High-intensity interval training (HIIT) is frequently used in sports training. The effects on cardiorespiratory and muscle systems have led scientists to consider its application in the field of cardiovascular diseases. The objective of this review is to report the effects and interest of HIIT in patients with coronary artery disease (CAD) and heart failure (HF), as well as in persons with high cardiovascular risk. A non-systematic review of the literature in the MEDLINE database using keywords 'exercise', 'high-intensity interval training', 'interval training', 'coronary artery disease', 'coronary heart disease', 'chronic heart failure' and 'metabolic syndrome' was performed. We selected articles concerning basic science research, physiological research, and randomized or non-randomized interventional clinical trials published in English. To summarize, HIIT appears safe and better tolerated by patients than moderate-intensity continuous exercise (MICE). HIIT gives rise to many short- and long-term central and peripheral adaptations in these populations. In stable and selected patients, it induces substantial clinical improvements, superior to those achieved by MICE, including beneficial effects on several important prognostic factors (peak oxygen uptake, ventricular function, endothelial function), as well as improving quality of life. HIIT appears to be a safe and effective alternative for the rehabilitation of patients with CAD and HF. It may also assist in improving adherence to exercise training. Larger randomized interventional studies are now necessary to improve the indications for this therapy in different populations.

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A long-term lifestyle intervention with optimized high-intensity interval exercise improves body composition, cardiometabolic risk, and exercise tolerance in obese subjects. This intervention seems safe, efficient, and well tolerated and could improve adherence to exercise training in this population.

BackgroundAngiopoietin like‐2 (angptl2), a proinflammatory protein, is overexpressed in endothelial cells (ECs) from patients with coronary artery disease (CAD). Whether angptl2 contributes to atherogenesis is unknown. We tested the hypothesis that angptl2 promotes inflammation and leukocyte adhesion onto ECs, thereby accelerating atherogenesis in preatherosclerotic dyslipidemic mice.Methods and ResultsIn ECs freshly isolated from the aorta, basal expression of TNF‐α and IL‐6 mRNA was higher in 3‐month‐old severely dyslipidemic mice (LDLr−/−; hApoB100+/+ [ATX]) than in control healthy wild‐type (WT) mice (P<0.05) and was increased in both groups by exogenous angptl2 (100 nmol/L). Angptl2 stimulated the adhesion of leukocytes ex vivo on the native aortic endothelium of ATX, but not WT mice, in association with higher expression of ICAM‐1 and P‐selectin in ECs (P<0.05). Antibodies against these endothelial adhesion molecules prevented leukocyte adhesion. Intravenous administration of angptl2 for 1 month in preatherosclerotic 3‐month‐old ATX mice increased (P<0.05) total cholesterol and LDL‐cholesterol levels, strongly induced (P<0.05) the expression of endothelial proinflammatory cytokines and adhesion molecules while accelerating atherosclerotic lesion formation by 10‐fold (P<0.05). Plasma and aortic tissue levels of angptl2 increased (P<0.05) with age and were higher in 6‐ and 12‐month‐old ATX mice than in age‐matched WT mice. Angptl2 accumulated to high levels in the atherosclerotic lesions (P<0.05). Finally, angptl2 was greatly expressed (P<0.05) in ECs cultured from CAD patients, and circulating angptl2 levels were 6‐fold higher in CAD patients compared with age‐matched healthy volunteers.ConclusionsAngptl2 contributes to the pathogenesis of atherosclerosis.

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Background-There is epidemiological evidence that omega-3 polyunsaturated fatty acids (PUFAs) reduce the risk of atrial fibrillation (AF), but clinical data are conflicting. The present study assessed the effects of PUFA on AF in experimental models. Methods and Results-We studied the effects of oral PUFA supplements in 2 experimental AF paradigms: electrical remodeling induced by atrial tachypacing (400 bpm for 1 week) and congestive heart failure-associated structural remodeling induced by ventricular tachypacing (240 bpm for 2 weeks). PUFA pretreatment did not directly change atrial effective refractory period (128Ϯ6 [meanϮSEM] versus 127Ϯ2 ms; all effective refractory periods at 300-ms cycle lengths) or burst pacing-induced AF duration (5Ϯ4 versus 34Ϯ18 seconds). Atrial tachypacing dogs had shorter refractory periods (73Ϯ6 ms) and greater AF duration (1185Ϯ300 seconds) than shams (119Ϯ5 ms and 20Ϯ11 seconds; PϽ0.01 for each). PUFAs did not significantly alter atrial tachypacing effects on refractory periods (77Ϯ8 ms) or AF duration (1128Ϯ412 seconds). PUFAs suppressed ventricular tachypacing-induced increases in AF duration (952Ϯ221 versus 318Ϯ249 seconds; PϽ0.05) and attenuated congestive heart failure-related atrial fibrosis (from 19.2Ϯ1.1% to 5.8Ϯ1.0%; PϽ0.001) and conduction abnormalities. PUFAs also attenuated ventricular tachypacing-induced hemodynamic dysfunction (eg, left ventricular end-diastolic and left atrial pressure from 12.2Ϯ0.5 and 11.4Ϯ0.6 mm Hg, respectively, to 6.4Ϯ0.5 and 7.0Ϯ0.8 mm Hg; PϽ0.01) and phosphorylation of mitogen-activated protein kinases (extracellular-signal related and P38 kinase). Conclusions-PUFAs