Blind defibrillation

Blind defibrillation

LETTERS TO TIE EDITOR CARDIAC PACING IN ACUTE MYOCARDIAL INFARCTION Waters and Mizgala,’ in their study of the role of cardiac pacing, conclude that ...

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LETTERS TO TIE EDITOR

CARDIAC PACING IN ACUTE MYOCARDIAL INFARCTION Waters and Mizgala,’ in their study of the role of cardiac pacing, conclude that “prophylactic temporary transvenous pacemaker insertion in patients with acute myocardial infarction complicated by incomplete bilateral bundle branch block is of little value.” It is dangerous to draw such a conclusion from the small number of patients analyzed. As the authors note, the overall mortality for patients with incomplete bilateral bundle branch block in their study is lower than that in other reported series. This discrepancy may be a result of the skilled application of prophylactic and emergency cardiac pacing in this group of patients. Of the group of 15 patients in whom complete heart block developed, 3 of 5 with a prophylactic pacemaker survived, whereas only 3 of 10 with a pacemaker implanted at the time of development of complete heart block survived hospitalization. One might conclude from this that prophylactic, as opposed to after-the-fact pacemaking significantly increases survival of patients in whom complete heart block develops. In addition, although the authors attribute one death to pacemaker manipulation, they document the possible salvage of six lives (three in prophylactic, three in after-the-fact group) by pacemaking. Of course, neither these nor the authors’ conclusions are justified, except as hypotheses for further study of this controversial subject. Waters and Mizgala’s view that the potential gain of pacemaking in these patients “may be counterbalanced by the frequent occurrence of serious ventricular arrhythmias” was previously postulated by Godman et a1.,2 but Post and Killip3 regard their incidence of pacemaker catheter-induced arrhythmias as atypically high. Perhaps because there is a widespread conviction that certain patients benefit from cardiac pacing, studies comparing patients with acute myocardial infarction who undergo cardiac pacing with exactly matched control groups have not appeared. When and if they do, interpretation will be further complicated by various estimates of the risks of cardiac pacing as related to variations in technique and skill. Calixto A. Romero, MD Department of Medicine/Cardiology The University of Chicago Chicago, Illinois References 1. Waters DD, Mlzgala HF: Long-term prognosis of patients with uxxxnplete bilateral bundle branch block complicating acute myocardial infarction. Role of cardiac pacing. Am J Cardiil34:1-6. 1974 2. Godman MJ. Latuers BW. Julian Do: Complete EBB complicating acute myocardial infarction. NEngl J Mad 282:237. 1970 3. Posf Ml?. Klffb T: Aoolication of cardiac pacuva to acute mvocardiil infarction. In. Textbook of C%rona~~Care (Meitzer LE. dunnin> AJ. ed). Philadelphia and Amsterdam, Charles Press and Excerpta Medica. 1972. p 348

to catheter

manipulation) and the other nine died of causes related to the severity of their coronary artery disease and to the extent of myocardial infarction. Of the patients in whom complete heart block developed in the absence of a prophylactic pacemaker, all survived long enough to have a pacemaker inserted. On the other hand, of the survivors, complete heart block never developed in nine whereas it did in six; of these six, all survived whether or not a prophylactic pacemaker had been inserted. We agree that once complete heart block appears in such patients, a pacemaker is indicated and indeed could be lifesaving. However, no data, ours included, indicate that ultimate survival in these patients is influenced by prophylactic insertion of a pacemaker. Thus, analysis of this group of patients, however small, tends to support the view that acute myocardial infarction complicated by incomplete bilateral bundle branch block points to very extensive myocardial damage and is complicated by a high incidence of ventricular brady- and tachyarrhythmias, congestive heart failure and cardiogenic shock. Survival seems to be unrelated to the use of prophylactic pacing but rather appears to be determined by the degree of myocardial reserve remaining after the acute event and is often accompanied by gradual regression of the conduction disturbances. All patients in our series were monitored during the acute phase of this illness and 24 hour lead II recordings were obtained. Analysis of these tracings clearly revealed an unusually high incidence of ventricular arrhythmias in all patients, not only in recipients of prophylactic pacemakers. Our reported high incidence of ventricular arrhythmias is therefore unrelated to the possibility of “variation in technique and skill” but rather to increased ventricular irritability, presumably related to the extensive infarction. Harry F. Mizgala, MD, FRCP (C), FACC lnstitut de Cardiologie de Montreal Montreal, Quebec, Canada

BLIND

Irving N. Wolfson, MD Division of Cardiology Worcester City Hospital Department of Medicine University of Massachusetts Medical School Worcester, Massachusetts

REPLY We agree that our series is small (27 cases), that our conclusions may not constitute the last word on this important subject and that further observations are necessary, as our purpose was to present some evidence for questioning the widespread belief that acute myocardial infarction complicated by incomplete bilateral bundle branch block must be treated with a prophylactic temporary pacemaker and, as suggested by some, eventually with a permanent pacemaker. Careful examination of the deaths in our series shows that none of the 12 patients who died succumbed for lack of a prophylactic pacemaker; three died of ventricular fibrillation (including one whose death was directly related

412

September 1975

The American Journal of CARDIOLOGY

DEFIBRILLATION

To the editorial on blind defibrillation by Grace et al.’ I would add: If a first blind defibrillation does not restore the heartbeat, a second one should be performed immediately. This suggestion is based upon the rare possibility that the initial cardiac arrest was due to ventricular tachycardia and the first blind defibrillation (since synchronizing the electrical impulse is not indicated) might have been triggered during the vulnerable period and resulted in ventricular fibrillation. In that case a second blind defibrillation might restore sinus rhythm.

Reference

1 GraceWJ,

Kennedy

RJ, Nolb

CT: Blind defibrillation.

Am J Cardiol 34:115-116.

1974

PREDICTIVE

VALUE

OF

MYOCARDIAL

ENZYME

STUDIES

IN

INFARCTION

Rose et al.’ suggest that serum glutamic oxaloacetic transaminase and creatine phosphokinase values above 200 and

Volume 36