Epidemiologically, HDL-Cholesterol has been found to correlate inversely with CAD events. Unfortunately interventional trials have not found that increasing HDL is clinically beneficial. Interesting to see the exponential rise in published HDL articles since mid 1970s (graph).
Please find below the NLA approach to HDL-Cholesterol. Guidelines were published in April 2015. Text has been slightly modified for easier and succinct reading.
EXCERPTS FROM THE GUIDELINES:
Epidemiologic evidence suggests that HDL is inversely associated with ASCVD, and the level of HDL is widely accepted as an important risk indicator and used in risk factor counting and quantitative ASCVD risk assessment. Low HDL is also a component of the metabolic syndrome. HDL particles have several properties that are expected to provide protection against ASCVD including reverse cholesterol transport, antioxidation, endothelial protection, antiplatelet activity, and anticoagulation, but a direct mechanistic relationship between low HDL and ASCVD is not fully understood.
It has been suggested that low HDL levels may simply be a reflection of the presence of other atherogenic factors, such as hypertriglyceridemia, particularly the degree of postprandial hypertriglyceridemia. A Mendelian randomization approach to examine the potential causality of the relationship between HDL level and reduced risk for myocardial infarction in case-control and prospective cohort studies found that single nucleotide polymorphisms that increase plasma HDL concentration in isolation (ie, without altering triglycerides or LDL-C) were not associated with reduced risk of myocardial infarction.
To date, clinical trials of agents that markedly raise HDL-C, including niacin and cholesteryl ester transfer protein inhibitors, have failed to demonstrate that they reduce all cause mortality, CHD mortality, myocardial infarction, or stroke in statin-treated patients. The NLA Expert Panel did not rule out the possibility of a potential ASCVD risk-reduction benefit with raising HDL or promoting HDL function, but at this time, HDL is not recommended as a target of therapy per se. The HDL level is often raised as a consequence of efforts to reduce atherogenic cholesterol through lifestyle and drug therapies.