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
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Items 401–500 of 6,144
Murphy, S. A., Pedersen, T. R., Gaciong, Z. A., Češka, R., Владиславович, Е. М., Connolly, D. L., Jukema, J. W., Tóth, K., Tikkanen, M. J., Im, K., et al. (2019) · JAMA Cardiology · doi:10.1001/jamacardio.2019.0886 · Cited by 105
Self-citationWong, N. D., Toth, P. P., & Amsterdam, E. A. (2019) · Trends in Cardiovascular Medicine · doi:10.1016/j.tcm.2019.11.013 · Cited by 105
ACC/AHA lipid guidelines: Personalized care to prevent cardiovascular disease
Reiter–Brennan, C., Osei, A. D., Uddin, S. M. I., Orimoloye, O. A., Obisesan, O. H., Mirbolouk, M., Blaha, M. J., & Dzaye, O. D. A. (2020) · Cleveland Clinic Journal of Medicine · doi:10.3949/ccjm.87a.19078 · Cited by 108
New and Emerging Therapies for Reduction of LDL-Cholesterol and Apolipoprotein B
Nurmohamed, N. S., Návar, A. M., & Kastelein, J. J. P. (2021) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2020.11.079 · Cited by 116
Safety and Efficacy of Obicetrapib in Patients at High Cardiovascular Risk
Nicholls, S. J., Nelson, A. J., Ditmarsch, M., Kastelein, J. J. P., Ballantyne, C. M., Ray, K. K., Návar, A. M., Nissen, S. E., Harada‐Shiba, M., Curcio, D. L., et al. (2025) · New England Journal of Medicine · doi:10.1056/nejmoa2415820 · Cited by 116
Clinical Efficacy and Safety of Evolocumab in High-Risk Patients Receiving a Statin
Giugliano, R. P., KEECH, A. C., Murphy, S. A., Huber, K., Tokgozoglu, S. L., Lewis, B. S., Ferreira, J., Pineda, A. L., Somaratne, R. M., Sever, P., et al. (2017) · JAMA Cardiology · doi:10.1001/jamacardio.2017.3944 · Cited by 105
Self-citationRay, K. K., Leiter, L. A., Müller‐Wieland, D., Cariou, B., Colhoun, H. M., Henry, R. R., Tinahones, F. J., Bujas‐Bobanovic, M., Domenger, C., Letierce, A., et al. (2018) · Diabetes Obesity and Metabolism · doi:10.1111/dom.13257 · Cited by 104
Cholesterol Mass Efflux Capacity, Incident Cardiovascular Disease, and Progression of Carotid Plaque
Shea, S., Stein, J. H., Jorgensen, N. W., McClelland, R. L., Tascau, L., Shrager, S., Heinecke, J. W., Yvan‐Charvet, L., & Tall, A. R. (2018) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/atvbaha.118.311366 · Cited by 109
Medical Therapy for Long-Term Prevention of Atherothrombosis Following an Acute Coronary Syndrome
Gallone, G., Baldetti, L., Pagnesi, M., Latib, A., Colombo, A., Libby, P., & Giannini, F. (2018) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2018.09.052 · Cited by 104
Hong, J. C., Blankstein, R., Shaw, L. J., Padula, W. V., Arrieta, A., Fialkow, J. A., Blumenthal, R. S., Blaha, M. J., Krumholz, H. M., & Nasir, K. (2017) · JACC: Cardiovascular Imaging · doi:10.1016/j.jcmg.2017.04.014 · Cited by 101
Marston, N., Gurmu, Y., Melloni, G. E. M., Bonaca, M. P., Gencer, B., Sever, P. S., Pedersen, T. R., KEECH, A. C., Roselli, C., Lubitz, S. A., et al. (2020) · Circulation · doi:10.1161/circulationaha.120.046397 · Cited by 104
Self-citationShokoples, B. G., Paradis, P., & Schiffrin, E. L. (2020) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/atvbaha.120.315116 · Cited by 104
