We developed a new animal model of ischemic mitral insufficiency in sheep and used it to test the hypothesis that the combination of posterior papillary muscle infarction and left ventricular dilatation was required to produce mitral regurgitation after acute inferior myocardial infarction of moderate size. In 12 sheep, ligation of the first two circumflex marginal coronary arteries infarcted 23% of the left ventricular mass, increased left ventricular cavitary area from 13.2 +/- 1.2 cm2 to 20.0 +/- 2.7 cm2 by 8 weeks and did not produce ischemic mitral regurgitation. In 13 sheep, ligation of the second and third circumflex marginal arteries infarcted 21% of the left ventricular mass and, in 11 of these sheep, the posterior papillary muscular mass as well. When the papillary muscle was included, this infarction produced progressively severe mitral regurgitation over 8 weeks, as left ventricular cavitary area increased from 12.5 +/- 2.6 cm2 to 22.8 +/- 3.8 cm2. We conclude that neither posterior papillary muscle infarction nor left ventricular dilatation alone produces ischemic mitral regurgitation after moderate-sized inferior wall infarction, but that the combination does.
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Cardiol Rev
January 2025
Departments of Cardiology and Medicine, New York Medical College and Westchester Medical Center, Valhalla, NY.
Right ventricular myocardial infarction (RVMI) is a significant and distinct form of acute myocardial infarction associated with considerable morbidity and mortality. It occurs most commonly due to proximal right coronary artery obstruction, often in conjunction with inferior myocardial infarction. RVMI poses unique diagnostic and therapeutic challenges due to the anatomical and functional differences between the right and left ventricles.
View Article and Find Full Text PDFPLoS One
January 2025
Department of Pathology, 906 Hospital of Joint Logistic Support Force of PLA, Ningbo, Zhejiang, China.
Objective: To investigate the effects and mechanisms of miRNA 221 on myocardial ischemia/reperfusion injury (MIRI) in mice through the regulation of phospholamban (PLB) expression.
Methods: The MIRI mouse model was created and mice were divided into sham, MIRI, MIRI+ 221, and MIRI+ scr groups, with miRNA 221 overexpression induced in the myocardium of MIRI mice by targeted myocardial injection. Quantitative RT-PCR analysis was performed to observe the variation in miRNA 221, PLB, SERCA2, RYR2, NCX1, Cyt C and caspase 3 mRNA levels in myocardium, while Western blot assessed the levels of PLB, p-PLB (Ser16), p-PLB (Thr17), SERCA2, RYR2, NCX1, Cyt C and caspase 3 proteins.
Phys Eng Sci Med
January 2025
School of Electrical Engineering and Electronic Information, Xihua University, Chengdu, China.
Hypertrophic cardiomyopathy (HCM), including obstructive HCM and non-obstructive HCM, can lead to sudden cardiac arrest in adolescents and athletes. Early diagnosis and treatment through auscultation of different types of HCM can prevent the occurrence of malignant events. However, it is challenging to distinguish the pathological information of HCM related to differential left ventricular outflow tract pressure gradients.
View Article and Find Full Text PDFHerzschrittmacherther Elektrophysiol
January 2025
Klinik für Elektrophysiologie/Rhythmologie, Ruhr-Universität Bochum, Bochum, Deutschland.
Atrial fibrillation (AF) ablation is associated with a lower likelihood of death and surgical heart failure (HF) interventions in patients with HF. This effect is mainly driven by reduced all cause and cardiovascular death following ablation. Ablation also results in improved left ventricular (LV) function, decreased AF burden and AF regression.
View Article and Find Full Text PDFMultimed Man Cardiothorac Surg
January 2025
Congenital Heart Center, Division of Cardiovascular Surgery, Department of Surgery, University of Florida, Gainesville, FL, USA.
The Berlin Heart EXCOR is a pulsatile paracorporeal ventricular assist device (VAD) for neonates, infants, children and adults with congenital or acquired severe ventricular dysfunction. Berlin Heart EXCOR VADs are routinely used as either a bridge to a cardiac transplantation, or occasionally as a bridge to ventricular recovery. Our programmatic philosophy is to bridge neonates and infants with functionally univentricular ductal-dependent systemic circulation or functionally univentricular ductal-dependent pulmonary circulation who are at high risk for staged palliation because of important cardiac risk factors with a single-ventricle VAD (sVAD) as a bridge to a cardiac transplant.
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