources say
- Supportedcites [57] source
The section on representation of racial and ethnic minority populations (indexed as Abstract; no page given) says inclusion in CMI trials was low: non-White participants made up 9% of EXPLORER-HCM and 11% of VALOR-HCM. It also says experience in this group is limited, supporting the citing sentence’s uncertainty about generalizability. (LLM, conf=0.93)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“patients with gene elusive hypertrophic cardiomyopathy tend to present at later ages than their genotype positive counterparts”
§ Current management of hypertrophic cardiomyopathy > Gene elusive hypertrophic cardiomyopathy
What the sources say
- Not checked — no full text of the sourcecites [72] source
- Supportedcites [73] source
The Results section states that patients with sarcomere variants were younger at diagnosis than those without them. Figure 1 reports a mean age at initial evaluation of 45.78 years for sarcomere-positive patients versus 53.05 years for sarcomere-negative patients; the Discussion also describes younger age at presentation among variant carriers. (LLM, conf=0.93)
- Supportedcites [84] source
The Results (Clinical Characteristics; page unavailable) define SARC− patients as having negative genetic testing and report that their median age at diagnosis was 51.1 years, versus 37.5 years for SARC+ patients. This supports the claim that gene-elusive patients tend to present later than genotype-positive patients. (LLM, conf=0.94)
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“In the EXPLORER trial, 5.6% of patients on mavacamten compared with 1.5% on placebo had a transient drop in ejection fraction to <50% during the trial, requiring treatment discontinuation and resumption at a lower dose.33”
§ Current management of hypertrophic cardiomyopathy > Cardiac myosin inhibitors
What the sources say
- Partly supportedcites [33] sourceExperimental — accuracy not yet measured
The Summary (p. 1) gives group sizes of 123 on mavacamten and 128 on placebo; the safety results (p. 9) report transient LVEF below 50% in seven and two patients, respectively, consistent with the quoted percentages. But only three of the seven mavacamten patients and both placebo patients had temporary treatment discontinuation during the trial. The passage says they resumed treatment, but does not say they resumed at a lower dose. (LLM, conf=0.92)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“The most common of the sarcomeric gene variants in hypertrophic cardiomyopathy are those affecting the thick filament proteins cardiac myosin binding protein C (MYBPC3) and β-myosin heavy chain (MYH7).”
§ Current management of hypertrophic cardiomyopathy > Genotype positive hypertrophic cardiomyopathy
What the sources say
- Could not verifycites [75] sourceExperimental — accuracy not yet measured
The passages available from our copy are bibliographic metadata (the title and Abstract-labeled record, with no substantive paper text or page-specific findings). Searches for MYBPC3, MYH7, and thick-filament proteins found no passage stating which sarcomeric gene variants are most common in hypertrophic cardiomyopathy. (LLM, conf=0.74)
- Supportedcites [76] source
In the ‘Specific genes implicated as causes of HCM’ section (page unavailable), the paper identifies MYH7 and MYBPC3 as the main thick-filament genes involved in HCM. The same section reports variants in each gene in approximately 20% of HCM cases, supporting the claim that they are the most common sarcomeric genes affected. (LLM, conf=0.94)
- Supportedcites [77] source
The Interpretation of Genotype-Negative HCM section calls MYH7 and MYBPC3 the predominant genes associated with HCM and identifies them as thick-filament genes. Table 1 in Genetic Associations names their proteins as beta-myosin heavy chain and myosin-binding protein C, respectively (page numbers unavailable). (LLM, conf=0.92)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Could not verify
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“In the long term follow-up MAVA_ LTE, 49 the incidence of atrial fibrillation adjusted for exposure was 4.5%.”
§ Current management of hypertrophic cardiomyopathy > Cardiac myosin inhibitors
What the sources say
- Partly supportedcites [49] sourceExperimental — accuracy not yet measured
The Results, under “Exposure-adjusted safety” (Table 3), report an atrial fibrillation incidence of 4.50 per 100 patient-years through Week 252, not 4.5%. The percentage of patients who experienced atrial fibrillation was 14.3%. The claim matches the exposure-adjusted number but gives it the wrong unit. (LLM, conf=0.90)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“better outcomes by multiple metrics”
§ Current management of hypertrophic cardiomyopathy > Gene elusive hypertrophic cardiomyopathy
What the sources say
- Not checked — no full text of the sourcecites [72] source
- Supportedcites [73] source
The Results (Effect of mutations in sarcomere genes; page unavailable) report more cardiovascular deaths and sudden death/ICD discharges among patients with sarcomere variants than among those without them. The genotype–phenotype Results also show higher risks for sarcomere-positive patients on both outcomes, supporting the claim of better outcomes by multiple metrics for the negative group. (LLM, conf=0.90)
- Supportedcites [84] source
The Results section defines SARC− as patients with negative genetic testing and reports that SARC+ patients had higher risks of death, heart failure, malignant arrhythmias, and atrial fibrillation than SARC− patients. The Discussion likewise concludes that sarcomeric HCM has worse outcomes than HCM without sarcomere mutations. Page numbers were not provided in our copy. (LLM, conf=0.93)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“LVOT obstruction has been identified as a predictor of sudden death in some but not all studies”
§ Current management of hypertrophic cardiomyopathy > Hypertrophic cardiomyopathy phenocopies
What the sources say
- Partly supportedcites [98] sourceExperimental — accuracy not yet measured
Model development (p. 4) reports that the maximal left ventricular outflow tract gradient was associated with sudden cardiac death, and Selection of predictor variables (p. 2) says candidate predictors had been independently associated with it in at least one prior analysis. Our copy does not establish the claim that other studies failed to identify LVOT obstruction as a predictor. (LLM, conf=0.82)
- Partly supportedcites [103] sourceExperimental — accuracy not yet measured
The paper’s risk-model equation (What Are the Clinical Implications?, page unavailable) includes the LVOT gradient as a positive predictor of sudden cardiac death risk, and reference 17 names a study treating obstruction as a risk factor. Our copy does not say that other studies failed to identify it as a predictor, so the “some but not all studies” qualification is unsupported. (LLM, conf=0.82)
- Not checked — no full text of the sourcecites [105] source
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“A recent meta-analysis of CMI trials did not show an increase in atrial fibrillation.55”
§ Current management of hypertrophic cardiomyopathy > Cardiac myosin inhibitors
What the sources say
- Supportedcites [55] source
The Results (Safety of mavacamten; page not provided) report no significant difference in atrial fibrillation between mavacamten and placebo (RR 0.90; 95% CI 0.26–3.13). The meta-analysis concerns mavacamten, a cardiac myosin inhibitor, in patients with hypertrophic cardiomyopathy; it does not establish a result for every inhibitor in the class. (LLM, conf=0.92)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Personal history of non-vagal syncope is also predictive, particularly if recent.”