PCSK9 Inhibition: From Current Advances to Evolving Future
Liu, C., Chen, J., Chen, H., Zhang, T., He, D., Luo, Q., Chi, J., Hong, Z., Liao, Y., Zhang, S., et al. (2022) · Cells · doi:10.3390/cells11192972 · Cited by 108
Can LDL cholesterol be too low? Possible risks of extremely low levels
OLSSON, A. G., Angelin, B., Assmann, G., Binder, C. J., Björkhem, I., Cedazo-Mı́nguez, Á., Cohen, J. C., von Eckardstein, A., Farinaro, E., Müller‐Wieland, D., et al. (2017) · Journal of Internal Medicine · doi:10.1111/joim.12614 · Cited by 102
Orringer, C. E., Jacobson, T. A., Saseen, J. J., Brown, A. S., Gotto, A. M., Ross, J. L., & Underberg, J. A. (2017) · Journal of clinical lipidology · doi:10.1016/j.jacl.2017.05.001 · Cited by 103
The PCSK9 revolution: Current status, controversies, and future directions
Warden, B. A., Fazio, S., & Shapiro, M. D. (2019) · Trends in Cardiovascular Medicine · doi:10.1016/j.tcm.2019.05.007 · Cited by 103
Schwartz, G. G., Steg, P. G., Bhatt, D. L., Bittner, V., Díaz, R., Goodman, S. G., Jukema, J. W., Kim, Y.-U., Li, Q. H., Manvelian, G. Z., et al. (2021) · Circulation · doi:10.1161/circulationaha.120.049447 · Cited by 102
Meta-Analysis of Inclisiran for the Treatment of Hypercholesterolemia
Khan, S. A., Naz, A., Qamar Masood, M., & Shah, R. (2020) · The American Journal of Cardiology · doi:10.1016/j.amjcard.2020.08.018 · Cited by 98
Inclisiran: a new promising agent in the management of hypercholesterolemia
Kosmas, C. E., Muñoz Estrella, A., Sourlas, A., Silverio, D., Hilario, E., Montan, P. D., & Guzman, E. (2018) · Diseases · doi:10.3390/diseases6030063 · Cited by 99
“To that effect, evolocumab and alirocumab, two human monoclonal antibodies directed against PCSK9, given on a background of statin therapy, have been shown to markedly decrease LDL-C levels and significantly reduce cardiovascular risk [14,15].”
BackgroundChamberlain, J. J., Johnson, E. L., Leal, S., Rhinehart, A. S., Shubrook, J. H., & Peterson, L. (2018) · Annals of Internal Medicine · doi:10.7326/m18-0222 · Cited by 105
Jang, H., Lee, S. E., Yang, J., Lee, H.-C., Shin, D., Lee, H., Lee, J., Jin, S., Kim, S., Lee, S. J., et al. (2019) · European Heart Journal · doi:10.1093/eurheartj/ehz566 · Cited by 100
Clonal hematopoiesis in cardiovascular disease and therapeutic implications
Tall, A. R., & Fuster, J. J. (2022) · Nature Cardiovascular Research · doi:10.1038/s44161-021-00015-3 · Cited by 104
Evidence of an anti-inflammatory effect of PCSK9 inhibitors within the human atherosclerotic plaque
Marfella, R., Prattichizzo, F., Sardu, C., Paolisso, P., D’Onofrio, N., Scisciola, L., Grotta, R. L., Frigé, C., Ferraraccio, F., Panarese, I., et al. (2023) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2023.06.971 · Cited by 103
Williams, M. C., Wereski, R., Tuck, C. E., Adamson, P. D., Shah, A. S. V., van Beek, E. J. R., Roditi, G., Berry, C., Boon, N. A., Flather, M., et al. (2025) · The Lancet · doi:10.1016/s0140-6736(24)02679-5 · Cited by 108
How to use Mendelian randomization to anticipate the results of randomized trials
Ference, B. A. (2018) · European Heart Journal · doi:10.1093/eurheartj/ehx462 · Cited by 96
