Niacin for primary and secondary prevention of cardiovascular events

Saccilotto, Ramon; Kasenda, Benjamin; Nordmann, Alain; Briel, Matthias

doi:10.1002/14651858.cd009744

Cited by 2 publications

(3 citation statements)

References 43 publications

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“…For example, trials adding fibrates and niacin to statins showed very small effects on LDL-C and no clinical outcomes benefit. 19,20 In sum, these studies suggested the need for new agents that have far greater LDL-C lowering effects.…”

Section: Limits Of Statin Therapymentioning

confidence: 99%

<p>Cardiovascular Outcomes and Proprotein Convertase Subtilisin/Kexin Type 9 Inhibitors: Current Data and Future Prospects</p>

Duprez¹,

Handelsman²,

Koren³

2020

VHRM

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Cardiovascular (CV) disease remains the leading cause of morbidity and mortality worldwide and poses an ongoing challenge with the aging population. Elevated lowdensity lipoprotein cholesterol (LDL-C) is an established risk factor for atherosclerotic cardiovascular disease (ASCVD), and the expert consensus is the use of statin therapy (if tolerated) as first line for LDL-C reduction. However, patients with ASCVD may experience recurrent ischemic events despite receiving maximally tolerated statin therapy, including those whose on-treatment LDL-C remains ≥70 mg/dL, patients with familial hypercholesterolemia, high-risk subgroups with comorbidities such as diabetes mellitus, and those who have an intolerance to statin therapy. Optimal therapeutic strategies for this unmet need should deploy aggressive lipid lowering to minimize the contribution of dyslipidemia to their CV risk, particularly for very high-risk populations with additional risk factors beyond hypercholesterolemia and established ASCVD. To understand the current clinical climate and guidelines regarding ASCVD, we primarily searched PubMed for articles published in English regarding lipid-lowering therapies and CV risk reduction, including emerging therapies, and CV outcomes trials with proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors. This review discusses the findings of recent clinical trial evidence for CV risk reduction with cholesterol-lowering therapies, with a focus on CV outcomes trials with PCSK9 inhibitors, and considers the impact of the study results for secondary prevention and future strategies in patients with hypercholesterolemia and CV risk despite maximally tolerated statin therapy.

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Section: Limits Of Statin Therapymentioning

confidence: 99%

<p>Cardiovascular Outcomes and Proprotein Convertase Subtilisin/Kexin Type 9 Inhibitors: Current Data and Future Prospects</p>

Duprez¹,

Handelsman²,

Koren³

2020

VHRM

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“…A review of the use of fibrates for primary prevention of CVD revealed a modest benefit over placebo for combined endpoints, but none for overall or non-CVD mortality [3]. A separate review of the efficacy of niacin with or without the addition of a statin demon-strated no reduction in overall mortality, cardiovascular mortality, or fatal or non-fatal myocardial infarctions when compared with placebo [4].While La Fountaine et al's article is cleanly written and argued, it underscores the need for a certain aggression in tackling cardio-metabolic disease in SCI. Rather than descriptive analyses of lipid profiles or discussion of how cardiovascular risk factors cluster in people with injuries [5], we need trials of interventions with hard and tangible outcomes.…”

mentioning

confidence: 99%

mentioning

confidence: 99%

Response to La Fountaine et al.

Stillman

Williams

2018

Spinal Cord

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La Fountaine et al. [1] recently compared the lipid profiles of 401 persons with chronic spinal cord injury (SCI) with those of 197 able-bodied controls. In so doing, they found that adverse serum triglyceride (TG) concentrations in people with SCI are lower than in those without, and reiterated previous insights into links between sympathetic nervous system input and circulating lipid levels.While this article is well reasoned-and each of its authors has substantively contributed to the physiatric literature-the reader is left questioning its clinical relevance. In concluding that clinicians should "consider instituting appropriate dietary, exercise, and/or pharmacological interventions" in patients with elevated TG concentrations, the authors obscure the fact that none of these has been shown to reduce atherosclerotic burden, risk of major adverse coronary events, or cardiac or overall mortality in people with SCI. There are simply no data upon which to base these recommendations.Further, while the authors rightly point to recent guidelines reaffirming that low high-density lipoprotein levels are a major risk factor for cardiovascular disease (CVD) and that TG levels ≥200 may identify individuals at increased risk (Grade B recommendation) [2], it is not clear what to do with this information. A review of the use of fibrates for primary prevention of CVD revealed a modest benefit over placebo for combined endpoints, but none for overall or non-CVD mortality [3]. A separate review of the efficacy of niacin with or without the addition of a statin demon-strated no reduction in overall mortality, cardiovascular mortality, or fatal or non-fatal myocardial infarctions when compared with placebo [4].While La Fountaine et al.'s article is cleanly written and argued, it underscores the need for a certain aggression in tackling cardio-metabolic disease in SCI. Rather than descriptive analyses of lipid profiles or discussion of how cardiovascular risk factors cluster in people with injuries [5], we need trials of interventions with hard and tangible outcomes. As CVD emerges as the leading cause of mortality among individuals with SCI, what can and ought we do to improve their health and longevity?Compliance with ethical standards

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Niacin for primary and secondary prevention of cardiovascular events

Cited by 2 publications

References 43 publications

<p>Cardiovascular Outcomes and Proprotein Convertase Subtilisin/Kexin Type 9 Inhibitors: Current Data and Future Prospects</p>

<p>Cardiovascular Outcomes and Proprotein Convertase Subtilisin/Kexin Type 9 Inhibitors: Current Data and Future Prospects</p>

Response to La Fountaine et al.

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