§ Current management of hypertrophic cardiomyopathy > Hypertrophic cardiomyopathy phenocopies
What the sources say
- Partly supportedcites [104] sourceExperimental — accuracy not yet measured
The Discussion reports that recent unexplained syncope predicted a higher risk of sudden death, while neurally mediated (vasovagal) syncope did not. This supports the distinction and the emphasis on recency, but the study concerns patients with hypertrophic cardiomyopathy; the claim does not state that population limit. (LLM, conf=0.82)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Variants in genes that encode for myofilament proteins of the cardiac sarcomere are found in 30-50% of patients with hypertrophic cardiomyopathy.[70][71][72][73][74]”
§ Current management of hypertrophic cardiomyopathy > Genotype positive hypertrophic cardiomyopathy
What the sources say
- Partly supportedcites [70] sourceExperimental — accuracy not yet measured
The introductory text under Conclusions reports that 30%–40% of HCM index patients carry disease-associated variants in recognized HCM genes. It also discusses sarcomeric disease genes, but does not give a 30%–50% prevalence for variants in genes encoding cardiac-sarcomere myofilament proteins. Its separate 30%–50% figure describes age-dependent penetrance in affected families, not the proportion of HCM patients with variants. (LLM, conf=0.84)
- Supportedcites [71] source
The Introduction states that mutations in genes encoding sarcomere contractile proteins accounted for approximately half of HCM cases, consistent with the claimed 30–50% range. The Results also report pathogenic mutations in 56 of 120 subjects, approximately 47%. (LLM, conf=0.90)
- Not checked — no full text of the sourcecites [72] source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“although one study did not find that genotype influenced clinical course.”
§ Current management of hypertrophic cardiomyopathy > Gene elusive hypertrophic cardiomyopathy
What the sources say
- Supportedcites [86] source
The Abstract Conclusions state that genotype was not a predictor of clinical course in this HCM cohort. The Discussion likewise reports no difference in mortality, progressive heart failure, or sudden-death events by genotype status. (LLM, conf=0.95)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“and 24% and 37% in relatives with positive genetics.”
§ Current management of hypertrophic cardiomyopathy > Gene elusive hypertrophic cardiomyopathy
What the sources say
- Partly supportedcites [87] sourceExperimental — accuracy not yet measured
The Discussion (page unavailable) reports that Christiaans et al. found HCM in 24% of mutation carriers at baseline, so the cited paper does report that figure. It does not report a 37% prevalence in genetically positive relatives; the nearby figure of 37 is the mean age, in years, of relatives in a different study. Its own Results report HCM at baseline in 18% of relatives from genotype-positive families. (LLM, conf=0.88)
- Partly supportedcites [88] sourceExperimental — accuracy not yet measured
The indexed abstract (page not specified) reports HCM in 136 of 446 predictively tested mutation carriers, supporting the general point that some genetically positive relatives have manifest disease. It gives 30%, not the claimed prevalences of 24% and 37%; searches for those figures found no supporting passage in our copy. (LLM, conf=0.82)
- Not checked — no full text of the sourcecites [89] source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Similarly, data from SEQUOIA-HCM show that patients taking aficamten had improvements in echocardiographic diastolic parameters compared with placebo.”
§ Current management of hypertrophic cardiomyopathy > Emerging treatments
What the sources say
- Supportedcites [152] source
The Results report that SEQUOIA-HCM enrolled 142 patients receiving aficamten and 140 receiving placebo. The paper’s Conclusions state that, compared with placebo, aficamten significantly improved measures of left ventricular diastolic function; the Abstract identifies improved eʹ velocities and E/eʹ among those measures. (LLM, conf=0.94)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“However, dose dependent editing of the wild type allele can lead to reduced contractile function.162”
§ Current management of hypertrophic cardiomyopathy > Targeted genetic therapies
What the sources say
- Supportedcites [162] source
In Results (“Eliminating mutant alleles with Cas9 nuclease to prevent HCM”; page unavailable), the paper reports dose-dependent loss of the wild-type allele and depressed contractile function after high-dose treatment in mice carrying the R403Q mutation. It concludes that the dysfunction likely reflected unintended disruption of the wild-type allele, consistent with the claim’s qualified wording. (LLM, conf=0.91)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Early, non-randomized data suggest that SGLT-1/2 inhibitors may reduce cardiovascular events in patients with hypertrophic cardiomyopathy”
§ Current management of hypertrophic cardiomyopathy > Emerging treatments
What the sources say
- Not checked — no full text of the sourcecites [157] source
- Partly supportedcites [158] sourceExperimental — accuracy not yet measured
The study reports that SGLT2 inhibitor use in patients with hypertrophic cardiomyopathy was associated with lower all-cause mortality, all-cause hospitalization, and documented cardiovascular symptoms over two years. Its electronic-health-record design and call for randomized trials support the claim’s cautious, non-randomized framing. However, the paper studies SGLT2 inhibitors, not the broader SGLT-1/2 class, and does not establish a reduction in cardiovascular events as such; it found no difference in acute heart-failure exacerbations. (LLM, conf=0.86)
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Pre-clinical studies in experimental murine models have shown that a single administration of adenoassociated virus 9 (AAV9)-MYBPC3 successfully prevented the development of cardiac hypertrophy and dysfunction, 159 as well as myocardial disarray and fibrosis.”
§ Current management of hypertrophic cardiomyopathy > Targeted genetic therapies
What the sources say
- Partly supportedcites [159] sourceExperimental — accuracy not yet measured
The Abstract and the section ‘Long-term prevention of LVH and dysfunction by gene therapy’ report that a single AAV9-Mybpc3 administration prevented cardiac hypertrophy and dysfunction in neonatal knock-in mice, with effects varying by dose. Our copy does not report prevention of myocardial disarray or fibrosis; its cardiac-section analysis concerns protein localization rather than those outcomes. (LLM, conf=0.86)
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“occurring in 4.7% of the vigorous and 4.6% of the non-vigorous exercisers (adjusted hazard ratio 1.01, upper 95% one sided confidence interval 1.48, below the pre-specified non-inferiority bound).”
§ Current management of hypertrophic cardiomyopathy > Exercise in hypertrophic cardiomyopathy
What the sources say
- Supportedcites [131] source
The Abstract Results report the composite endpoint in 33 vigorous exercisers (4.7%) and 44 non-vigorous exercisers (4.6%). The Results > Primary Analysis gives the adjusted hazard ratio as 1.01 and the upper one-sided 95% confidence limit as 1.48, below the prespecified non-inferiority boundary of 1.5. (LLM, conf=0.94)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“In experimental models, use of adeno-associated viruses for delivery of gene editing materials has shown beneficial effects as a proof of concept, with prevention of the development of the functional, histopathological, and molecular phenotypes of hypertrophic cardiomyopathy including prevention of hypertrophy.161 162”
§ Current management of hypertrophic cardiomyopathy > Targeted genetic therapies
What the sources say
- Supportedcites [161] source
The Results section reports that dual AAV9 delivered the base editor and guide RNA to humanized mice. Treated mice had echocardiographic measurements, cardiac dimensions, heart weight, and collagen area similar to controls, supporting prevention of functional abnormalities, hypertrophy, and histopathological remodeling. The Discussion also reports reduced pathogenic transcripts, supporting the molecular component of the claim. (LLM, conf=0.91)
- Supportedcites [162] source
The Main section states that AAV9-delivered genomic editing prevented the functional, histopathological, and molecular phenotypes of HCM in mouse models. It also reports that AAV9-delivered Cas9 prevented left ventricular hypertrophy, although that strategy had dose-dependent adverse effects on contractile function. (LLM, conf=0.94)
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Rests on an assumption: Missense variants in MYH7 and other sarcomere genes cause hypertrophic cardiomyopathy mostly through gain-of-function mechanisms.