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BackgroundResultGutierrez, J. A., Aday, A. W., Patel, M. R., & Jones, W. S. (2019) · Circulation Cardiovascular Interventions · doi:10.1161/circinterventions.119.007385 · Cited by 103
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Ugovšek, S., & Šebeštjen, M. (2021) · Biomolecules · doi:10.3390/biom12010026 · Cited by 102
Tremblay, F., Xiong, Q., Shah, S. S., Ko, C., Kelly, K., Morrison, M. S., Giancarlo, C., Ramírez, R. N., Hildebrand, E. M., Voytek, S. B., et al. (2025) · Nature Medicine · doi:10.1038/s41591-025-03508-x · Cited by 116
The Interplay of Lipids, Lipoproteins, and Immunity in Atherosclerosis
Pirillo, A., Bonacina, F., Norata, G. D., & Catapano, A. L. (2018) · Current Atherosclerosis Reports · doi:10.1007/s11883-018-0715-0 · Cited by 97
Wang, X., Yan, J., Wang, L., Pan, D., Xu, Y., Wang, F., Sheng, J., Li, X., & Yang, M. (2020) · Theranostics · doi:10.7150/thno.47601 · Cited by 97
JCS 2018 Guideline on Diagnosis of Chronic Coronary Heart Diseases
Yamagishi, M., Tamaki, N., Akasaka, T., Ikeda, T., Ueshima, K., Uemura, S., Otsuji, Y., Kihara, Y., Kimura, K., Kimura, T., et al. (2021) · Circulation Journal · doi:10.1253/circj.cj-19-1131 · Cited by 100
Williams, S. A., Ostroff, R., Hinterberg, M. A., Coresh, J., Ballantyne, C. M., Matsushita, K., Mueller, C. E., Walter, J., Jonasson, C., Holman, R. R., et al. (2022) · Science Translational Medicine · doi:10.1126/scitranslmed.abj9625 · Cited by 97
Anti-inflammatory Nanomedicine for Cardiovascular Disease
Katsuki, S., Matoba, T., Koga, J., Nakano, K., & Egashira, K. (2017) · Frontiers in Cardiovascular Medicine · doi:10.3389/fcvm.2017.00087 · Cited by 97
Effect of Access to Prescribed PCSK9 Inhibitors on Cardiovascular Outcomes
Myers, K. D., Farboodi, N., Mwamburi, M., Howard, W. H. R., Staszak, D., Gidding, S. S., Baum, S. J., Wilemon, K. A., & Rader, D. J. (2019) · Circulation Cardiovascular Quality and Outcomes · doi:10.1161/circoutcomes.118.005404 · Cited by 96
Amarenco, P. (2020) · New England Journal of Medicine · doi:10.1056/nejmcp1908837 · Cited by 96
A Comprehensive Review of PCSK9 Inhibitors
Coppinger, C., Movahed, M. R., Azemawah, V., Peyton, L., Gregory, J., & Hashemzadeh, M. (2022) · Journal of Cardiovascular Pharmacology and Therapeutics · doi:10.1177/10742484221100107 · Cited by 103
Atherosclerosis With Immune Checkpoint Inhibitor Therapy
Suero‐Abreu, G. A., Zanni, M. V., & Neilan, T. G. (2022) · JACC CardioOncology · doi:10.1016/j.jaccao.2022.11.011 · Cited by 104
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Emdin, C. A., Khera, A. V., Chaffin, M. D., Klarin, D. M., Natarajan, P., Aragam, K. G., Haas, M. E., Bick, A. G., Zekavat, S. M., Nomura, A., et al. (2018) · Nature Communications · doi:10.1038/s41467-018-03911-8 · Cited by 90
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Katzmann, J. L., Packard, C. J., Chapman, M. J., Katzmann, I., & Laufs, U. (2020) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2020.05.070 · Cited by 99
Cognition After Lowering LDL-Cholesterol With Evolocumab
