Search

Background: Inflammation and coagulation may contribute to the increased risk for atherosclerotic cardiovascular disease (ASCVD) associated with high lipoprotein(a). The association of lipoprotein(a) with ASCVD is stronger in individuals with high versus low high-sensitivity C-reactive protein (hs-CRP), a marker of inflammation., Objectives: Determine the association of lipoprotein(a) with incident ASCVD by levels of coagulation Factor VIII controlling for hs-CRP., Methods: We analyzed data from 6,495 men and women 45 to 84 years of age in the Multi-Ethnic Study of Atherosclerosis (MESA) without prevalent ASCVD at baseline (2000-2002). Lipoprotein(a) mass concentration, Factor VIII coagulant activity, and hs-CRP were measured at baseline and categorized as high or low (≥75 th or <75 th percentile of the distribution). Participants were followed for incident coronary heart disease (CHD) and ischemic stroke through 2015., Results: Over a median follow-up of 13.9 years, there were 390 CHD and 247 ischemic stroke events. The hazard ratio (95%CI) for CHD associated with high lipoprotein(a) (≥40.1 versus <40.1 mg/dL) including adjustment for hs-CRP among participants with low and high Factor VIII was 1.07 (0.80-1.44) and 2.00 (1.33-3.01), respectively (p-value for interaction 0.016). The hazard ratio (95%CI) for CHD associated with high lipoprotein(a) including adjustment for Factor VIII was 1.16 (0.87-1.54) and 2.00 (1.29-3.09) among participants with low and high hs-CRP, respectively (p-value for interaction 0.042). Lp(a) was not associated with ischemic stroke regardless of Factor VIII or hs-CRP levels., Conclusion: High lipoprotein(a) is a risk factor for CHD in adults with high levels of hemostatic or inflammatory markers., (Copyright © 2023. Published by Elsevier Inc.)

Background: Adults with atherosclerotic cardiovascular disease (ASCVD) at very high-risk for recurrent events who have low-density lipoprotein cholesterol ≥ 70 mg/dL despite maximally-tolerated statin therapy are recommended to initiate ezetimibe or a proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitor., Objective: Compare the initiation of ezetimibe and a PCSK9 inhibitor after a myocardial infarction (MI) among very high-risk ASCVD patients by race/ethnicity and sex., Methods: We analyzed data from 374,786 adults ≥ 66 years of age with Medicare fee-for-service coverage who had an MI between July 1, 2015 and December 31, 2018, were not taking ezetimibe or a PCSK9 inhibitor, and had very high-risk ASCVD defined by the 2018 American Heart Association/American College of Cardiology multi-society cholesterol guideline. Pharmacy claims through December 31, 2018 were used to determine ezetimibe and PCSK9 inhibitor initiation., Results: Overall, 6980 (1.9%) beneficiaries initiated ezetimibe, and 1433 (0.4%) initiated a PCSK9 inhibitor. Adjusted hazard ratios (aHR) for ezetimibe initiation among non-Hispanic Black, Hispanic, and Asian versus non-Hispanic White beneficiaries were 0.77 (95% confidence interval [95%CI]: 0.70-0.86), 0.92 (95%CI: 0.76-1.11) and 0.73 (95%CI: 0.59-0.89), respectively. Compared to non-Hispanic White beneficiaries, the aHRs for PCSK9 inhibitor initiation were 0.63 (95%CI: 0.48-0.81) among non-Hispanic Black, 0.70 (95%CI: 0.43-1.13) among Hispanic, and 0.93 (95%CI: 0.62-1.39) among Asian beneficiaries. The aHRs for ezetimibe and PCSK9 inhibitor initiation comparing women to men were 1.11 (95%CI: 1.06-1.17) and 1.13 (95%CI: 1.01-1.25), respectively., Conclusion: There are race/ethnic and sex disparities in the initiation of ezetimibe and a PCSK9 inhibitor following MI among very high-risk ASCVD patients., (Copyright © 2021 National Lipid Association. Published by Elsevier Inc. All rights reserved.)

Background: High-intensity statins, beta-blockers, angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, and antiplatelet agents (ie, intensive medical management) reduce coronary heart disease (CHD) risk after myocardial infarction (MI)., Objective: The objective of the study was to determine the risk of CHD events or death despite receiving intensive medical management after MI., Methods: We studied 16,853 United States adults with health insurance in the MarketScan and Medicare databases who underwent percutaneous coronary intervention while hospitalized for MI between January 1, 2014 and June 30, 2015 and received intensive medical management within 30 days after hospital discharge. MI, CHD, and all-cause mortality rates from 30 days after hospital discharge through December 31, 2015 were compared with 67,412 individuals in each of three groups: (1) the general MarketScan and Medicare populations, (2) with diabetes, and (3) with a CHD history., Results: Among beneficiaries intensively medically managed after their MI, recurrent MI, CHD events, and all-cause mortality rates were 47.1, 72.0, and 57.5 per 1000 person-years, respectively. The multivariable-adjusted hazard ratio (95% CI) comparing intensively medically managed beneficiaries after MI to the general population, those with diabetes, and those with a history of CHD were 8.54 (7.52-9.70), 7.40 (6.61-8.28), and 5.45 (4.92-6.05), respectively, for recurrent MI; 7.82 (7.07-8.64), 6.27 (5.74-6.86), and 4.45 (4.10-4.82), respectively, for CHD events; and 1.15 (1.05-1.25), 1.05 (0.97-1.14), and 1.06 (0.97-1.15), respectively, for all-cause mortality., Conclusion: Substantial residual risk for MI and CHD events remains despite intensive medical management after MI., (Copyright © 2020 National Lipid Association. Published by Elsevier Inc. All rights reserved.)

