The DOI matches its Crossref record; 34 of the 34 references it cites were found in a registry or an index; 17 of the 26 sources its claims cite were checked for support.
Evolocumab and Clinical Outcomes in Patients with Cardiovascular Disease
Open accessAbstract
BACKGROUND: Evolocumab is a monoclonal antibody that inhibits proprotein convertase subtilisin-kexin type 9 (PCSK9) and lowers low-density lipoprotein (LDL) cholesterol levels by approximately 60%. Whether it prevents cardiovascular events is uncertain. METHODS: We conducted a randomized, double-blind, placebo-controlled trial involving 27,564 patients with atherosclerotic cardiovascular disease and LDL cholesterol levels of 70 mg per deciliter (1.8 mmol per liter) or higher who were receiving statin therapy. Patients were randomly assigned to receive evolocumab (either 140 mg every 2 weeks or 420 mg monthly) or matching placebo as subcutaneous injections. The primary efficacy end point was the composite of cardiovascular death, myocardial infarction, stroke, hospitalization for unstable angina, or coronary revascularization. The key secondary efficacy end point was the composite of cardiovascular death, myocardial infarction, or stroke. The median duration of follow-up was 2.2 years. RESULTS: At 48 weeks, the least-squares mean percentage reduction in LDL cholesterol levels with evolocumab, as compared with placebo, was 59%, from a median baseline value of 92 mg per deciliter (2.4 mmol per liter) to 30 mg per deciliter (0.78 mmol per liter) (P<0.001). Relative to placebo, evolocumab treatment significantly reduced the risk of the primary end point (1344 patients [9.8%] vs. 1563 patients [11.3%]; hazard ratio, 0.85; 95% confidence interval [CI], 0.79 to 0.92; P<0.001) and the key secondary end point (816 [5.9%] vs. 1013 [7.4%]; hazard ratio, 0.80; 95% CI, 0.73 to 0.88; P<0.001). The results were consistent across key subgroups, including the subgroup of patients in the lowest quartile for baseline LDL cholesterol levels (median, 74 mg per deciliter [1.9 mmol per liter]). There was no significant difference between the study groups with regard to adverse events (including new-onset diabetes and neurocognitive events), with the exception of injection-site reactions, which were more common with evolocumab (2.1% vs. 1.6%). CONCLUSIONS: In our trial, inhibition of PCSK9 with evolocumab on a background of statin therapy lowered LDL cholesterol levels to a median of 30 mg per deciliter (0.78 mmol per liter) and reduced the risk of cardiovascular events. These findings show that patients with atherosclerotic cardiovascular disease benefit from lowering of LDL cholesterol levels below current targets. (Funded by Amgen; FOURIER ClinicalTrials.gov number, NCT01764633 .).
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Claims the paper makes
17 of 26 cited sources checked · 9 supported · 0 flagged · accuracy not yet measured
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“However, there were little more than 100 events in these studies combined.”
§ From the Thrombolysis in Myocardial Infarction (TIMI > 1714
What the sources say
- Partly supportedcites [9] sourceExperimental — accuracy not yet measured
The Results passage reproduced in the Discussion reports 29 cardiovascular events in the evolocumab group and 31 in the standard-therapy group—60 in the combined OSLER trials. The paper identifies these as follow-up trials for participants from phase 2 and phase 3 studies, but it does not establish the claimed total of little more than 100 events across the studies referred to by the citing sentence. (LLM, conf=0.84)
- Could not verifycites [10] sourceExperimental — accuracy not yet measured
The indexed copy’s Abstract reports cardiovascular-event rates for one alirocumab trial (1.7% versus 3.3%), but gives no combined event count across PCSK9-inhibitor studies. Searches for a pooled count and for phase 2 and phase 3 trials found no passage establishing that there were little more than 100 events. (LLM, conf=0.72)
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Moreover, exploratory data from longer-term follow-up in phase 2 and phase 3 trials of PCSK9 inhibitors showed significant reductions in cardiovascular outcomes.9,10”
§ From the Thrombolysis in Myocardial Infarction (TIMI > 1714
What the sources say
- Supportedcites [9] source
The Methods describe longer-term follow-up of patients from phase 2 and phase 3 evolocumab trials, with cardiovascular events assessed in a prespecified exploratory analysis. The Cardiovascular Events section reports a significantly lower event rate with evolocumab than with standard therapy (0.95% versus 2.18% at one year; P=0.003). Page numbers are not available in our copy. (LLM, conf=0.93)
- Could not verifycites [10] sourceExperimental — accuracy not yet measured
The indexed results contain repository metadata and an Abstract passage, but no eligible full-text passage about exploratory cardiovascular outcomes. Searches for longer-term follow-up, post hoc analysis, and cardiovascular events did not locate the relevant findings outside the abstract. (LLM, conf=0.68)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Likewise, these observations are supported by data from a recent mendelian randomization study in which variants in PCSK9 and variants in HMGCR were associated with nearly identical lower risks of cardiovascular events per unit reduction in LDL cholesterol.29”
§ From the Thrombolysis in Myocardial Infarction (TIMI > Table 3. Adverse Events and Laboratory Test Results.
What the sources say
- Supportedcites [29] source
The Results (p. 1) report nearly identical protective associations for PCSK9 and HMGCR variants per 10 mg/dL decrease in LDL cholesterol, with an odds ratio of 0.81 for each. The paper also describes its approach as mendelian randomization (Abstract, p. 2). (LLM, conf=0.95)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“and compares favorably to the rates that have been found with atorvastatin at a dose of 80 mg daily (1.5% per year) and with ezetimibe (1.1% per year) in other trials.14,15”
§ From the Thrombolysis in Myocardial Infarction (TIMI > Table 3. Adverse Events and Laboratory Test Results.
What the sources say
- Supportedcites [14] source
The Safety section (p. 9) reports that 7.2% of patients receiving atorvastatin 80 mg discontinued because of treatment-related adverse events. The paper reports a median follow-up of 4.9 years (p. 5); 7.2% over 4.9 years is approximately 1.5% per year. This source supports the atorvastatin comparison; the ezetimibe figure is attributed to the other citation. (LLM, conf=0.90)
- Partly supportedcites [15] sourceExperimental — accuracy not yet measured
The Safety section reports discontinuation owing to an adverse event in 10.6% of patients receiving simvastatin–ezetimibe, versus 10.1% receiving simvastatin alone. It does not report the cited 1.1% per-year rate or identify those adverse events as caused by ezetimibe. The atorvastatin comparison is not a finding of this trial. (LLM, conf=0.85)
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“In an observation consistent with previous trials of more intensive LDL cholesterol-lowering therapy as compared with moderate-intensity statin therapy, 15,25 we found no effect of additional lowering of LDL cholesterol levels on cardiovascular mortality.”
§ From the Thrombolysis in Myocardial Infarction (TIMI > Table 3. Adverse Events and Laboratory Test Results.
What the sources say
- Supportedcites [15] source
The citation supports the sentence’s comparison with previous trials, not the citing authors’ finding in FOURIER. The Discussion reports no observed difference in cardiovascular mortality in IMPROVE-IT and says this was consistent with trials of intensive-dose versus standard-dose statin therapy. (LLM, conf=0.91)
- Supportedcites [25] source
The citation supports the comparison with previous trials, not the citing authors’ finding in FOURIER. In the Results (page unavailable), the five trials comparing more- with less-intensive statin therapy showed a nonsignificant 7% reduction in coronary death (p=0.2), consistent with no demonstrated mortality benefit. This does not establish that the true effect was exactly zero. (LLM, conf=0.84)
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“These observations are in accord with meta-analyses of data from clinical trials of different lipid-lowering interventions, which show consistent clinical benefits per unit reduction in LDL cholesterol.28”
§ From the Thrombolysis in Myocardial Infarction (TIMI > Table 3. Adverse Events and Laboratory Test Results.
What the sources say
- Supportedcites [28] source
The Results (page not available in our copy) report that five established intervention classes showed similar reductions in major vascular events per unit of LDL-C lowering. The paper describes this as consistent clinical benefit relative to the magnitude of LDL-C reduction, regardless of treatment class within that group. (LLM, conf=0.91)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“The advent of increasingly sensitive cardiac troponin assays probably makes cardiac ischemia increasingly questionable as the true cause of a hospitalization for chestpain symptoms without biochemical evidence of myocyte injury.27”
§ From the Thrombolysis in Myocardial Infarction (TIMI > Table 3. Adverse Events and Laboratory Test Results.
