INFARCT SIZE AS ESTIMATED FROM PEAK CREATINE-KINASE AND LACTATE-DEHYDROGENASE IS PROBABLY REDUCED IN PATIENTS USING CALCIUM-ANTAGONISTS AT THE ONSET OF SYMPTOMS

In animal models, calcium antagonists (Ca-A) administered before ische mia. and reperfusion reduced myocardial necrosis, attenuated postische mic contractile dysfunction, and reduced tissue calcium. In 753 patien ts with acute myocardial infarction (AMI), we examined if use of Ca-A at the onset of symptoms (n = 127 patients) reduced infarct size as es timated hom peak creatine kinase (CKmax) and lactate dehydrogenase (LD max) activities. The study had an observational exposed/nonexposed des ign, and both erode and adjusted effects were investigated. Crude effe cts: In the restricted cohort of patients not receiving thrombolytic t reatment (thr- pts; n = 411 patients), CKmax and LDmax were lower in C a-A+ patients than in Ca-A- patients, being 643 versus 887 U/l (2 p = 0.004) and 708 versus 867 U/l (2 p = 0.005), respectively. When using log (CKmax) and log (LKmax) as outcomes, the same results were found ( 2 p = 0.002). More of the restricted cohort of thr-pts used Ca-A in th e lower quartiles of CKmax and LDmax (p for linear trend = 0.005 and 0 .004 for CKmax and LDmax, respectively). Adjusted effects: Thrombolysi s was an effect modifier of the association between Ca-A and peak enzy me levels. In thr-pts, the coefficients of Ca-A were negative and bord erline significant for log (CKmax; 2 p = 0.088) and negative and highl y significant for log (LDmax; 2 p = 0.010) when adjusting for confound ers. The present observational study indicates that the use of a Ca-A at the onset of AMI reduces infarct size, as estimated from CKmax and LDmax activities.