Abstract:Aim To apply coronary angiography derived index of microcirculatory resistance (caIMR) to evaluate the effect of coronary microcirculation perfusion on myocardial remodeling after interventional therapy in patients with acute anterior ST segment elevation myocardial infarction (STEMI). Methods This was a cross-sectional study.The analysis was performed among the patients who were hospitalized for acute anterior STEMI in the First Department of the Second Affiliated Hospital of Dalian Medical University from January 2021 to July 2022 and received percutaneous coronary intervention (PCI) with regtelar follow-up visits. The patients were divided into low caIMR (L-caIMR) group, medium caIMR (M-caIMR) group and high caIMR (H-caIMR) group according to the results of caIMR. The results of echocardiography at perioperative period, 1 month, 3 months, 6 months and 1 year were analyzed and compared, including left atrial diameter (LAD), left ventricular end-diastolic diameter (LVEDD), interventricular septum thickness (IVST), mitral orifice flow velocity E/A, mitral annular septum e′ and mitral annular wall e′, etc. The difference of interleukin-1β (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α) and other inflammatory factors in peripheral blood of the three groups were also compared. Results A total of 75 patients diagnosed with acute anterior STEMI were recruited, including 55 males. The L-caIMR group, M-caIMR group, and H-caIMR group had 6,6 and 23 cases, respectively. Compared with the L-caIMR group, the LAD and IVST in the M-caIMR group and the H-caIMR group exhibited an increasing tendency one month after PCI, and the increase in the H-caIMR group was more significant than that in the M-caIMR group (P＜0.05). The ejection fraction in the H-caIMR group was notably lower than that in the L-caIMR group and the M-caIMR group at 1 and 3 months after PCI (P＜0.05). Compared with the L-caIMR group, the mitral flow velocity E/A at 6 months after PCI, and the e′ at the septal side and the lateral wall of the mitral annulus at 1,3, and 6 months after PCI were significantly reduced in the M-caIMR and H-caIMR groups(P＜0.05). Compared with the L-caIMR group, the levels of IL-1β, IL-6, and TNF-α showed an increasing trend in the M-caIMR group and the H-caIMR group, and the increase was greater in the H-caIMR group than that in the M-caIMR group (P＜0.05). Multivariate analysis revealed that caIMR was a factor influencing the levels of IL-1 β and IL-6 (P＜0.05). Conclusion CMD may be involved in the process of myocardial remodeling in patients with acute anterior STEMI after PCI, in which inflammation plays a role.

Abstract:Myocardial infarction is the most common cause of heart failure, and myocardial remodeling can occur after infarction, thus contributing to the progression of heart failure. The occurrence of post-infarction ventricular remodeling is closely related to m6A methylation. m6A methylation is a reversible and highly dynamic process. This process is mainly mediated by m6A methylation positive and negative regulatory enzymes and is involved in the occurrence of post-infarction myocardial remodeling through mechanisms such as cellular autophagy. This article mainly reviews relevant literature in recent years. Firstly, a brief introduction is given to m6A methylation, followed by an introduction to the role of m6A methylase in regulating myocardial remodeling. Finally, a summary analysis is conducted on the mechanism of m6A methylation in regulating myocardial remodeling from the perspectives of autophagy, inflammation, cell apoptosis, calcium ion homeostasis, extracellular matrix remodeling, and ferroptosis. The feasibility of using m6A methylation serological detection as a diagnostic tool for myocardial remodeling after myocardial infarction is discussed, in order to provide reference for related research.

Abstract:Myocardial remodeling after myocardial infarction is a complex pathological process, which seriously affects the prognosis of patients. CTRP9 is a newly discovered adipokine in recent years. A large number of studies have shown that CTRP9 can inhibit myocardial remodeling after myocardial infarction. This article reviews the related research of CTRP9 on myocardial remodeling after myocardial infarction.

Abstract:Klotho is an important endogenous pluripotent protein involved in pathophysiological processes such as aging and calcium/phosphorus metabolism, which is closely correlated with cardiovascular diseases. Recent clinical studies have found that low levels of Klotho expression are associated with more cardiovascular risk factors and predict cardiovascular risk; Basic studies have also shown that Klotho plays a pivotal role in maintaining vascular homeostasis and heart function. Klotho can promote nitric oxide (NO) production, reduce the expression of inflammatory factors and adhesion molecules, mediate the biological effects of anti-oxidation, anti-apoptosis, and anti-aging, alleviate atherosclerosis and vascular calcification, and inhibit cardiac hypertrophy and fibrosis. Klotho may serve as a new interventional target and provide new insights for the prevention and treatment of cardiovascular diseases. This review aims to summarize the association of Klotho with cardiovascular diseases and its underlying biological mechanisms.

Abstract:Recent studies have shown that angiotensin-converting enzyme-2 (ACE2) plays an important role in the pathogenesis of atherosclerosis, aneurysm, coronary heart disease, diabetic cardiomyopathy and adriamycin cardiomyopathy. There is increasing support for the belief that ACE2 has a significant role in inhibiting vascular and myocardial remodeling, which is of great significance in the prevention and treatment of cardiovascular diseases.