Gencer, B., Mach, F., Guo, J., Im, K., Ruzza, A., Wang, H., Kurtz, C. E., Pedersen, T. R., KEECH, A. C., Ott, B. R., et al. (2020) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2020.03.039 · Cited by 94
Self-citationColchicine’s Role in Cardiovascular Disease Management
Buckley, L. F., & Libby, P. (2024) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/atvbaha.124.319851 · Cited by 99
Impact of Apolipoprotein(a) Isoform Size on Lipoprotein(a) Lowering in the HPS2-THRIVE Study
Parish, S., Hopewell, J. C., Hill, M. R., Marcovina, S., Valdes-Marquez, E., Haynes, R., Offer, A., Pedersen, T. R., Baigent, C., Collins, R., et al. (2018) · Circulation: Genomic and Precision Medicine · doi:10.1161/circgen.117.001696 · Cited by 93
Self-citationGenetic and In Vitro Inhibition of PCSK9 and Calcific Aortic Valve Stenosis
Perrot, N., Valerio, V., Moschetta, D., Boekholdt, S. M., Dina, C., Chen, H. Y., Abner, E., Martinsson, A., Manikpurage, H. D., Rigade, S., et al. (2020) · JACC: Basic to Translational Science · doi:10.1016/j.jacbts.2020.05.004 · Cited by 91
“PCSK9 inhibitors have been shown to substantially lower LDL-C levels in various populations and reduce the risk of adverse cardiovascular outcomes in patients at high cardiovascular risk (10,11).”
BackgroundPhysiological and therapeutic regulation of PCSK9 activity in cardiovascular disease
Glerup, S., Schulz, R., Laufs, U., & Schlüter, K. (2017) · Basic Research in Cardiology · doi:10.1007/s00395-017-0619-0 · Cited by 95
Clark, D., Nicholls, S. J., John, J. S., Elshazly, M. B., Kapadia, S. R., Tuzcu, E. M., Nissen, S. E., & Puri, R. (2018) · European Heart Journal · doi:10.1093/eurheartj/ehy209 · Cited by 93
Kaasenbrood, L., Bhatt, D. L., Dorresteijn, J. A. N., Wilson, P. W. F., D’Agostino, R. B., Massaro, J. M., van der Graaf, Y., Cramer, M. J., Kappelle, L. J., de Borst, G. J., et al. (2018) · Journal of the American Heart Association · doi:10.1161/jaha.118.009217 · Cited by 102
PCSK9 Inhibitors: Mechanism of Action, Efficacy, and Safety
Roth, E. M., & Davidson, M. H. (2018) · Reviews in Cardiovascular Medicine · doi:10.3909/ricm19s1s0002 · Cited by 100
Advances in rehabilitation for chronic diseases: improving health outcomes and function
Richardson, C. R., Franklin, B. A., Moy, M. L., & Jackson, E. A. (2019) · BMJ · doi:10.1136/bmj.l2191 · Cited by 102
Ray, K. K., Corral, P., Morales, E., & Nicholls, S. J. (2019) · The Lancet · doi:10.1016/s0140-6736(19)31950-6 · Cited by 94
D’Onofrio, N., Prattichizzo, F., Marfella, R., Sardu, C., Martino, E., Scisciola, L., Marfella, L., Grotta, R. L., Frigé, C., Paolisso, G., et al. (2023) · Theranostics · doi:10.7150/thno.80289 · Cited by 93
Adverse Events Associated With PCSK 9 Inhibitors: A Real‐World Experience
Gürgöze, M. T., Muller-Hansma, A. H. G., Schreuder, M. M., Galema‐Boers, A. M. H., Boersma, E. H., & van Lennep, J. E. R. (2018) · Clinical Pharmacology & Therapeutics · doi:10.1002/cpt.1193 · Cited by 92
Lipoprotein(a) and Cardiovascular Disease in Chinese Population
Li, J., Ma, C.-S., Zhao, D. H., Yan, X.-W., Li, J., Ma, C., Zhao, D. H., Yan, X.-W., Ye, P., Chen, H., et al. (2022) · JACC Asia · doi:10.1016/j.jacasi.2022.08.015 · Cited by 96