What the sources say
- Partly supportedcites [27] sourceExperimental — accuracy not yet measured
The Conclusions (page unavailable) say that more sensitive troponin assays have reduced the proportion of patients classified as having unstable angina and that it is unclear whether acute coronary syndrome events occur without some troponin increase. That supports questioning an acute coronary syndrome diagnosis when sensitive testing shows no increase, but the paper does not extend that inference to cardiac ischemia as the cause of every chest-pain hospitalization; it also discusses angina without myocardial infarction. (LLM, conf=0.79)
Strength:hedged· not yet calibratedCausal:conditional· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“A delay between the onset of LDL cholesterol lowering and the emergence of the full clinical benefit of the intervention in terms of clinical risk reduction has been well documented in trials of statins, ezetimibe, and other LDL cholesterollowering therapies.15,[21][22][23][24]”
§ From the Thrombolysis in Myocardial Infarction (TIMI > Discussion
What the sources say
- Partly supportedcites [15] sourceExperimental — accuracy not yet measured
The Efficacy End Points and Discussion sections report that the clinical benefit of adding ezetimibe to simvastatin appeared after about one year, while the Lipid Data section documents LDL lowering. This supports a delayed clinical benefit in this trial, but the paper does not establish that the same delay is well documented across trials of statins and other LDL-lowering therapies. (LLM, conf=0.84)
- Not matchedcites [21][22][23][24]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“The major limitation of this trial was a relatively short duration of follow-up as compared with that in other lipid-lowering trials, in which follow-up periods have averaged approximately 5 years.28”
§ From the Thrombolysis in Myocardial Infarction (TIMI > Table 3. Adverse Events and Laboratory Test Results.
What the sources say
- Partly supportedcites [28] sourceExperimental — accuracy not yet measured
The Results report a mean follow-up of 4.3 years across 49 lipid-lowering trials, supporting the comparison to approximately five years. The paper does not assess FOURIER or identify its follow-up duration as a limitation, so it supports only the comparison, not the claim about FOURIER. (LLM, conf=0.88)
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes- Partly supported
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The median LDL cholesterol level at baseline was 92 mg per deciliter (interquartile range, 80 to 109) (2.4 mmol per liter [interquartile range, 2.1 to 2.8]).”
§ From the Thrombolysis in Myocardial Infarction (TIMI > Lipid Data
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes
- It may state two separate claims as one. 15
- Probably not a substantial claim. 11
Every source the paper cites for this claim was checked and supports it.
In the paper
“The size of the patient population in the trial was based on the key secondary end point, and we estimated that 1630 such end-point events were required to provide 90% power to detect a 15% relative risk reduction with evolocumab as compared with placebo.11”
§ From the Thrombolysis in Myocardial Infarction (TIMI > Statistical Analysis
What the sources say
- Supportedcites [11] source
The indexed study-design passage (page not specified) identifies the key secondary end point and says the trial was planned to continue until at least 1,630 patients experienced it, providing 90% power to detect a relative reduction of at least 15%. The same passage describes randomization to evolocumab or matching placebo, supporting the stated comparison. (LLM, conf=0.92)
Load-bearingStrength:hedged· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt 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
“Genetic studies have shown that carriage of PCSK9 loss-of-function alleles is associated with lower LDL cholesterol levels and a reduced risk of myocardial infarction.7,8”
§ From the Thrombolysis in Myocardial Infarction (TIMI > 1714
What the sources say
- Partly supportedcites [7] sourceExperimental — accuracy not yet measured
The Discussion (page unavailable) reports that LDL-lowering PCSK9 variants were associated with reduced coronary heart disease. The Methods (page unavailable) define that outcome as a composite including myocardial infarction, CHD death, and coronary revascularization; the paper does not report a separate reduction in myocardial infarction risk. (LLM, conf=0.85)
- Supportedcites [8] source
In the correspondence, the authors state that a PCSK9 loss-of-function allele decreases LDL cholesterol and protects against myocardial infarction. Their own myocardial-infarction analysis specifically concerns the R46L allele and early-onset cases; the cited sentence makes the same association without claiming a broader trial result. (LLM, conf=0.94)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt 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
“More recently, the addition of ezetimibe to statin therapy in the Improved Reduction of Outcomes: Vytorin Efficacy International Trial (IMPROVE-IT) lowered LDL cholesterol levels from 70 mg per deciliter (1.8 mmol per liter) to 54 mg per deciliter (1.4 mmol per liter) and significantly reduced major cardiovascular events.”
§ From the Thrombolysis in Myocardial Infarction (TIMI > Discussion
What the sources say
- Supportedcites [15] source
The Results report median LDL cholesterol levels of 69.5 mg/dL with simvastatin alone versus 53.7 mg/dL with simvastatin plus ezetimibe, matching the rounded 70-to-54 comparison. The same Results passage reports a significantly lower primary cardiovascular event rate with ezetimibe (32.7% versus 34.7%; P=0.016). (LLM, conf=0.94)
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
- Supported
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
“The risk of new-onset diabetes in our trial appeared to be similar in the two groups, although the 95% confidence intervals did not exclude the point estimates observed with statins.30,31”
§ From the Thrombolysis in Myocardial Infarction (TIMI > Table 3. Adverse Events and Laboratory Test Results.
What the sources say
Strength:hedged· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In the evolocumab group, new binding antibodies developed in 43 patients (0.3%), and development of neutralizing antibodies did not occur in any patient.”
§ From the Thrombolysis in Myocardial Infarction (TIMI > Safety
Strength:plain· not yet calibratedn = 43Tests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The large majority of reactions (approximately 90% in each group) were classified as mild, and only 0.1% of the patients in each group stopped receiving the study agent because of an injection-site reaction.”
§ From the Thrombolysis in Myocardial Infarction (TIMI > Safety
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“as compared with placebo, at 48 weeks, evolocumab had reduced non-HDL cholesterol levels by 52% and apolipoprotein B levels by 49% (P<0.001 for both).”
§ From the Thrombolysis in Myocardial Infarction (TIMI > Characteristics
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt 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
“Finally, the rate of urgent coronary revascularization appeared to be more modifiable than that of elective revascularization.”
§ From the Thrombolysis in Myocardial Infarction (TIMI > Table 3. Adverse Events and Laboratory Test Results.
Strength:hedged· not yet calibratedCausal:conditional· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“No significant between-group differences were seen in the overall rates of adverse events, serious adverse events, or adverse events thought to be related to the study agent and leading to discontinuation of the study regimen (Table 3).”
§ From the Thrombolysis in Myocardial Infarction (TIMI > Safety
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The benefit of evolocumab was also consistent across levels of intensity of statin therapy, regardless of ezetimibe use, and with both the dosing regimen of 140 mg every 2 weeks and that of 420 mg monthly.”
§ From the Thrombolysis in Myocardial Infarction (TIMI > Efficacy End Points
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“in which the rates of cardiovascular mortality were one third of the rates in the Scandinavian Simvastatin Survival Study (4S).26”
§ From the Thrombolysis in Myocardial Infarction (TIMI > Table 3. Adverse Events and Laboratory Test Results.
What the sources say
- Not matchedcites [26] Scandinavian Simvastatin Survival Study Group, 1994, Lancet
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
- Not matched
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Injection-site reactions were rare, but they were more frequent with evolocumab (2.1% vs. 1.6%).”
§ From the Thrombolysis in Myocardial Infarction (TIMI > Safety
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Achievement of these very low LDL cholesterol levels with evolocumab did not lead to any significant differences between the two study groups in the overall rates of adverse events or in rates of study-regimen discontinuation.”
§ From the Thrombolysis in Myocardial Infarction (TIMI > Table 3. Adverse Events and Laboratory Test Results.
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Randomization was performed in a double-blinded manner with the use of a central computerized system, with stratification according to the final screening LDL cholesterol level (<85 or ≥85 mg per deciliter [<2.2 or ≥2.2 mmol per liter]) and region.”
§ From the Thrombolysis in Myocardial Infarction (TIMI > Randomization and Study Agents
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim. It may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Premature permanent discontinuation of the study regimen occurred in 12.5% of patients (5.7% per year), withdrawal of consent in 0.7% (0.3% per year), and loss to follow-up in less than 0.1% (0.03% per year), with similar rates in the two study groups”
§ From the Thrombolysis in Myocardial Infarction (TIMI > Patients
Strength:plain· not yet calibratedn = 27,525Tests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“A central clinicalevents committee led by the TIMI Study Group, whose members were unaware of study-group assignments and lipid levels, adjudicated all potential efficacy end-point events and cases of new-onset diabetes.”
§ From the Thrombolysis in Myocardial Infarction (TIMI > End Points
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“All efficacy analyses were conducted on an intentionto-treat basis.”
§ From the Thrombolysis in Myocardial Infarction (TIMI > Statistical Analysis
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“The FOURIER trial was a randomized, doubleblind, placebo-controlled, multinational clinical trial in which patients at 1242 sites in 49 countries underwent randomization”
§ From the Thrombolysis in Myocardial Infarction (TIMI > Trial Design and Oversight
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“The raw database was provided to the Thrombolysis in Myocardial Infarction (TIMI) Study Group, which conducted data analyses independently of the sponsor.”
§ From the Thrombolysis in Myocardial Infarction (TIMI > Trial Design and Oversight
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“A total of 27,525 patients (99.9%) received at least one dose of a study agent.”
