[Myocardial lactate extraction during programmed ventricular stimulation and its value for etiologically-related therapy of ischemic ventricular tachyarrhythmia].

UNLABELLED

Ischemia is considered to be one of the most important trigger mechanisms of ventricular tachyarrhythmias, i.e., tachycardia (VT) and fibrillation (VF) in coronary artery disease (CAD). The aim of the study was 1) to investigate the relationship between ischemia and inducibility of VT/VF, and 2) to address the question, if removal of ischemia leads 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 myocardial lactate extraction (MLE) was calculated by measuring the arterio venous coronary lactate difference simultaneously during programmed ventricular stimulation. Eighteen pts (group A, "lactate-positive") showed a significant decrease of MLE from +16 +/- 13% at rest to -18 +/- 24% during stimulation just before induction of VT/VF (p < 0.0005). During 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 recovery. Compared to group B pts, group A pts demonstrated a significantly higher number and degree of coronary lesions as well as regions with reversible ischemia during 201Tl- 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 noninducible during post interventional PVS in 94%, showing also a normalized MLE in 87% of cases. In group B only 4/12 pts were suitable for revascularization and could be rendered noninducible in only 50% of cases. With respect to the success-rate of the anti-ischemic therapy in terms of arrhythmia suppression, a lactate-positive result during primary PVS had a sensitivity of 89%, a specificity of 75%, a positive predictive value of 94%, and a negative predictive value of 60%.

IN CONCLUSION

in about 60% of pts with VT/VF and significant CAD a correlation between ischemia and inducibility could be demonstrated. MLE during PVS has a highly significant predictive value for the effect of an antiischemic intervention on arrhythmia induction.