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Nicholas George Kounis is professor emeritus of cardiology in the University of Patras and scientific cardiology advisor at Saint Andrews (Agios Andreas) State General Hospital Patras and at the Department of cardiology of University of Patras Medical School, Patras, Greece.
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He was born in Patras from Greek parents after his father's return from the United States of America where he emigrated in 1914, became an American citizen, served in the American Army, fought and injured in action in France during the 1st World War. This enabled Dr Kounis to get also the American citizenship. After bright elementary and Lyceum studies he passed the entrance examinations and entered first of all candidates in the Athens University Medical School. There, he had also a bright undergraduate career and qualified first of all students after 5 and a half years (normally the course lasts 6 years) as MD. Following this, he served the compulsory military service in the Greek Army for 2 and a half years as a Medical Lieutenant in various army units and areas including Cyprus. After finishing the army service, he performed the compulsory service as a medical practitioner in rural Greek areas.
In 1971, he moved to the United Kingdom where he undertook postgraduate medical training first in medicine and later in adult and pediatric cardiology as house officer, senior house officer, registrar, senior registrar and clinical tutor for 10 years under famous teachers including the Queen's physician David Somerset Short of Aberdeen University, Scotland and professor James Francis "Frank" Pantridge of Queen's University of Belfast, Northern Ireland. During this period he passed the board specialty examinations in medicine, the board specialty examinations in Cardiology and received his doctorate in 1976 from Athens University with doctoral thesis: Contribution to the prevention and treatment of chronic thromboembolism with a new regimen including Arvin, heparin, phenformin, orabolin and warfarin. [1] [2]
On his return to Greece, in 1981, he was appointed consultant cardiologist and director of the Intensive Care Unit at “Saint Andrews University Hospital”, Department of medicine, University of Patras Medical School. It was during this period when he treated two patients who developed angina progressing to acute myocardial infarction following an allergic reaction after shellfish ingestion. Following this observation, Paris Constantinides MD Vienna, Austria and PhD Montreal, Canada who was the first to discover that the junctions between endothelial cells that line human atheromatous plaques are open in contrast to closed junctions over the normal arterial intima, in an editorial in the journal “Circulation” raised the possibility that “even ordinary reactions could promote plaque disruption”.
One of his contributions to medical science is describing the Kounis syndrome, [3] [4] the name given to "anaphylactic CHD [coronary heart disease] including patients with drug eluting coronary stents". [5] He received his MD and PhD from Athens Medical School. He worked in various hospitals in Greece including a 10-year term as consultant and director of the Intensive Care Unit of the department of cardiology of the University of Patras Medical School and culminating in an appointment to Patras Highest Institute of Education and Technology Department of Medical Sciences [ATEI of Patras, now University of Patras] in 1988. [6]
Kounis is an emeritus professor of medicine, research advisor to the Cardiology department of University of Patras, Greece, Chief Editor of the medical Journal "Achaiki Iatriki" and is doing some private practice sessions. He lives in Patras, Achaia, Greece with his wife, daughter, son and a grandson.[ citation needed ]
His description of Kounis syndrome, denoting for the first time a hypersensitivity blow up inside the coronary, cerebral and mesenteric arteries, might have profound clinical and therapeutic implications because he discovered that the same mediators, released during acute allergic episodes, are increased in blood or urine of patients with acute coronary syndromes of nonallergic etiology. [7] [8] Consequently, the same substances from the same cells are present in both acute allergic episodes and acute coronary syndromes. Drugs and natural molecules which stabilize mast cell membrane, monoclonal antibodies that protect mast cell surface and drugs that are targeting at stem cell factor which is essential for mast cell growth, proliferation, survival, adhesion, homing and differentiation could emerge as novel therapeutic modalities capable of preventing acute coronary, cerebrovascular and other arterial events. [9]
Angina, also known as angina pectoris, is chest pain or pressure, usually caused by insufficient blood flow to the heart muscle (myocardium). It is most commonly a symptom of coronary artery disease.
An antiplatelet drug (antiaggregant), also known as a platelet agglutination inhibitor or platelet aggregation inhibitor, is a member of a class of pharmaceuticals that decrease platelet aggregation and inhibit thrombus formation. They are effective in the arterial circulation where classical Vitamin K antagonist anticoagulants have minimal effect.
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.
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.
Variant angina, also known as Prinzmetal angina,vasospastic angina, angina inversa, coronary vessel spasm, or coronary artery vasospasm, is a syndrome typically consisting of angina. Variant angina differs from stable angina in that it commonly occurs in individuals who are at rest or even asleep, whereas stable angina is generally triggered by exertion or intense exercise. Variant angina is caused by vasospasm, a narrowing of the coronary arteries due to contraction of the heart's smooth muscle tissue in the vessel walls. In comparison, stable angina is caused by the permanent occlusion of these vessels by atherosclerosis, which is the buildup of fatty plaque and hardening of the arteries.
Unstable angina is a type of angina pectoris that is irregular or more easily provoked. It is classified as a type of acute coronary syndrome (ACS).