- Supported
In the paper
“Mavacamten decreased need or eligibility for SRT.At 16 weeks: 76.8% of patients on placebo and 17.9% of those on mavacamten met criteria for SRT (difference 58.9%, CI 44% to 73.9%).”
§ Current management of hypertrophic cardiomyopathy > Abstract
What the sources say
- Not matchedcites Desai 35
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Not matched
In the paper
“Aficamten: 1.8 (95% CI 1.2 to 2.3) mL/kg/min; placebo: 0.0 (-0.5 to 0.5).mL/kg/min”
§ Current management of hypertrophic cardiomyopathy > Abstract
What the sources say
- Not matchedcites Maron 36
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Not matched
In the paper
“Aficamten showed improvement in peak oxygen uptake compared with placebo.”
§ Current management of hypertrophic cardiomyopathy > Abstract
What the sources say
- Not matchedcites Maron 36
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Not matched
In the paper
“Despite a paucity of randomized data, on the basis of data from series and crossover studies, non-vasodilating β blockers and CCBs remain the first line treatments for symptomatic hypertrophic cardiomyopathy.22”
§ Current management of hypertrophic cardiomyopathy > Sources and selection criteria
What the sources say
- Not checked — no full text of the sourcecites [22] source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“Alcohol use has been shown to increase LVOT obstruction and should be minimized [20][21][22]”
§ Current management of hypertrophic cardiomyopathy > Sources and selection criteria
What the sources say
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Echocardiography with provocative maneuvers including Valsalva and exercise is important in determining the presence of obstruction, as only one third of patients with hypertrophic cardiomyopathy have outflow tract obstruction at rest.16”
§ Current management of hypertrophic cardiomyopathy > Sources and selection criteria
What the sources say
- Not checked — no full text of the sourcecites [16] source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“At 128 weeks, 15.7% patients in total study sample (108 patients) met composite endpoint”
§ Current management of hypertrophic cardiomyopathy > Abstract
What the sources say
- Not matchedcites Desai 35
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plainn = 108- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Not matched
In the paper
“The 2024 AHA/ACC guidelines give a class 1 recommendation to the use of CMIs, disopyramide, or SRT in patients who have symptoms despite first line therapy (table 2).22”
§ Current management of hypertrophic cardiomyopathy > Cardiac myosin inhibitors
What the sources say
- Not checked — no full text of the sourcecites [22] source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“All guidelines recommend ICDs for patients with hypertrophic cardiomyopathy who have survived a cardiac arrest or hemodynamically significant ventricular tachycardia.”
§ Current management of hypertrophic cardiomyopathy > Hypertrophic cardiomyopathy phenocopies
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“A magnetic resonance imaging (MRI) sub-study showed that mavacamten had a favorable effect on cardiac remodeling; specifically, significant reductions in absolute intracellular myocardial mass index as well as left ventricular mass index, maximum left ventricular wall thickness, and left atrial volume index were seen.48”
§ Current management of hypertrophic cardiomyopathy > Cardiac myosin inhibitors
What the sources say
- Not checked — no full text of the sourcecites [48] source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Several dose adjustments may be needed, and CYP2C19 genotyping is required in the UK to determine the initial dose.56”
§ Current management of hypertrophic cardiomyopathy > Cardiac myosin inhibitors
What the sources say
- Not checked yetcites [56] National Institute for Health and Care Excellence. Mavacamten for treating symptomatic obstructive hypertrophic cardiomyopathy. 2023. https://www.nice.org.uk/guidance/ta913.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“Non-sustained ventricular tachycardia (NSVT) seen on 24-48 hours of ambulatory monitoring is predictive of risk of arrhythmia.”
§ Current management of hypertrophic cardiomyopathy > Hypertrophic cardiomyopathy phenocopies
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“These data suggest that in appropriately selected patients with severe symptoms, CMIs can be considered as an alternative to SRT.”
§ Current management of hypertrophic cardiomyopathy > Cardiac myosin inhibitors
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“An exploratory substudy from VALOR data suggests that mavacamten improves echocardiographic parameters of diastolic dysfunction.”
§ Current management of hypertrophic cardiomyopathy > Emerging treatments
What the sources say
- Not checked — no full text of the sourcecites [151] source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“a smaller subset of patients (7-10%) 139 progress to experience advanced heart failure symptoms characterized by severe functional limitation and refractory heart failure symptoms in the absence of LVOT obstruction.”
§ Current management of hypertrophic cardiomyopathy > Management of advanced heart failure in hypertrophic cardiomyopathy
What the sources say
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“Subanalyses of the CMI trials have shown that, in addition to reduction in LVOT gradient, CMIs affect cardiac structural parameters and diastolic function.”
§ Current management of hypertrophic cardiomyopathy > Emerging treatments
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- It may state two separate claims as one. 47
- Probably not a substantial claim. 18
Some cited sources support this claim and some don’t — read each source’s verdict below.
In the paper
“In EXPLORER-LTE, the number of patients with drop in ejection fraction to <50% was 8.7%, 49 and in VALOR-LTE it was 15.7%, 50 although clinical heart failure was much less common.”
