Coronary artery disease is caused by plaque buildup in the wall of the arteries that supply blood to the heart and is the most common heart disease in the United States. Angioplasty or coronary stent procedures are current treatment options to open coronary arteries to improve blood flow to the heart muscle.
The research program in the Cardiovascular Research Center at Rhode Island Hospital seeks to understand the regulation of the microcirculation in health and disease, ischemic injury and inflammation during cardiac surgery, collateral vascular formation in chronic myocardial ischemia, and the use of growth factors, cell therapy and modulation of subcellular oxidant levels to increase blood flow to ischemic myocardium.
Researchers are investigating potential signaling pathways including nitric oxide and reactive oxygen species that alter the function of coronary artery endothelial cells, focusing on the development of novel therapeutic modalities for ischemic heart diseases.
Clinical research in the Cardiovascular Research Center also focuses on optimizing outcomes after cardiac surgery, the reduction of bleeding and transfusion, and neurocognitive dysfunction and atrial fibrillation after surgery. In addition, the research program focuses on vascular/endothelial biology and cardiovascular diseases associated with metabolic syndrome, diabetes, hypertension and related cellular and electrical signaling to advance understanding of coronary heart diseases, particularly macrovascular and microvascular diseases caused by metabolic syndrome, diabetes, and hypertension; and to develop novel therapeutic strategies to effectively treat patients with metabolic syndrome, diabetes, hypertension and coronary artery diseases.
Enhanced coronary arteriolar contraction to vasopressin in patients with diabetes after cardiac surgery (https://pubmed.ncbi.nlm.nih.gov/30057184/)
Clinical Application of Novel Therapies for Coronary Angiogenesis: Overview, Challenges, and Prospects (https://pubmed.ncbi.nlm.nih.gov/33918396/)
Chronic Inhibition of mROS Protects Against Coronary Endothelial Dysfunction in Mice With Diabetes
“Metabolic regulation of endothelial SK channels and human coronary microvascular function” (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7388214/)
“Inhibition of mitochondrial reactive oxygen species protects against coronary endothelial function following cardioplegic hypoxia/reoxygenation” (https://pubmed.ncbi.nlm.nih.gov/34274141/)
“Assessments of microvascular function in organ systems” (https://pubmed.ncbi.nlm.nih.gov/35333121/)
“Mechanisms and clinical implications of endothelium-dependent vasomotor dysfunction in coronary microvasculature” (https://pubmed.ncbi.nlm.nih.gov/35333122/)
“Extracellular vesicles improve diastolic function and substructure in normal and high-fat diet models of chronic myocardial ischemia” (https://pubmed.ncbi.nlm.nih.gov/34756431/)
“Optimization of mito-roGFP protocol to measure mitochondrial oxidative status in human coronary artery endothelial cells” (https://pubmed.ncbi.nlm.nih.gov/34458871/)
“Mitochondrial redox plays a critical role in the paradoxical effects of NAPDH oxidase-derived ROS on coronary endothelium” (https://pubmed.ncbi.nlm.nih.gov/28088753/)
Frank W. Sellke
M. Ruhul Abid