There is robust epidemiological evidence dating back to the original Framingham Heart Study from 1977 that indicates an important inverse relationship between high-density lipoprotein cholesterol (HDL-C) and risk of incident coronary artery disease (CAD). Despite this body of scientific information demonstrating that low levels of HDL-C are an independent predictor of subsequent CAD events, multiple therapeutic attempts to raise HDL-C levels have failed to demonstrate a consistent reduction in prognostically important endpoints such as death, myocardial infarction (MI), and stroke. Recently, several major randomized trials using different therapeutic interventions have raised appropriate concerns about our basic understanding of HDL-C and whether the "HDL hypothesis" of lowering cardiovascular events through therapeutic interventions directed at raising HDL-C is a scientifically viable one. While two recent randomized controlled trials (AIM-HIGH and HPS2-THRIVE) failed to show a reduction in cardiovascular events in patients treated to optimally low levels of low-density lipoprotein cholesterol (LDL-C) at baseline with extended-release niacin on a background of simvastatin, these clinical trials studied specific populations of stable ischemic heart disease patients. The data from these two contemporary trials cannot be extrapolated to all patient populations, such as those with acute coronary syndromes or myocardial infarction or those with significant residual mixed dyslipidemia not treated with optimal doses of intensive statin therapy, as these patients were excluded by trial design in both studies. Therefore, at the present time, there is insufficient evidence from clinical trials to recommend HDL-targeted therapy for additional event reduction in CAD patients. However, we will review the relevant data from recent major trials (AIM-HIGH, HPS2-THRIVE, ILLUMINATE, and dal-OUTCOMES) and highlight the potential clinical implications of these trials in modern pharmacotherapy as it relates to HDL-C raising and potential cardiovascular event reduction.

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Primary meningococcal pericarditis (PMP) is a rare form of acute purulent pericarditis that often evolves into cardiac tamponade and usually requires pericardial drainage. PMP is a rare, difficult to diagnose, rapidly progressive form of meningococcal infections. PMP is typically caused by Neisseria meningitidis of serotype C, or, less commonly, B or W135. We report the second case of PMP caused by Neisseria meningitidis of serotype Y. Our patient was not critically ill at presentation, and her presentation could have been consistent with viral uncomplicated pericarditis with the exception of the mild leukocytosis with a left shift in the differential. Clinicians should be aware that early in the course of PMP, the illness may not be severe. Mild leukocytosis with a left shift or bandemia in the setting of what otherwise seems to be a case of uncomplicated viral pericarditis should prompt suspicion for PMP and further evaluation and/or monitoring.

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