The association of ventricular tachycardia and endothelial dysfunction in the setting of acute myocardial infarction with ST elevation

Background Ventricular tachycardia (VT) is frequently seen in ischemic settings like acute myocardial infarction with ST segment elevation (STEMI). Endothelial dysfunction (ED) represents inflammation and the loss of all protective features of the endothelium. We aimed to examine the association between VT and ED in patients with STEMI. Material/Methods The study included 90 subjects (30 with VT and acute STEMI, 30 with STEMI without VT, and 30 controls). Sera of all subjects were tested on ED markers by enzyme immunoassay: sICAM-1 (intracellular adhesive molecule-1), sVCAM-1 (vascular adhesive molecule-1), P- and E-selectins, and VEGF (vascular endothelial growth factor). In addition, CRP (C-reactive protein) was detected. Results Significantly increased values of low-density lipoprotein, triglycerides, leukocytes, creatinine, and the number of cigarettes smoked were observed among patients with VT+STEMI in comparison to controls. The levels of E-selectin were significantly lower in the VT+STEMI group than in the other groups, while the levels of VCAM-1 were significantly higher in the groups with STEMI and VT+STEMI compared to the controls. Lower levels of VEGF were recorded in STEMI and VT+STEMI groups compared to the control group. A significant correlation between CRP and VCAM-1 in patients with VT +STEMI was demonstrated. Conclusions We showed that ED may have a role in the immunopathogenesis of VT in patients with STEMI. The role of sE-selectin and correlation of sVCAM-1 with CRP as possible ED predictive markers in patients with VT+STEMI should be further investigated in a large cohort of patients.

[1]  M. Arshad PRIMARY ANGIOPLASTY IN MYOCARDIAL INFARCTION (PAMI) , 2014 .

[2]  M. Portolés,et al.  Sum of effects of myocardial ischemia followed by electrically induced tachycardia on myocardial function , 2013, Medical science monitor basic research.

[3]  Jin Zhang,et al.  C-reactive protein (CRP) gene polymorphisms, CRP levels and risk of incident essential hypertension: findings from an observational cohort of Han Chinese , 2012, Hypertension Research.

[4]  A. Markotić,et al.  Electrocardiographic changes in hospitalized patients with leptospirosis over a 10-year period , 2011, Medical science monitor : international medical journal of experimental and clinical research.

[5]  Dariusz Janusek,et al.  Risk assessment of ventricular arrhythmia using new parameters based on high resolution body surface potential mapping , 2011, Medical science monitor : international medical journal of experimental and clinical research.

[6]  S. Ogawa,et al.  Role of ischemic preconditioning and inflammatory response in the development of malignant ventricular arrhythmias after reperfused ST-elevation myocardial infarction. , 2009, Journal of cardiac failure.

[7]  P. Armstrong,et al.  Incidence of and outcomes associated with ventricular tachycardia or fibrillation in patients undergoing primary percutaneous coronary intervention. , 2009, JAMA.

[8]  J. Piccini,et al.  Early sustained ventricular arrhythmias complicating acute myocardial infarction. , 2008, The American journal of medicine.

[9]  A. Postadzhiyan,et al.  Circulating soluble adhesion molecules ICAM-1 and VCAM-1 and their association with clinical outcome, troponin T and C-reactive protein in patients with acute coronary syndromes. , 2008, Clinical biochemistry.

[10]  S. Collot-Teixeira,et al.  The dialogue between endothelial cells and monocytes/macrophages in vascular syndromes. , 2007, Current pharmaceutical design.

[11]  A. Esen,et al.  Relationship between endothelial function and coronary risk factors in patients with stable coronary artery disease. , 2007, Circulation journal : official journal of the Japanese Circulation Society.

[12]  G. Biondi-Zoccai,et al.  Prognostic role of post-infarction C-reactive protein in patients undergoing implantation of cardioverter-defibrillators: design of the C-reactive protein Assessment after Myocardial Infarction to GUide Implantation of DEfibrillator (CAMI GUIDE) study , 2007, Journal of cardiovascular medicine.

[13]  J. Mehta,et al.  Inflammatory markers, angiographic severity of coronary artery disease, and patient outcome. , 2007, The American journal of cardiology.

[14]  A. Lerman Restenosis: another "dysfunction" of the endothelium. , 2005, Circulation.

[15]  K. Harjai,et al.  Sustained ventricular tachycardia or fibrillation in the cardiac catheterization laboratory among patients receiving primary percutaneous coronary intervention: incidence, predictors, and outcomes. , 2004, Journal of the American College of Cardiology.

[16]  Gregory Y H Lip,et al.  The adhesion molecule P-selectin and cardiovascular disease. , 2003, European heart journal.

[17]  L. Rallidis,et al.  Usefulness of elevated levels of soluble vascular cell adhesion molecule-1 in predicting in-hospital prognosis in patients with unstable angina pectoris. , 2003, The American journal of cardiology.

