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Stephen E. Epstein is the Head of Translational and Vascular Biology Research at the MedStar Heart and Vascular Institute, MedStar Washington Hospital Center and Clinical Professor of Medicine at the Georgetown University School of Medicine. [1] [2] [3] [4] [5] [6] [7]
After graduating summa cum laude from Columbia College and elected to Phi Beta Kappa, Epstein took his medical training at Cornell University Medical College. [1] He was elected to AOA, the medical honor society. Epstein interned at the New York Hospital, New York, NY. [1]
Epstein served for over 30 years as Chief of the Cardiology Branch of the NHLBI at the National Institutes of Health in Bethesda, MD. [2] [3] [8] [5] [9] [10] He then served as Executive Director of the Cardiovascular Research Institute and Director of Vascular Biology Research, at the MedStar Health Research Institute, Washington Hospital Center. He currently serves as Head of Translational Research at the MedStar Heart and Vascular Institute, MedStar Washington Hospital Center. [1] [2] [3] [8] [4] [5] [7]
With more than 500 publications in peer‐reviewed medical journals, Epstein is a recognized international authority on angiogenesis and on the application of stem cell strategies for cardiovascular therapeutics. [1] [2] [3] [8] [4] [5] [9] [7] His recent work on stem cell therapy [4] [5] [11] [10] [7] has demonstrated that mesenchymal stem cells (MSCs) when administered intravenously to mice with acute myocardial infarction and to mice with ischemic cardiomyopathy, markedly attenuate the progressive development of adverse left ventricular remodeling and deterioration in LV function. He and his associates have also demonstrated that one of the mechanisms responsible for these beneficial effects is a modulation of the excessive immune and inflammatory responses that are triggered by the presence of an injured left ventricle. These observations resulted in the initiation of two clinical trials testing the efficacy of the intravenous injection of MSCs in patients with heart failure. The observations are now being used to inform the development of novel monoclonal antibody strategies to modulate inflammation for treating patients with myocardial infarctions, patients with heart failure, and patients with various autoimmune diseases. [2]
Epstein and his colleagues have developed a biomarker strategy that identifies patients with coronary artery disease who are at very high near-term risk of experiencing death or an acute myocardial infarction. [8] [6]
Epstein served on two National Heart, Lung, and Blood Institute (NHLBI) committees: Vice‐Chairman of the Data Safety Management Board (DSMB) for Programs of Excellence in Gene and Cell Therapy for the Heart, Lung, and Blood Institute, and Chairman of the DSMB for Specialized Centers for Clinically Oriented Research in Cardiac Dysfunction and Disease. [1]
Epstein is also a Fellow of the American Heart Association, a member of the Association of American Physicians, and an Honorary Fellow of the American College of Chest Physicians. He is the recipient of the Distinguished WELCOME Lecturer award, was selected for the Pfizer Visiting Professor Program. [1]
Atherosclerosis is a pattern of the disease arteriosclerosis, characterized by development of abnormalities called lesions in walls of arteries. This is a chronic inflammatory disease involving many different cell types and driven by elevated levels of cholesterol in the blood. These lesions may lead to narrowing of the arterial walls due to buildup of atheromatous plaques. At the onset there are usually no symptoms, but if they develop, symptoms generally begin around middle age. In severe cases, it can result in coronary artery disease, stroke, peripheral artery disease, or kidney disorders, depending on which body part(s) the affected arteries are located in the body.
Thrombolysis, also called fibrinolytic therapy, is the breakdown (lysis) of blood clots formed in blood vessels, using medication. It is used in ST elevation myocardial infarction, stroke, and in cases of severe venous thromboembolism.
Pericarditis is inflammation of the pericardium, the fibrous sac surrounding the heart. Symptoms typically include sudden onset of sharp chest pain, which may also be felt in the shoulders, neck, or back. The pain is typically less severe when sitting up and more severe when lying down or breathing deeply. Other symptoms of pericarditis can include fever, weakness, palpitations, and shortness of breath. The onset of symptoms can occasionally be gradual rather than sudden.