§ Current management of hypertrophic cardiomyopathy > Cardiac myosin inhibitors
What the sources say
- Supportedcites [49] source
The Results (Safety results) report that 20 patients (8.7%) in the EXPLORER cohort had a transient drop in LVEF below 50%. Only one of those 20 had a serious cardiac-failure event. The separate 15.7% VALOR-LTE figure is attached to another citation and is not attributed to this paper. (LLM, conf=0.93)
- Disputedcites [50] sourceExperimental — accuracy not yet measured
The Results > Safety section reports LVEF falling below 50% in 15 patients (13.9%), not 15.7%. The 15.7% figure in the Results section refers instead to a composite septal-reduction endpoint. The Discussion says the 12 patients who temporarily interrupted treatment for reduced LVEF remained asymptomatic, consistent with the claim that clinical heart failure was less common. (LLM, conf=0.88)
Checked by a reasoning model — may be wrong.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Both the 2024 ACC/AHA and 2023 ESC guidelines give non-dihydropyridine CCBs a class I recommendation for patients in whom β blockers are ineffective or not well tolerated (table 2). 1 22”
§ Current management of hypertrophic cardiomyopathy > Sources and selection criteria
What the sources say
- Partly supportedcites [1] sourceExperimental — accuracy not yet measured
Section 7.1.4.1 says verapamil can be used when beta-blockers are contraindicated or ineffective, and diltiazem should be considered when beta-blockers and verapamil are not tolerated or are contraindicated. The retrieved passages do not establish a Class I recommendation for both drugs, and the diltiazem condition is narrower than the claim states. This verdict addresses only the cited ESC guideline, not the ACC/AHA guideline. (LLM, conf=0.76)
- Not checked — no full text of the sourcecites [22] source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Depending on the cohort studied, 30-60% of patients harbor genetic variants inherited as autosomal dominant traits, whereas no pathogenic variant is identified in around 40%. 12”
§ Current management of hypertrophic cardiomyopathy > Epidemiology
What the sources say
- Partly supportedcites [12] sourceExperimental — accuracy not yet measured
The Diagnostic testing section reports positive genetic-test results in over 60% of patients with a family history of HCM and informative results in approximately 30% of those without one. The Genetics of Hypertrophic Cardiomyopathy section describes sarcomeric HCM as autosomal dominant. The copy does not give an overall figure of around 40% with no identified pathogenic variant; its reported yields vary by family history. (LLM, conf=0.85)
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Women with the disease have higher rates of heart failure and mortality.14”
§ Current management of hypertrophic cardiomyopathy > Epidemiology
What the sources say
- Supportedcites [14] source
The Results (Meta-Analysis of Sex Differences in Adverse Outcomes; page unavailable) report higher risks of heart-failure events and all-cause mortality among women with hypertrophic cardiomyopathy than among men. Both parts of the claim are supported by the paper’s pooled findings. (LLM, conf=0.94)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“ASA is associated with higher rates of post-procedural pacemaker implantation and has a significantly higher risk of re-intervention compared with patients undergoing surgery.66”
§ Current management of hypertrophic cardiomyopathy > Obstructive disease
What the sources say
- Supportedcites [66] source
The Patient Selection and Specialized Care section reports permanent pacemaker implantation in 1 in 10 ASA patients versus 1 in 25 myectomy patients, and a fivefold higher risk of reintervention after ASA. The Effect section adds that studies with long-term follow-up found a higher need for reintervention, although an earlier meta-analysis did not find a significant difference. (LLM, conf=0.90)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“To date, variants in eight different sarcomeric genes have been identified as definitively causative of hypertrophic cardiomyopathy, and variants in several other genes show at least moderate evidence of pathogenicity (table 4; fig 2).[75][76][77]”
§ Current management of hypertrophic cardiomyopathy > Genotype positive hypertrophic cardiomyopathy
What the sources say
- Could not verifycites [75] sourceExperimental — accuracy not yet measured
Searches for the eight sarcomeric genes and for definitive or moderate evidence returned no relevant body-text passage. The only related text retrieved was labeled Abstract, which does not establish the claim's definitive and moderate evidence classifications under the stipulated evidence rule. (LLM, conf=0.63)
- Partly supportedcites [76] sourceExperimental — accuracy not yet measured
The ‘Specific genes implicated as causes of HCM’ section identifies sarcomeric genes with established roles in HCM and discusses additional implicated genes. It does not establish a count of eight definitively causal sarcomeric genes or classify several other genes as having at least moderate evidence of pathogenicity; it cautions that the pathogenicity of individual variants requires assessment. Page numbers are unavailable in our copy. (LLM, conf=0.84)
- Supportedcites [77] source
The Genetic Associations section calls eight sarcomeric genes validated and says ClinGen classified their association with HCM as definitive. It also lists several other genes with strong or moderate evidence for an HCM association (Table 3). (LLM, conf=0.93)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Could not verify
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Family history of sudden death in first degree relatives before age 40-50, long considered a marker of risk, has been validated in one study showing a similar rate of ICD interventions for those implanted for only this risk factor compared with those with other risk factors, 102 as well as in multivariable models of risk.”
§ Current management of hypertrophic cardiomyopathy > Hypertrophic cardiomyopathy phenocopies
What the sources say
boostedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“In centers with experienced operators, it is associated with an improvement in symptoms in 90-95% of patients and a mortality rate of <1%. 59”
§ Current management of hypertrophic cardiomyopathy > Obstructive disease
What the sources say
- Partly supportedcites [59] sourceExperimental — accuracy not yet measured
The paper’s Abstract and Table 1 report 0.4% 30-day operative mortality for septal myectomy at experienced hypertrophic cardiomyopathy centers. The Abstract describes relief of heart-failure symptoms but does not give the claimed 90–95% improvement rate. Its mortality data concern surgical myectomy, not septal reduction therapy generally; passage page numbers are not available in our copy. (LLM, conf=0.88)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Left ventricular dysfunction, which for patients with hypertrophic cardiomyopathy is considered to be ejection fraction <50%, is present in 8% of patients with hypertrophic cardiomyopathy and is associated with adverse outcomes, particularly in those with sarcomeric variants.”
§ Current management of hypertrophic cardiomyopathy > Hypertrophic cardiomyopathy phenocopies
What the sources say
- Supportedcites [106] source
Split into 2 atoms — 2 confirmed, 0 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Mitral valve repair is preferred to replacement and is associated with improved survival.63”
§ Current management of hypertrophic cardiomyopathy > Obstructive disease
What the sources say
- Supportedcites [63] source
The Abstract concludes that when patients with hypertrophic obstructive cardiomyopathy require a mitral valve procedure, repair is preferred because survival is better than with replacement. It reports 10-year survival of 80.0% after repair versus 55.2% after replacement. (LLM, conf=0.94)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Sudden cardiac death is less common in patients over 60 with hypertrophic cardiomyopathy, and individualized risk assessment is less well defined in this group.”
§ Current management of hypertrophic cardiomyopathy > Hypertrophic cardiomyopathy phenocopies
What the sources say
- Partly supportedcites [84] sourceExperimental — accuracy not yet measured
The Discussion (Morbidity and Mortality in HCM; page unavailable) reports that ventricular arrhythmias and sudden death were rare among patients diagnosed after age 60. It also calls for further study of whether age at diagnosis improves sudden-death risk assessment, but does not specifically say individualized assessment is less well defined for this older group. The claim also describes patients over 60 generally, rather than patients diagnosed after 60. (LLM, conf=0.87)
- Supportedcites [101] source
The Discussion reports a low sudden-death event rate of 0.20% per year in patients aged ≥60 and says reaching older age may convey relative protection. The Abstract says guidance for preventive defibrillator decisions remains uncertain in older patients, supporting the claim that individual risk assessment is less well defined for this group. (LLM, conf=0.93)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Arrhythmic sudden cardiac death and heart failure represent the two most common modes of death related to hypertrophic cardiomyopathy, with an overall low annual mortality rate in contemporary community based populations of 1.5-2%.”
