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Effects of indomethacin during experimental myocardial ischemia
1082
Letters
to the
December, 1@81 American Heart Journal
Editor
must show a progressive twisting of the pointes (QRS and T), yielding a modulated sinus curve with small-size QRS complexes and possibly normal widths of those portions of the curve with the least amplitude. The question regarding the QT interval has already been dealt with in our reply to Drs. Motro and Neufeld. We agree that atypical ventricular tachycardia described as torsades de pointes usually starts as a single premature beat with subsequent complexes representing large-size reentrant waves which appear to have different pathways involving different areas.: Therefore we do not feel that this premature beat must have a fixed and prolonged coupling interval. G. Cocco, M.D. D. Chu, Ph.D. C. Stroesi, M.D. Cardiology Division, Clinica Medica University of Ferrara Ferraru, Italy Address for correspondence: Giuseppe Cocco, M.D. Postfach 290, CH-4103 Bottmingen, Switzerland REFERENCES 1.
2.
Kossmann CE: Torsades de pointes: An additional to the nosography of ventricular tachycardia. Am J Cardiol 42:1054, 1978. Wiggers CJ: The mechanism and nature of ventricular fibrillation. AM HEART J 20:399, 1940.
EFFECTS OF lND\OMETHAClN EXf’ERlMENTAL MYOCARDIAL
DURING ISCHEMA
To the Editor: The report in the JOURNAL by Berman et al1 concerning the management of symptomatic pericarditis associated with acute myocardial infarction (AMI) includes excellent observations on the clinical setting, presentation, and successful management of this annoying complication. In a well executed study, the authors nicely demonstrated equality of effect of aspirin and indomethatin. Successful management with indomethacin is in accord with our group’s experience. However, about 2 years ago we reluctantly ceased using it, owing to the report of Jugdutt et al.z who demonstrated increase in myocardial necrosis after experimental coronary occlusion in dogs pretreated with indomethacin. Since E-type prostaglandins appear to preserve the integrity of ischemic myocardial tissuei any potential deleterious effect of indomethacin might be attributed to prostaglandin inhibition. Subsequently, it was also shown experimentally that indomethatin appears to have a coronary vasoconstrictor effect’; it
increased myocardial oxygen demand by increasing mean arterial pressure and coronary blood flow declined as coronary vascular resistance increased. Although the work cited was carried out in experimental animals,:-’ it made our group reluctant to use indomethacin in the presence of coronary heart disease and particularly in the setting of AMI. David H. Spodick, M.D. Division of Cardiology St. Vincent Hospital Worcester, MA 01604 REFERENCES Berman J, Haffajee CL Alpert JS: Therapy of symptomatic pericarditis after myocardial infarction: Retrospective and prospective studies of aspirin, indomethacin, prednisone and spontaneous resolutionAM HEART J 101:756, 1981. Juedutt BI. Becker LC. Bulklev BH. Hutchins GM: Prostaglandin inhibition increases infarct size after coronary artery occlusion in conscious dogs. Am J Cardiol41:359, 1978. Ogletree ML, Lefer AM: Prostaglandin-induced preservation of the ischemic myocardium. Circ Res 42:218, 1978. Brown EJ, Friedman PL, Gunther S, Alexander RW, Barry WH, Grossman W, Mudge GH: Coronary vasoconstrictor effect of indomethacin in patients with coronary artery disease. Circulation 82(Suppl 111):325, 1980.
REPLY To the Editor: We thank Dr. Spodick for his timely remarks in response to our article in the recent issue of the JOURNAL. Despite the two experimental studies to which Dr. Spodick refers, many cardiologists still employ indomethacin in the treatment of postmyocardial infarction pericarditis. In fact, our study was initiated because of confusion on the part of our medical residents over which agent to use in this setting. Despite the experimental studies to which Dr. Spodick refers, we are unaware of any untoward effect of indomethacin in patients with acute myocardial infarction. This agent continues to be the preferred form of therapy for post-myocardial infarction pericarditis in many coronary care units in this country and abroad. We have found no evidence of infarct extension or increasing myocardial ischemia subsequent to initiating indomethacin therapy in our patients. Further observations concerning the clinical significance of the cited animal experiments would clearly be of interest. Joseph S. Alpert, M.D. Jay Berman, M.D. Division of Cardiovascular Medicine Department of Medicine University of Massachusetts Medical School Worcester, MA 01605
Letters
to the
December, 1@81 American Heart Journal
Editor
must show a progressive twisting of the pointes (QRS and T), yielding a modulated sinus curve with small-size QRS complexes and possibly normal widths of those portions of the curve with the least amplitude. The question regarding the QT interval has already been dealt with in our reply to Drs. Motro and Neufeld. We agree that atypical ventricular tachycardia described as torsades de pointes usually starts as a single premature beat with subsequent complexes representing large-size reentrant waves which appear to have different pathways involving different areas.: Therefore we do not feel that this premature beat must have a fixed and prolonged coupling interval. G. Cocco, M.D. D. Chu, Ph.D. C. Stroesi, M.D. Cardiology Division, Clinica Medica University of Ferrara Ferraru, Italy Address for correspondence: Giuseppe Cocco, M.D. Postfach 290, CH-4103 Bottmingen, Switzerland REFERENCES 1.