Coronary thrombosis is defined as the formation of a blood clot inside a blood vessel of the heart. This blood clot may then restrict blood flow within the heart, leading to heart tissue damage, or a myocardial infarction, also known as a heart attack.
Cardiac markers are biomarkers measured to evaluate heart function. They can be useful in the early prediction or diagnosis of disease. Although they are often discussed in the context of myocardial infarction, other conditions can lead to an elevation in cardiac marker level.
Acute coronary syndrome (ACS) is a syndrome due to decreased blood flow in the coronary arteries such that part of the heart muscle is unable to function properly or dies. The most common symptom is centrally located pressure-like chest pain, often radiating to the left shoulder or angle of the jaw, and associated with nausea and sweating. Many people with acute coronary syndromes present with symptoms other than chest pain, particularly women, older people, and people with diabetes mellitus.
Percutaneous coronary intervention (PCI) is a minimally invasive non-surgical procedure used to treat narrowing of the coronary arteries of the heart found in coronary artery disease. The procedure is used to place and deploy coronary stents, a permanent wire-meshed tube, to open narrowed coronary arteries. PCI is considered 'non-surgical' as it uses a small hole in a peripheral artery (leg/arm) to gain access to the arterial system; an equivalent surgical procedure would involve the opening of the chest wall to gain access to the heart area. The term 'coronary angioplasty with stent' is synonymous with PCI. The procedure visualises the blood vessels via fluoroscopic imaging and contrast dyes. PCI is performed by an interventional cardiologists in a catheterization laboratory setting.
Paul M. Ridker is a cardiovascular epidemiologist and biomedical researcher. He is currently the Eugene Braunwald Professor of Medicine at Harvard University and Brigham and Women's Hospital, where he directs the Center for Cardiovascular Disease Prevention. Ridker also holds an appointment as Professor in the Department of Epidemiology at the Harvard T.H. Chan School of Public Health.
Désiré, Baron Collen is a Belgian physician, chemist, biotechnology entrepreneur and life science investor. He made several discoveries in thrombosis, haemostasis and vascular biology in many of which serendipity played a significant role. His main achievement has been his role in the development of tissue-type plasminogen activator (t-PA) from a laboratory concept to a life-saving drug for dissolving blood clots causing acute myocardial infarction or acute ischemic stroke. Recombinant t-PA was produced and marketed by Genentech Inc as Activase and by Boehringer Ingelheim GmbH as Actilyse, and is considered biotechnology's first life saving drug.
Troponin I is a cardiac and skeletal muscle protein family. It is a part of the troponin protein complex, where it binds to actin in thin myofilaments to hold the actin-tropomyosin complex in place. Troponin I prevents myosin from binding to actin in relaxed muscle. When calcium binds to the troponin C, it causes conformational changes which lead to dislocation of troponin I. Afterwards, tropomyosin leaves the binding site for myosin on actin leading to contraction of muscle. The letter I is given due to its inhibitory character. It is a useful marker in the laboratory diagnosis of heart attack. It occurs in different plasma concentration but the same circumstances as troponin T - either test can be performed for confirmation of cardiac muscle damage and laboratories usually offer one test or the other.
A coronary stent is a tube-shaped device placed in the coronary arteries that supply blood to the heart, to keep the arteries open in patients suffering from coronary heart disease. The vast majority of stents used in modern interventional cardiology are drug-eluting stents (DES). They are used in a medical procedure called percutaneous coronary intervention (PCI). Coronary stents are divided into two broad types: drug-eluting and bare metal stents. As of 2023, drug-eluting stents were used in more than 90% of all PCI procedures. Stents reduce angina and have been shown to improve survival and decrease adverse events after a patient has suffered a heart attack—medically termed an acute myocardial infarction.
A myocardial infarction (MI), commonly known as a heart attack, occurs when blood flow decreases or stops in one of the coronary arteries of the heart, causing infarction to the heart muscle. The most common symptom is retrosternal chest pain or discomfort that classically radiates to the left shoulder, arm, or jaw. The pain may occasionally feel like heartburn. This is the dangerous type of Acute coronary syndrome.
The JUPITER trial was a clinical trial aimed at evaluating whether statins reduce heart attacks and strokes in people with normal cholesterol levels.