Background: The Atherothrombosis Intervention in Metabolic Syndrome with Low HDL/High Triglycerides and Impact on Global Health Outcomes trial showed no incremental benefit of extended-release niacin (ERN) therapy added to simvastatin in subjects with cardiovascular disease (CVD)., Objectives: To examine the effects of ERN treatment on lipoprotein particles and GlycA, a new marker of systemic inflammation, and their relations with incident CVD events including mortality., Methods: GlycA and very low-density lipoprotein, low-density lipoprotein (LDL), and high-density lipoprotein (HDL) particle subclasses were quantified by nuclear magnetic resonance spectroscopy using available stored baseline (n = 2754) and 1-year in-trial (n = 2581) samples. Associations with CVD events and all-cause mortality were assessed using multivariable Cox proportional hazards regression adjusted for age, sex, diabetes, treatment assignment, and lipoproteins., Results: Compared to placebo, ERN treatment lowered very low-density lipoprotein and LDL and increased HDL particle concentrations, increased LDL and HDL particle sizes (all P < .0001), but did not affect GlycA. Baseline and in-trial GlycA levels were associated with increased risk of CVD events: hazard ratio (HR) per SD increment, 1.17 (95% confidence interval [CI], 1.06-1.28) and 1.13 (1.02-1.26), respectively. However, none of the lipoprotein particle classes or subclasses was associated with incident CVD. By contrast, all-cause mortality was significantly associated with both GlycA (baseline HR: 1.46 [1.22-1.75]; in-trial HR: 1.41 [1.24-1.60]) and low levels of small HDL particles (baseline HR: 0.69 [0.56-0.86]; in-trial HR: 0.69 [0.56-0.86])., Conclusions: This Atherothrombosis Intervention in Metabolic Syndrome with Low HDL/High Triglycerides and Impact on Global Health Outcomes trial post hoc substudy indicates that inflammation, as indexed by GlycA, is unaffected by ERN treatment but is significantly associated with the residual risk of CVD and death in patients treated to low levels of LDL cholesterol., (Copyright © 2018 National Lipid Association. Published by Elsevier Inc. All rights reserved.)

The National Lipid Association's Safety Task Force convened a consensus conference of experts to develop a position statement on cognitive function to revise and update that published originally by the Association in the 2006 assessment of statin safety by a panel of neurologists. The current expert panel was charged with addressing the specific issue of potential adverse cognitive effects attributable to statins. Search strategies recently used in systematic reviews were used to identify relevant evidence using keywords and topics via Medline searches from 1966 to December 2013. Manual searches of bibliographies were also conducted. Panel members were asked to use the evidence to formulate answers to a series of questions of relevance to the subject matter. The strength of recommendations and quality of evidence were graded using accepted contemporary definitions and procedures. Recommendations to patients, health professionals, and researchers were put forth by the panel to aid in daily clinical decision making, and in future research endeavors., (Copyright © 2014 National Lipid Association. Published by Elsevier Inc. All rights reserved.)

Background: Although low-density lipoprotein cholesterol (LDL-C) is recommended as the primary marker to guide lipid-lowering therapy, some data suggest non-high-density lipoprotein cholesterol (non-HDL-C) may better reflect coronary heart disease risk. Discordance between these measures has not been evaluated., Methods: We used data from the National Health and Nutrition Examination Surveys 2005-2010 (n = 4986) to examine the discordance between these lipid parameters. Elevated levels of non-HDL-C and LDL-C were defined by using the 2004 Adult Treatment Panel III guidelines., Results: The prevalence of high non-HDL-C and LDL-C was 22.7% and 24.5%, respectively. Of participants with high non-HDL-C, 9.7% had normal LDL-C, whereas 15.7% of participants with high LDL-C had normal non-HDL-C. We estimate 3.9 million US adults had high non-HDL-C and normal LDL-C, whereas 6.8 million US adults had high LDL-C and normal non-HDL-C. Persons with high non-HDL-C and normal LDL-C were older, more likely to be men, Hispanic, and have impaired fasting glucose, diabetes metabolic syndrome, and more risk factors for coronary heart disease., Conclusions: Substantial discordance exists between high non-HDL-C and high LDL-C among US adults. Reliance on either single measure could result in failure to classify cardiovascular heart disease risks appropriately., (Copyright © 2014 National Lipid Association. Published by Elsevier Inc. All rights reserved.)

Early coronary revascularization has been shown to reduce major adverse cardiovascular events in patients with acute coronary syndromes. In patients with stable coronary heart disease (CHD), however, coronary revascularization does not reduce death or myocardial infarction compared to intensive medical therapy. The Clinical Outcomes Utilizing Revascularization and Aggressive Drug Evaluation (COURAGE) trial was the first to study whether coronary revascularization performed in addition to medical therapy, rather than as an alternative, would reduce death or myocardial infarction in patients with stable CHD. Between 1999 and 2004, 2287 patients were enrolled in 50 centers throughout Canada and the United States. After a median follow-up of 4.6 years, revascularization performed in addition to intensive medical therapy did not result in reduced mortality or myocardial infarction compared to medical therapy alone. At the end of follow-up, anginal control was similar in both groups, although patients receiving medical therapy only did require more antianginal medications, and one-third ultimately required revascularization. We review the strengths, limitations, and clinical relevance of the COURAGE trial in the context of the current literature on the benefits of medical management and coronary revascularization in patients with stable CHD.