Goldstein, L. B., Toth, P. P., Dearborn, J. L., Giugliano, R. P., Hirsh, B. J., Peña, J. M., Selim, M. H., & Woo, D. (2023) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/atv.0000000000000164 · Cited by 99
Self-citationCarotid Artery Stenosis: Medical Therapy, Surgery, and Stenting
Dharmakidari, S., Bhattacharya, P. D., & Chaturvedi, S. (2017) · Current Neurology and Neuroscience Reports · doi:10.1007/s11910-017-0786-2 · Cited by 91
Fonarow, G. C., van Hout, B., Villa, G., Arellano, J., & Lindgren, P. (2019) · JAMA Cardiology · doi:10.1001/jamacardio.2019.1647 · Cited by 91
Kim, N. H., Han, K. H., Choi, J., Lee, J., & Kim, S. G. (2019) · BMJ · doi:10.1136/bmj.l5125 · Cited by 95
High Sensitivity C-reactive Protein (hsCRP) and its Implications in Cardiovascular Outcomes
Denegri, A., & Boriani, G. (2020) · Current Pharmaceutical Design · doi:10.2174/1381612826666200717090334 · Cited by 98
Zarić, B. L., Radovanović, J., Gluvic, Z. M., Stewart, A. J., Essack, M., Motwalli, O., Gojobori, T., & Isenović, E. R. (2020) · Frontiers in Immunology · doi:10.3389/fimmu.2020.551758 · Cited by 94
Cardiorenal diseases in type 2 diabetes mellitus: clinical trials and real-world practice
Lim, L.-L., Chow, E., & Chan, J. C. N. (2023) · Nature Reviews Endocrinology · doi:10.1038/s41574-022-00776-2 · Cited by 91
Cui, D., Yu, X., Guan, Q., Shen, Y., Liao, J., Liu, Y., & Su, Z. (2025) · Molecular Biomedicine · doi:10.1186/s43556-025-00321-3 · Cited by 126
Remnant lipoproteins: are they equal to or more atherogenic than LDL?
Salinas, C. A. A., & Chapman, M. J. (2020) · Current Opinion in Lipidology · doi:10.1097/mol.0000000000000682 · Cited by 87
LPA Variants Are Associated With Residual Cardiovascular Risk in Patients Receiving Statins
Wei, W., Li, X., Feng, Q., Kubo, M., Kullo, I. J., Peissig, P. L., Karlson, E. W., Jarvik, G. P., Lee, M. T. M., Shang, N., et al. (2018) · Circulation · doi:10.1161/circulationaha.117.031356 · Cited by 93
Apaijai, N., Moisescu, D. M., Palee, S., McSweeney, C. M., Saiyasit, N., Maneechote, C., Boonnag, C., Chattipakorn, N., & Chattipakorn, S. C. (2019) · Journal of the American Heart Association · doi:10.1161/jaha.118.010838 · Cited by 90
Toth, P. P., & Banach, M. (2019) · Methodist DeBakey Cardiovascular Journal · doi:10.14797/mdcj-15-1-23 · Cited by 99
PCSK9 and LRP5 in macrophage lipid internalization and inflammation
Badimón, L., Luquero, A., Crespo, J., Peña, E., & Borrell-Pagés, M. (2020) · Cardiovascular Research · doi:10.1093/cvr/cvaa254 · Cited by 91
PCSK9 and atherosclerosis: Looking beyond LDL regulation
Ragusa, R., Basta, G., Neglia, D., Caterina, R. D., Turco, S. D., & Caselli, C. (2020) · European Journal of Clinical Investigation · doi:10.1111/eci.13459 · Cited by 92
Rubino, J., MacDougall, D. E., Sterling, L. R., Hanselman, J. C., & Nicholls, S. J. (2020) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2020.12.023 · Cited by 96
Krychtiuk, K. A., Ahrens, I., Drexel, H., Halvorsen, S., Hassager, C., Huber, K., Kurpas, D., Niessner, A., Schiele, F., Semb, A. G., et al. (2022) · European Heart Journal Acute Cardiovascular Care · doi:10.1093/ehjacc/zuac123 · Cited by 100