Spontaneous coronary artery dissection (SCAD) is an uncommon but potentially lethal condition in which one of the coronary arteries that supply the heart, spontaneously develops a blood collection, or hematoma, within the artery wall due to a tear in the wall. SCAD is one of the arterial dissections that can occur.
Cardiovascular Cell Therapy Research Network (CCTRN) is a network of physicians, scientists, and support staff dedicated to studying stem cell therapy for treating heart disease. The CCTRN is funded by the National Institutes of Health (NIH) and includes expert researchers with experience in cardiovascular care at seven stem cell centers in the United States. The goals of the Network are to complete research studies that will potentially lead to more effective treatments for patients with cardiovascular disease, and to share knowledge quickly with the healthcare community.
A diagnosis of myocardial infarction is created by integrating the history of the presenting illness and physical examination with electrocardiogram findings and cardiac markers. A coronary angiogram allows visualization of narrowings or obstructions on the heart vessels, and therapeutic measures can follow immediately. At autopsy, a pathologist can diagnose a myocardial infarction based on anatomopathological findings.
Management of acute coronary syndrome is targeted against the effects of reduced blood flow to the affected area of the heart muscle, usually because of a blood clot in one of the coronary arteries, the vessels that supply oxygenated blood to the myocardium. This is achieved with urgent hospitalization and medical therapy, including drugs that relieve chest pain and reduce the size of the infarct, and drugs that inhibit clot formation; for a subset of patients invasive measures are also employed. Basic principles of management are the same for all types of acute coronary syndrome. However, some important aspects of treatment depend on the presence or absence of elevation of the ST segment on the electrocardiogram, which classifies cases upon presentation to either ST segment elevation myocardial infarction (STEMI) or non-ST elevation acute coronary syndrome (NST-ACS); the latter includes unstable angina and non-ST elevation myocardial infarction (NSTEMI). Treatment is generally more aggressive for STEMI patients, and reperfusion therapy is more often reserved for them. Long-term therapy is necessary for prevention of recurrent events and complications.
Varespladib is an inhibitor of the IIa, V, and X isoforms of secretory phospholipase A2 (sPLA2). The molecule acts as an anti-inflammatory agent by disrupting the first step of the arachidonic acid pathway of inflammation. From 2006 to 2012, varespladib was under active investigation by Anthera Pharmaceuticals as a potential therapy for several inflammatory diseases, including acute coronary syndrome and acute chest syndrome. The trial was halted in March 2012 due to inadequate efficacy. The selective sPLA2 inhibitor varespladib (IC50 value 0.009 μM in chromogenic assay, mole fraction 7.3X10-6) was studied in the VISTA-16 randomized clinical trial (clinicaltrials.gov Identifier: NCT01130246) and the results were published in 2014. The sPLA2 inhibition by varespladib in this setting seemed to be potentially harmful, and thus not a useful strategy for reducing adverse cardiovascular outcomes from acute coronary syndrome. Since 2016, scientific research has focused on the use of Varespladib as an inhibitor of snake venom toxins using various types of in vitro and in vivo models. Varespladib showed a significant inhibitory effect to snake venom PLA2 which makes it a potential first-line drug candidate in snakebite envenomation therapy. In 2019, the U.S. Food and Drug Administration (FDA) granted varespladib orphan drug status for its potential to treat snakebite.
Circulating endothelial cells (CECs) are endothelial cells that have been shed from the lining of the vascular wall into the blood stream. Endothelial cells normally line blood vessels to maintain vascular integrity and permeability, but when these cells enter into the circulation, this could be a reflection of vascular dysfunction and damage. There are many factors involved in the process of creating CECs, including: reduced interaction between the endothelial cells and basement membrane proteins, damaged endothelial cellular adhesion molecules, mechanical injury, decreased survival of cytoskeletal proteins, and inflammation.
Nehal N. Mehta, is an American cardiologist at the National Heart, Lung, and Blood Institute (NHLBI) in Bethesda, Maryland where he studies the role of innate immunity and inflammation in the development of cardiovascular and metabolic diseases.
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