§ Current management of hypertrophic cardiomyopathy > Hypertrophic cardiomyopathy phenocopies
What the sources say
- Partly supportedcites [93] sourceExperimental — accuracy not yet measured
The Changing Epidemiology section identifies sudden arrhythmic death and heart failure as HCM-related causes of death, noting that advanced heart failure is now emerging as the predominant cause. But Historical Context assigns the 1.5%–2.0% annual mortality rate to community-based populations in the pre-ICD era; it reports approximately 0.5% per year with contemporary treatment. Page numbers are unavailable in our copy. (LLM, conf=0.88)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“The 2023 ESC guidelines assigned a class 2a recommendation to use of CMIs in patients with symptomatic hypertrophic cardiomyopathy with LVOT obstruction, in addition to β blockers or CCBs or as monotherapy when β blockers, CCBs, or disopyramide are not tolerated or contraindicated, before considering SRT. 1”
§ Current management of hypertrophic cardiomyopathy > Cardiac myosin inhibitors
What the sources say
- Supportedcites [1] source
The “Cardiac myosin ATPase inhibitors” section recommends these drugs as second-line therapy for symptomatic obstructive HCM, permits coadministration with beta-blockers or calcium antagonists, and allows monotherapy when beta-blockers, calcium antagonists, and disopyramide are contraindicated or not tolerated. The “Invasive treatment of left ventricular outflow tract” section places consideration of septal reduction therapy after maximally tolerated drug therapy. The recommendation’s “should be considered” wording is consistent with Class IIa. (LLM, conf=0.85)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. It may state two separate claims as one.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Postoperative atrial fibrillation and increasing age are associated with worse short term outcomes.62”
§ Current management of hypertrophic cardiomyopathy > Obstructive disease
What the sources say
- Partly supportedcites [62] sourceExperimental — accuracy not yet measured
The Outcomes and Survival Analysis section identifies residual postoperative atrial fibrillation and increasing age as predictors of long-term outcomes. The Discussion separately reports low short-term event rates, but does not establish that either factor predicts short-term outcomes. The claim changes the time frame of the finding. (LLM, conf=0.90)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“In appropriately selected patients, the procedure is associated with an improvement in NYHA class, five year survival free from cardiovascular events of 98.6%, and 10 year survival free from cardiovascular events of 92.3%.67”
§ Current management of hypertrophic cardiomyopathy > Obstructive disease
What the sources say
- Partly supportedcites [67] sourceExperimental — accuracy not yet measured
The long-term follow-up passage reports improved clinical symptoms in 94.3% of patients, consistent with improvement in functional status. The Acute Results passage reports 98.6% survival free of cardiovascular events at five years, but 96.5% at ten years; 92.3% is the fifteen-year estimate, not the ten-year estimate. Our copy does not specifically report a change in NYHA class in these passages. (LLM, conf=0.94)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“US guidelines primarily take a dichotomized, algorithmic approach, 22 whereas the European guidelines advise use of the HCM Risk-SCD calculator”
§ Current management of hypertrophic cardiomyopathy > Hypertrophic cardiomyopathy phenocopies
What the sources say
- Not checked — no full text of the sourcecites [22] source
- Supportedcites [1] source
Section 7.1.5.6 says the ESC Task Force maintains use of the validated HCM Risk-SCD tool as the first step in sudden-death prevention for patients aged 16 or older. That supports the claim about the European guidelines; the passage contrasts this with the AHA/ACC approach. (LLM, conf=0.92)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
Every source the paper cites for this claim was checked and supports it.
In the paper
“NSVT carries more risk in young people, 110 and it thus carries a 2a indication for ICD in children and 2B in adults in the US guidelines.”
§ Current management of hypertrophic cardiomyopathy > Hypertrophic cardiomyopathy phenocopies
What the sources say
- Supportedcites [110] source
Citation 110 is attached to the claim that NSVT carries greater risk in young people, not to the subsequent statement about US guideline indications. The Treatments and interventional procedures section reports that the relative risk of sudden death associated with NSVT was highest in patients aged 30 or younger; no page number is provided in our copy. (LLM, conf=0.93)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“This benefit persisted up to 128 weeks and included patients from the placebo arm who crossed over to mavacamten at the end of the randomized study period.50”
§ Current management of hypertrophic cardiomyopathy > Cardiac myosin inhibitors
What the sources say
- Supportedcites [50] source
The Methods and Study Population sections state that patients initially assigned to placebo crossed over to mavacamten at week 16 and were included in the week 128 evaluation. The Discussion reports sustained benefits through week 128, and Results > Study End Points reports outcomes for both treatment groups. (LLM, conf=0.93)
plaindirectn = 112- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“A retrospective comparison suggested improved mortality with myectomy over ASA, but referral bias cannot be excluded.65”
§ Current management of hypertrophic cardiomyopathy > Obstructive disease
What the sources say
- Supportedcites [65] source
The Abstract reports higher 10-year all-cause mortality after ASA than after myectomy, including after adjustment for age, sex, and comorbidities. The Study Limitations section says the retrospective design may introduce selection bias and that unmeasured differences between groups may have affected the results, supporting the caution about referral bias. (LLM, conf=0.92)
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Concurrent β blocker use did not affect functional capacity, reduction in LVOT gradients, symptoms, or biomarkers, but patients on β blockers had lower peak VO 2 and chronotropic incompetence.52”
§ Current management of hypertrophic cardiomyopathy > Cardiac myosin inhibitors
What the sources say
- Partly supportedcites [52] sourceExperimental — accuracy not yet measured
The Discussion reports that beta-blocker use did not alter mavacamten’s benefits for LVOT gradients, symptoms, or cardiac biomarkers, and the Chronotropic incompetence section reports a higher prevalence among beta-blocker users. However, the Functional capacity section reports smaller improvements in peak VO₂, peak METs, and exercise time with beta-blocker use. The claim that functional capacity was unaffected is therefore too broad. (LLM, conf=0.90)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Patients receiving mavacamten experienced improvement in symptoms and reduction in need for SRT from 76.8% of the placebo group to 17.9% of those treated with mavacamten (confidence interval for difference 44 to 74).”
§ Current management of hypertrophic cardiomyopathy > Cardiac myosin inhibitors
What the sources say
- Partly supportedcites [50] sourceExperimental — accuracy not yet measured
The Discussion and Conclusions report sustained symptom improvement and reduced need for septal reduction therapy with mavacamten. However, the Results > Study End Points section reports 15.7% meeting the composite endpoint at week 128, after the placebo group had crossed over to mavacamten; our copy does not report the claimed 76.8% versus 17.9% comparison or its 44-to-74 confidence interval (searched those figures and the week-16 comparison). Page numbers were not available in the indexed copy. (LLM, conf=0.88)
plaindirectn = 112- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Patients with multiple pathogenic variants tend to have more severe phenotypes and earlier ages of presentation.74 82”
§ Current management of hypertrophic cardiomyopathy > Genotype positive hypertrophic cardiomyopathy
What the sources say
- Partly supportedcites [74] sourceExperimental — accuracy not yet measured
In “Probands with multiple variants” (page unavailable), the paper reports a tendency toward younger age at referral for genetic testing among probands with two or more pathogenic or likely pathogenic variants, compared with those with one (29 versus 39 years; P = 0.29). Age at testing is not necessarily age of presentation, and the passage does not establish that these probands had more severe phenotypes. (LLM, conf=0.85)
- Partly supportedcites [82] sourceExperimental — accuracy not yet measured
The Results (‘Pathogenic variants shared by siblings’; page not provided) report that the siblings carried an additional MYL2 variant and had more severe HCM than their mother. The Results also give earlier diagnosis ages for the siblings (about 41 and 43) than for their mother (63), but this single-family comparison does not establish a general tendency for patients with multiple variants to present earlier or have more severe disease. (LLM, conf=0.85)
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“initially validated in 2013.”
