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Myocardial bridging of coronary artery
LETTERS
larly in the patient with uncomplicated infarction. During the past 5 years, at a time when the mortality rate after acute myocardial infarction has been declining, the role of hemodynamic monitoring has gained wide acceptance. Our experience does not indicate that the biomedical instrumentation itself is responsible for the accelerated heart rate or less favorable prognosis of some patients. Rather, as Peel et al.5 emphasized many years ago, the persistence of sinus tachycardia after infarction forebodes a compromise in ventricular function and a corresponding poor prognosis. We have merely confirmed this finding and perhaps provided additional information with which to assess the severity of ventricular dysfunction by pointing out the importance of left ventricular filling pressure. It is this compromised, high risk patient who can best be identified hemodynamically. Karl T. Weber, MD, FACC Joseph S. Janicki, PhD Richard 0. Russell, MD, FACC Charles E. Rackley, MD, FACC Hospital of the University of Pennsylvania Philadelphia, Pennsylvania
TO
THE
EDITOR
Figure 2B, which was described as showing a normal mid left anterior descending artery during diastole, has a significant narrowing of at least 50 percent in diameter and 75 percent in cross-sectional area in the segment denoted by the arrows, indicative of significant atherosclerotic obstruction. Although a still print from a cinearteriogram sometimes fails to reproduce the true appearance of the coronary artery, the frame the authors chose in this case certainly was not representative of a normal vessel during diastole. Perhaps the authors wish to review the cinecoronary arteriogram of their first patient to see if a frame showing a normal mid left anterior descending artery during diastole could actually be identified. The authors’ observation that the left anterior descending coronary artery felt stiff at operation would further suggest that the vessel was indeed not normal. Tsung 0. Cheng, MD, FACC
case,
Division of Cardiology Department of Medicine George Washington University Medical Center Washington, D. C.
References
Reierence
1. Kllllp 1, Kknball JT: Treatment of rnyocardial infarction in a coronary care unit. A two year experience with 250 patients. Am J Cardiol 20:457-464. 1967 2. Rackley CE, Roger8 WJ, Mantle JA, McDaniel HG, Russell RO: Hemodynamic. metabolic and anatomic abncxmallties in patients with uncomplicated acute myocardial infarction. Circulation 56:Suppl111:111-220. 1977 3. Forwstn JS, Diamond GA, Swan HJC: Correlative classification of clinical and hemcdynamic function after acute myocardial infarction. Am J Cardiol 39:137-145, 1977 4. Mlr~wskl M, Israel W, Ardonopoulos AGo, Mower MM, Mendeloff Al: Treatment of myocardial infarction in a community hospital coronary care unit. Arch Intern Med 138:210-215. 1976 5. Pm AAF. m T, Wang I, Lancaster WM, Dal1 JLO: A coronary prognostic index for grading the severity of infarction. Br Heart J 24:745-760. 1962
1. Faruqul AMA, M&y WC, F&w JM, Schlanf RC, Logan WD, Symbar P: Symptomatic myocardial bridging of coronary artwy. Am J Cardiol 41~1305-1310. 1976
REBUTTAL
Weber’s reply fails to address the issue, which is the negligible mortality in class I patients managed noninuasiuely and the 10 percent mortality rate reported in his study of class I patients managed inuasiuely. This highly significant difference in mortality still remains to be explained, and the basis for Weber’s “strong exception” to the possibility that biomedical instrumentation itself might be responsible remains to be clarified. Is it not possible that the excessive mortality may be a result of the invasive monitoring itself? Although the insertion of a Swan-Ganz catheter is a relatively simple procedure, it is not devoid of complications. In addition, the frequent checks and measurements required by cardiac care unit personnel using this procedure may be a cause for anxiety in some patients, resulting in increased sympathetic nervous system activity. This cannot be casually dismissed as totally innocuous. Weber claims that he is identifying a high risk subset of class I patients. I maintain that it is just as likely that he is creating a high risk subset of class I patients and, on the basis of his data, there is certainly no justification for recommending invasive monitoring in patients with clinically uncomplicated acute myocardial infarction. Sanford S. Zevon, MD, FACC
