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Aim: Left ventricular remodeling (LVR) after myocardial infarction (MI) can lead to heart failure, arrhythmia, and death. We aim to describe adverse LVR patterns at 6 months post-MI and their relationships with subsequent outcomes and to determine baseline.
Methods And Results: A multicenter cohort of 410 patients (median age 57 years, 87% male) with reperfused MI and at least 3 akinetic LV segments on admission was analyzed. All patients had transthoracic echocardiography performed 4 days and 6 months post-MI, and 214 also had cardiac magnetic resonance imaging performed on day 4. To predict LVR, machine learning methods were employed in order to handle many variables, some of which may have complex interactions. Six months post-MI, echocardiographic increases in LV end-diastolic volume (LVEDV), LV end-systolic volume (LVESV), and LV ejection fraction (LVEF) were 14.1% [interquartile range 0.0, 32.0], 5.0% [- 14.0, 25.8], and 8.7% [0.0, 19.4], respectively. At 6 months, ≥ 15% or 20% increases in LVEDV were observed in 49% and 42% of patients, respectively, and 37% had an LVEF < 50%. The rate of death or new-onset HF at the end of 5-year follow-up was 8.8%. Baseline variables associated with adverse LVR were determined best by random forest analysis and included stroke volume, stroke work, necrosis size, LVEDV, LVEF, and LV afterload, the latter assessed by Ea or Ea/Ees. In contrast, baseline clinical and biological characteristics were poorly predictive of LVR. After adjustment for predictive baseline variables, LV dilation > 20% and 6-month LVEF < 50% were significantly associated with the risk of death and/or heart failure: hazard ratio (HR) 2.12 (95% confidence interval (CI) 1.05-4.43; p = 0.04) and HR 2.68 (95% CI 1.20-6.00; p = 0.016) respectively.
Conclusion: Despite early reperfusion and cardioprotective therapy, adverse LVR remains frequent after acute MI and is associated with a risk of death and HF. A machine learning approach identified and prioritized early variables that are associated with adverse LVR and which were mainly hemodynamic, combining LV volumes, estimates of systolic function, and afterload.
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http://dx.doi.org/10.1007/s00392-023-02331-z | DOI Listing |
Eur Heart J Imaging Methods Pract
July 2025
Division of Cardiology, Medical University of Vienna, Waehringer Guertel 18-20, Vienna 1090, Austria.
Aims: Cardiac miR-132 has been proposed as a target for heart failure (HF) therapy. CDR132L, a rationally designed synthetic oligonucleotide inhibitor of miR-132 has proved pre-clinical efficacy in non-ischaemic and ischaemic large animal HF models. The safety and tolerability of CDR132L were tested in chronic HF patients in a Phase 1b study (NCT04045405) and is currently being tested in a Phase 2 trial in post-MI HF patients (NCT05350969).
View Article and Find Full Text PDFVascul Pharmacol
September 2025
Department of Thromboembolic Disorders, Institute of Cardiology, Jagiellonian University Medical College, 31-202 Krakow, Poland; Krakow Center for Medical Research and Technologies, St. John Paul II Hospital, 31-202 Krakow, Poland. Electronic address:
Background: Serum lipopolysaccharide (LPS), a marker of gut dysbiosis and endotoxemia is associated with myocardial infarction (MI). We investigated factors affecting LPS changes in MI patients treated with percutaneous coronary intervention (PCI) and aimed to establish factors associated with the degree of LPS decrease following MI.
Methods: In 46 PCI-treated MI patients (mean age 57.
BMC Cardiovasc Disord
July 2025
Nutrition Research Center, Department of Public Health, School of Health, Shiraz University of Medical Sciences, Shiraz, Shiraz, Iran.
Introduction: Myocardial Infarction (MI) ranks among the major causes of death and disability globally. The modifiable risk factors are very important not only for its prevention, but also for its long-term management. Adherence to self-care plays a very important part in improving outcomes following MI.
View Article and Find Full Text PDFAm J Physiol Heart Circ Physiol
August 2025
Division of Cardiovascular Sciences, Department of Internal Medicine, Morsani College of Medicine, Heart Institute, University of South Florida, Tampa, Florida, United States.
Heart failure (HF) is a major outcome in cardiovascular disease resulting from myocardial infarction (MI). Preclinical studies use MI-induced HF rodent models with either permanent coronary occlusion (PO) or transient ligation to induce ischemia-reperfusion (I/R). Comparisons of inflammation-resolution signaling in these models are understudied.
View Article and Find Full Text PDFAtherosclerosis
September 2025
Vascular Research Centre, Lifelong Health Theme, South Australian Health and Medical Research Institute, Adelaide, Australia; Adelaide Medical School, Faculty of Health and Medical Sciences, The University of Adelaide, Adelaide, Australia; Department of Cardiology, Central Adelaide Local Health Netw
Background And Aims: The measurement of lipid species in blood holds promise for identifying new biomarkers associated with coronary atherosclerosis. Here, we examined for relationships between circulating lipid species and coronary plaque changes following acute myocardial infarction (MI) in patients on guideline-recommended treatment.
Methods: In this post-hoc analysis of the INFLAME study, patients presenting with MI underwent serum lipidomic analysis and coronary computed tomography angiography (CCTA) during admission and at 6-month follow-up.