* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
Download JAOK HAN, MD, PH.D.
Saturated fat and cardiovascular disease wikipedia , lookup
Cardiac contractility modulation wikipedia , lookup
Remote ischemic conditioning wikipedia , lookup
Quantium Medical Cardiac Output wikipedia , lookup
Drug-eluting stent wikipedia , lookup
Mitral insufficiency wikipedia , lookup
Hypertrophic cardiomyopathy wikipedia , lookup
Heart failure wikipedia , lookup
History of invasive and interventional cardiology wikipedia , lookup
Electrocardiography wikipedia , lookup
Cardiac surgery wikipedia , lookup
Jatene procedure wikipedia , lookup
Coronary artery disease wikipedia , lookup
Management of acute coronary syndrome wikipedia , lookup
Arrhythmogenic right ventricular dysplasia wikipedia , lookup
430 LETTERS TO THE EDITOR decreasing the arterial pressure and coronary blood flow. JAOK HAN, M.D., PH.D. Department of Medicine Albany Medical College Albany, New York Downloaded from http://circ.ahajournals.org/ by guest on August 3, 2017 References 1. EPSTEIN SE, REDWOOD DR, SMITH ER: Atropine and acute myocardial infarction. Circulation 45: 1273, 1972 2. HAN J, DETRAGLIA J, MILLET D, MOE GK: Incidence of ectopic beats as a function of basic rate in the ventricle. Amer Heart J 72: 632, 1966 3. HAN J: Mechanisms of ventricular arrhythmias associated with myocardial infarction, Amer J Cardiol 24: 800, 1969 4. SCHERLAG BJ, HELFANT RH, HAFr JI, DAMATO AN: Electrophysiology underlying ventricular arrhythmias due to coronary ligation. Amer J Physiol 219: 1665, 1970 5. HAN J, GOEL BG, HANSON CS: Re-entrant beats induced in the ventricle during coronary occlusion. Amer Heart J 80: 778, 1970 6. HAN J: The concepts of reentrant activity responsible for ectopic rhythms. Amer J Cardiol 28: 253, 1971 7. HAN J: Ventricular ectopic activity in myocardial infarction. In Cardiac Arrhythmias, edited by Han J. Springfield, Illinois, Charles C Thomas, 1972, p 171 8. HAN J: Ventricular vulnerability during acute coronary occlusion. Amer J Cardiol 24: 857, 1969 9. KENT KM, SMITH ER, REDWOOD DR, EPSTEIN SE: The deleterious electrophysiologic effects produced by increasing heart rate during experimental coronary occlusion. (Abstr) Clin Res 20: 379, 1972 10. LOWN B, KLEIN MD, HERSHBERG PI: Coronary and precoronary care. Amer J Med 46: 705, 1969 The authors reply: To the Editor: We appreciate the opportunity of responding to some of the questions raised by Dr. Han in his letter. Dr. Han makes a very important point when he emphasizes that his own observations (demonstrating that slower heart rates during experimental acute myocardial infarction increase the incidence of ventricular premature beats) were made mainly within the first 1-3 min of onset of acute coronary occlusion.' We certainly do not question the importance of these results, given this time frame and the fact that open-chest anesthetized dogs were used with the attendant increase in circulating catecholamines, faster control heart rates, etc. However, it is questionable how relevant the data are to the problem we were mainly concerned with; i.e., the advisability of giving atropine to the patient with bradycardia and acute myocardial infarction. In this circumstance, practical considerations make it virtually impossible for any therapeutic intervention to be applied for the first few minutes after onset of infarction. It therefore seems to us that this important clinical question relates not so much to the first 3 min of the onset of myocardial infarction but to the effects of increasing heart rate on the incidence of ventricular premature contractions and ventricular fibrillation over the course of the first 1-3 hours after onset of acute infarction. Dr. Han is not entirely accurate in suggesting that the time course of onset of ventricular arrhythmias after coronary occlusion between his and Dr. Scherlag's studies1' 2 was very different. Moreover, although interpretation of Dr. Scherlag's paper is complicated when evaluating the results following the very fastpaced heart rates, Dr. Han neglects to mention another phase of the study in which these investigators reported that ventricular slowing produced by vagal stimulation caused disappearance of ventricular ectopic beats in all instances. Nevertheless, interpretative difficulties do remain since this study was not specifically designed to answer the question we were interested in exploring. We therefore investigated the effects of atropine (using a randomized study design) on ventricular arrhythmias over the first few hours of acute coronary occlusion in the closed-chest conscious dog.3 This model was chosen so that the relative