High-Density Lipoprotein and Coronary Heart Disease

Abstract

Coronary heart disease remains a major cause of worldwide morbidity and mortality despite therapeutic advances that control many risk factors such as low-density lipoprotein cholesterol to levels lower than previously possible. Population studies have consistently demonstrated an inverse association between high-density lipoprotein cholesterol (HDL-C) levels with the risk of coronary heart disease. As a result, HDL-C is gaining increasing interest as a therapeutic target. In this review, we explore the protective mechanisms of HDL and how current and future therapies harness these beneficial properties. We offer a biological framework to understand treatment strategies as well as their resultant successes and failures to guide management and future directions. At present, raising HDL-C level holds great promise, on the basis of epidemiology and initial trials, but we await the outcomes of the many large clinical outcomes trials currently under way to define the clinical role of older and novel therapies to raise HDL-C level.

miR-33 links SREBP-2 induction to repression of sterol transporters

“…This model is in apparent contradiction with data from large clinical trials that show a modest, but significant, increase in plasma HDL-cholesterol levels in patients treated with statins (recently reviewed in ref. 32). Interestingly, these latter studies show great variability between individuals, and the effects of some statins on HDL-cholesterol are not always dose-dependent.…”

Orthotopic Liver Transplantation in an Adult with Cholesterol Ester Storage Disease

“…Although statin therapy led to a reduction in total cholesterol, the low HDL cholesterol reversed only following liver transplantation. Multiple studies in healthy subjects have demonstrated the predictive importance of low HDL cholesterol in future cardiac and cerebrovascular outcome (Natarajan et al 2010). Indeed a recent consensus statement on defining the metabolic syndrome has used a cut-off of less than 1.3 mmol/L as abnormal in a female population (Alberti et al 2009).…”

Portal hypertension-related inflammatory phenotypes: From a vitelline and amniotic point of view

“…On the contrary, during cardiovascular inflammation cholesterol esters may be transferred from HDL to apolipoprotein B-containing particles, such as LDL or VLDL [62]. Trapping of apolipoprotein B containing particles within the arterial wall is unquestionably the essential initiating event for the development of complex atherosclerotic lesions [50].…”