§ From the Thrombolysis in Myocardial Infarction (TIMI > Patients
Strength:plain· not yet calibratedn = 27,525Tests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Most but not all of the patients in the trial received high-intensity statin therapy”
§ From the Thrombolysis in Myocardial Infarction (TIMI > Table 3. Adverse Events and Laboratory Test Results.
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“and ezetimibe use was infrequent.”
§ From the Thrombolysis in Myocardial Infarction (TIMI > Table 3. Adverse Events and Laboratory Test Results.
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Although the median follow-up period in FOURIER was originally planned to be approximately 4 years, an event rate that was approximately 50% higher than had been postulated led to a shorter required duration of follow-up to accrue the prespecified number of events.”
§ From the Thrombolysis in Myocardial Infarction (TIMI > Table 3. Adverse Events and Laboratory Test Results.
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
The paper relies on this without support.
The reduction in cardiovascular events with evolocumab is mediated by the lowering of LDL cholesterol.
“These findings show that patients with atherosclerotic cardiovascular disease benefit from lowering of LDL cholesterol levels below current targets.”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The cited source doesn’t support the claim as written.
In the citing paper
“Regarding the persistence phase, the FOURIER open-label extension study reported a 14.0% overall premature discontinuation rate over 5 years among 6,635 patients randomized to evolocumab.115,116”
From Adherence to PCSK9 Inhibitors in Clinical Practice (2026) · cites this paper as [115]
Checked by a reasoning model — may be wrong.
Experimental — accuracy not yet measuredThe cited source doesn’t support the claim as written.
In the citing paper
“The relative and absolute reductions in MACE observed in our analysis are similar in magnitude to those observed for the seminal IMPROVE-IT [3] and FOURIER [4] trials for ezetimibe and evolocumab respectively, with similarly non-significant reductions in all-cause and cardiovascular mortality.”
From The Clinical Efficacy and Safety of Bempedoic Acid in Patients at Elevated Risk of Cardiovascular Disease: A Meta-Analysis of Randomized Clinical Trials (2024) · cites this paper as [4]
Checked by a reasoning model — may be wrong.
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Serious safety concerns were also not observed with evolocumab in the FOURIER (Further Cardiovascular Outcomes Research with PCSK9 Inhibition in Subjects with Elevated Risk) trial, 11 which had no lower limit for allowable LDL cholesterol levels”
From Alirocumab and Cardiovascular Outcomes after Acute Coronary Syndrome (2018) · cites this paper as [11]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“This change is not necessarily a toxicity signal, because clinically approved PCSK9-targeting antibodies, including evolocumab and alirocumab, systemically reduce LDL-C and have shown acceptable tolerability in large cardiovascular outcome studies [ 65-67 ].”
From Restores Aβ Clearance by Overcoming PCSK9–LRP1 Dysregulation and TRIB3‐Mediated Autophagy Blockade in Alzheimer's Disease (2026) · cites this paper as [65]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Both have unequivocally shown that PCSK9 inhibition safely lowers LDL-C levels [56 mg/dl absolute reduction (95% confidence interval 55–57) or 59% relative reduction (95% confidence interval 58–60)] alone or on top of maximally tolerated lipid-lowering therapies (i.e. high-doses statins with or without ezetimibe) and reduces the number of cardiovascular events.”
From PCSK9 and the nervous system: a no-brainer? (2023) · cites this paper as [9]
Experimental — accuracy not yet measured
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Trials of PCSK9 inhibitors in cardiovascular populations consistently showed substantial reductions in LDL cholesterol without negative cognitive effects [11,22].”
From The Roles of PCSK9 in Alzheimer’s Disease: A Systematic Review of Clinical, Genetic, and Preclinical Evidence (2025) · cites this paper as [11]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“This suggests that any protective effects seen in laboratory studies probably occur through an indirect route. The benefits likely stem from improved systemic cholesterol levels and better overall vascular health, rather than from the drugs acting directly within the brain [11,27,50].”
From The Roles of PCSK9 in Alzheimer’s Disease: A Systematic Review of Clinical, Genetic, and Preclinical Evidence (2025) · cites this paper as [11]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Intensive therapy is indicated because cardiovascular event rates are increased in people with diabetes and established ASCVD, and it has been shown to be of benefit in multiple large meta-analyses and randomized cardiovascular outcomes trials (99,100,108,119,121).”
From 10. Cardiovascular Disease and Risk Management: Standards of Care in Diabetes—2025 (2025) · cites this paper as [121]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“In addition, no change in cognitive function has been reported in studies with the addition of ezetimibe (119) or PCSK9 inhibitors (121,170) to statin therapy, including among individuals treated to very low LDL cholesterol levels.”
From 10. Cardiovascular Disease and Risk Management: Standards of Care in Diabetes—2025 (2025) · cites this paper as [121]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“When added to a maximally tolerated statin, these agents reduced LDL cholesterol by ∼60% (115) and significantly reduced the risk of major adverse cardiovascular events by 15–20% in the FOURIER (evolocumab) and ODYSSEY OUTCOMES (Evaluation of Cardiovascular Outcomes After an Acute Coronary Syndrome During Treatment With Alirocumab) trials (115,117,122).”
From 10. Cardiovascular Disease and Risk Management: Standards of Care in Diabetes—2026 (2026) · cites this paper as [115]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“When added to a maximally tolerated statin, these agents reduced LDL cholesterol by ∼60% (115) and significantly reduced the risk of major adverse cardiovascular events by 15–20% in the FOURIER (evolocumab) and ODYSSEY OUTCOMES (Evaluation of Cardiovascular Outcomes After an Acute Coronary Syndrome During Treatment With Alirocumab) trials (115,117,122).”
From 10. Cardiovascular Disease and Risk Management: Standards of Care in Diabetes—2026 (2026) · cites this paper as [115]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“In addition, no change in cognitive function has been reported in studies with the addition of ezetimibe (112) or PCSK9 monoclonal antibodies (115,164) to statin therapy, including among individuals treated to very low LDL cholesterol levels.”
From 10. Cardiovascular Disease and Risk Management: Standards of Care in Diabetes—2026 (2026) · cites this paper as [115]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“PCSK9 inhibition has emerged as a potent therapeutic modality, with large outcome trials showing that the addition of injectable agents like evolocumab or alirocumab to intensive statin therapy lowers LDL-C by roughly 50–60% and reduces major adverse cardiovascular events in high-risk populations [2,3].”
From Oral PCSK9 inhibitors for elevated LDL-C: A systematic review and meta-analysis of randomized trials (2026) · cites this paper as [2]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“However, BA increased the risk of gout, renal impairment, and cholelithiasis, none of which were significantly increased with ezetimibe or evolocumab.”
From The Clinical Efficacy and Safety of Bempedoic Acid in Patients at Elevated Risk of Cardiovascular Disease: A Meta-Analysis of Randomized Clinical Trials (2024) · cites this paper as [4]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Accordingly, PCSK9 inhibitory antibodies and siRNA potently reduce LDL cholesterol to unprecedented low levels and are approved for treatment of hypercholesterolemia.”
From PCSK9 deficiency alters brain lipid composition without affecting brain development and function (2023) · cites this paper as Sabatine et al., 2017
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Accordingly, PCSK9 siRNA and monoclonal antibodies blocking the PCSK9/LDLR interaction potently lower LDL cholesterol and reduce the risk of adverse cardiovascular events (Sabatine et al., 2017; Schwartz et al., 2018; Ray et al., 2020).”
From PCSK9 deficiency alters brain lipid composition without affecting brain development and function (2023) · cites this paper as Sabatine et al., 2017
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“targeted PCSK9 inhibition restores hepatic LDLR levels, decreases plasma LDL-C levels and improves cardiovascular outcomes.7,9–11”
From Sirtuin-1 directly binds and deacetylates hepatic PCSK9 thereby promoting the inhibition of LDL receptor degradation (2025) · cites this paper as [10]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“Two of these agents were reported to reduce the risk of ischemic cardiovascular events in patients who had stable atherosclerotic disease or high cardiovascular risk and an elevated level of atherogenic lipoproteins despite statin treatment, 11,13”
From Alirocumab and Cardiovascular Outcomes after Acute Coronary Syndrome (2018) · cites this paper as [11]
The cited source says what the claim attributes to it.
In the citing paper
“These findings have led to the development of monoclonal antibodies to PCSK9 that produce substantial reductions in LDL cholesterol when administered alone or with a statin. 8-12”
From Alirocumab and Cardiovascular Outcomes after Acute Coronary Syndrome (2018) · cites this paper as [11]
The cited source says what the claim attributes to it.
In the citing paper
“however, that trial had a shorter median follow-up, and very few patients were followed for 3 or more years.”
From Alirocumab and Cardiovascular Outcomes after Acute Coronary Syndrome (2018) · cites this paper as [11]
The cited source says what the claim attributes to it.
