HDL as a prognostic biomarker for coronary atherosclerosis: the role of inflammation

<p><b>Introduction</b>: Emerging evidence suggests that the role of high density lipoprotein (HDL) in the atherosclerotic process is not as clear as previously thought, since atheroprotective HDL becomes atherogenic in states of increased inflammatory processes.</p> <p><b>Areas covered</b>: In this review we aim to elucidate the role of HDL as a prognostic biomarker and we discuss therapeutic approaches that aim to increase HDL and their possible clinical benefit.</p> <p><b>Expert opinion</b>: Given the structural variability and biological complexity of the HDL particle, its role in the atherosclerotic process is far from clear. According to current evidence, the atheroprotective role of HDL turns atherogenic in states of increased inflammatory processes, while even minor alterations in systemic inflammation are likely to hinder the endothelial protective effects of HDL. In accordance, significant data have revealed that HDL-related drugs may be effective in reducing cardiovascular mortality; however they are not as encouraging or unanimous as expected. Possible future goals could be to quantify either HDL subclasses or functions in an attempt to reach safer conclusions as to the prognostic importance of HDL in coronary atherosclerosis. Having achieved that, a more targeted therapy that would aim to raise either HDL functionality or to remodel HDL structure would be more easily designed.</p

Phenotype, outcomes and natural history of early‐stage non‐ischaemic cardiomyopathy

AimsTo characterize the phenotype, clinical outcomes and rate of disease progression in patients with early‐stage non‐ischaemic cardiomyopathy (early‐NICM).Methods and resultsWe conducted a prospective observational cohort study of patients with early‐NICM assessed by late gadolinium enhancement cardiovascular magnetic resonance (CMR). Cases were classified into the following subgroups: isolated left ventricular dilatation (early‐NICM H−/D+), non‐dilated left ventricular cardiomyopathy (early‐NICM H+/D−), or early dilated cardiomyopathy (early‐NICM H+/D+). Clinical follow‐up for major adverse cardiovascular events (MACE) included non‐fatal life‐threatening arrhythmia, unplanned cardiovascular hospitalization or cardiovascular death. A subset of patients (n = 119) underwent a second CMR to assess changes in cardiac structure and function. Of 254 patients with early‐NICM (median age 46 years [interquartile range 36–58], 94 [37%] women, median left ventricular ejection fraction [LVEF] 55% [52–59]), myocardial fibrosis was present in 65 (26%). There was no difference in the prevalence of fibrosis between subgroups (p = 0.90), however fibrosis mass was lowest in early‐NICM H−/D+, higher in early‐NICM H+/D− and highest in early‐NICM H+/D+ (p = 0.03). Over a median follow‐up of 7.9 (5.5–10.0) years, 28 patients (11%) experienced MACE. Non‐sustained ventricular tachycardia (hazard ratio [HR] 5.1, 95% confidence interval [CI] 2.36–11.00, p < 0.001), myocardial fibrosis (HR 3.77, 95% CI 1.73–8.20, p < 0.001) and diabetes mellitus (HR 5.12, 95% CI 1.73–15.18, p = 0.003) were associated with MACE in a multivariable model. Only 8% of patients progressed from early‐NICM to dilated cardiomyopathy with LVEF <50% over a median of 16 (11–34) months.ConclusionEarly‐NICM is not benign. Fibrosis develops early in the phenotypic course. In‐depth characterization enhances risk stratification and might aid clinical management.</p