2.
Kossmann CE: Torsades de pointes: An additional to the nosography of ventricular tachycardia. Am J Cardiol 42:1054, 1978. Wiggers CJ: The mechanism and nature of ventricular fibrillation. AM HEART J 20:399, 1940.
EFFECTS OF lND\OMETHAClN EXf’ERlMENTAL MYOCARDIAL
DURING ISCHEMA
To the Editor: The report in the JOURNAL by Berman et al1 concerning the management of symptomatic pericarditis associated with acute myocardial infarction (AMI) includes excellent observations on the clinical setting, presentation, and successful management of this annoying complication. In a well executed study, the authors nicely demonstrated equality of effect of aspirin and indomethatin. Successful management with indomethacin is in accord with our group’s experience. However, about 2 years ago we reluctantly ceased using it, owing to the report of Jugdutt et al.z who demonstrated increase in myocardial necrosis after experimental coronary occlusion in dogs pretreated with indomethacin. Since E-type prostaglandins appear to preserve the integrity of ischemic myocardial tissuei any potential deleterious effect of indomethacin might be attributed to prostaglandin inhibition. Subsequently, it was also shown experimentally that indomethatin appears to have a coronary vasoconstrictor effect’; it
increased myocardial oxygen demand by increasing mean arterial pressure and coronary blood flow declined as coronary vascular resistance increased. Although the work cited was carried out in experimental animals,:-’ it made our group reluctant to use indomethacin in the presence of coronary heart disease and particularly in the setting of AMI. David H. Spodick, M.D. Division of Cardiology St. Vincent Hospital Worcester, MA 01604 REFERENCES Berman J, Haffajee CL Alpert JS: Therapy of symptomatic pericarditis after myocardial infarction: Retrospective and prospective studies of aspirin, indomethacin, prednisone and spontaneous resolutionAM HEART J 101:756, 1981. Juedutt BI. Becker LC. Bulklev BH. Hutchins GM: Prostaglandin inhibition increases infarct size after coronary artery occlusion in conscious dogs. Am J Cardiol41:359, 1978. Ogletree ML, Lefer AM: Prostaglandin-induced preservation of the ischemic myocardium. Circ Res 42:218, 1978. Brown EJ, Friedman PL, Gunther S, Alexander RW, Barry WH, Grossman W, Mudge GH: Coronary vasoconstrictor effect of indomethacin in patients with coronary artery disease. Circulation 82(Suppl 111):325, 1980.
REPLY To the Editor: We thank Dr. Spodick for his timely remarks in response to our article in the recent issue of the JOURNAL. Despite the two experimental studies to which Dr. Spodick refers, many cardiologists still employ indomethacin in the treatment of postmyocardial infarction pericarditis. In fact, our study was initiated because of confusion on the part of our medical residents over which agent to use in this setting. Despite the experimental studies to which Dr. Spodick refers, we are unaware of any untoward effect of indomethacin in patients with acute myocardial infarction. This agent continues to be the preferred form of therapy for post-myocardial infarction pericarditis in many coronary care units in this country and abroad. We have found no evidence of infarct extension or increasing myocardial ischemia subsequent to initiating indomethacin therapy in our patients. Further observations concerning the clinical significance of the cited animal experiments would clearly be of interest. Joseph S. Alpert, M.D. Jay Berman, M.D. Division of Cardiovascular Medicine Department of Medicine University of Massachusetts Medical School Worcester, MA 01605