§ Current management of hypertrophic cardiomyopathy > Hypertrophic cardiomyopathy phenocopies
What the sources say
- Supportedcites [98] source
The Model validation section (p. 4) reports validation results for HCM Risk-SCD, and the Discussion (p. 7) calls it the first validated SCD risk prediction model for patients with HCM. The paper was published online on 14 October 2013 (p. 1), supporting the stated year. (LLM, conf=0.88)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“In a single center study, apical myectomy increased stroke volume and improved postoperative measurements of left ventricular compliance.69”
§ Current management of hypertrophic cardiomyopathy > Non-obstructive disease
What the sources say
- Supportedcites [69] source
The Methods describe patients who underwent apical myectomy at Mayo Clinic, Rochester, establishing the single-center setting. The Results report increased stroke volume and increased end-diastolic volume alongside reduced end-diastolic pressure; the Discussion interprets these postoperative measurements as improved effective operative left ventricular compliance. The paper does not claim a direct measurement of intrinsic ventricular compliance. (LLM, conf=0.92)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Left ventricular dysfunction is uncommon, developing in 7.5% over 15 years, but once this occurs 35% progress to death, transplant, or mechanical assist device over median of 8.4 years, as shown in a cohort of more than 6500 patients in the SHARE registry”
§ Current management of hypertrophic cardiomyopathy > Management of advanced heart failure in hypertrophic cardiomyopathy
What the sources say
- Supportedcites [106] source
Split into 2 atoms — 2 confirmed, 0 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
plaincorrelationaln = 6,500- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“patients with atrial fibrillation have more symptoms, 115 with greater functional limitation, particularly with progression to permanent atrial fibrillation.”
§ Current management of hypertrophic cardiomyopathy > Management of atrial fibrillation
What the sources say
- Partly supportedcites [115] sourceExperimental — accuracy not yet measured
The Results report that patients with atrial fibrillation in this hypertrophic cardiomyopathy cohort were more symptomatic and had worse exercise tolerance than those without it. The Conclusions include both paroxysmal and permanent atrial fibrillation, but do not report greater functional limitation specifically with progression to permanent atrial fibrillation. Page numbers are not available in our copy. (LLM, conf=0.88)
- Not checked — no full text of the sourcecites [113] source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Survival outcomes after transplantation in hypertrophic cardiomyopathy remain similar to those for other forms of advanced heart failure, with one year survival of approximately 91%.”
§ Current management of hypertrophic cardiomyopathy > Management of advanced heart failure in hypertrophic cardiomyopathy
What the sources say
- Supportedcites [144] source
The HEART TRANSPLANTATION section reports that, since adoption of the current allocation policy, one-year post-transplantation survival was similar for HCM and non-HCM patients: 91.2% versus 91.0%. This supports both the comparison and the approximately 91% figure. (LLM, conf=0.94)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Although the overall success rate of ablation of atrial fibrillation in maintaining sinus rhythm without recurrence is lower in patients with hypertrophic cardiomyopathy than those without it (39% v 50% for one procedure), rates are similar for those with paroxysmal left ventricular and/or a non-dilated left atrium.”
§ Current management of hypertrophic cardiomyopathy > CMR=cardiovascular magnetic resonance; ECG=electrocardiogram; EF=ejection fraction; FH=family history; HCM=hypertrophic cardiomyopathy; ICD=implantable cardioverter-defibrillator;
What the sources say
- Partly supportedcites [118] sourceExperimental — accuracy not yet measured
Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“In a large observational database, patients with hypertrophic cardiomyopathy treated with DOACs had similar rates of stroke or systemic embolism to those treated with warfarin and nonsignificantly lower rates of major bleeding.”
§ Current management of hypertrophic cardiomyopathy > CMR=cardiovascular magnetic resonance; ECG=electrocardiogram; EF=ejection fraction; FH=family history; HCM=hypertrophic cardiomyopathy; ICD=implantable cardioverter-defibrillator;
What the sources say
- Supportedcites [123] source
The study describes an observational analysis of patients with hypertrophic cardiomyopathy and atrial fibrillation in a large insurance database. Table 1 reports similar stroke or systemic embolism rates for NOACs and warfarin (1.93 versus 2.03 per 100 person-years); the main text reports a nonsignificant trend toward lower major bleeding rates with NOACs (4.18 versus 5.38). (LLM, conf=0.94)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
In the paper
“Hypertrophic cardiomyopathy has a global presence with an estimated prevalence of 1 in 500.”
§ Current management of hypertrophic cardiomyopathy > Epidemiology
What the sources say
- Not matchedcites 8 9
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Not matched
In the paper
“It has been described in at least 125 countries and has a similar prevalence in men and women.8 9”
§ Current management of hypertrophic cardiomyopathy > Epidemiology
What the sources say
- Not matchedcites 8 9
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
- Not matched
In the paper
“Many patients with non-obstructive hypertrophic cardiomyopathy have symptoms, with 8% in New York Heart Association (NYHA) class III or IV, and mortality rates are similar to those of patients with obstructive hypertrophic cardiomyopathy.40”
§ Current management of hypertrophic cardiomyopathy > Management of acute hypotension
What the sources say
- Not checked — no full text of the sourcecites [40] source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Mavacamten was associated with a significant reduction in LVOT gradient and improvement in quality of life as measured by the Kansas City Cardiomyopathy Questionnaire, compared with placebo.47”
§ Current management of hypertrophic cardiomyopathy > Cardiac myosin inhibitors
What the sources say
- Not checked — no full text of the sourcecites [47] source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“No randomized trials have evaluated the use of ICDs for primary prevention in hypertrophic cardiomyopathy, so guidelines are based on series showing risk predictors in this population.”
§ Current management of hypertrophic cardiomyopathy > Hypertrophic cardiomyopathy phenocopies
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Extensive fibrosis (typical threshold ≥15%), detected by late gadolinium enhancement, doubles the risk of sudden cardiac death in patients with no other risk factors, with an estimated risk for life threatening arrhythmia of 6% at five years.”
§ Current management of hypertrophic cardiomyopathy > Hypertrophic cardiomyopathy phenocopies
What the sources say
- Not checked — no full text of the sourcecites [107] source
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Efficacy of the implantable cardioverter-defibrillator (ICD) for primary prevention in patients with hypertrophic cardiomyopathy was first reported in 2000”
§ Current management of hypertrophic cardiomyopathy > Hypertrophic cardiomyopathy phenocopies
What the sources say
- Not checked — no full text of the sourcecites [94] source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“current European guidelines recommend a combined approach, using the risk score for an initial stratification, with further delineation of the need for an ICD, based on presence of other clinical factors for patients with calculator estimated low (five year <4%) risk.”
§ Current management of hypertrophic cardiomyopathy > Hypertrophic cardiomyopathy phenocopies
What the sources say
- Not checked yetcites [1] source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim.
In the paper
“Most pathogenic variants in hypertrophic cardiomyopathy are missense with dominant negative effects, although haploinsufficiency related to truncating variants (nonsense, frameshift, and splice site) is the prevailing mechanism in hypertrophic cardiomyopathy related to MYBPC3.78”
§ Current management of hypertrophic cardiomyopathy > Genotype positive hypertrophic cardiomyopathy
What the sources say
- Not checked — no full text of the sourcecites [78] source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Overall, these observations suggest that gene elusive hypertrophic cardiomyopathy is largely a phenotypically distinct entity that is most often nonfamilial with non-mendelian inheritance.”
