Open AccessSIN‐1 has no direct myocardial anti‐ischemic action
Author(s) -
Kober G.,
Bender M.,
Vallbracht C.,
Sievert H.,
Klepzig H.
Publication year - 1993
Publication title -
clinical cardiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.263
H-Index - 72
eISSN - 1932-8737
pISSN - 0160-9289
DOI - 10.1002/clc.4960161006
Subject(s) - medicine , molsidomine , preload , afterload , cardiology , peripheral , angina , placebo , myocardial infarction , hemodynamics , anesthesia , nitric oxide , alternative medicine , pathology
Anti‐ischemic drugs may develop their cardiac activity via peripheral (reduction in preload and/or afterload) or cardiac (coronary vasculature, myocardial cell metabolism) effects. The aim of the study was to investigate whether SIN‐1, the active metabolite of molsidomine, develops a direct myocardial anti‐ischemic property. Three groups of seven patients each were treated with 0.4 mg SIN‐1 administered via either the intracoronary (IC) or intravenous (IV) route, or with placebo in a double‐blind randomized investigation. SIN‐1 had no influence on either the ischemic parameters in the surface electrocardiogram (ECG) or the intracoronary ECG. There was also no change in peripheral or central hemodynamics or in the severity of angina following this low IC or IV dosage. There is no evidence of a direct myocardial anti‐ischemic response of SIN‐1. The well known anti‐ischemic activity of SIN‐1 or molsidomine has to be attributed to the proven peripheral and cardiac vascular responses.