O’Connell, E. M., & Lohoff, F. W. (2020) · Frontiers in Neuroscience · doi:10.3389/fnins.2020.00609 · Cited by 93
Annemans, L., Packard, C. J., Briggs, A. H., & Ray, K. K. (2017) · European Heart Journal · doi:10.1093/eurheartj/ehx710 · Cited by 91
Karagiannis, A. D., Liu, M., Toth, P. P., Zhao, S., Agrawal, D. K., Libby, P., & Chatzizisis, Y. S. (2018) · Current Atherosclerosis Reports · doi:10.1007/s11883-018-0718-x · Cited by 93
Observational study of the medical management of patients with peripheral artery disease
Saratzis, A. N., Jaspers, N. E. M., Gwilym, B. L., Thomas, O., Tsui, A., Lefroy, R., Parks, M., Htun, Mera, Z., Thatcher, A. J., et al. (2019) · British journal of surgery · doi:10.1002/bjs.11214 · Cited by 87
Penson, P. E., Long, D. L., Howard, G., Toth, P. P., Muntner, P., Howard, V. J., Safford, M. M., Jones, S. R., Martin, S. S., Mazidi, M., et al. (2018) · European Heart Journal · doi:10.1093/eurheartj/ehy533 · Cited by 89
RNA Therapeutics in Cardiovascular Precision Medicine
Laina, A., Gatsiou, A., Georgiopoulos, G. A., Stamatelopoulos, K. S., & Stellos, K. (2018) · Frontiers in Physiology · doi:10.3389/fphys.2018.00953 · Cited by 90
Novel strategies to target proprotein convertase subtilisin kexin 9: beyond monoclonal antibodies
Seidah, N. G., Prat, A., Pirillo, A., Catapano, A. L., & Norata, G. D. (2019) · Cardiovascular Research · doi:10.1093/cvr/cvz003 · Cited by 91
Sinnaeve, P., Schwartz, G. G., WOJDYLA, D. M., et al. (2019) · European Heart Journal · doi:10.1093/eurheartj/ehz809 · Cited by 88
Qian, S., You, S., Sun, Y.-M., Wu, Q., Wang, X., Tang, W., Dong, X.-F., Liu, C.-F., Xu, T., Cao, Y.-J., et al. (2021) · Circulation Cardiovascular Imaging · doi:10.1161/circimaging.120.010953 · Cited by 69
Inflammation and Cardiovascular Disease: The Future
Arnold, N., Lechner, K., Waldeyer, C., Shapiro, M. D., & Köenig, W. (2021) · European Cardiology Review · doi:10.15420/ecr.2020.50 · Cited by 93
IL-1 family cytokines in cardiovascular disease
Pfeiler, S., Winkels, H., Kelm, M., & Gerdes, N. (2017) · Cytokine · doi:10.1016/j.cyto.2017.11.009 · Cited by 88
Fox, K. M., Tai, M., Kostev, K., Hatz, M., Qian, Y., & Laufs, U. (2017) · Clinical Research in Cardiology · doi:10.1007/s00392-017-1193-z · Cited by 89
PCSK9 inhibition alters the lipidome of plasma and lipoprotein fractions
Hilvo, M., Simolin, H., Metso, J., Ruuth, M., Öörni, K., Jauhiainen, M., Laaksonen, R., & Baruch, A. (2018) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2018.01.004 · Cited by 87
Gragnano, F., & Calabrò, P. (2018) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2018.01.012 · Cited by 89
PCSK9 Inhibition: Insights From Clinical Trials and Future Prospects
Katzmann, J. L., Gouni‐Berthold, I., & Laufs, U. (2020) · Frontiers in Physiology · doi:10.3389/fphys.2020.595819 · Cited by 91
Atherosclerotic plaque stabilization and regression: a review of clinical evidence
Sarraju, A., & Nissen, S. E. (2024) · Nature Reviews Cardiology · doi:10.1038/s41569-023-00979-8 · Cited by 96
Mazhar, F., Faucon, A., Fu, E. L., Szummer, K. E., Mathisen, J., Gerward, S., Reuter, S. B., Marx, N., Mehran, R., & Carrero, J. J. (2024) · European Heart Journal · doi:10.1093/eurheartj/ehae557 · Cited by 95
