1,148 research outputs found
What More Can Be Delivered to Future Patients with Coronary Syndromes?
No full textCoronary artery disease (CAD) is a major cardiovascular disease that imposes substantial clinical and socioeconomic burdens worldwide [...
Collective Knowledge Used to Unveil Cardiovascular Injury Emerged during COVID-19
No full textTwo years have passed since the unprecedented breakout of the global pandemic of the coronavirus disease COVID-19, which began at the end of 2019 [...
So‐far overlooked HFpEF patients with normal natriuretic peptide level need more evidence
No full textThe role of vascular failure in coronary artery spasm
No full textSummaryCoronary artery spasm plays an important role in the pathogenesis of angina pectoris as well as acute coronary syndrome and sudden death. The prevalence of coronary spasm is greater in East Asian populations than in other parts of the world. Although the mechanism of coronary spasm is still unclear, both endothelial and smooth muscle dysfunction have been reported to play a role. We recently proposed a new concept termed ‘vascular failure’ that represents an integration of endothelial and smooth muscle abnormalities. Thus, vascular failure is the primary cause of coronary artery spasm
Postprandial hyperglycemia as an etiological factor in vascular failure
No full textAbstract Postprandial hyperglycemia is characterized by hyperglycemic spikes that induce endothelial dysfunction, inflammatory reactions and oxidative stress, which may lead to progression of atherosclerosis and occurrence of cardiovascular events. Emerging data indicate that postprandial hyperglycemia or even impaired glucose tolerance may predispose to progression of atherosclerosis and cardiovascular events. There is evidence that postprandial hyperglycemia, but not fasting hyperglycemia, independently predicts the occurrence of cardiovascular events. We proposed a concept of 'vascular failure' as a comprehensive syndrome of vascular dysfunction extending from risk factors to advanced atherosclerotic disease. Postprandial hyperglycemia is therefore one of the very important pathophysiological states contributing to vascular failure. Accordingly, controlling postprandial hyperglycemia should be the focus of future clinical investigation as a potential target for preventing vascular failure.</p
Exploration of the clinical benefits of sodium glucose co-transporter 2 inhibitors in diabetic patients with concomitant heart failure
No full textAbstract Prevention and treatment strategies for heart failure (HF) in diabetes have not been fully established, at least partly due to lack of recognition of a pathological link between the two and effective antidiabetic agents for HF. Recent cardiovascular (CV) outcomes trials demonstrated that treatment with sodium glucose co-transporter 2 (SGLT2) inhibitors greatly improved major CV adverse events in type 2 diabetes (T2D) patients at high risk for CV events, seemingly driven by risk reduction in HF-related outcomes. The beneficial effects of SGLT2 inhibitors on such outcomes and the heart itself are unique characteristics among antidiabetic agents, and SGLT2 inhibitors are expected to be a promising therapeutic option for CV disease and HF care. However, because a limited number of T2D patients with concomitant HF were included in the CV outcomes trials, the treatment effects of SGLT2 inhibitors for such conditions have not been fully investigated. Moreover, there has been little evidence to suggest SGLT2 inhibitor mediated effects on CV function and relevant biomarkers. Januzzi et al. (J Am Coll Cardiol 70: 704–712, 2017) reported that canagliflozin treatment could delay the escalation of cardiac biomarkers in older T2D patients, suggesting direct CV protection by SGLT2 inhibitors in this population. Whether SGLT2 inhibitors can exert similar benefits in T2D patients with concomitant HF will likely be the next big issue of medical concern. Furthermore, newer clinical trials are currently ongoing to investigate whether SGLT2 inhibitors exhibit beneficial effects for HF, both in the presence and absence of T2D. Such trials may potentially identify novel approaches for treating HF
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