In the citing paper
“large cardiovascular trials of PCSK9 antibodies such as evolocumab have not demonstrated cognitive harm10,43”
From Small-molecule PCSK9 inhibition enhances BBB amyloid-β clearance and suppresses microglial inflammation in Alzheimer’s disease models (2026) · cites this paper as [10]
The cited source says what the claim attributes to it.
In the citing paper
“This innovative approach, calibrated and validated against major outcome trials such as FOURIER19 and ORION-10, estimated that inclisiran could reduce the risk of 3-point MACE by 25% over 5 years compared to placebo, when added to high-intensity statins with or without ezetimibe.”
From Small Interfering RNA for LDL-Cholesterol Reduction (2026) · cites this paper as [19]
The cited source says what the claim attributes to it.
In the citing paper
“Injectable proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors are an established strategy to lower low-density lipoprotein cholesterol (LDL-C) and reduce atherosclerotic cardiovascular disease risk.”
From Oral PCSK9 inhibitors for elevated LDL-C: A systematic review and meta-analysis of randomized trials (2026) · cites this paper as [2]
The cited source says what the claim attributes to it.
In the citing paper
“In comparison, evolocumab reduced LDL-C by ∼59% and alirocumab by ∼60% in the FOURIER and ODYSSEY OUTCOMES trials, respectively [2,3]”
From Oral PCSK9 inhibitors for elevated LDL-C: A systematic review and meta-analysis of randomized trials (2026) · cites this paper as [2]
The cited source says what the claim attributes to it.
In the citing paper
“The main alternative treatments indicated to lower LDL-C and cardiovascular risk are ezetimibe, evolocumab, and alirocumab based on the IMPROVE-IT [3], FOURIER [4], and ODYSSEY Outcomes [5] trials respectively, wherein the 3 treatments resulted in significant reductions in LDL-C and cardiovascular events.”
From The Clinical Efficacy and Safety of Bempedoic Acid in Patients at Elevated Risk of Cardiovascular Disease: A Meta-Analysis of Randomized Clinical Trials (2024) · cites this paper as [4]
The cited source says what the claim attributes to it.
In the citing paper
“In fact, PCSK9 has emerged as a key target for the treatment and prevention of FH with successful preclinical studies in macaques132 and human clinical trials for Evolocumab133.”
From Pathways and Molecular Mechanisms Governing LDL Receptor Regulation (2025) · cites this paper as [133]
The check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“evolocumab in the FOURIER trial reduced Lp(a) by a median of 26.9% at 48 weeks[2,25], and alirocumab in ODYSSEY OUTCOMES showed a median relative reduction of −23% by 4 months[3,26].”
From Oral PCSK9 inhibitors for elevated LDL-C: A systematic review and meta-analysis of randomized trials (2026) · cites this paper as [2]
Experimental — accuracy not yet measuredIn the citing paper
“In particular, evolocumab showed a 17% RR reduction of a composite primary endpoint of CV death, MI, stroke, hospitalization for unstable angina, or coronary revascularization in patients with diabetes included in the FOURIER trial (HR 0.83; 95% CI, 0.75-0.93;P = 0.0008).263”
From 2023 ESC guidelines for the management of cardiovascular disease in patients with diabetes. (2023) · cites this paper as [263]
In the citing paper
“the cumulative data from the FOURIER and ODYSSEY OUTCOMES trials suggest that PCSK9 inhibitors effectively lower LDL-C and cardiovascular risk in individuals with CAD regardless of diabetes mellitus status.”
From Clinical management of stable coronary artery disease in patients with type 2 diabetes mellitus: a scientific statement from the American Heart Association (2020) · cites this paper as [125]
In the citing paper
“Although neither PCSK9 inhibitor reduced cardiovascular mortality in these trials,125,126”
From Clinical management of stable coronary artery disease in patients with type 2 diabetes mellitus: a scientific statement from the American Heart Association (2020) · cites this paper as [125]
In the citing paper
“However, the best evidence to support lower LDL cholesterol targets in people with diabetes and established cardiovascular disease derives from multiple large randomized trials investigating the benefi ts of adding nonstatin agents to statin therapy.”
From 10. Cardiovascular Disease and Risk Management: Standards of Care in Diabetes—2023 (2023) · cites this paper as [108]
In the citing paper
“Because cardiovascular event rates are increased in people with diabetes and established ASCVD, intensive therapy is indicated and has been shown to be of bene fi t in multiple large meta-analyses and randomized cardiovascular outcomes trials (91,99,105,107,108).”
From 10. Cardiovascular Disease and Risk Management: Standards of Care in Diabetes—2023 (2023) · cites this paper as [108]
In the citing paper
“During the median follow-up of 2.2 years, the composite outcome of cardiovascular death, MI, stroke, hospitalization for angina, or revascularization occurred in 11.3% vs. 9.8% of the placebo and evolocumab groups, respectively, representing a 15% relative risk reduction (P < 0.001).”
From 10. Cardiovascular Disease and Risk Management: Standards of Care in Diabetes—2023 (2023) · cites this paper as [108]
In the citing paper
“Evolocumab reduced LDL cholesterol by 59% from a median of 92 to 30 mg/dL in the treatment arm.”
From 10. Cardiovascular Disease and Risk Management: Standards of Care in Diabetes—2023 (2023) · cites this paper as [108]
In the citing paper
“The combined end point of cardiovascular death, MI, or stroke was reduced by 20%, from 7.4 to 5.9% ( P < 0.001).”
From 10. Cardiovascular Disease and Risk Management: Standards of Care in Diabetes—2023 (2023) · cites this paper as [108]
In the citing paper
“Each trial found a signi fi cant bene fi t in the reduction of ASCVD events that was directly related to the degree of further LDL cholesterol lowering.”
From 10. Cardiovascular Disease and Risk Management: Standards of Care in Diabetes—2023 (2023) · cites this paper as [108]
Citations
Cites
Stone, N. J., Robinson, J. G., Lichtenstein, A. H., Bairey Merz, C. N., Blum, C. B., Eckel, R. H., Goldberg, A. C., Gordon, D., Levy, D., Lloyd-Jones, D. M., et al. (2014) · Circulation · doi:10.1161/01.cir.0000437738.63853.7a · Cited by 7,081
Cholesterol Treatment Trialists' (CTT) Collaboration (2010) · The Lancet · doi:10.1016/s0140-6736(10)61350-5 · Cited by 6,550
Intensive versus Moderate Lipid Lowering with Statins after Acute Coronary Syndromes
Cannon, C. P., Braunwald, E., McCabe, C. H., Rader, D. J., Rouleau, J. L., Belder, R., Joyal, S. V., Hill, K. A., Pfeffer, M. A., & Skene, A. M. (2004) · New England Journal of Medicine · doi:10.1056/nejmoa040583 · Cited by 4,938
Ezetimibe Added to Statin Therapy after Acute Coronary Syndromes
Cannon, C. P., Blazing, M. A., Giugliano, R. P., McCagg, A., White, J. A., Theroux, P., Darius, H., Lewis, B. S., Ophuis, T. O., Jukema, J. W., et al. (2015) · New England Journal of Medicine · doi:10.1056/nejmoa1410489 · Cited by 4,487
Self-citationHelsinki Heart Study: Primary-Prevention Trial with Gemfibrozil in Middle-Aged Men with Dyslipidemia
Frick, M. H., Elo, O., Haapa, K., Heinonen, O. P., Heinsalmi, P., Helo, P., Huttunen, J. K., Kaitaniemi, P., Koskinen, P., Manninen, V., et al. (1987) · New England Journal of Medicine · doi:10.1056/nejm198711123172001 · Cited by 3,881
Intensive Lipid Lowering with Atorvastatin in Patients with Stable Coronary Disease
LaRosa, J. C., Grundy, S. M., Waters, D. D., Shear, C., Barter, P., Fruchart, J.-C., Gotto, A. M., Greten, H., Kastelein, J. J. P., Shepherd, J., et al. (2005) · New England Journal of Medicine · doi:10.1056/nejmoa050461 · Cited by 3,489
Sequence Variations in PCSK9, Low LDL, and Protection against Coronary Heart Disease
Cohen, J. C., Boerwinkle, E., Mosley, T. H., & Hobbs, H. H. (2006) · New England Journal of Medicine · doi:10.1056/nejmoa054013 · Cited by 3,181
Statins and risk of incident diabetes: A collaborative meta-analysis of randomised statin trials
Sattar, N., Preiss, D., Murray, H. M., Welsh, P., Buckley, B. M., de Craen, A. J., Seshasai, S. R. K., McMurray, J. J., Freeman, D. J., Jukema, J. W., et al. (2010) · The Lancet · doi:10.1016/s0140-6736(09)61965-6 · Cited by 2,436
Self-citationEfficacy and Safety of Alirocumab in Reducing Lipids and Cardiovascular Events
Robinson, J. G., Farnier, M., Krempf, M., Bergeron, J., Luc, G., Averna, M., Stroes, E. S., Langslet, G., Raal, F. J., El Shahawy, M., et al. (2015) · New England Journal of Medicine · doi:10.1056/nejmoa1501031 · Cited by 2,296
Flagged first, then by citations
Research works printed but not linked: 4
- Landmesser U, Eur Heart J
- Sabatine MS, Eur Heart J
- Scandinavian Simvastatin Survival Study Group, 1994, Lancet, 344, 1383
- Koren MJ, JAMA Cardiol
Cited by
Sorted by citations
Items 101–200 of 6,144
O’Sullivan, J. W., Raghavan, S., Márquez‐Luna, C., Luzum, J. A., Damrauer, S. M., Ashley, E. A., O’Donnell, C. J., Willer, C. J., & Natarajan, P. (2022) · Circulation · doi:10.1161/cir.0000000000001077 · Cited by 443
Advancing human genetics research and drug discovery through exome sequencing of the UK Biobank
Szustakowski, J. D., Balasubramanian, S., Kvikstad, E., Khalid, S., Bronson, P. G., Sasson, A., Wong, E., Liu, D., Wade Davis, J., Haefliger, C., et al. (2021) · Nature Genetics · doi:10.1038/s41588-021-00885-0 · Cited by 401
Soppert, J., Lehrke, M., Marx, N., Jankowski, J., & Noels, H. (2020) · Advanced Drug Delivery Reviews · doi:10.1016/j.addr.2020.07.019 · Cited by 440
Long-term evolocumab in patients with established atherosclerotic cardiovascular disease
O’Donoghue, M. L., Giugliano, R. P., Wiviott, S. D., Atar, D., Keech, A., Kuder, J. F., Im, K., Murphy, S. A., Flores-Arredondo, J. H., López, J. A. G., et al. (2022) · Circulation · doi:10.1161/circulationaha.122.061620 · Cited by 410
Self-citation2017 EACTS Guidelines on perioperative medication in adult cardiac surgery
Sousa‐Uva, M., Head, S. J., Milojevic, M., Collet, J., Landoni, G., Castellà, M., Dunning, J., Guðbjartsson, T., Linker, N., Sandoval, E., et al. (2017) · European Journal of Cardio-Thoracic Surgery · doi:10.1093/ejcts/ezx314 · Cited by 415
Fernández-Friera, L., Fuster, V., López-Melgar, B., Oliva, B., García-Ruiz, J. M., Mendiguren, J., Bueno, H., Pocock, S., Ibáñez, B., Fernández-Ortiz, A., et al. (2017) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2017.10.024 · Cited by 378
“This hypothesis is consistent with recent lipidlowering trials, in which adverse clinical outcomes were significantly reduced when LDL-C levels were lowered below current targets (37).”
