Nicholas Kounis

Nicholas George Kounis (MD, PhD, FESC, FAHA, FACC), born in Patras, Greece, is professor emeritus of cardiology in the Technological Educational Institute of Patras and scientific cardiology advisor at Saint Andrews (Agios Andreas) State General Hospital Patras.

One of his contributions to medical science is describing the Kounis syndrome,[1][2] the name given to "anaphylactic CHD [coronary heart disease] including patients with drug eluting coronary stents".[3] He received his MD and PhD from Athens Medical School with a thesis entitled Contribution to the prevention and treatment of chronic thromboembolism with a new regimen including Arvin, phenformin and orabolin. He worked in various hospitals in Greece, starting in 1966, 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] in 1988. He has also held, for 10 years, salaried hospital appointments in England, Scotland and Northern Ireland as house officer, senior house officer, registrar, clinical tutor and senior registrar.

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 suffering from acute coronary syndromes of nonallergic etiology.[4][5] 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.[6]

Selected publications

  1. "Atropine and bradycardia after myocardial infarction". Kounis NG, Chopra RK. Ann Intern Med 1974; 81: 117-8.
  2. "Oxytetracycline-induced thrombocytopenic purpura". Kounis NG. JAMA. 1975; 231: 734-5.
  3. Micturition syncope, hypokalemia, and atrial fibrillation. Kounis NG, Kenmure AC. JAMA 1976; 236: 954
  4. "Iliacus hematoma syndrome." Kounis N G, Macauley MB, Ghorbal MS. Canadian Medical Association Journal 1975; 112: 872-873.
  5. "Cardiopathia Fantastica: Munchhausen syndrome with cardiac symptoms." Kounis NG. British Journal of Clinical Practice 1979; 33: 77-72.
  6. "Kounis syndrome (allergic angina and allergic myocardial infarction): A natural paradigm?" Kounis NG. International Journal of Cardiology 2006; 110: 7-14.
  7. "Coronary Artery Stents" Kounis NG, Kounis GN, Kouni SN. N Engl J Med 2006; 354: 2076-8
  8. "Drug-eluting stent thrombosis: the Kounis hypersensitivity-associated acute coronary syndrome revisited". Chen JP, Hou D, Pendyala L, Goudevenos JA, Kounis NG. JACC Cardiovasc Interv 2009; 2: 583-93. Review.
  9. Everolimus-eluting versus paclitaxel-eluting stents. Kounis NG, Goudevenos JA. Lancet 2010;375:1160-3.

References

  1. ↑ Kounis NG. Kounis syndrome (allergic angina and allergic myocardial infarction): A natural paradigm? International Journal of Cardiology 2006; 110: 7-14.
  2. ↑ Kounis NG, Kourelis T, Hahalis G, Manola M, Theoharides TC. Kounis syndrome (allergic angina and allergic myocardial infarction). Angina Pectoris. Etiology, Pathogenesis and Treatment. New York:Nova Biomedical; 2008. p. 77–150. ISBN 978-1-60456-674-1.
  3. ↑ Cetrulo, Kyle (2009). Perinatal Stem Cells. John Wiley and Sons. p. 121. ISBN 978-0-470-42084-3. http://books.google.com/books?id=BnDd7MPaXnoC&pg=PT121.
  4. ↑ Sakata V, Komamura K, Hirayama A, et al. Elevation of plasma histamine concentration in the coronary circulation in patients with variant angina. Am J Cardiol 1996;77:1121–6.
  5. ↑ Cuculo A, Summaria F, Schiavino D, et al. Tryptase levels are elevated during spontaneous ischemic episodes in unstable angina but not after ergonovine test in variant angina. Cardiologia 1998; 43:189–93.
  6. ↑ Kaartinen M, Penttila A, Kovanen PT. Accumulation of activated mast cells in the shoulder region of human coronary atheroma, the prediction site of atheromatous rupture. Circulation 1994;90:1669–78.
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