Coronary angiography is the gold standard for the diagnosis of coronary artery disease. Coronary artery Gensini scoring systems measure both the extent and the degree of stenosis of coronary artery and therefore, give clinicians a more accurate, objective, and comprehensive assessment of the severity of coronary artery disease. Using Gensini scoring systems in combination with statistical analysis, we found that five variables, namely, Brachial-ankle pulse wave velocity (PWV), ankle-brachial index (ABI), carotid artery intima-media thickness (IMT), blood sugar, and high density lipoprotein cholesterol (HDL-C), were all significantly different among groups of patients with different Gensini scores. All five variables can be used for early screening and assessment of coronary artery disease as independent prognostic factors for the morbidity and mortality from cardiovascular conditions. With the progression of coronary artery disease, the levels of PWV, IMT, and blood glucose are gradually increasing whereas the levels of ABI and HDL-C are gradually decreasing. These changes can be treated as warning signs and can also be helpful in evaluating the severity of coronary artery diseases. It is highly recommended to perform these five non-invasive tests as early as possible in order to identify high-risk patients at their subclinical stages. This would allow timely intervention and thereby lead to reduced morbidity and mortality from cardiovascular diseases.
Gestational zinc deficiency is a cause of congenital heart disease in the fetus, and sentrin/small ubiquitin-like modifier (SUMO)-specific proteases (SENPs) as deSUMOylation enzymes play a crucial role in the development of cardiac structures. However, current studies of the regulation and function of SENP in zinc-deficient status during heart development remain limited. In this study, SUMO1 modification was found to gradually decrease during heart development, and the level of SENP5 exhibited a similar trend to SUMO1 conjugation. In addition, zinc deficiency resulted in cardiac dysplasia, increased cell apoptosis, decreased cell viability, and differentiation inhibition of hiPSC-CMs. In order to investigate the function of SENP5 in zinc deficiency, hiPSC-CMs were transfected with SENP5 small interfering RNA. The negative effects of zinc lacking conditions were reversed with depletion of SENP5. It was confirmed that zinc deficiency induced abnormal differentiation of hiPSCs and increased apoptosis of hiPSC-CMs by promoting SENP5 overexpression, which led to cardiac dysplasia. Thus, it was concluded that SENP5 regulates the SUMO1 deconjugation during heart development and zinc deficiency may reduce conjugated SUMO by promoting SENP5 overexpression, which induces abnormal development of the myocardium.
Moderate hypothermia plays a major role in myocardial cell death as a result of hypoxia/reoxygenation (H/r) injury. However, few studies have investigated the molecular mechanisms of hypothermic cardioprotection. Several responses to stress and other cell functions are regulated by post-translational protein modifications controlled by small ubiquitin-like modifier (SUMO). Previous studies have established that high SuMoylation of proteins potentiates the ability of cells to withstand hypoxic-ischemic stress. The level to which moderate hypothermia affects SuMoylation is not fully understood, as the functions of SuMoylation in the heart have not been studied in depth. The aim of the present study was to investigate the effect of moderate hypothermia (33˚C) on the protective functions of SuMoylation on myocardial cells. Hl-1 and H9c2 cells were treated with the hypoxia-mimetic chemical cocl 2 and complete medium to simulate H/r injury. Hypothermia intervention was then administered. a cell counting kit-8 assay was used to analyze cell viability. Mitochondrial membrane potential and the generation of reactive oxygen species (roS) were used as functional indexes of mitochondria dysfunction. Bcl-2 and caspase-3 expression levels were analyzed by western blotting. The present results suggested that moderate hypothermia significantly increased SuMo1 and Bcl-2 expression levels, as well as the mitochondrial membrane potential, but significantly decreased the expression levels of caspase-3 and mitochondrial roS. Thus, moderate hypothermia may enhance SuMoylation and attenuate myocardial H/r injury. Moreover, a combination of SuMoylation and moderate hypothermia may be a potential cardiovascular intervention.
DEB plus BMS was better than BMS alone in reducing LLL and MACEs, especially when dilatation was performed after stenting for de-novo coronary lesions, but it was inferior to DES. Therefore, the treatment strategy with DEB plus BMS should not be recommended for de-novo coronary lesions, except for patients who have contraindications for DES.
Objective Patients with non-ST elevation acute coronary syndrome (NSTE-ACS) benefit from coronary intervention, but the optimal timing for an invasive strategy is not well defined. This study aimed to determine whether an early invasive strategy (<12 hours) is superior to a delayed invasive strategy. Methods Twelve studies of nine randomized, controlled trials of 8586 patients were included. Results There were no significant differences in all-cause death (risk ratio [95% confidence interval]) (0.90, [0.77–1.06), re-myocardial infarction (re-MI) (0.95 [0.70–1.29]), major bleeding (0.97 [0.77–1.23]), and refractory ischemia (0.74 [0.53–1.05]) when we compared use of early and delayed invasive strategies. Furthermore, analysis of the effect of the chosen strategy on high-risk patients showed that the rate of composite death or re-MI was significantly decreased in patients with either a Global Registry of Acute Coronary Events (GRACE) risk score >140 or with elevated troponin levels (risk ratio 0.82 [0.72–0.92]; risk ratio 0.84 [0.76–0.93], respectively). Conclusions This meta-analysis shows that an early angiographic strategy does not improve clinical outcome in patients with NSTE-ACS. An early invasive strategy might reduce the rate of composite death or re-MI in high-risk patients with GRACE risk scores >140 or elevated cardiac markers.
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