In the acute phase of ST-elevation myocardial infarction (STEMI) viability imaging techniques are not validated and/or not available.This study aimed to evaluate the ability of strain parameters assessed in the acute phase of STEMI, to predict myocardial viability after revascularization.Thirty-one STEMI patients whose culprit coronary artery was recanalized and in whom baseline echocardiogram showed an akinesia in the infarcted area, were prospectively included. Bidimensional left ventricular global longitudinal strain (GLS), and territorial longitudinal strain (TLS) in the territory of the infarct related artery were obtained within 24 hours from admission. Delayed enhancement (DE) cardiac magnetic resonance imaging (CMR) was used as a reference test to assess post-revascularization myocardial viability. DE-CMR was performed 3 months after percutaneous coronary intervention. According to myocardial viability, patients were divided into 2 groups; CMR viable myocardium patients with more than half of infarcted segments having a DE <50% (group V) and CMR nonviable myocardium patients with half or more of the infarcted segments having a DE >50% (group NV).GLS and TLS were lower in group V compared to group NV (respectively: -14.4% ± 2.9% vs -10.9% ± 2.4%, P = .002 and -11.0 ± 4.1 vs -3.2 ± 3.1, P = .001). GLS was correlated with DE-CMR (r = 0.54, P = .002) and a cut off value of -13.9% for GLS predicted viability with 86% sensitivity (Se) and 78% specificity (Sp). TLS showed the strongest correlation with DE-CMR (r = 0.69, P < .001). A cut off value of -9.4% for TLS yielded a Se of 78% and a Sp of 95% to predict myocardial viability.GLS and TLS measured in the acute phase of STEMI predicted myocardial viability assessed by 3 months DE-CMR. They are prognostic indicators and they can be used to guide the priority and usefulness of percutaneous coronary intervention in these patients.
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http://dx.doi.org/10.1097/MD.0000000000019528 | DOI Listing |
Eur J Pharmacol
January 2025
Academy of Integrated Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, China. Electronic address:
Dihydrotanshinone I (DHT) is an active ingredient derived from Salvia miltiorrhiza. Previous studies have demonstrated that DHT can improve cardiac function in rats with myocardial ischemia-reperfusion injury (IR). However, the mechanism by which DHT improves myocardial injury in rats still requires further research.
View Article and Find Full Text PDFInt Rev Immunol
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Department of Cardiology, Loudi Central Hospital, Loudi City, Hunan Province, China.
Objective: Heart failure (HF) causes structural and functional changes in the heart, with the pyroptosis-mediated inflammatory response as the core link in HF pathogenesis. E3 ubiquitin ligases participate in cardiovascular disease progression. Here, we explored the underlying molecular mechanisms of E3 ubiquitin ligase Smurf1 in governing HF.
View Article and Find Full Text PDFCardiovasc Drugs Ther
January 2025
Department of Anesthesiology, Hainan Hosiptal of Chinese PLA General Hospital, No.80 Jianglin Street, Haitang District, Sanya City, Hainan Province, China.
Purpose: Myocardial ischemia/reperfusion injury (MIRI) is closely associated with ferroptosis. Dexmedetomidine (Dex) has good therapeutic effects on MIRI. This study investigates whether dexmedetomidine (Dex) regulates ferroptosis during MIRI by affecting ferroportin1 (FPN) levels and elucidates the underlying mechanisms.
View Article and Find Full Text PDFSci Rep
January 2025
Geriatric Center, Affiliated Hospital of Inner Mongolia Medical University, No.1 Tongdao North Street, Huimin District, Hohhot, 010050, China.
Myocardial ischemia/reperfusion injury (MIRI) is a serious clinical complication that is caused by reperfusion therapy following myocardial infarction (MI). Mitochondria-related genes (Mito-RGs) play important roles in multiple diseases. However, the role of mitochondria-related genes in MIRI remains largely unknown.
View Article and Find Full Text PDFInt J Med Sci
January 2025
Guang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing 100053, China.
This study investigates the role of Fundc1 in cardiac protection under high-altitude hypoxic conditions and elucidates its underlying molecular mechanisms. Using cardiomyocyte-specific knockout ( ) mice, we demonstrated that deficiency exacerbates cardiac dysfunction under simulated high-altitude hypoxia, manifesting as impaired systolic and diastolic function. Mechanistically, we identified that Fundc1 regulates cardiac function through the mitochondrial unfolded protein response (mito-UPR) pathway.
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