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Metabolic syndrome (MetS), a cluster of metabolic dysregulations, is recognized as a significant risk factor for the development of heart failure (HF). The pathophysiological mechanisms linking MetS to HF are complex and multifaceted, with the components of MetS contributing to cardiac deterioration through impaired myocardial energy metabolism, increased inflammation, and endothelial dysfunction. Numerous clinical studies have confirmed the relationship between MetS and HF. Multiple studies have demonstrated that the impact of MetS on HF varies by sex and age. Metabolic disorders, including MetS, have a greater impact on HF incidence in younger adults compared to the elderly population and in women compared to men. Although the reasons for these differences are not yet fully understood, recognizing the sex- and age-related variations is crucial for developing targeted strategies to prevent HF in individuals with MetS. Future research should continue to investigate the underlying mechanisms behind these variations and identify optimal management approaches that account for both sex and age in reducing HF risk. [ABSTRACT FROM AUTHOR]

Limited data are available regarding the effect of metabolic syndrome on heart failure (HF) development in young individuals. Utilizing data from the Korean National Health Insurance Service, we included a total of 1,958,284 subjects in their 40s who underwent health screening between January 2009 and December 2009 in Korea. Subjects were classified into three groups: normal, pre-metabolic syndrome (Pre-MetS), and metabolic syndrome (MetS). MetS was identified in 10.58% of males and 5.21% of females. The hazard ratio for HF in subjects with MetS was 1.968 (95% CI: 1.526–2.539) for males and 2.398 (95% CI: 1.466–3.923) for females. For those with Pre-MetS, the hazard ratio was 1.607 (95% CI: 1.293–1.997) in males and 1.893 (95% CI: 1.43–2.505) in females. Additionally, acute myocardial infarction and low hemoglobin levels were identified as significant risk factors for HF in both genders. MetS approximately doubled the risk of developing HF in individuals in their 40s. Pre-MetS was also a significant risk factor for HF in this population. [ABSTRACT FROM AUTHOR]

Introduction: Early recognition and risk stratification of cardiovascular events are necessary in patients after ischemic stroke. Recent evidence suggests that elevated high-sensitive cardiac troponin is a predictor of mortality and vascular events. Therefore, we aimed to explore the prognostic role of high-sensitive cardiac troponin I (hs-TnI) on mortality and cardiovascular outcomes in patients after ischemic stroke. Methods: From August 2014 to July 2017, 1,506 patients with acute ischemic stroke were pulled consecutively in a retrospective single-center registry. Of these, 1,019 patients were selected and classified into the elevated or non-elevated hs-TnI groups according to hs-TnI level of 99th percentile upper reference limit (URL) at the time of admission for ischemic stroke. The primary outcome was a major adverse cardiac and cerebrovascular event (MACCE) during follow-up. Results: Among 1,019 patients, 708 patients were non-elevated hs-TnI group (<99th percentile URL of hs-TnI) and 311 patients were elevated hs-TnI group (≥99th percentile URL of hs-TnI). The median follow-up period was 22.5 (interquartile range 5.0–38.8) months. In a multivariable Cox regression model, the elevated hs-TnI group has a higher risk of MACCE (adjusted hazard ratio [HR]: 3.12; 95% confidence interval [CI]: 2.33–4.17; p < 0.01), all-cause mortality (adjusted HR: 4.15; 95% CI: 2.47–6.99; p < 0.01) and readmission caused by coronary revascularization (adjusted HR: 3.12; 95% CI: 1.41–6.90; p < 0.01), heart failure (adjusted HR: 2.76; 95% CI: 1.38–5.51; p < 0.01), and stroke (adjusted HR: 1.73; 95% CI: 1.07–2.78; p = 0.02) compared with the non-elevated hs-TnI group. Conclusions: Elevated hs-TnI is independently associated with higher mortality and cardiac and cerebrovascular events in patients with ischemic stroke and may serve as a valuable prognostic factor in management after ischemic stroke. [ABSTRACT FROM AUTHOR]

Oxidative stress is associated with many cardiovascular diseases, such as hypertension and arteriosclerosis. Oxidative stress reportedly activates the L-type voltage-gated calcium channel (VDCCL) and elevates [Ca2+]i in many cells. However, how oxidative stress activates VDCCL under clinical setting and the consequence for arteries are unclear. Here, we examined the hypothesis that hydrogen peroxide (H2O2) regulates membrane potential (Em) by altering Na+ influx through cation channels, which consequently activates VDCCL to induce vasoconstriction in rat mesenteric arteries. To measure the tone of the endothelium-denuded arteries, a conventional isometric organ chamber was used. Membrane currents and Em were recorded by the patch-clamp technique. [Ca2+]i and [Na+]i were measured with microfluorometry using Fura2-AM and SBFI-AM, respectively. We found that H2O2 (10 and 100 µM) increased arterial contraction, and nifedipine blocked the effects of H2O2 on isometric contraction. H2O2 increased [Ca2+]i as well as [Na+]i, and depolarised Em. Gd3+ (1 µM) blocked all these H2O2-induced effects including Em depolarisation and increases in [Ca2+]i and [Na+]i. Although both nifedipine (30 nM) and low Na+ bath solution completely prevented the H2O2-induced increase in [Na+], they only partly inhibited the H2O2-induced effects on [Ca2+]i and Em. Taken together, the results suggested that H2O2 constricts rat arteries by causing Em depolarisation and VDCCL activation through activating Gd3+-and nifedipine-sensitive, Na+-permeable channels as well as Gd3+-sensitive Ca2+-permeable cation channels. We suggest that unidentified Na+-permeable cation channels as well as Ca2+-permeable cation channels may function as important mediators for oxidative stress-induced vascular dysfunction. [ABSTRACT FROM AUTHOR]