Backer, G. D., Jankowski, P., Kotseva, K., Mirrakhimov, E. M., Reiner, Ž., Rydén, L., Tokgözoğlu, L. S., Wood, D., Bacquer, D. D., Backer, G. D., et al. (2019) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2019.03.014 · Cited by 391
Lloyd‐Jones, D. M., Morris, P. B., Ballantyne, C. M., Birtcher, K. K., Daly, D. D., DePalma, S. M., Minissian, M., Orringer, C. E., & Smith, S. C. (2017) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2017.07.745 · Cited by 398
Athyros, V. G., Doumas, M. N., Imprialos, K. P., Stavropoulos, K., Georgianou, E., Katsimardou, A., & Karagiannis, A. I. (2018) · HORMONES · doi:10.1007/s42000-018-0014-8 · Cited by 384
Dyslipidemia and cardiovascular disease risk among the MASHAD study population
Hedayatnia, M., Asadi, Z., Zare‐Feyzabadi, R., Yaghooti‐Khorasani, M., Ghazizadeh, H., Zirak, R. G., Tirkani, A. N., Mohammadi‐Bajgiran, M., Rohban, M., Sadabadi, F., et al. (2020) · Lipids in Health and Disease · doi:10.1186/s12944-020-01204-y · Cited by 406
Lipoprotein(a) and its Significance in Cardiovascular Disease
Lau, F. D., & Giugliano, R. P. (2022) · JAMA Cardiology · doi:10.1001/jamacardio.2022.0987 · Cited by 377
Self-citationPCSK9 inhibitors: clinical evidence and implementation
Sabatine, M. S. (2019) · Nature Reviews Cardiology · doi:10.1038/s41569-018-0107-8 · Cited by 338
Self-citationAssociation Between Obesity and Cardiovascular Outcomes
Riaz, H., Khan, M. S., Siddiqi, T. J., Usman, M., Shah, N. P., Goyal, A., Khan, S. S., Mookadam, F., Krasuski, R. A., & Ahmed, H. M. (2018) · JAMA Network Open · doi:10.1001/jamanetworkopen.2018.3788 · Cited by 378
Diversity and inclusion in genomic research: why the uneven progress?
Bentley, A. R., Callier, S., & Rotimi, C. N. (2017) · Journal of Community Genetics · doi:10.1007/s12687-017-0316-6 · Cited by 357
“…and alirocumab, have been approved widely for use either alone or in combination with statins after demonstrating that they are well tolerated and effective at reducing LDLC (Gouni-Berthold et al. 2016; Roth et al. 2016) and, for evolucumab, risk of cardiovascular outcomes (Sabatine et al., 2017).”
Lipid Management for the Prevention of Atherosclerotic Cardiovascular Disease
Michos, E. D., McEvoy, J. W., & Blumenthal, R. S. (2019) · New England Journal of Medicine · doi:10.1056/nejmra1806939 · Cited by 354
Summary of Updated Recommendations for Primary Prevention of Cardiovascular Disease in Women
Cho, L., Davis, M. B., Elgendy, I. Y., Epps, K., Lindley, K. J., Mehta, P. K., Michos, E. D., Minissian, M., Pepine, C. J., Vaccarino, V., et al. (2020) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2020.03.060 · Cited by 363
Japanese Clinical Practice Guideline for Diabetes 2019
Araki, E., Goto, A., Kondo, T., Noda, M., Noto, H., Origasa, H., Osawa, H., Taguchi, A., Tanizawa, Y., Tobe, K., et al. (2020) · Journal of Diabetes Investigation · doi:10.1111/jdi.13306 · Cited by 346
10. Cardiovascular Disease and Risk Management: Standards of Care in Diabetes—2025
American Diabetes Association Professional Practice Committee, ElSayed, N. A., McCoy, R. G., Aleppo, G., Balapattabi, K., Beverly, E. A., Briggs Early, K., Bruemmer, D., Das, S. R., Echouffo-Tcheugui, J. B., et al. (2025) · Diabetes Care · doi:10.2337/dc25-s010 · Cited by 339
Using Mendelian Randomization to Improve the Design of Randomized Trials
Ference, B. A., Holmes, M. V., & Smith, G. D. (2021) · Cold Spring Harbor Perspectives in Medicine · doi:10.1101/cshperspect.a040980 · Cited by 338
“This is precisely what the landmark FOURIER and ODYSSEY trials showed (Sabatine et al. 2017; Schwartz et al. 2018).”