§ Current management of hypertrophic cardiomyopathy > Gene elusive hypertrophic cardiomyopathy
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Patients receiving aficamten showed significantly improved peak VO 2 (1.8 mL/min/kg improvement, compared with 0.0 mL/min/kg in patients receiving placebo; P<0.001 for between group difference), with similar low rates of adverse events (5.6% in aficamten group, none thought to be due to drug, versus 9.3% for placebo).36”
§ Current management of hypertrophic cardiomyopathy > Cardiac myosin inhibitors
What the sources say
- Not checked yetcites [36] source
Checked before — its earlier verdict is held back until a new check runs.
plaindirectn = 282- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Not checked yet
In the paper
“Cardiac MRI can be used in conjunction with genetic testing to differentiate causes of left ventricular hypertrophy and is an ACC/AHA class 1 recommendation in this setting.”
§ Current management of hypertrophic cardiomyopathy > Hypertrophic cardiomyopathy phenocopies
What the sources say
- Not checked — no full text of the sourcecites [92] source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Risk of sudden cardiac death is higher in children and has different risk predictors”
§ Current management of hypertrophic cardiomyopathy > Hypertrophic cardiomyopathy phenocopies
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: unclear — It is unclear why the paper says it holds.
It may state two separate claims as one.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“I-metaiodobenzylguanidine have shown associations with ventricular arrhythmias, 164 as well as with progression of myocardial damage.165”
§ Current management of hypertrophic cardiomyopathy > Molecular
What the sources say
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Specifically with LVAD therapy, small left ventricular dimensions can increase the probability of inflow cannula suction increasing the chances of device suction and arrhythmia.”
§ Current management of hypertrophic cardiomyopathy > Management of advanced heart failure in hypertrophic cardiomyopathy
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: unclear — It is unclear why the paper says it holds.
It may state two separate claims as one.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“Radiotracers based on fibroblast activation protein inhibitor (for example, 18 F-FAPI) measure levels of fibroblast activation in the myocardium, reflecting an active fibrotic process, which has correlated with myocardial function, 166 as well as with sudden cardiac death.167”
§ Current management of hypertrophic cardiomyopathy > Molecular
What the sources say
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“For patients with advanced disease, advances in MCS and cardiac transplantation offer an opportunity for improved survival in an increasing number of patients.”
§ Current management of hypertrophic cardiomyopathy > Molecular
plainconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“Atrial fibrillation is common in hypertrophic cardiomyopathy, being present in 5% at the time of diagnosis and developing in another 10-22% during follow-up.”
§ Current management of hypertrophic cardiomyopathy > Management of atrial fibrillation
What the sources say
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“After 16 weeks, the 67 participants randomized to the moderate intensity training showed improved exercise capacity with higher peak VO 2 compared with the usual activity group (n=69), with a between group difference of 1.27 (95% confidence interval 0.17 to 2.37; P=0.02), as well as subjective improvement, with no arrhythmic events.”
§ Current management of hypertrophic cardiomyopathy > Exercise in hypertrophic cardiomyopathy
What the sources say
- Not checked yetcites [130] source
Checked before — its earlier verdict is held back until a new check runs.
plaindirectn = 67 ·- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Not checked yet
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“CMI therapy has changed the treatment paradigm for obstructive hypertrophic cardiomyopathy.”
§ Current management of hypertrophic cardiomyopathy > Molecular
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper may give no reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“recent developments on multiple fronts have led to more treatment options and improved quality of life for patients.”
§ Current management of hypertrophic cardiomyopathy > Molecular
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Hypertrophic cardiomyopathy is a common genetic cardiomyopathy with a global presence that remains underdiagnosed and undertreated.”
§ Current management of hypertrophic cardiomyopathy > Molecular
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds. It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“first line medical and surgical therapy has been largely unchanged over the past half century”
§ Current management of hypertrophic cardiomyopathy > Molecular
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
In the paper
“Only 30% of patients with hypertrophic cardiomyopathy with heart failure will have an LVEF <50% at presentation, with most patients having normal LVEF with restrictive physiology.”
§ Current management of hypertrophic cardiomyopathy > Management of advanced heart failure in hypertrophic cardiomyopathy
What the sources say
- Not checked — no full text of the sourcecites [140] source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Specifically, CPET parameters such as peak oxygen consumption (pVO 2 ), ventilatory efficiency (VE/VCO 2 slope), and anaerobic threshold can be useful for prognosis independent of LVEF and guide the need for advanced heart failure therapies such as cardiac transplantation.”
§ Current management of hypertrophic cardiomyopathy > Management of advanced heart failure in hypertrophic cardiomyopathy
What the sources say
- Not checked — no full text of the sourcecites [145] source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Our understanding of the management of arrhythmias, risk of sudden cardiac death, and recommendations for exercise has evolved.”
§ Current management of hypertrophic cardiomyopathy > Molecular
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds. It may state two separate claims as one.
The paper relies on this without support.
No current medical therapy improves survival in hypertrophic cardiomyopathy.
“To date, no data suggest that any current medical therapy improves survival.”
The paper relies on this without support.
No data support initiation of gradient reduction therapy in patients without symptoms.
“Similarly, no data support initiation of gradient reduction therapy in patients without symptoms.”
The paper relies on this without support.
Limited evidence exists to guide medical therapy for patients with non-obstructive hypertrophic cardiomyopathy.
“Limited evidence exists to guide medical therapy for these patients.”
The paper relies on this without support.
Genotype-phenotype correlations in hypertrophic cardiomyopathy are generally modest.
“However, genotype-phenotype correlations in hypertrophic cardiomyopathy are generally modest, with significant phenotypic heterogeneity among patients with similar genetics.”
The paper relies on this without support.
Alcohol septal ablation and septal myectomy have comparable rates of 30-day survival, sudden cardiac death, and long-term survival in published studies.
“ASA and septal myectomy have comparable rates of 30 day survival, sudden cardiac death, and long term survival in published studies, although no RCT has ever been done.”
The paper relies on this without support.
A polygenic contribution to hypertrophic cardiomyopathy is increasingly recognized in patients with gene-elusive hypertrophic cardiomyopathy.
“Increasingly, a polygenic contribution to hypertrophic cardiomyopathy is recognized in these patients.”
The paper relies on this without support.
Gene therapeutics for hypertrophic cardiomyopathy is in early phase trials, with the most significant limitation being cardiac directed delivery.
“Gene therapeutics for hypertrophic cardiomyopathy is in early phase trials, with the most significant limitation being cardiac directed delivery.”
The paper relies on this without support.
Current adeno-associated virus vectors transduce the heart but need high titers that necessitate aggressive immunosuppressive regimens to reduce the risk of systemic toxicity.
“Current adeno-associated virus vectors transduce the heart but need high titers that necessitate aggressive immunosuppressive regimens to reduce the risk of systemic toxicity.”
The paper relies on this without support.
Missense variants in MYH7 and other sarcomere genes cause hypertrophic cardiomyopathy mostly through gain-of-function mechanisms.
