The left ventricular (LV) scar size detected by cardiac magnetic resonance (CMR) imaging in ischemic cardiomyopathy (IC) has been correlated with mortality. However, the associations among myocardial fibrosis, ventricular geometry, and physiologic measures of myocardial performance remain to be defined. A retrospective analysis of patients with stable chronic IC (LV ejection fraction ≤50%) who underwent CMR imaging from 2004 to 2010 and had plasma B-type natriuretic peptide (BNP) measured within 14 days of the CMR study was undertaken. A total of 38 patients met the criteria (mean age 66 ± 10 years; 31 men [82%]). The duration of IC was 67 ± 69 months. The CMR characteristics included LV dilation (LV end-diastolic dimension 62 ± 8 mm) and severe systolic dysfunction (LV ejection fraction 28 ± 11%). The average quantitated myocardial fibrosis was 20 ± 12% of the LV mass. When stratified by fibrotic mass, increased myocardial scar size was associated with increased LV cavity size (p = 0.007), lower LV ejection fraction (p = 0.04), and higher BNP (p = 0.013). In comparison, when stratified by median BNP (475 pg/ml), an elevated BNP level was associated, not only with LV size, function, and degree of fibrosis, but also with increased meridional wall stress (p = 0.002) and worse New York Heart Association functional class (p = 0.006). In conclusion, in chronic IC, quantitated myocardial fibrosis is associated with CMR structural and functional LV abnormalities. Elevated BNP levels are related to high-risk structural and functional CMR abnormalities and wall stress and functional status. Myocardial fibrosis appears to be related to plasma BNP through the processes of ventricular remodeling.
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http://dx.doi.org/10.1016/j.amjcard.2011.09.027 | DOI Listing |
Cell Signal
January 2025
Department of Cardiovascular Surgery, The Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China; Future Medical laboratory, The Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China. Electronic address:
Background: Dichloroacetate (DCA) has shown potential in modulating cellular metabolism and inflammation, particularly in cardiac conditions. This study investigates DCA's protective effects in a mouse model of myocardial infarction (MI), focusing on its ability to enhance cardiac function, reduce inflammation, and shift macrophage polarization from the pro-inflammatory M1 to the anti-inflammatory M2 phenotype.
Methods: An acute MI model was created using left anterior descending coronary artery ligation.
Eur J Prev Cardiol
January 2025
St Vincent's Institute of Medical Research, 9 Princes St Fitzroy VIC 3065 Australia.
Aim: To define the association between severe coronary artery disease and widespread atherosclerosis in younger individuals.
Methods: Individuals aged 1-50 years with sudden cardiac death (SCD) from 2019-23, autopsy-proven to be due to coronary artery disease, were identified using the state-wide EndUCD registry. Presence of extra-coronary atherosclerosis greater than modified American Heart Association class III was assessed in 5 arterial beds (intra-cerebral vessels, aorta, carotid, renal and femoral arteries).
Front Biosci (Landmark Ed)
January 2025
Department of Biomedical Sciences, Grand Valley State University, Allendale, MI 49401, USA.
Background: Diabetes mellitus is associated with morphological and functional impairment of the heart primarily due to lipid toxicity caused by increased fatty acid metabolism. Extracellular signal-regulated protein kinases 1 and 2 (ERK1/2) have been implicated in the metabolism of fatty acids in the liver and skeletal muscles. However, their role in the heart in diabetes remains unclear.
View Article and Find Full Text PDFMedicina (Kaunas)
December 2024
Clinic for Gastroenterology and Hepatology, University Clinical Centre of Serbia, 11 000 Belgrade, Serbia.
Cirrhotic cardiomyopathy (CCM) is a diagnostic entity defined as cardiac dysfunction (diastolic and/or systolic) in patients with liver cirrhosis, in the absence of overt cardiac disorder. Pathogenically, CCM stems from a combination of systemic and local hepatic factors that, through hemodynamic and neurohormonal changes, affect the balance of cardiac function and lead to its remodeling. Vascular changes in cirrhosis, mostly driven by portal hypertension, splanchnic vasodilatation, and increased cardiac output alongside maladaptively upregulated feedback systems, lead to fluid accumulation, venostasis, and cardiac dysfunction.
View Article and Find Full Text PDFBiomolecules
January 2025
Heart and Vascular Institute, Pennsylvania State University Hershey Medical Center, Hershey, PA 17033, USA.
Immuno-fibrotic networks and their protein mediators, such as cytokines and chemokines, have increasingly been appreciated for their critical role in cardiac healing and fibrosis during cardiomyopathy. Immune activation, trafficking, and extravasation are tightly regulated to ensure a targeted and effective response against non-self antigens/pathogens while preserving tolerance towards self-antigens and coordinate fibrotic responses for efficient scar formation, a distinction that is severely compromised during chronic diseases. It is clear that immune cells are not only the critical regulators of post-infarct healing and scarring but are also the key players in regulating fibroblast activation during left-ventricular (LV) remodeling.
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