arrhythmic potential of a physiologic range of heart rate could be evaluated. We found that the incidence of serious ventricular arrhythmias was directly related to the spontaneous heart rate; i.e., slower heart rates (< 60 beats/min) were accompanied by a lower incidence of ventricular ectopic activity and ventricular fibrillation. Moreover, we found that when compared to a saline-treated control group the incidence of ventricular arrhythmias and ventricular fibrillation was higher in dogs whose baseline heart rates were increased from a mean of 88-107 beats/min by an infusion of atropine. A second aspect of the problem raised in Dr. Han's letter is the influence of heart rate on electrophysiologic parameters that may influence the incidence of ventricular arrhythmias. Dr. Han and his co-workers demonstrated that both ischemia and bradyeardia independently increase the disparity of the length of ventricular refractory periods (thereby favoring development of reentrant arrhythmias) and decrease ventricular fibrillation threshold.4 While we do not question these experimental results, we do wonder whether some of the conclusions derived from these results are entirely valid. For example, several authors have interpreted these data as supporting the hypothesis that increasing the heart rate of a patient with an acute myocardial infarction who has bradyeardia will diminish the risk of arrhythmic death. Although this may be true, it appeared somewhat tenuous to us to extrapolate data obtained in the absence of ischemia to the ischemic situation since, to our knowledge, Dr. Han has never published studies showing that a slower heart rate during acute myocardial infarction leads to deleterious electrophysiologic effects (with the exception of a figure5 illustrating temporal dispersion data obtained from only a single dog). Our own skepticism originated from the finding that increasing heart rate, even from rates as slow as 30-40/min, increased the degree of ischemic injury in the closed-chest conscious dog,6 a result which suggested to us that altering heart rate might have very different electrophysiologic effects in the presence of ischemia. When this hypothesis was tested, we indeed Circuiation, Volume XLVII, February 1973 LETTERS TO THE EDITOR Downloaded from http://circ.ahajournals.org/ by guest on August 3, 2017 found that the results in the absence of ischemia were opposite to those found during ischemia. Thus, increasing heart rate during ischemia increased the dispersion of recovery of refractory periods and decreased fibrillation threshold.7 More recently, we demonstrated that when heart rate was increased from 50-60 to 90 beats/min by lowering the intensity of vagal stimulation, ventricular fibrillation threshold during ischemia consistently decreased; the mean decrease was 37%.8 In addition, over this same heart rate range, disparity of recovery of refractory periods increased in half of the animals tested. Thus, our results clearly indicate that during acute coronary occlusion in the dog, increasing heart rate within a range similar to that present during acute myocardial infarction in man causes electrophysiologic effects that would favor development of reentrant arrhythmias and increase the heart's vulnerability to ventricular fibrillation. We would certainly agree with Dr. Han that atropine and cardiac pacing have a definite place in the management of bradyeardia in the setting of a coronary care unit, but would add the proviso that these interventions are clearly indicated only when severe bradycardia is complicated by excessive hypotension or excessive ventricular ectopic activity. The point we wish to emphasize is that we do not know the precise definitions of "severe" or "excessive," nor what the limits of safety are when heart rate is increased, since our own studies would indicate that relatively modest increases in heart rate may produce deleterious effects. Nor do we know whether increasing modest levels of hypotension by increasing heart rate is truly beneficial. For example, although hypotension has been shown experimentally to increase the degree of ischemic injury produced by coronary occlusion,6 9 patients with acute myocardial infarction observed in a coronary care unit who had hypotension unassociated with clinical evidence of vasoconstriction or impaired regional perfusion were reported not to have a significantly higher mortality than patients without hypotension.10 It therefore is not clear whether under these circumstances the net effect on ischemic injury of modest increases in pressure at the expense of an increased heart rate diminishes or augments the degree of ischemic