MYOCARDIAL
BRIDGING OF CORONARY
ARTERY
Faruqui et al.’ presented two cases of myocardial bridging of the left anterior descending coronary artery. In their first
REPLY
The angiogram in question was reviewed by several of the authors prior to publication. If the area under consideration is compared with the proximal anterior descending artery, the caliber is smaller. However, several branches including a large diagonal and a large septal perforator branch are given off before the area of bridging begins. Keeping this in mind and having the benefit of reviewing the vessel in motion rather than in a still frame, we still believe that there is no significant luminal obstruction present in diastole. Azhar M. A. Faruqui, MD, FACC National Institute of Cardiovascular Diseases Karachi, Pakistan
DISOPYRAMIDE-INDUCED
SYNCOPE
In their excellent review article on new antiarrhythmic agents Zipes and Troupi state that marked Q-T prolongation and syncope resulting from ventricular tachyarrhythmias have not been reported with disopyramide when administered at usual maintenance doses despite the drug’s electrophysiologic similarities to quinidine. They made reference, however, to a patient with a history of quinidine syncope who manifested a prolonged Q-T interval and ventricular fibrillation while receiving 300 mg of disopyramide every 6 hours. We recently saw a patient with normal hepatic and renal function in whom marked Q-T prolongation and syncope developed secondary to ventricular tachycardia while she was receiving quinidine. She subsequently had an identical complication while receiving only 100 mg of disopyramide every 6 hours. The initial Q-Tc interval of 0.42 second increased to 0.65 second with disopyramide administration. It had previously increased to 0.62 second when she was receiving quinidine. A somewhat similar case of a patient who manifested a Q-Tc interval of 0.44 second and recurrent ventricular fibrillation while receiving 150 mg of disopyramide every 6 hours was reported by Frieden.
August 1979
The American Journal of CARDIOLOGY
Volume 44
391
larly in the patient with uncomplicated infarction. During the past 5 years, at a time when the mortality rate after acute myocardial infarction has been declining, the role of hemodynamic monitoring has gained wide acceptance. Our experience does not indicate that the biomedical instrumentation itself is responsible for the accelerated heart rate or less favorable prognosis of some patients. Rather, as Peel et al.5 emphasized many years ago, the persistence of sinus tachycardia after infarction forebodes a compromise in ventricular function and a corresponding poor prognosis. We have merely confirmed this finding and perhaps provided additional information with which to assess the severity of ventricular dysfunction by pointing out the importance of left ventricular filling pressure. It is this compromised, high risk patient who can best be identified hemodynamically. Karl T. Weber, MD, FACC Joseph S. Janicki, PhD Richard 0. Russell, MD, FACC Charles E. Rackley, MD, FACC Hospital of the University of Pennsylvania Philadelphia, Pennsylvania
TO
THE
EDITOR
Figure 2B, which was described as showing a normal mid left anterior descending artery during diastole, has a significant narrowing of at least 50 percent in diameter and 75 percent in cross-sectional area in the segment denoted by the arrows, indicative of significant atherosclerotic obstruction. Although a still print from a cinearteriogram sometimes fails to reproduce the true appearance of the coronary artery, the frame the authors chose in this case certainly was not representative of a normal vessel during diastole. Perhaps the authors wish to review the cinecoronary arteriogram of their first patient to see if a frame showing a normal mid left anterior descending artery during diastole could actually be identified. The authors’ observation that the left anterior descending coronary artery felt stiff at operation would further suggest that the vessel was indeed not normal. Tsung 0. Cheng, MD, FACC
case,
Division of Cardiology Department of Medicine George Washington University Medical Center Washington, D. C.
