Background: Left ventricular (LV) remodeling after acute myocardial infarction has still to be clarified in the thrombolytic era.
Methods: To evaluate timing and the magnitude and pattern of postinfarct LV remodeling, a subset of 614 patients enrolled in the Gruppo Italiano per lo Studio della Sopravvivenza nell'Infarto Miocardico-3 Echo Substudy underwent serial 2-dimensional echocardiograms at 24 to 48 hours from symptom onset (S1), at hospital discharge (S2), at 6 weeks (S3), and at 6 months (S4) after acute myocardial infarction.
Results: During the study period the end-diastolic volume index (EDVi) increased (P <.001) and wall motion abnormalities (%WMA) decreased (P <.001), whereas ejection fraction (EF) remained unchanged. Nineteen percent of patients showed a > 20% increase in EDVi at S2 compared with S1 (severe early dilation), and 16% of patients showed a > 20% dilation at S4 compared with S2 (severe late dilation). Independent predictors of severe in-hospital LV dilation were relatively small EDVi (odds ratio [OR] 0.961, 95% confidence interval [CI] 0.947-0.974, P =.0001) and relatively large %WMA (OR 1.030, 95% CI 1.013-1.048, P =.0005). Similarly, smaller predischarge EDVi (OR 0.975, 95% CI 0. 963-0.987, P =.0001), greater %WMA (OR 1.026, 95% CI 1.008-1.045, P =.0042), and moderate to severe mitral regurgitation (OR 2.261, 95% CI 1.031-4.958, P = 0.0417) independently predicted severe late dilation. Importantly, 92% of the patients with severe early dilation did not have further dilation at S4, and 91% of patients with severe late dilation did not have in-hospital dilation. EF was unchanged over time in patients with early dilation, whereas it significantly decreased in those with late dilation.
Conclusions: Although in-hospital LV enlargement is not predictive of subsequent dilation and dysfunction, late remodeling is associated with progressive deterioration of global ventricular function over time: patients with extensive %WMA and not significantly enlarged ventricular volume before discharge are at higher risk for progressive dilation and dysfunction.
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http://dx.doi.org/10.1067/mhj.2001.111260 | DOI Listing |
Eur J Prev Cardiol
January 2025
Department of Occupational and Environmental Medicine, Bispebjerg Hospital, Copenhagen, Denmark.
Aims: Exposure to air pollution including diesel engine exhaust (DEE) is associated with increased risk of acute myocardial infarction (AMI). Few studies have investigated the risk of AMI according to occupational exposure to DEE. The aim of this study was to evaluate the association between occupational exposure to DEE and the risk of first-time AMI.
View Article and Find Full Text PDFCell Commun Signal
January 2025
Department of Vascular & Cardiology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Purpose: Cardiomyocyte death is a major cytopathologic response in acute myocardial infarction (AMI) and involves complex inflammatory interactions. Although existing reports indicating that mixed lineage kinase domain-like protein (MLKL) is involved in macrophage necroptosis and inflammasome activation, the downstream mechanism of MLKL in necroptosis remain poorly characterized in AMI.
Methods: MLKL knockout mice (MLKL), RIPK3 knockout mice (RIPK3), and macrophage-specific MLKL conditional knockout mice (MLKL) were established.
BMC Public Health
January 2025
Grupo de Investigación en Servicios Sanitarios de Aragón (GRISSA), Fundación Instituto de Investigación Sanitaria de Aragón (IIS Aragón), Zaragoza, Spain.
Background: European guidelines recommend the prescription of certain drugs after acute myocardial infarction (AMI). The existence of gender differences in pharmacological treatment after an AMI has been described. This study aims to describe and analyse, using real-world data (RWD), whether there are gender differences in the prescribing patterns and initiation of treatment in secondary prevention after a first AMI, and which are the factors that explain these differences.
View Article and Find Full Text PDFInt J Cardiovasc Imaging
January 2025
Department of Cardiovascular Medicine, Chiba University Graduate School of Medicine, Chiba, Japan.
Can J Cardiol
January 2025
University of Montreal Hospital Center (CHUM) Cardiovascular Center & Research Center (CRCHUM), University of Montreal, Montreal, Quebec, Canada. Electronic address:
Despite concerted efforts to rapidly identify patients with cardiogenic shock complicating acute myocardial infarction (AMI-CS) and provide timely revascularization, early mortality remains stubbornly high. While artificially augmenting systemic flow through the use of temporary mechanical circulatory support (tMCS) devices would be expected to reduce the rate of progression to multi-organ dysfunction and thereby enhance survival, reliable evidence for benefit has remained elusive with lingering questions regarding the appropriate selection of both patients and devices, as well as the timing of device implantation relative to other critical interventions. Further complicating matters are the resource-intensive multidisciplinary systems of care that must be brought to bear in this complex patient population.
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