[18]  M. Entman,et al.  Soluble adhesion molecules and the search for biomarkers for atherosclerosis. , 2002, Circulation.

[19]  J. Janowska,et al.  Serum levels of selected adhesion molecules in patients with coronary artery disease. , 2002, International journal of cardiology.

[20]  L. Bouter,et al.  Why is soluble intercellular adhesion molecule‐1 related to cardiovascular mortality? , 2002, European journal of clinical investigation.

[21]  P. Wilson,et al.  Diabetes mellitus and coronary heart disease. , 2001, Endocrinology and metabolism clinics of North America.

[22]  J. Danesh,et al.  Soluble adhesion molecules and prediction of coronary heart disease: a prospective study and meta-analysis , 2001, The Lancet.

[23]  S. Blankenberg,et al.  Impact of Viral and Bacterial Infectious Burden on Long-Term Prognosis in Patients With Coronary Artery Disease , 2001, Circulation.

[24]  B. Gersh,et al.  Cell adhesion molecules and inflammation in acute coronary syndromes: markers and emerging risk factors. , 2001, European heart journal.

[25]  P. Crean,et al.  Risk stratification in unstable angina and non-Q wave myocardial infarction using soluble cell adhesion molecules , 2001, Heart.

[26]  P. Ridker,et al.  Soluble P-Selectin and the Risk of Future Cardiovascular Events , 2001, Circulation.

[27]  A. Siegbahn,et al.  Markers of myocardial damage and inflammation in relation to long-term mortality in unstable coronary artery disease. FRISC Study Group. Fragmin during Instability in Coronary Artery Disease. , 2000, The New England journal of medicine.

[28]  P. Crean,et al.  Evidence of prolonged inflammation in unstable angina and non-Q wave myocardial infarction. , 2000, Journal of the American College of Cardiology.

[29]  T. Murohara,et al.  Increased circulating soluble intercellular adhesion molecule-1 in acute myocardial infarction: A possible predictor of reperfusion ventricular arrhythmias , 2000, Critical care medicine.

[30]  Eric J. Topol,et al.  Manual of Cardiovascular Medicine , 2000 .

[31]  K. Norowitz,et al.  Lymphocyte activation in angina pectoris. , 1999, Clinical immunology.

[32]  C. Held,et al.  Elevated serum intercellular adhesion molecule-1 and vascular adhesion molecule-1 among patients with stable angina pectoris who suffer cardiovascular death or non-fatal myocardial infarction. , 1999, European heart journal.

[33]  A. Rebuzzi,et al.  Incremental prognostic value of serum levels of troponin T and C-reactive protein on admission in patients with unstable angina pectoris. , 1998, The American journal of cardiology.

[34]  E. Antman,et al.  C-Reactive Protein Is a Potent Predictor of Mortality Independently of and in Combination With Troponin T in Acute Coronary Syndromes: A TIMI 11A Substudy , 1998 .

[35]  P. Vallance,et al.  Inflammatory cytokines impair endothelium-dependent dilatation in human veins in vivo. , 1997, Circulation.

[36]  D. Collen,et al.  Thrombosis and atherosclerosis , 1997, Current opinion in lipidology.

[37]  H. Wysocki,et al.  The release of soluble adhesion molecules ICAM-1 and E-selectin after acute myocardial infarction and following coronary angioplasty. , 1997, International journal of cardiology.

[38]  P. Libby,et al.  Molecular Determinants of Atherosclerotic Plaque Vulnerability a , 1997, Annals of the New York Academy of Sciences.

[39]  M. Nieminen,et al.  Infection and inflammation as risk factors for myocardial infarction. , 1993, European heart journal.

[40]  D. Celermajer,et al.  Cigarette Smoking Is Associated With Dose‐Related and Potentially Reversible Impairment of Endothelium‐Dependent Dilation in Healthy Young Adults , 1993, Circulation.

[41]  D. Krikler,et al.  Heart disease: A textbook of cardiovascular medicine , 1992 .

[42]  W. Weintraub,et al.  Elevation of C-reactive protein in "active" coronary artery disease. , 1990, The American journal of cardiology.

[43]  H. Kammermeier,et al.  Catecholamine Induced Cardiac Necroses are Mediated by Thrombocytes , 1983 .

[44]  T. Killip,et al.  Treatment of myocardial infarction in a coronary care unit. A two year experience with 250 patients. , 1967, The American journal of cardiology.

[45]  S. Chien,et al.  Effects of disturbed flow on vascular endothelium: pathophysiological basis and clinical perspectives. , 2011, Physiological reviews.

[46]  K. Mizia-Stec Cytokines and adhesive molecules in detection of endothelial dysfunction. , 2006, Pharmacological reports : PR.

[47]  E. Antman,et al.  C-reactive protein is a potent predictor of mortality independently of and in combination with troponin T in acute coronary syndromes: a TIMI 11A substudy. Thrombolysis in Myocardial Infarction. , 1998, Journal of the American College of Cardiology.