References
Reierence
1. Kllllp 1, Kknball JT: Treatment of rnyocardial infarction in a coronary care unit. A two year experience with 250 patients. Am J Cardiol 20:457-464. 1967 2. Rackley CE, Roger8 WJ, Mantle JA, McDaniel HG, Russell RO: Hemodynamic. metabolic and anatomic abncxmallties in patients with uncomplicated acute myocardial infarction. Circulation 56:Suppl111:111-220. 1977 3. Forwstn JS, Diamond GA, Swan HJC: Correlative classification of clinical and hemcdynamic function after acute myocardial infarction. Am J Cardiol 39:137-145, 1977 4. Mlr~wskl M, Israel W, Ardonopoulos AGo, Mower MM, Mendeloff Al: Treatment of myocardial infarction in a community hospital coronary care unit. Arch Intern Med 138:210-215. 1976 5. Pm AAF. m T, Wang I, Lancaster WM, Dal1 JLO: A coronary prognostic index for grading the severity of infarction. Br Heart J 24:745-760. 1962
1. Faruqul AMA, M&y WC, F&w JM, Schlanf RC, Logan WD, Symbar P: Symptomatic myocardial bridging of coronary artwy. Am J Cardiol 41~1305-1310. 1976
REBUTTAL
Weber’s reply fails to address the issue, which is the negligible mortality in class I patients managed noninuasiuely and the 10 percent mortality rate reported in his study of class I patients managed inuasiuely. This highly significant difference in mortality still remains to be explained, and the basis for Weber’s “strong exception” to the possibility that biomedical instrumentation itself might be responsible remains to be clarified. Is it not possible that the excessive mortality may be a result of the invasive monitoring itself? Although the insertion of a Swan-Ganz catheter is a relatively simple procedure, it is not devoid of complications. In addition, the frequent checks and measurements required by cardiac care unit personnel using this procedure may be a cause for anxiety in some patients, resulting in increased sympathetic nervous system activity. This cannot be casually dismissed as totally innocuous. Weber claims that he is identifying a high risk subset of class I patients. I maintain that it is just as likely that he is creating a high risk subset of class I patients and, on the basis of his data, there is certainly no justification for recommending invasive monitoring in patients with clinically uncomplicated acute myocardial infarction. Sanford S. Zevon, MD, FACC
MYOCARDIAL
BRIDGING OF CORONARY
ARTERY
Faruqui et al.’ presented two cases of myocardial bridging of the left anterior descending coronary artery. In their first
REPLY
The angiogram in question was reviewed by several of the authors prior to publication. If the area under consideration is compared with the proximal anterior descending artery, the caliber is smaller. However, several branches including a large diagonal and a large septal perforator branch are given off before the area of bridging begins. Keeping this in mind and having the benefit of reviewing the vessel in motion rather than in a still frame, we still believe that there is no significant luminal obstruction present in diastole. Azhar M. A. Faruqui, MD, FACC National Institute of Cardiovascular Diseases Karachi, Pakistan
DISOPYRAMIDE-INDUCED
SYNCOPE
In their excellent review article on new antiarrhythmic agents Zipes and Troupi state that marked Q-T prolongation and syncope resulting from ventricular tachyarrhythmias have not been reported with disopyramide when administered at usual maintenance doses despite the drug’s electrophysiologic similarities to quinidine. They made reference, however, to a patient with a history of quinidine syncope who manifested a prolonged Q-T interval and ventricular fibrillation while receiving 300 mg of disopyramide every 6 hours. We recently saw a patient with normal hepatic and renal function in whom marked Q-T prolongation and syncope developed secondary to ventricular tachycardia while she was receiving quinidine. She subsequently had an identical complication while receiving only 100 mg of disopyramide every 6 hours. The initial Q-Tc interval of 0.42 second increased to 0.65 second with disopyramide administration. It had previously increased to 0.62 second when she was receiving quinidine. A somewhat similar case of a patient who manifested a Q-Tc interval of 0.44 second and recurrent ventricular fibrillation while receiving 150 mg of disopyramide every 6 hours was reported by Frieden.
August 1979
The American Journal of CARDIOLOGY
Volume 44
391