Percutaneous coronary intervention (PCI) is a non-surgical procedure used to treat narrowing of the coronary arteries of the heart found in coronary artery disease. The process involves combining coronary angioplasty with stenting, which is the insertion of a permanent wire-meshed tube that is either drug eluting (DES) or composed of bare metal (BMS). The stent delivery balloon from the angioplasty catheter is inflated with media to force contact between the struts of the stent and the vessel wall, thus widening the blood vessel diameter. After accessing the blood stream through the femoral or radial artery, the procedure uses coronary catheterization to visualise the blood vessels on X-ray imaging. After this, an interventional cardiologist can perform a coronary angioplasty, using a balloon catheter in which a deflated balloon is advanced into the obstructed artery and inflated to relieve the narrowing; certain devices such as stents can be deployed to keep the blood vessel open. Various other procedures can also be performed.
P2Y12 is a chemoreceptor for adenosine diphosphate (ADP) that belongs to the Gi class of a group of G protein-coupled (GPCR) purinergic receptors. This P2Y receptor family has several receptor subtypes with different pharmacological selectivity, which overlaps in some cases, for various adenosine and uridine nucleotides. The P2Y12 receptor is involved in platelet aggregation and is thus a biological target for the treatment of thromboembolisms and other clotting disorders. Two transcript variants encoding the same isoform have been identified for this gene.
A drug-eluting stent (DES) is a peripheral or coronary stent placed into narrowed, diseased peripheral or coronary arteries that slowly release a drug to block cell proliferation. This prevents fibrosis that, together with clots (thrombi), could otherwise block the stented artery, a process called restenosis. The stent is usually placed within the peripheral or coronary artery by an interventional cardiologist or interventional radiologist during an angioplasty procedure.
Bivalirudin (Bivalitroban), sold under the brand names Angiomax and Angiox and manufactured by The Medicines Company, is a direct thrombin inhibitor (DTI).
The history of invasive and interventional cardiology is complex, with multiple groups working independently on similar technologies. Invasive and interventional cardiology is currently closely associated with cardiologists, though the development and most of its early research and procedures were performed by diagnostic and interventional radiologists.
Alan W. Heldman is an American interventional cardiologist. Heldman graduated from Harvard College, University of Alabama School of Medicine, and completed residency and fellowship training at Johns Hopkins University School of Medicine. He held positions on the faculty of Johns Hopkins from 1995 to 2007. In 2007, he became clinical chief of cardiology at the University of Miami's Leonard M. Miller School of Medicine.
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 the treatment of coronary heart disease. It is used in a procedure called percutaneous coronary intervention (PCI). Coronary stents are now used in more than 90% of PCI procedures. Stents reduce angina and have been shown to improve survival and decrease adverse events in an acute myocardial infarction.
A myocardial infarction (MI), commonly known as a heart attack, occurs when blood flow decreases or stops in the coronary artery of the heart, causing damage to the heart muscle. The most common symptom is chest pain or discomfort which may travel into the shoulder, arm, back, neck or jaw. Often it occurs in the center or left side of the chest and lasts for more than a few minutes. The discomfort may occasionally feel like heartburn. Other symptoms may include shortness of breath, nausea, feeling faint, a cold sweat or feeling tired. About 30% of people have atypical symptoms. Women more often present without chest pain and instead have neck pain, arm pain or feel tired. Among those over 75 years old, about 5% have had an MI with little or no history of symptoms. An MI may cause heart failure, an irregular heartbeat, cardiogenic shock or cardiac arrest.
Reperfusion therapy is a medical treatment to restore blood flow, either through or around, blocked arteries, typically after a heart attack. Reperfusion therapy includes drugs and surgery. The drugs are thrombolytics and fibrinolytics used in a process called thrombolysis. Surgeries performed may be minimally-invasive endovascular procedures such as a percutaneous coronary intervention (PCI), which involves coronary angioplasty. The angioplasty uses the insertion of a balloon and/or stents to open up the artery. Other surgeries performed are the more invasive bypass surgeries that graft arteries around blockages.
Francis Miller Fesmire was an American emergency physician and a nationally recognized expert in myocardial infarction. He authored numerous academic articles and assisted in the development of clinical guidelines on the standard of care in treating patients with suspected myocardial infarction by the American College of Emergency Physicians and the American Heart Association/American College of Cardiology. He performed numerous research investigations in chest pain patients, reporting the usefulness of continuous 12-lead ECG monitoring, two-hour delta cardiac marker testing, and nuclear cardiac stress testing in the emergency department. The culmination of his studies was The Erlanger Chest Pain Evaluation Protocol published in the Annals of Emergency Medicine in 2002. In 2011 he published a novel Nashville Skyline that received a 5 star review by ForeWord Reviews. His most recent research involved the risk stratification of chest pain patients in the emergency department.
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.
Kounis syndrome is defined as acute coronary syndrome caused by an allergic reaction or a strong immune reaction to a drug or other substance. It is a rare syndrome with authentic cases reported in 130 males and 45 females, as reviewed in 2017; however, the disorder is suspected of being commonly overlooked and therefore much more prevalent. Mast cell activation and release of inflammatory cytokines as well as other inflammatory agents from the reaction leads to spasm of the arteries leading to the heart muscle or a plaque breaking free and blocking one or more of those arteries.
Alfredo E. Rodríguez is an Argentine interventional cardiologist, clinical researcher, and author. He is the Chief of Interventional Cardiology Service at Otamendi Hospital and Director and Founder of the Cardiovascular Research Center (CECI) a non -profit Research Organization in Buenos Aires Argentina.