Cardiovascular diseases, especially coronary artery disease (CAD), are the leading causes of death in patients with chronic obstructive pulmonary disease (COPD). There is a high prevalence of common risk factors in the COPD/CAD patient population including smoking, sedentary lifestyle and low socio-economic status. However, various studies have shown that airflow limitation is an independent risk factor for cardiovascular diseases. Chronic low-grade systemic inflammation, oxidative stress and increased platelet activation have been widely reported to be pathophysiological links between COPD and atherosclerosis. Statins and inhaled corticosteroids have been investigated as potential therapeutic interventions in COPD that may lower cardiovascular risk. The goals of this review are to examine the evidence for increased cardiovascular risk in COPD patients, the possible mechanisms linking these two chronic conditions, to discuss possible predictors or markers of poor outcomes among patients diagnosed with both COPD and CAD, and the therapeutic options aimed at reducing cardiovascular risks associated with COPD.

Despite rapid advances in cardiovascular research and therapeutic strategies, ischemic heart disease (IHD) remains the leading cause of mortality worldwide. MicroRNAs (miRNAs) are small, noncoding RNAs which post transcriptionally regulate gene expression. In the past few years, miRNAs have emerged as key tools for the understanding of the pathophysiology of IHD, with potential uses as new biomarkers and therapeutic targets. Several studies report a regulatory role of miRNAs, with regard to fundamental components of IHD pathogenesis and progression, such as lipoprotein metabolism, atherogenesis, vascular calcification, platelet function, and angiogenesis. Due to their high stability in biofluids, circulating miRNAs have attracted attention as promising biomarkers of IHD, especially in cardiovascular risk prediction and the diagnosis of myocardial infarction. Furthermore, experimental studies have demonstrated the potential of miRNA-targeted therapy in improving hyperlipidemia, atherosclerosis, and angiogenesis. In this review, the current knowledge on the role of miRNAs in IHD and translational perspectives of their use is discussed.

Aims:The association of frailty with coronary plaque phenotype among older patients with non-ST-elevation acute coronary syndrome (NSTEACS) is not known. The aim of this study was to evaluate the association of frailty with coronary plaque phenotype among older patients with NSTEACS.Methods and results: Older patients with NSTEACS who underwent invasive angiography were recruited. Frailty was measured using the Fried frailty score. Following angiography, patients underwent greyscale and virtual histology intravascular ultrasound (VH-IVUS) imaging. Of the 90 patients, 26 (28.9%) were robust, 49 (54.4%) patients were pre-frail, and 15 (16.7%) were frail. Mean age was 80.9±3.8 years; 59 (65.6%) were male. Compared to robust patients, the pre-frail group had a significantly greater presence of high-risk lesions including VH thin-cap fibroatheroma (TCFA, p=0.011), minimum lumen area (MLA) ≤4 mm 2 (p=0.016), TCFA+MLA ≤4 mm 2 (p=0.005), TCFA+plaque burden (PB) ≥70% (p=0.005) and TCFA+PB ≥70%+MLA ≤4 mm 2 (p=0.003). By age-and sex-adjusted logistic regression analysis, frailty was found to be strongly and independently associated with the presence of TCFA (odds ratio [OR] 2.81, 95% confidence interval [CI]:1.06-7.48, p=0.039).Conclusions: This is the first study to report the relationship between frailty phenotype and coronary plaque morphology among frail older NSTEACS patients. ClinicalTrials.gov Identifier: NCT01933581

Sudden cardiac death is the leading cause of mortality among young athletes with an incidence of 1-2 per 100,000 athletes per annum. It is described as 'an event that is non-traumatic, non-violent, unexpected, and resulting from sudden cardiac arrest within six hours of previously witnessed normal health'. Most predisposed athletes have no symptoms and there is no warning for the impending tragic event. The majority of cases are caused by an underlying structural cardiac abnormality, most commonly hypertrophic cardiomyopathy. More recently, the understanding of non-structural causes such as long QT syndrome and Brugada syndrome has grown and diagnostic criteria have been developed. This review presents the known aetiologies of sudden cardiac death among athletes and outlines their identification and management including implications for future sporting participation as laid out in the consensus documents produced by the European Society of Cardiology and the 36th Bethesda Conference.