Genetics, Dyslipidemia, and Cardiovascular Disease: New Insights
Stein, R., Ferrari, F., & Scolari, F. (2019) · Current Cardiology Reports · doi:10.1007/s11886-019-1161-5 · Cited by 83
Nomura, A., Won, H., Khera, A. V., Takeuchi, F., Ito, K., McCarthy, S., Emdin, C. A., Klarin, D. M., Natarajan, P., Zekavat, S. M., et al. (2017) · Circulation Research · doi:10.1161/circresaha.117.311145 · Cited by 86
Harvey, P. D., Sabbagh, M. N., Harrison, J., Ginsberg, H. N., Chapman, M. J., Manvelian, G. Z., Moryusef, A., Mandel, J., & Farnier, M. (2017) · European Heart Journal · doi:10.1093/eurheartj/ehx661 · Cited by 89
Lipid and Non-lipid Factors Affecting Macrophage Dysfunction and Inflammation in Atherosclerosis
Gibson, M. S., Domingues, N. S., & Vieira, O. V. (2018) · Frontiers in Physiology · doi:10.3389/fphys.2018.00654 · Cited by 82
PCSK9 inhibitors for treating hypercholesterolemia
Pasta, A., Cremonini, A. L., Pisciotta, L., Buscaglia, A., Porto, I., Barra, F., Ferrero, S., Brunelli, C., & Rosa, G. M. (2020) · Expert Opinion on Pharmacotherapy · doi:10.1080/14656566.2019.1702970 · Cited by 88
Handelsman, Y., & Lepor, N. E. (2018) · Journal of the American Heart Association · doi:10.1161/jaha.118.008953 · Cited by 88
PCSK9 inhibition in the management of familial hypercholesterolemia
Ogura, M. (2018) · Journal of Cardiology · doi:10.1016/j.jjcc.2017.07.002 · Cited by 84
“Regarding adverse reactions, while there were slightly more injection site reactions in the evolocumab group, no difference was observed between the groups regarding new-onset diabetes and cognitive impairment [16].”
BackgroundNutraceuticals as therapeutic agents for atherosclerosis
Moss, J. W. E., Williams, J. O., & Ramji, D. P. (2018) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2018.02.006 · Cited by 89
Short-Term Global Cardiovascular Disease Risk Prediction in Older Adults
Saeed, A., Nambi, V., Sun, W., Virani, S. S., Taffet, G. E., Deswal, A. M., Selvin, E., Matsushita, K., Wagenknecht, L. E., Hoogeveen, R. C., et al. (2018) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2018.02.050 · Cited by 86
Oesterle, A., & Liao, J. K. (2018) · Current Vascular Pharmacology · doi:10.2174/1570161116666180817155058 · Cited by 82
Dyslipidemia Management in Adults With Diabetes
Lazarte, J., & Hegele, R. A. (2019) · Canadian Journal of Diabetes · doi:10.1016/j.jcjd.2019.07.003 · Cited by 88
Lipoprotein(a) in atherosclerosis: from pathophysiology to clinical relevance and treatment options
Likozar, A. R., Zavrtanik, M., & Šebeštjen, M. (2020) · Annals of Medicine · doi:10.1080/07853890.2020.1775287 · Cited by 91
Management of Dyslipidemia in Patients with Non-Alcoholic Fatty Liver Disease
Martin, A., Lang, S., Goeser, T., Demir, M., Steffen, H., & Kasper, P. (2022) · Current Atherosclerosis Reports · doi:10.1007/s11883-022-01028-4 · Cited by 93
Existing and emerging strategies to lower Lipoprotein(a)
Schwartz, G. G., & Ballantyne, C. M. (2022) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2022.04.020 · Cited by 86
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
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