injury. In conclusion, our own orientation toward this very important question is that the role of atropine in the treatment of bradyeardia in acute myocardial infarction is uncertain, insofar as the specific situations in which atropine may result in a net beneficial effect; and those in which it may result in a net deleterious effect still must be defined. STEPHEN E. EPsTEIN, M.D. DAVID R. REDWOOD, M.B., M.R.C.P. Cardiology Branch National Heart and Lung Institute Bethesda, Maryland ELDON R. SMITH, M.D. Department of Medicine Victoria General Hospital Halifax, Nova Scotia Circulation, Volume XLVII, February 1973 431 References 1. HAN J, DETRAGLIA J, MILLET D, MOE GK: Incidence of ectopic beats as a function of basic rate in the ventricle. Amer Heart J 72: 632, 1966 2. SCHERLAG BJ, HELFANT RH, HAFT JI, DAMATO AN: Electrophysiology underlying ventricular arrhythmias due to coronary ligation. Amer J Physiol 219: 1665, 1970 3. KARSH RB, ORLANDO M, NORMAN D, EPSTEIN SE: Ineffectiveness of prophylactic atropine in decreasing arrhythmias and enhancing survival following acute coronary artery occlusion in conscious dogs. (Abstr) Amer J Cardiol 29: 273, 1972 4. HAN J, MILLET D, CHIZZONITTI B, MOE GK: Temporal dispersion of recovery of excitability in atrium and ventricle as a function of heart rate. Amer Heart J 71: 481, 1966 5. HAN J: The concepts of reentrant activity responsible for ectopic rhythms. Amer J Cardiol 28: 253, 1971 6. REDWOOD DR, SMiTH ER, EPSTEIN SE: Coronary artery occlusion in the conscious dog: Effects of alterations in heart rate and arterial pressure on the degree of myocardial ischemia. Circulation 46: 323, 1972 7. KENT KM, SMITH ER, REDWOOD DR, EPSTEIN SE: The deleterious electrophysiologic effects produced by increasing heart rate during experimental coronary occlusion. (Abstr) Clin Res 20: 379, 1972 8. KENT KM, SMITH ER, REDWOOD DR, EPSTEIN SE: Electrical stability of acutely ischemic myocardium: Influences of heart rate and vagal stimulation. Circulation 47: 291, 1973 9. MAROKO PR, KjEKCSHUs JK, SOBEL BE, WATANABE T, COVELL JW, Ross J JR, BRAUNWALD E: Factors influencing infarct size following experimental coronary artery occlusions. Circulation 43: 67, 1971 10. LOWN B, VASSAUX C, HooD WB JR, FAKHRO AM, KAPLINSKY E, ROBERGE C: Unresolved problems in coronary care. Amer J Cardiol 20: 494, 1967 Echocardiographic Pattern of Right Ventricular Diastolic Volume Overload in Children To the Editor: This article (CIRCULATION 46: 36, 1972) is quite good and does confirm previous observations having been made by echocardiography. I would like to comment on the three cases of right ventricular volume overload that had normal septal motion by echocardiography. Two of these are illustrated in the article. Case 13 was illustrated as having normal septal motion and is a case of anomalous pulmonary venous connection. The echocardiogram illustrated is taken from low in the left ventricle near the apex, and there is no evidence of the mitral valve being present. Past experience with scanning technics involving a strip chart recorder rather than Polaroid films has shown that in people with atrial septal defects with abnormal septal motion as you scan near the apex you tend to get a normal septal motion. I feel strongly that in order to make the diagnosis of abnormal septal motion you must Atropine and Acute Myocardial Infarction: The authors reply: STEPHEN E. EPSTEIN, DAVID R. REDWOOD and ELDON R. SMITH Circulation. 1973;47:430-431 doi: 10.1161/01.CIR.47.2.430 Downloaded from http://circ.ahajournals.org/ by guest on August 3, 2017 Circulation is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231 Copyright © 1973 American Heart Association, Inc. All rights reserved. Print ISSN: 0009-7322. Online ISSN: 1524-4539 The online version of this article, along with updated information and services, is located on the World Wide Web at: http://circ.ahajournals.org/content/47/2/430.citation Permissions: Requests for permissions to reproduce figures, tables, or portions of articles originally published in Circulation can be obtained via RightsLink, a service of the Copyright Clearance Center, not the Editorial Office. Once the online version of the published article for which permission is being requested is located, click Request Permissions in the middle column of the Web page under Services. Further information about this process is available in the Permissions and Rights Question and Answer document. Reprints: Information about reprints can be found online at: http://www.lww.com/reprints Subscriptions: Information about subscribing to Circulation is online at: http://circ.ahajournals.org//subscriptions/