title: Pacing-induced myocardial ischemia does not affect the endothelial release of coagulant and fibrinolytic factors into the coronary circulation.
abstract: The present study addresses the potential effects of pacing-induced myocardial ischemia on the secretion of coagulant and fibrinolytic factors within the coronary circulation. In 6 patients undergoing programmed ventricular stimulation with repeated induction of clinical ventricular tachycardia, the coronary release of tissue-type plasminogen activator (t-PA) antigen, plasminogen activator inhibitor (PAI) capacity, von Willebrand factor antigen (WF:Ag), and prostacyclin (6-keto-PGF 1a) was measured. Blood samples were collected simultaneously from the ascending aorta and the coronary sinus at baseline and immediately after the induction of ventricular tachycardia. The occurrence of pacing-induced myocardial ischemia was established by myocardial net lactate production. Myocardial ischemia was induced in every patient by repeated pacing trials. Pacing-induced ischemia did not affect the coronary release of any of the above factors. Consequently, there was no alteration of transcardiac gradients of thrombin-antithrombin complexes and D-dimer. The present results indicate that pacing-induced myocardial ischemia does not affect the release of coagulant and fibrinolytic endothelial factors or prostacyclin into the coronary circulation.
authors.affiliation: Division of Cardiology, University of Vienna, Austria.
authors.forename: H D
authors.initials: HD
authors.lastname: Gössinger
authors.forename: W
authors.initials: W
authors.lastname: Speiser
authors.forename: P
authors.initials: P
authors.lastname: Siostrzonek
authors.forename: M
authors.initials: M
authors.lastname: Jung
authors.forename: P A
authors.initials: PA
authors.lastname: Kyrle
authors.forename: M
authors.initials: M
authors.lastname: Heistinger
authors.forename: K
authors.initials: K
authors.lastname: Lechner
authors.forename: H
authors.initials: H
authors.lastname: Mösslacher
mesh_terms: D015121:6-Ketoprostaglandin F1 alpha / Q000097:blood; D000368:Aged; D000990:Antithrombin III / Q000032:analysis; D001011:Aorta; D001779:Blood Coagulation Factors / Q000032:analysis* / Q000493:pharmacokinetics; D006328:Cardiac Catheterization; D005117:Cardiac Complexes, Premature / Q000503:physiopathology; D002304:Cardiac Pacing, Artificial; D003326:Coronary Circulation / Q000502:physiology; D003327:Coronary Disease / Q000378:metabolism* / Q000503:physiopathology; D003331:Coronary Vessels / Q000378:metabolism*; D004562:Electrocardiography; D004730:Endothelium, Vascular / Q000378:metabolism*; D005260:Female; D005343:Fibrinolytic Agents / Q000097:blood* / Q000493:pharmacokinetics; D006801:Humans; D007773:Lactates / Q000097:blood; D008297:Male; D010447:Peptide Hydrolases / Q000032:analysis; D013610:Tachycardia / Q000503:physiopathology; D010959:Tissue Plasminogen Activator / Q000097:blood; D014841:von Willebrand Factor / Q000032:analysis
chemical_list: D001779:Blood Coagulation Factors; D005343:Fibrinolytic Agents; D007773:Lactates; C046193:antithrombin III-protease complex; D014841:von Willebrand Factor; D015121:6-Ketoprostaglandin F1 alpha; D000990:Antithrombin III; D010447:Peptide Hydrolases; D010959:Tissue Plasminogen Activator