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Full-Text Articles in Cardiovascular Diseases
Cardiac Fibroblast-Dependent Extracellular Matrix Accumulation Is Associated With Diastolic Stiffness In Type 2 Diabetes., Kirk R. Hutchinson, C. Kevin Lord, T. Aaron West, James A. Stewart
Cardiac Fibroblast-Dependent Extracellular Matrix Accumulation Is Associated With Diastolic Stiffness In Type 2 Diabetes., Kirk R. Hutchinson, C. Kevin Lord, T. Aaron West, James A. Stewart
College of Arts and Sciences Publications and Scholarship
Cardiovascular complications are a leading cause of death in patients with type 2 diabetes mellitus (T2DM). Diastolic dysfunction is one of the earliest manifestations of diabetes-induced changes in left ventricular (LV) function, and results from a reduced rate of relaxation and increased stiffness. The mechanisms responsible for increased stiffness are not completely understood. Chronic hyperglycemia, advanced glycation endproducts (AGEs), and increased levels of proinflammatory and profibrotic cytokines are molecular pathways known to be involved in regulating extracellular matrix (ECM) synthesis and accumulation resulting in increased LV diastolic stiffness. Experiments were conducted using a genetically-induced mouse model of T2DM generated by …
Loss Of Dystrophin Staining In Cardiomyocytes: A Novel Method For Detection Early Myocardial Infarction, Satwat Hashmi, Suhail Al-Salam
Loss Of Dystrophin Staining In Cardiomyocytes: A Novel Method For Detection Early Myocardial Infarction, Satwat Hashmi, Suhail Al-Salam
Department of Biological & Biomedical Sciences
Myocardial infarction (MI) is the most frequent diagnosis made in majority of sudden death cases subjected to clinical and medicolegal autopsies. When sudden death occurs at a very early stage of MI, traditional macroscopic examination, or histological stains cannot easily detect the myocardial changes. For this reason we propose a new method for detecting MI at an early stage. Murine model of MI was used to induce MI through permanent ligation of left anterior descending branch of left coronary artery. Five groups of C57B6/J mice were used for inducing MI, which includes 20 minutes, 30 minutes, one hour, four hours …
Early Hemodynamic And Biochemical Changes In Overloaded Swine Ventricle.Early Hemodynamic And Biochemical Changes In Overloaded Swine Ventricle, Sandro Gelsomino, Fabiana Lucà, Chiara Nediani, Sandra Zecchi Orlandini, Daniele Bani, Antonio S Rubino, Attilio Renzulli, Roberto Lorusso, Andrea Consolo, Antonino Lo Cascio, Jos Maessen, Gian Franco Gensini
Early Hemodynamic And Biochemical Changes In Overloaded Swine Ventricle.Early Hemodynamic And Biochemical Changes In Overloaded Swine Ventricle, Sandro Gelsomino, Fabiana Lucà, Chiara Nediani, Sandra Zecchi Orlandini, Daniele Bani, Antonio S Rubino, Attilio Renzulli, Roberto Lorusso, Andrea Consolo, Antonino Lo Cascio, Jos Maessen, Gian Franco Gensini
The Texas Heart Institute Journal
The present study was undertaken to investigate, in an animal model, the relationship between sarcoplasmic reticulum Ca2+-ATPase (SERCA2a) activity, phospholamban phosphorylation, acylphosphatase activity, and hemodynamic changes that occur in the early phase of pressure overload. In 54 study-group pigs, weighing 40±5 kg each, an aortic stenosis was created with a band of umbilical tape tied around the aorta; 18 sham-operated pigs formed our control group. Eight animals (6 study and 2 control) were randomly assigned to each experimental time (0.5, 3, 6, 12, 24, 48, 72, 96, and 168 hr). All indices of left ventricular function declined significantly, with a …
The Pathobiology Of Acute Coronary Syndromes: Clinical Implications And Central Role Of The Mitochondria, L Maximilian Buja
The Pathobiology Of Acute Coronary Syndromes: Clinical Implications And Central Role Of The Mitochondria, L Maximilian Buja
The Texas Heart Institute Journal
Ongoing investigation has provided new insights into the pathobiology of myocardial ischemic injury. These include an improved understanding of the roles of the major modes of cell injury and death, including oncosis, apoptosis, and unregulated autophagy, as well as the central role of the mitochondria in the progression of myocardial ischemic injury, reperfusion injury, and myocardial conditioning. This understanding is providing insights for developing new pathophysiologic, pharmacologic, and cell-based therapies, alone or in combination with percutaneous coronary interventions, for better preservation of myocardium and reduction of morbidity and mortality rates from ischemic heart disease.