ResultA decade of genome-wide association studies for coronary artery disease: the challenges ahead
Erdmann, J., Kessler, T., Venegas, L. M., & Schunkert, H. (2018) · Cardiovascular Research · doi:10.1093/cvr/cvy084 · Cited by 331
Ray, K. K., Troquay, R. P. T., Visseren, F. L. J., Leiter, L. A., Scott Wright, R., Vikarunnessa, S., Talloczy, Z., Zang, X., Maheux, P., Lesogor, A., et al. (2023) · The Lancet Diabetes & Endocrinology · doi:10.1016/s2213-8587(22)00353-9 · Cited by 328
on behalf of the China Kadoorie Biobank Collaborative Group, Sun, L., Clarke, R., Bennett, D., Yu, C., Walters, R. G., Hill, M., Parish, S., Millwood, I. Y., Bian, Z., et al. (2019) · Nature Medicine · doi:10.1038/s41591-019-0366-x · Cited by 318
2023 ESC Guidelines for the management of acute coronary syndromes
Byrne, R. A., Rosselló, X., Coughlan, J. J., Barbato, E., Berry, C., Chieffo, A., Claeys, M. J., Dan, G., Dweck, M. R., Galbraith, M., et al. (2023) · European Heart Journal Acute Cardiovascular Care · doi:10.1093/ehjacc/zuad107 · Cited by 373
Residual Cardiovascular Risk at Low LDL: Remnants, Lipoprotein(a), and Inflammation
Hoogeveen, R. C., & Ballantyne, C. M. (2020) · Clinical Chemistry · doi:10.1093/clinchem/hvaa252 · Cited by 322
Brunner, F. J., Waldeyer, C., Ojeda, F., Salomaa, V. V., Kee, F., Sans, S., Thorand, B., Giampaoli, S., Brambilla, P., Tunstall‐Pedoe, H., et al. (2019) · The Lancet · doi:10.1016/s0140-6736(19)32519-x · Cited by 322
Arnold, S. V., Bhatt, D. L., Barsness, G. W., Beatty, A. L., Deedwania, P. C., Inzucchi, S. E., Kosiborod, M., Leiter, L. A., Lipska, K. J., Newman, J. D., et al. (2020) · Circulation · doi:10.1161/cir.0000000000000766 · Cited by 304
Okamura, T., Tsukamoto, K., Arai, H., Fujioka, Y., Ishigaki, Y., Koba, S., Ohmura, H., Shoji, T., Yokote, K., Yoshida, H., et al. (2023) · Journal of Atherosclerosis and Thrombosis · doi:10.5551/jat.gl2022 · Cited by 345
The therapeutic potential of mesenchymal stem cells for cardiovascular diseases
Guo, Y., Yu, Y., Hu, S., Chen, Y., & Shen, Z. (2020) · Cell Death and Disease · doi:10.1038/s41419-020-2542-9 · Cited by 302
Garber, A. J., Abrahamson, M. J., Barzilay, J. I., Blonde, L., Bloomgarden, Z. T., Bush, M. A., Dagogo-Jack, S., DeFronzo, R. A., Einhorn, D., Fonseca, V. A., et al. (2019) · Endocrine Practice · doi:10.4158/cs-2018-0535 · Cited by 297
“In the FOURIER (Further Cardiovascular Outcomes Research with PCSK9 Inhibition in Subjects with Elevated Risk) study, evolocumab significantly reduced the risk of myocardial infarction, stroke, and coronary revascularization (143), and similar effects were seen with alirocumab in ODYSSEY Outcomes (Evaluation of Cardio…”
Karczewski, K. J., Solomonson, M., Chao, K. R., Goodrich, J. K., Tiao, G., Lu, W., Riley-Gillis, B. M., Tsai, E. A., Kim, H. I., Zheng, X., et al. (2022) · Cell Genomics · doi:10.1016/j.xgen.2022.100168 · Cited by 284
Cardiomyopathy in obesity, insulin resistance and diabetes
Nakamura, M., & Sadoshima, J. (2019) · The Journal of Physiology · doi:10.1113/jp276747 · Cited by 294
Koskinas, K. C., Windecker, S., Pedrazzini, G., Mueller, C. E., Cook, S., Matter, C. M., Müller, O., Häner, J. D., Gencer, B., Crljenica, C., et al. (2019) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2019.08.010 · Cited by 296
Inflammatory and Cholesterol Risk in the FOURIER Trial
Bohula, E. A., Giugliano, R. P., Leiter, L. A., Verma, S., Park, J.-G., Sever, P. S., Lira Pineda, A., Honarpour, N., Wang, H., Murphy, S. A., et al. (2018) · Circulation · doi:10.1161/circulationaha.118.034032 · Cited by 280
Self-citationGaudet, D., Karwatowska-Prokopczuk, E., Baum, S. J., Hurh, E., Kingsbury, J., Bartlett, V. J., Figueroa, A. L., Piscitelli, P., Singleton, W., Witztum, J. L., et al. (2020) · European Heart Journal · doi:10.1093/eurheartj/ehaa689 · Cited by 279
“Despite significant evidence that low-density lipoprotein cholesterol (LDL-C)-targeted therapies reduce cardiovascular (CV) events, residual CV risk remains high.(1,2) There is increasing evidence that this residual CV risk is in part related to increased levels of plasma triglycerides and remnant lipoproteins.”
BackgroundPCSK9: From Basic Science Discoveries to Clinical Trials
Shapiro, M. D., Tavori, H., & Fazio, S. (2018) · Circulation Research · doi:10.1161/circresaha.118.311227 · Cited by 285
Diabetes and peripheral artery disease: A review
Soyoye, D. O., Abiodun, O. O., Ikem, R. T., Kolawole, B. A., & Akintomide, A. O. (2021) · World Journal of Diabetes · doi:10.4239/wjd.v12.i6.827 · Cited by 337
Residual Inflammatory Risk on Treatment With PCSK9 Inhibition and Statin Therapy
Pradhan, A. D., Aday, A. W., Rose, L. M., & Ridker, P. M. (2018) · Circulation · doi:10.1161/circulationaha.118.034645 · Cited by 258
Hallmarks of cardiovascular ageing
Abdellatif, M., Rainer, P. P., Sedej, S., & Kroemer, G. (2023) · Nature Reviews Cardiology · doi:10.1038/s41569-023-00881-3 · Cited by 305
Lipid management in patients with chronic kidney disease
Ferro, C. J., Mark, P. B., Kanbay, M., Sarafidis, P. A., Heine, G. H., Rossignol, P., Massy, Z. A., Mallamaci, F., Valdivielso, J. M., Małyszko, J., et al. (2018) · Nature Reviews Nephrology · doi:10.1038/s41581-018-0072-9 · Cited by 281
Diagnosis and Treatment of Heterozygous Familial Hypercholesterolemia
McGowan, M. P., Dehkordi, S. H. H., Moriarty, P. M., & Duell, P. B. (2019) · Journal of the American Heart Association · doi:10.1161/jaha.119.013225 · Cited by 293
Cholesterol Review: A Metabolically Important Molecule
Schade, D. S., Shey, L., & Eaton, R. P. (2020) · Endocrine Practice · doi:10.4158/ep-2020-0347 · Cited by 298
Apolipoprotein B and Cardiovascular Disease: Biomarker and Potential Therapeutic Target
Behbodikhah, J., Ahmed, S., Elyasi, A., Kasselman, L. J., Leon, J. D., Glass, A. D., & Reiss, A. B. (2021) · Metabolites · doi:10.3390/metabo11100690 · Cited by 299
Anticytokine Agents: Targeting Interleukin Signaling Pathways for the Treatment of Atherothrombosis
Ridker, P. M. (2019) · Circulation Research · doi:10.1161/circresaha.118.313129 · Cited by 260
Floege, J., Barbour, S. J., Cattran, D. C., Hogan, J. J., Nachman, P. H., Tang, S. C. W., Wetzels, J. F. M., Cheung, M., Wheeler, D. C., Winkelmayer, W. C., et al. (2019) · Kidney International · doi:10.1016/j.kint.2018.10.018 · Cited by 263
“, evolocumab, alirocumab) need to be studied in the GN population.(46) Evidence that lipid-lowering therapy in children is beneficial is of poor quality but needs to be explored given their expected longevity.”
BackgroundLanglois, M. R., Chapman, M. J., Cobbaert, C., Mora, S., Remaley, A. T., Ros, E., Watts, G. F., Borén, J., Baum, H., Bruckert, E., et al. (2018) · Clinical Chemistry · doi:10.1373/clinchem.2018.287037 · Cited by 260
Marston, N. A., Giugliano, R. P., Melloni, G. E. M., Park, J.-G., Morrill, V., Blazing, M. A., Ference, B., Stein, E., Stroes, E. S., Braunwald, E., et al. (2022) · JAMA Cardiology · doi:10.1001/jamacardio.2021.5083 · Cited by 262
Self-citationSabatine, M. S., De Ferrari, G. M., Giugliano, R. P., Huber, K., Lewis, B. S., Ferreira, J., Kuder, J. F., Murphy, S. A., Wiviott, S. D., Kurtz, C. E., et al. (2018) · Circulation · doi:10.1161/circulationaha.118.034309 · Cited by 255
Self-citationEffects of Icosapent Ethyl on Total Ischemic Events
Bhatt, D. L., Steg, P. G., Miller, M., Brinton, E. A., Jacobson, T. A., Ketchum, S. B., Doyle, R. T., Juliano, R. A., Jiao, L., Granowitz, C., et al. (2019) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2019.02.032 · Cited by 259
Neurocognitive Function after Cardiac Surgery
Berger, M., Terrando, N., Smith, S. K., Browndyke, J. N., Newman, M. F., & Mathew, J. P. (2018) · Anesthesiology · doi:10.1097/aln.0000000000002194 · Cited by 271
Handelsman, Y., Jellinger, P. S., Guerin, C. K., Bloomgarden, Z. T., Brinton, E. A., Budoff, M. J., Davidson, M. H., Einhorn, D., Fazio, S., Fonseca, V. A., et al. (2020) · Endocrine Practice · doi:10.4158/cs-2020-0490 · Cited by 248
“Outcomes trials with proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors in which achieved LDL-C levels were substantially lower than those in statin trials further reinforced the notion that “lower is better” (24,25).”
