[Reduction in CK- and CKMB-measured infarct size by verapamil].
In a prospective, randomized and controlled study, 29 patients received i.v. verapamil, 5-10 mg/h for two days, at a mean of eight hours after onset of myocardial infarction. In a control group, 25 patients received no specific treatment. In all patients, left ventricular end-diastolic pressure was initially less than 15 mm Hg. The two groups were comparable as to age, infarct site and haemodynamics (measured via Swan-Ganz catheter). CK and CKMB peaks were significantly lower in the verapamil than the control group (CK 547 vs 703 U/1, P less than 0.05; CKMB 51 vs 68 U/1, P less than 0.025), as well as infarct weight (CK = 48 vs 65 g-equivalent; P less than 0.03; CKMB = 31 vs 49 g-equivalent; P less than 0.005). Arterial blood pressure was lower by 10 mm Hg than in the control group. Peripheral resistance and filling pressure remained unchanged. In patients without left ventricular failure verapamil reduces the infarct size by about 30%. The most prominent haemodynamic change is a reduction in blood pressure.
D001794:Blood Pressure / Q000187:drug effects; D003402:Creatine Kinase / Q000378:metabolism*; D004305:Dose-Response Relationship, Drug; D005665:Furosemide / Q000627:therapeutic use; D006327:Heart Block / Q000139:chemically induced; D006339:Heart Rate / Q000187:drug effects; D006801:Humans; D007527:Isoenzymes; D008012:Lidocaine / Q000627:therapeutic use; D009203:Myocardial Infarction / Q000188:drug therapy / Q000201:enzymology*; D005996:Nitroglycerin / Q000627:therapeutic use; D014700:Verapamil / Q000009:adverse effects / Q000627:therapeutic use*
D007527:Isoenzymes; D005665:Furosemide; D008012:Lidocaine; D014700:Verapamil; D003402:Creatine Kinase; D005996:Nitroglycerin
Reduktion der CK- und CKMB-Infarktgrösse durch Verapamil.