MYOCARDIAL LACTATE EXTRACTION DURING PROG RAMMED VENTRICULAR STIMULATION IN PATIENTS WITH VENTRICULAR TACHYARRHYTHMIAS DUE TO CORONARY HEART-DISEASE - IS IT RELEVANT FOR A CAUSATIVE ANTIISCHEMIC TREATMENT

Ischemia is considered to be one of the most important trigger mechani sms of ventricular tachyarrhythmias, i. e., tachycardia (VT) and fibri llation (VF) in coronary artery disease (CAD). The aim of the study wa s 1) to investigate the relationship between ischemia and inducibility of VT/VF, and 2) to address the question, if removal of ischemia lead s to suppression, resp. noninducibility of arrhythmias. In 30 patients (pts) with CAD (healed myocardial infarction in 73%, acute myocardial infarction excluded) and sustained malignant ventricular arrhythmias (VF in 47%, VT in 37%, and arrhythmogenic syncope in 16%) the myocardi al lactate extraction (MLE) was calculated by measuring the arterio ve nous coronary lactate difference simultaneously during programmed vent ricular stimulation. Eighteen pts (group A, ''lactate-positive'') show ed a significant decrease of MLE from +16 +/- 13% at rest to -18 +/- 2 4% during stimulation just before induction of VT/VF (p < 0.0005). Dur ing recovery up to 10 min following termination of VT/VF MLE returned to normal range (+19 +/- 16%). In 12 pts (group B, ''lactate-negative' ') MLE showed no significant change between rest, stimulation, and rec overy. Compared to group B pts, group A pts demonstrated a significant ly higher number and degree of coronary lesions as well as regions wit h reversible ischemia during Tl-201-scintigraphy. Lactate-positive pts presented spontaneous arrhythmias of higher frequency and had usually a two- or three-vessel disease, while lactate-negative pts presented arrhythmias of lower frequency and had more often a one-vessel disease with ventricular aneurysm. 17/18 (94%) group A pts underwent coronary bypass grafting (11) or balloon angioplasty (6) and were rendered non inducible during post interventional PVS in 94%, showing also a normal ized MLE in 87% of cases. In group B only 4/12 pts were suitable for r evascularization and could be rendered noninducible in only 50% of cas es. With respect to the success-rate of the antiischemic therapy in te rms of arrhythmia suppression, a lactate-positive result during primar y PVS had a sensitivity of 89%, a specificity of 75%, a positive predi ctive value of 94%, and a negative predictive value of 60%. In conclus ion: in about 60% of pts with VT/VF and significant CAD a correlation between ischemia and inducibility could be demonstrated. MLE during PV S has a highly significant predictive value for the effect of an antii schemic intervention on arrhythmia induction.