InfluentialDiabetes, heart failure, and renal dysfunction: The vicious circles
D, E. B. M. (2019) · Progress in Cardiovascular Diseases · doi:10.1016/j.pcad.2019.07.003 · Cited by 252
Fiolet, A. T. L., Opstal, T. S. J., Mosterd, A., Eikelboom, J. W., Jolly, S. S., KEECH, A. C., Kelly, P. J., Tong, D. C., Layland, J. J., Nidorf, S. M., et al. (2021) · European Heart Journal · doi:10.1093/eurheartj/ehab115 · Cited by 263
Self-citationKoskinas, K. C., Siontis, G. C. M., Piccolo, R., Mavridis, D., Räber, L., Mach, F., & Windecker, S. (2017) · European Heart Journal · doi:10.1093/eurheartj/ehx566 · Cited by 257
ESVM Guideline on peripheral arterial disease
Frank, U., Nikol, S., Belch, J. J. F., Boc, V., Brodmann, M., Carpentier, P., Chraim, A., Canning, C., Dimakakos, E. P., Gottsäter, A., et al. (2019) · VASA · doi:10.1024/0301-1526/a000834 · Cited by 275
Ryan, D. H., Lingvay, I., Colhoun, H. M., Deanfield, J., Emerson, S. S., Kahn, S. E., Kushner, R. F., Marso, S., Plutzky, J., Brown-Frandsen, K., et al. (2020) · American Heart Journal · doi:10.1016/j.ahj.2020.07.008 · Cited by 249
HEART UK consensus statement on Lipoprotein(a): A call to action
Cegla, J., Neely, R. D. G., France, M. W., Ferns, G. A., Byrne, C. D., Halcox, J., Datta, D. B. N., Capps, N. E., Shoulders, C. C., Qureshi, N., et al. (2019) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2019.10.011 · Cited by 248
Qi, Z., Hu, L., Zhang, J., Yang, W., Liu, X., Jia, D., Yao, Z., Chang, L., Pan, G., Zhong, H., et al. (2021) · Circulation · doi:10.1161/circulationaha.120.046290 · Cited by 268
2026 ACC/AHA/AACVPR/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Dyslipidemia
Blumenthal, R. S., Morris, P. B., Gaudino, M., Johnson, H. M., Anderson, T. S., Bittner, V. A., Blankstein, R., Brewer, L. C., Cho, L., de Ferranti, S. D., et al. (2026) · JACC · doi:10.1016/j.jacc.2025.11.016 · Cited by 304
2020 Clinical practice guidelines for Acute ST-segment elevation myocardial infarction
Russian Society of Cardiology (2020) · Russian Journal of Cardiology · doi:10.15829/29/1560-4071-2020-4103 · Cited by 271
Cannon, C. P., de Lemos, J. A., Rosenson, R. S., Ballantyne, C. M., Liu, Y., Gao, Q., Palagashvili, T., Alam, S., Mues, K. E., Bhatt, D. L., et al. (2021) · JAMA Cardiology · doi:10.1001/jamacardio.2021.1810 · Cited by 250
Lee, R. G., Mazzola, A. M., Braun, M. C., Platt, C., Vafai, S. B., Kathiresan, S., Rohde, E., Bellinger, A. M., & Khera, A. V. (2022) · Circulation · doi:10.1161/circulationaha.122.062132 · Cited by 254
Stone, P., Libby, P., & Boden, W. (2022) · JAMA cardiology · doi:10.1001/jamacardio.2022.3926 · Cited by 241
Damask, A., Steg, P. G., Schwartz, G. G., Szarek, M. J., Hagström, E., Badimón, L., Chapman, M. J., Boileau, C., Tsimikas, S., Ginsberg, H. N., et al. (2019) · Circulation · doi:10.1161/circulationaha.119.044434 · Cited by 241
Genetics of Common, Complex Coronary Artery Disease
Musunuru, K., & Kathiresan, S. (2019) · Cell · doi:10.1016/j.cell.2019.02.015 · Cited by 246
PCSK9 and inflammation: role of shear stress, pro-inflammatory cytokines, and LOX-1
Ding, Z., Pothineni, N. V. K., Goel, A., Lüscher, T. F., & Mehta, J. L. (2019) · Cardiovascular Research · doi:10.1093/cvr/cvz313 · Cited by 240
Bartha, I., di Iulio, J., Venter, J. C., & Telenti, A. (2017) · Nature Reviews Genetics · doi:10.1038/nrg.2017.75 · Cited by 234
Coronary heart disease risk: Low-density lipoprotein and beyond
Shaya, G. E., Leucker, T. M., Jones, S. R., Martin, S. S., & Toth, P. P. (2021) · Trends in Cardiovascular Medicine · doi:10.1016/j.tcm.2021.04.002 · Cited by 247
Wright, R. S., Ray, K. K., Raal, F. J., Kallend, D. G., Jaros, M., Koenig, W., Leiter, L. A., Landmesser, U., Schwartz, G. G., Friedman, A., et al. (2021) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2020.12.058 · Cited by 229
Wilson, P. W. F., Polonsky, T. S., Miedema, M. D., Khera, A., Kosinski, A. S., & Kuvin, J. T. (2018) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2018.11.004 · Cited by 239
Orringer, C. E., Blaha, M. J., Blankstein, R., Budoff, M. J., Goldberg, R. B., Gill, E. A., Maki, K. C., Mehta, L. S., & Jacobson, T. A. (2020) · Journal of clinical lipidology · doi:10.1016/j.jacl.2020.12.005 · Cited by 236
The Multifaceted Biology of PCSK9
Seidah, N. G., & Prat, A. (2022) · Endocrine Reviews · doi:10.1210/endrev/bnab035 · Cited by 232
Hepatic cholesterol transport and its role in non-alcoholic fatty liver disease and atherosclerosis
Li, H., Yu, X.-H., Ou, X., Ouyang, X.-P., & Tang, C. (2021) · Progress in Lipid Research · doi:10.1016/j.plipres.2021.101109 · Cited by 237
Dawson, J., Béjot, Y., Christensen, L. M., Marchis, G. M. D., Dichgans, M., Hagberg, G., Heldner, M. R., Milionis, H. J., Li, L., Pezzella, F. R., et al. (2022) · European Stroke Journal · doi:10.1177/23969873221100032 · Cited by 260
Nonalcoholic fatty liver disease in adults: current concepts in etiology, outcomes, and management
Marjot, T., Moolla, A., Cobbold, J. F., Hodson, L., & Tomlinson, J. W. (2020) · Endocrine Reviews · doi:10.1210/endrev/bnz009 · Cited by 228
2021 Clinical Practice Guidelines for Diabetes Mellitus of the Korean Diabetes Association
Hur, K. Y., Moon, M. K., Park, J. S., Kim, S., Lee, S., Yun, J., Baek, J. H., Noh, J., Lee, B., Oh, T. J., et al. (2021) · Diabetes & Metabolism Journal · doi:10.4093/dmj.2021.0156 · Cited by 233
Inclisiran and cardiovascular events: a patient-level analysis of phase III trials
Ray, K. K., Raal, F. J., Kallend, D. G., Jaros, M. J., Köenig, W., Leiter, L. A., Landmesser, U., Schwartz, G. G., Lawrence, D., Friedman, A., et al. (2022) · European Heart Journal · doi:10.1093/eurheartj/ehac594 · Cited by 239
Wein, T. H., Lindsay, M. P., Côté, R., Foley, N. C., Berlingieri, J., Bhogal, S. K., Bourgoin, A., Buck, B. H., Cox, J. L., Davidson, D., et al. (2017) · International Journal of Stroke · doi:10.1177/1747493017743062 · Cited by 227
2023 Chinese guideline for lipid management
Li, J., Zhao, S., Zhao, D. H., Lü, G., Peng, D., Liu, J., Chen, Z., Guo, Y., Wu, N., Yan, S.-K., et al. (2023) · Frontiers in Pharmacology · doi:10.3389/fphar.2023.1190934 · Cited by 241
Piepoli, M. F., Abreu, A., Albus, C., Ambrosetti, M., Brotons, C., Catapano, A. L., Corrà, U., Cosyns, B., Deaton, C., Graham, I. M., et al. (2019) · European Journal of Preventive Cardiology · doi:10.1177/2047487319893035 · Cited by 226
Disorders of lipid metabolism. Clinical Guidelines 2023
Владиславович, Е. М., Kukharchuk, V. V., Сергиенко, И. В., Alieva, A. S., Antsiferov, M. B., Ansheles, A. A., Arabidze, G. G., Dm, A., Arutyunov, G. P., Ахмеджанов, Н. М., et al. (2023) · Russian Journal of Cardiology · doi:10.15829/1560-4071-2023-5471 · Cited by 270
Marston, N., Kamanu, F., Nordio, F., Gurmu, Y., Roselli, C., Sever, P., Pedersen, T. R., KEECH, A. C., Wang, H., Pineda, A. L., et al. (2019) · Circulation · doi:10.1161/circulationaha.119.043805 · Cited by 219
Self-citationWalker, V. M., Smith, G. D., Davies, N. M., & Martin, R. M. (2017) · International Journal of Epidemiology · doi:10.1093/ije/dyx207 · Cited by 216
Paik, D. T., Chandy, M., & Wu, J. C. (2019) · Pharmacological Reviews · doi:10.1124/pr.116.013003 · Cited by 219
Karatasakis, A., Danek, B. A., Karacsonyi, J., Rangan, B. V., Roesle, M. K., Knickelbine, T., Miedema, M. D., Khalili, H., Ahmad, Z., Abdullah, S., et al. (2017) · Journal of the American Heart Association · doi:10.1161/jaha.117.006910 · Cited by 215
