PIERUGO CARBONIN, M.D. MARCO Di GENNARO, M.D. Instituto di Patologia Medica, UniversitA Cattolica, Rome, Italy FRANCEsCo FURLANELLO, M.D. Divisione di Cardiologia, Ospedale S’Chiara, Trento, Italy
1. Kerin NZ, Rubenfire M, Naini M, Wajszczuk WJ, Patamat A, Cascade PN: Arrhythmias in variant angina pectoris.
Relationship of arrhythmias to ST-segment elevation and Rwave changes. Circulation 60: 1343, 1979
2. Bigger JT, Dresdale RH, Heinsenbuttel FM, Weld FM, Wit AL: Ventricular arrhythmia in ischemic heart disease:
Mechanism, prevalence, significance, and management. Prog Cardiovasc Dis 19: 255, 1977
3. Bricknell OL, Opie LH: Effects of substrates on tissue metabolic changes in the isolated rat heart during underperfusion
and on the release of lactate dehydrogenase and arrhythmias during reperfusion. Circ Res 43: 102, 1978
4.DiGennaro M, Valle R, Carbonin PU: Electrocardiographic differences between underperfusion and anoxia in isolated rat
heart. in Proceedings of Florence International Meeting on Myocardial Infarction, edited by Mason DT, Neri serneri GG.
Amsterdam, Excerpta Medica. in press
5. Carbonin PU, Di Gennaro M, Valle R: R wave increase in partial and global ischemia. J Electrocardiol 13: 99, 1980
6. Holland PR, Brooks H: the QRS complex during myocardial ischemia. An experimental analysis in the porcine heart. J Clin
7. Carbonin PU, Di Gennaro M, Valle R, Bernabei R, Abed H: Intracellular calcium and electrogram during ischemic perfusion
of isolated rat heart. Am J Physiol. in press
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occlusion: a useful index of myocardial injury. J Electrocardiol
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of spasm in the pathogenesis of ischemic heart disease. Am J Cardiol 44: 788, 1979
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reperfusion. J Electrocardiol 13: 49, 1980
To the Editor: the excellent paper of Kerin et al.’ demonstrates that ventricular tachyarrhythmias (VTAs) are related to ST-segment elevation and R-wave amplitude (V) during the variant angina attacks. Evidence suggests that these VTAs can be provoked by a reflow mechanism observed that the occurrence of VTAs is related to the increase of V. in experimental ischemia, increased V can be considered a marker of severity of myocardial damage. the dynamics of the phenomenon are characterized, in order of succession, by inhibition of oxidative metabolism, augmentation of intracellular calcium and, as a consequence, of potassium conductance, and hyperpolarization of the cardiac cells.7 furthermore, the V ischemic increase is significantly inversely correlated with reduction of the coronary flow rate.5 7′ On the contrary, VTAs occurring during the first phase of experimental infarction seem independent of the duration, and then of the severity, of myocardial ischemia, because they are frequent during the first 5-10 minutes after the coronary artery ligation and, successively, subside for many hours.2
The hypothesis that, in variant angina, several types of VTAs are provoked by a reperfusion mechanism is important from a practical point of view. it has been demonstrated that VTAs can be induced by reflow after coronary artery spasm.9 Reperfusion VTAs, then, should probably be managed differently from VTAs beginning during the ischemic period. in fact, the mechanism of the reperfusion VTAs is different from that of ischemic VTAs.`0 the former respond to verapamil and not to lidocaine or propranolol.10 Therefore, treatment of variant angina with calcium antagonists seems to be justified not only for counteracting the coronary spasm but also for reducing the risk of reperfusion VTAs and sudden death.
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The authors reply: to the Editor: Dr. P. Carbonin et al. have raised a pertinent issue regarding our article. this issue regards the possibility of reperfusion as a mechanism of dysrhythmias in variant angina pectoris. we heartily agree with Dr. Carbonin et al. that dysrhythmias induced by reperfusion may occur during episodes of variant angina pectoris. we reviewed our 36 cases of variant angina pectoris and found that reperfusion might explain three of 13 cases with dysrhythmias (20%) (Kerin NZ, Rubenfire M, Wajszczuk WJ, Willens H: unpublished data). we analyzed the time relation to dysrhythmias to the ST-segment elevation during dysrhythmias. the occlusive dysrhythmias were considered those developing close to or at the acme of ST-segment elevation, while the dysrhythmias occurred during the resolution of ST-segment normalization. There is ample evidence that reflow dysrhythmias occur when the ST-segment elevation will remain on a plateau (from a few seconds2 to minutes3) or during the resolution of the ST segment before returning to the isoelectric line. the reperfusion dysrhythmias occurred in our cases during the resolution of ST-segment elevation in one case and in two cases, within seconds of ST normalization. the fact that only a few cases had reperfusion dysrhythmias was nor surprising. Suzuk et al.4 observed that in dogs, reperfusion dysrhythmias were commonly elicited after 20-24 minutes of coronary occlusion. the average clinical episode of variant angina pectoris lasting 5-15 minutes may not be long enough to cause dysrhythmias during early coronary reperfusion. we analyzed the time relationship between the onset of the rhythm disturbance and the peak or acme of ST-segment elevation as well as the total duration of ST-segment elevation in the groups with and without dysrhythmias. the average time to onset of dysrhythmias from the beginning of ST-segment elevation was 4.94 ± 1.52 minutes (seven episodes), while the duration of episodes in patients without dysrhythmias was 0.86 ± 0.53 minutes (six episodes).
Although the R wave increases during the occlusive phase of STsegment elevation with its normalization immediately after the restoration of the coronary flow,5’6 the R wave may decrease during the episodes of coronary occlusion by ligation3 or during spontaneous episodes of coronary spasm.’ changes of the AR of more than 10% were seen in 17 of 30 patients (57%). in patients with dysrhythmias, AR changes occurred more frequently and were seen n 1 1 of 13 patients (85%). Although R-wave augmentation occurs during the occlusion of the coronary artery by coronary spasm, we did not find this sign very useful as a definitive criterion of separating the type of dysrhythmia occurring during the episodes of variant angina pectoris.Vari
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