Post-myocardial infarction (MI) ventricular septal defect (VSD) is a rare but potentially catastrophic mechanical complication that occurs in <1% of patients following a myocardial infarction and it is associated with a high morbidity and mortality despite improvements in medical and surgical therapies. Post-MI VSD is a medical emergency and outcome is very poor in medically treated patients. Treatment of choice remains surgical closure of defect and transcatheter defect closure less so. We performed a comprehensive review of the clinical presentation and management options of post-MI VSD.
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http://dx.doi.org/10.1016/j.carrev.2018.11.017 | DOI Listing |
Rev Cardiovasc Med
January 2025
Department of Cardiology, Hospital Clinico Universitario de Valencia, 46010 Valencia, Spain.
Background: Exercise-based cardiac rehabilitation programs (CRP) are recommended for patients following acute coronary syndrome to potentially improve high-density lipoprotein cholesterol (HDL-C) levels and prognosis. However, not all patients reach target HDL-C levels. Here we analyze the dynamics and predictors of HDL-C increase during CRP in patients following ST-segment elevation myocardial infarction or occlusion myocardial infarction.
View Article and Find Full Text PDFPharmacoecon Open
January 2025
Optimax Access Ltd, Kenneth Dibben House, Enterprise Rd, Chilworth, Southampton University Science Park, Southampton, UK.
Background: Patients with a left ventricular ejection fraction ≤ 35% are at increased risk of sudden cardiac death (SCD) within the first months after a myocardial infarction (MI). The wearable cardioverter defibrillator (WCD) is an established, safe and effective solution which can protect patients from SCD during the first months after an MI, when the risk of SCD is at its peak. This study aimed to evaluate the cost-effectiveness of WCD combined with guideline-directed medical therapy (GDMT) compared to GDMT alone, after MI in the English National Health Service (NHS).
View Article and Find Full Text PDFNPJ Regen Med
January 2025
Department of Cardiovascular Surgery, Université Paris Cité, INSERM U970, PARCC Hôpital Européen Georges Pompidou, 75015, Paris, France.
Myocardial infarction (MI) causes the loss of millions of cardiomyocytes, and current treatments do not address this root issue. New therapies focus on stimulating cardiomyocyte division in the adult heart, inspired by the regenerative capacities of lower vertebrates and neonatal mice. This review explores strategies for heart regeneration, offers insights into cardiomyocyte proliferation, evaluates in vivo models, and discusses integrating in vitro human cardiac models to advance cardiac regeneration research.
View Article and Find Full Text PDFFront Cardiovasc Med
January 2025
Department of Cardiology, Liuzhou Workers' Hospital, The Fourth Affiliated Hospital of Guangxi Medical University, Liuzhou, China.
Background: Fibroblasts in the fibrotic heart exhibit a heterogeneous biological behavior. The specific subsets of fibroblasts that contribute to progressive cardiac fibrosis remain unrevealed. Our aim is to identify the heart fibroblast (FB) subsets that most significantly promote fibrosis and the related critical genes as biomarkers for ischemic heart disease.
View Article and Find Full Text PDFFront Cardiovasc Med
January 2025
Department of Cardiology, Shibei Hospital of Jing'an District, Shanghai, China.
Objective: To investigate the effects of dapagliflozin, in addition to standard therapy, on heart rate variability (HRV), soluble growth stimulation expressed gene 2 protein (sST2), N-terminal pro B-type natriuretic peptide (NT-proBNP), and echocardiographic parameters in patients with early-onset post-myocardial infarction heart failure (HF).
Methods: A total of 98 patients with early-onset post-myocardial infarction HF were enrolled and randomly divided into a control group ( = 48, receiving standard therapy) and an observation group ( = 50, receiving standard therapy plus dapagliflozin 10 mg daily). HRV, cardiac function, and echocardiographic parameters were measured at baseline and after 24 weeks of treatment.
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