Atherosclerotic cardiovascular disease prevention in rheumatoid arthritis
Semb, A. G., Ikdahl, E., Wibetoe, G., Crowson, C. S., & Rollefstad, S. (2020) · Nature Reviews Rheumatology · doi:10.1038/s41584-020-0428-y · Cited by 221
2024 Clinical practice guidelines for Hypertension in adults
Кобалава, Ж. Д., Конради, А. О., Nedogoda, S. V., Shlyakhto, E. V., Arutyunov, G. P., Баранова, Е. И., Барбараш, О. Л., Bobkova, N. V., Boytsov, S. A., Bubnova, M. G., et al. (2024) · Russian Journal of Cardiology · doi:10.15829/1560-4071-2024-6117 · Cited by 274
2018 Guidelines for the management of dyslipidemia
Rhee, E., Kim, H. C., Kim, J. H., Lee, E. Y., Kim, B. J., Kim, E. M., Song, Y., Lim, J. H., Kim, B. J., Choi, S., et al. (2019) · The Korean Journal of Internal Medicine · doi:10.3904/kjim.2019.188 · Cited by 221
Evidence-Based Medical Management of Peripheral Artery Disease
Bevan, G. H., & Solaru, K. W. (2020) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/atvbaha.119.312142 · Cited by 241
Efficacy and safety of evolocumab in chronic kidney disease in the FOURIER trial
Charytan, D. M., Sabatine, M. S., Pedersen, T. R., Im, K., Park, J.-G., Pineda, A. L., Wasserman, S. M., Deedwania, P., Olsson, A. G., Sever, P. S., et al. (2019) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2019.03.513 · Cited by 210
Self-citationBergmark, B. A., Marston, N. A., Bramson, C. R., Curto, M., Ramos, V., Jevne, A., Kuder, J. F., Park, J.-G., Murphy, S. A., Verma, S., et al. (2022) · Circulation · doi:10.1161/circulationaha.122.059266 · Cited by 216
Self-citationGuedeney, P., Giustino, G., Sorrentino, S., Claessen, B. E., Camaj, A., Kalkman, D. N., Vogel, B., Sartori, S., De Rosa, S., Baber, U., et al. (2022) · European Heart Journal · doi:10.1093/eurheartj/ehz430 · Cited by 208
The Lancet Commission on rethinking coronary artery disease: moving from ischaemia to atheroma
Zaman, S. J., Wasfy, J. H., Kapil, V., Ziaeian, B., Parsonage, W. A., Sriswasdi, S., Chico, T., Capodanno, D., Colleran, R., Sutton, N. R., et al. (2025) · The Lancet · doi:10.1016/s0140-6736(25)00055-8 · Cited by 236
PCSK9 monoclonal antibodies for the primary and secondary prevention of cardiovascular disease
Schmidt, A. F., Pearce, L. S., Wilkins, J. T., Overington, J. P., Hingorani, A. D., & Casas, J. P. (2017) · Cochrane Database of Systematic Reviews · doi:10.1002/14651858.cd011748.pub2 · Cited by 203
Sabatine, M. S., Wiviott, S. D., Im, K., Murphy, S. A., & Giugliano, R. P. (2018) · JAMA Cardiology · doi:10.1001/jamacardio.2018.2258 · Cited by 214
Self-citationWelsh, C., Celis-Morales, C. A., Brown, R., Mackay, D. F., Lewsey, J., Mark, P. B., Gray, S. R., Ferguson, L. D., Anderson, J. J., Lyall, D. M., et al. (2019) · Circulation · doi:10.1161/circulationaha.119.041149 · Cited by 191
Liu, L., Li, Z., Zhou, H., Duan, W., Huo, X., Xu, W., Li, S., Nie, X., Liu, H., Liu, J., et al. (2023) · Stroke and Vascular Neurology · doi:10.1136/svn-2023-002998 · Cited by 227
Landmesser, U., Chapman, M. J., Stock, J. K., Amarenco, P., Belch, J. J. F., Borén, J., Farnier, M., Ference, B. A., Gielen, S., Graham, I., et al. (2018) · European Heart Journal · doi:10.1093/eurheartj/ehx549 · Cited by 200
Unmet Need for Adjunctive Dyslipidemia Therapy in Hypertriglyceridemia Management
Ganda, O. P., Bhatt, D. L., Mason, R. P., Miller, M., & Boden, W. E. (2018) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2018.04.061 · Cited by 195
“With the recent availability of proprotein convertase subtilisin/kexin type 9 inhibitors for intensive LDL-C reduction beyond statins (3,72,73), it is worth considering the potential impact of OM3FA supplementation on further reducing residual risk.”
BackgroundTurner, R. M., & Pirmohamed, M. (2019) · Journal of Clinical Medicine · doi:10.3390/jcm9010022 · Cited by 206
Causal Inference in Cancer Epidemiology: What Is the Role of Mendelian Randomization?
Yarmolinsky, J., Wade, K. H., Richmond, R. C., Langdon, R., Bull, C. J., Tilling, K. M., Relton, C. L., Lewis, S. J., Smith, G. D., & Martin, R. M. (2018) · Cancer Epidemiology Biomarkers & Prevention · doi:10.1158/1055-9965.epi-17-1177 · Cited by 189
Metadata
- Authors
- Sabatine, M. S., Giugliano, R. P., Keech, A. C., Honarpour, N., Wiviott, S. D., Murphy, S. A., Kuder, J. F., Wang, H., Liu, T., Wasserman, S. M., Sever, P. S., & Pedersen, T. R.
- Affiliations
- Oslo University Hospital (NO)
- ORCID
- Venue
- New England Journal of Medicine
- Publisher
- Massachusetts Medical Society
- Published
- 2017-05-04
- Volume
- 376
- Issue
- 18
- Pages
- 1713-1722
- ISSN
- 0028-4793 (ISSN-L)
- 1533-4406
- OpenAlex
- W2596179513
- Semantic Scholar
- 993698ddc1fcdfd3e66edebf1904b360eca3b4a8
- Cited by
- 6,138
- References
- 28
- Citations by year
- 2026: 628 · 2025: 589 · 2024: 608 · 2023: 635 · 2022: 623 · 2021: 632 · 2020: 658 · 2019: 637 · 2018: 669 · 2017: 443
- FWCI
- 674.25
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- New England Journal of Medicine (publishedVersion)
- PubMed (publishedVersion)
- Archive ouverte UNIGE (University of Geneva) (publishedVersion, other-oa)
- SZTE Publicatio Repozitórium (University of Szeged) (acceptedVersion, other-oa)
- Zurich Open Repository and Archive (University of Zurich) (acceptedVersion, cc-by-nc)
- IRIS Research product catalog (Sapienza University of Rome) (submittedVersion, other-oa)
- HAL (submittedVersion)
- Ghent University Academic Bibliography (Ghent University) (submittedVersion)
- BOA (University of Milano-Bicocca) (submittedVersion)
- Deakin Research Online (Deakin University) (submittedVersion)
- Figshare (submittedVersion)
- Open Repository and Bibliography (University of Liège) (submittedVersion)
- Archivio Istituzionale della Ricerca - Università degli Studi dell Aquila (submittedVersion)
- Spiral (Imperial College London) (submittedVersion)
- Archive ouverte UNIGE (University of Geneva) (submittedVersion, cc-by)
- Use Siena air (University of Siena) (submittedVersion)
- NORA - Norwegian Open Research Archives (submittedVersion, other-oa)
- Zurich Open Repository and Archive (University of Zurich) (submittedVersion, cc-by-nc)
- Zurich Open Repository and Archive (University of Zurich)
- Funders
- National Institute for Health and Care Research (NF-SI-0513-10059)
- Medical Research Council (MC_EX_MR/M009203/1, MC_PC_14089)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipoproteins and Cardiovascular Health
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Acute Myocardial Infarction Research
- Keywords
- evolocumab, PCSK9 inhibition, LDL cholesterol lowering, atherosclerotic cardiovascular disease, cardiovascular events, myocardial infarction, stroke, cardiovascular mortality, statin therapy, LDL cholesterol levels, new-onset diabetes, injection site reactions, primary prevention of cardiovascular disease, LDL-C lowering therapy
- MeSH terms
- Proprotein Convertase 9, PCSK9 Inhibitors, Aged, Antibodies, Monoclonal, Anticholesteremic Agents, Cardiovascular Diseases, Double-Blind Method, Drug Therapy, Combination, Female, Follow-Up Studies, Humans, Hypercholesterolemia, Cholesterol, LDL, Male, Middle Aged, Incidence, Least-Squares Analysis, Hydroxymethylglutaryl-CoA Reductase Inhibitors, Atherosclerosis, Antibodies, Monoclonal, Humanized
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.
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