Left ventricular remodelling after ST‐segment elevation myocardial infarction: sex differences and prognosis

Abstract

Aims Left ventricular (LV) remodelling after ST-segment elevation myocardial infarction (STEMI) worsens outcome. The effect of sex on LV post-infarct remodelling is unknown. We therefore investigated the sex distribution and long-term prognosis of LV post-infarct remodelling after STEMI in the contemporary era of primary percutaneous coronary intervention (PCI) and optimal pharmacotherapy. Methods and results Data were obtained from an ongoing primary PCI STEMI registry. LV remodelling was defined as ≥20% increase in LV end-diastolic volume at either 3, 6, or 12 months post-infarct, and LV remodelling impact on outcome was evaluated with a log-rank test. A total population of 1995 STEMI patients were analysed (mean age 60 ± 12 years): 1527 (77%) men and 468 (23%) women. The mean age of male patients was 60±11 versus 63±13 years for women (P < 0.001). A total of 953 (48%) patients experienced LV remodelling in the first 12 months of follow-up, and it was equally frequent amongst men (n = 729, 48%) and women (n = 224, 48%). After a median follow-up of 94 (interquartile range 69-119) months, 225 patients died: 171 (11%) men and 54 (12%) women. No survival difference was seen between remodellers and non-remodellers in the male (P = 0.113) and female (P = 0.920) groups. Conclusion LV post-infarct remodelling incidence, as well as long-term survival of LV remodellers and non-remodellers, was similar in men and women who were treated with primary PCI and optimal pharmacotherapy post-STEMI. Figure 2 Kaplan-Meier survival curves, according to sex and remodelling status. Time to cumulative survival in men (A) and women (B), according to the presence of left ventricular remodelling in the first 12 months after ST-segment elevation myocardial infarction. Post-STEMI remodelling, sex and outcome 479 ESC Heart Failure 2020; 7: 474-481

Effects and Safety of Sacubitril/Valsartan for Patients with Myocardial Infarction: A Systematic Review and Meta-Analysis

“…In recent years, due to the continuous expansion of chest pain centers in China, the mortality rate of AMI patients is significantly lower than before [ 2 ]. Although emergency PCI can revascularize and save part of dying and damaged myocardium, some patients could still experience left ventricular remodeling postmyocardial infarction [ 3 , 4 ]. Ventricular remodeling includes myocardial hypertrophy, interstitial fibrosis, increased cardiac volume, and reduced diastolic function.…”

Sonothrombolysis Augments Reperfusion in ST-Elevation Myocardial Infarction With Primary Percutaneous Coronary Intervention: Insights From the SONOSTEMI Study

“…We observed a high rate of ≥50% ST-segment resolution post PCI (a marker of myocardial perfusion)greater than expected in STEMI 5 , and may be a reflection of enhanced microvascular function with sonothrombolysis. Finally, the enhancement in left ventricular performance at 3-months is notable given the degree of improvement in WMSI and LV function when compared to remodeling findings in STEMI 6 . Our results are notable and provide further data to support this novel technique in augmenting reperfusion in STEMI both at the epicardial and myocardial level, which we believe translates to enhanced left ventricular performance.…”

Deep Learning Analyses to Delineate the Molecular Remodeling Process after Myocardial Infarction

“…During the procedure, IV fentanyl (0.75 mg/kg/45 min) (Fentanest ® , Kern Pharma, Madrid, Spain) was administered as an analgesic, and IV atracurium besylate (1.5 mg/kg bolus) (Tracrium ® , GlaxoSmithKline, Brentford, UK) was used 3) We used the information to generate a map of proteins regulated by the obtained experimental data. (4) We fed the mathematical models to identify patterns in the data, (5) identify key regulatory proteins, and (6) predict new mechanisms of action. (7) The final result included a scientific justification of every prediction.…”

“…(3) We used the information to generate a map of proteins regulated by the obtained experimental data. (4) We fed the mathematical models to identify patterns in the data, (5) identify key regulatory proteins, and (6) predict new mechanisms of action. (7) The final result included a scientific justification of every prediction.…”

“…Myocardial infarction (MI) occurs when blood flow suddenly stops due to occlusion of a coronary artery, leading to local ischemia in the heart [ 1 , 2 , 3 ]. This condition triggers an adverse myocardial remodeling response involving a wide variety of signaling pathways, potentially including extracellular matrix (ECM) dysregulation, cardiomyocyte apoptosis, and cardiogenic processes, such as myocyte concentric and eccentric hypertrophy, slippage, accumulation of interstitial tissue, a molecular shift towards an embryonic pattern, and loss of cardiac energy reserves [ 4 , 5 ]. Cardiac remodeling secondary to MI is a well-defined process that may ultimately lead to heart failure (HF) [ 6 , 7 , 8 ], but the specific dynamic molecular mechanisms underlying this progression have not been fully characterized.…”