“Missense variants in MYH7 and other sarcomere genes are believed to cause hypertrophic cardiomyopathy mostly through gain of function mechanisms.”
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
Each contradiction between two passages listed here was confirmed by an independent check.
Rated minor: it would not touch a result — a value no result rests on, a p-value that stays on the same side of the significance level, or a conflict that is clerical, resolved elsewhere in the paper, or outside its own findings.
In the paper
§ Current management of hypertrophic cardiomyopathy > Abstract
“SRT=stereotactic radiotherapy.”
§ Current management of hypertrophic cardiomyopathy > PATIENT INVOLVEMENT
“SRT-septal reduction therapy”
Citations
Cites
Shared decision making — The pinnacle of patient-centered care
Barry, M. J., & Edgman-Levitan, S. (2012) · New England Journal of Medicine · doi:10.1056/nejmp1109283 · Cited by 3,433
2023 ESC guidelines for the management of cardiomyopathies
Arbelo, E., Protonotarios, A., Gimeno, J. R., Arbustini, E., Barriales-Villa, R., Basso, C., Bezzina, C. R., Biagini, E., Blom, N. A., de Boer, R. A., et al. (2023) · European Heart Journal · doi:10.1093/eurheartj/ehad194 · Cited by 2,844
Early Rhythm-Control Therapy in Patients with Atrial Fibrillation
Kirchhof, P. F., Camm, A. J., Goette, A., Brandes, A., Eckardt, L., Elvan, A., Fetsch, T., Gelder, I. C. V., Haase, D., Haegeli, L., et al. (2020) · New England Journal of Medicine · doi:10.1056/nejmoa2019422 · Cited by 2,227
Mehra, M. R., Canter, C. E., Hannan, M. M., Semigran, M. J., Uber, P. A., Baran, D. A., Danziger‐Isakov, L. A., Kirklin, J. K., Kirk, R., Kushwaha, S. S., et al. (2016) · The Journal of Heart and Lung Transplantation · doi:10.1016/j.healun.2015.10.023 · Cited by 1,424
New Perspectives on the Prevalence of Hypertrophic Cardiomyopathy
Semsarian, C., Ingles, J., Maron, M. S., & Maron, B. J. (2015) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2015.01.019 · Cited by 1,405
Hypertrophic Cardiomyopathy: Genetics, Pathogenesis, Clinical Manifestations, Diagnosis, and Therapy
Marian, A. J., & Braunwald, E. (2017) · Circulation Research · doi:10.1161/circresaha.117.311059 · Cited by 1,403
Olivotto, I., Oreziak, A., Barriales-Villa, R., Abraham, T. P., Masri, A., Garcia-Pavia, P., Saberi, S., Lakdawala, N. K., Wheeler, M. T., Owens, A., et al. (2020) · The Lancet · doi:10.1016/s0140-6736(20)31792-x · Cited by 1,296
Maron, M. S., Olivotto, I., Betocchi, S., Casey, S. A., Lesser, J. R., Losi, M. A., Cecchi, F., & Maron, B. J. (2003) · New England Journal of Medicine · doi:10.1056/nejmoa021332 · Cited by 1,259
O'Mahony, C., Jichi, F., Pavlou, M., Monserrat, L., Anastasakis, A., Rapezzi, C., Biagini, E., Gimeno, J. R., Limongelli, G., McKenna, W. J., et al. (2014) · European Heart Journal · doi:10.1093/eurheartj/eht439 · Cited by 1,251
Chan, R. H., Maron, B. J., Olivotto, I., Pencina, M. J., Assenza, G. E., Haas, T., Lesser, J. R., Gruner, C., Crean, A. M., Rakowski, H., et al. (2014) · Circulation · doi:10.1161/circulationaha.113.007094 · Cited by 962
Research works printed but not linked: 3
- 10.1161/circresaha.121.318346 · DOI · Paper page
- 10.1161/circulationaha.117.033200 · DOI · Paper page
- 10.1161/circheartfailure.114.001843 · DOI · Paper page
Cited by
Sorted by citations
Ni, L., Lu, B., Peng, G., Ma, W., Guo, Z., Huang, L., Zhang, Y., Gao, F., Wang, Z., & Cai, W. (2025) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2025.07.024 · Cited by 13
Electromechanically Optimized Right Ventricular Pacing for Obstructive Hypertrophic Cardiomyopathy
Mohal, J. S., Whinnett, Z. I., MOHIDDIN, S. A., Malcolmson, J. W., Elliot, P. M., Ormerod, J. O. M., Prasad, S., Ware, J. S., Cooper, R. M., Tanner, M. A., et al. (2025) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2025.08.050 · Cited by 3
Yang, W., Shi, H., Chang, S., Zhang, Y., Jixiang, A., Wu, C., Qian, J., Ge, J., & Zhang, S. (2026) · Cardiovascular Therapeutics · doi:10.1155/cdr/5690104 · Cited by 2
Multimodality Imaging in Hypertrophic Cardiomyopathy
Escribano, D., Díaz-Peláez, E., & Delgado, V. (2026) · Cardiac failure review · doi:10.15420/cfr.2025.14 · Cited by 2
Zhang, S., Yuan, Q., Zhu, Z., Deng, L., Nie, H., Liang, T., & Wang, X. (2025) · The Annals of Thoracic Surgery · doi:10.1016/j.athoracsur.2025.12.009 · Cited by 1
Metadata
- Authors
- Sikand, N., Stendahl, J., Sen, S., Lampert, R., & Day, S.
- Affiliations
- Yale University (US)
- University of Pennsylvania (US)
- Corresponding author
- Lampert, Rachel
- Venue
- BMJ
- Publisher
- BMJ
- Published
- 2025-05-27
- Volume
- 389
- Pages
- e077274
- ISSN
- 1756-1833 (ISSN-L)
- OpenAlex
- W4410774547
- Cited by
- 26
- References
- 156
- Citations by year
- 2026: 19 · 2025: 7
- FWCI
- 4.15
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.bmj.com/company/legal-information/terms-conditions/legal-information/tdm-licencepolicy (tdm)
- Locations
- BMJ (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiomyopathy and Myosin Studies
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Effects of Exercise
- Health Sciences › Medicine › Infectious Diseases › Viral Infections and Immunology Research
- Keywords
- hypertrophic cardiomyopathy, left ventricular hypertrophy, hypertrophic obstructive cardiomyopathy, non-obstructive hypertrophic cardiomyopathy, cardiac myosin inhibitor, septal reduction therapy, sarcomeric gene variants, gene therapy, sudden cardiac death risk, implantable cardioverter-defibrillator, atrial fibrillation, anticoagulation, physical activity limitation, advanced heart failure, heart transplantation
- MeSH terms
- Atrial Fibrillation, Cardiomyopathy, Hypertrophic, Humans, Risk Factors, Death, Sudden, Cardiac, Defibrillators, Implantable
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
A language model drew the claims from the paper on 2026-11-09, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).
A second model labelled each claim on 2026-11-09 (model jev-1.13-20260917, definition revision gold-guideline-v0.2).
Cited sources are checked with a language model’s help (gpt-6-sol).
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
