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Spontaneous rupture of abdominal aneurysm
LETTERS TO THE EDITOR
Bennett for rescuing me from categorization as a false prophet by providing the first incontrovertible evidence to support the prediction made. Bennett's successful management of his case with propranolol should be noted by all who treat arrhythrajas. Charles E. Kossmann, MD, FACC University of Tennessee College of Medicine Memphis, Tennessee
2. Kossmann CE. Torsade de pointes: an addition to the nosography of ventricular taehy. oardia. 3. Ranquln R, Parizel G. Ventricular fibrillo-flutter ("torsade de pointe"): an established electrocardiographic and clinica) entity. Angiology 1977; 28:115-8. 4. Oessert'enne F. La tachycardie ventriculaire a deux foyers opposes variables. Arch Mal Coeur 1966; 59:263. 5. Slama R, Metre G, Coumel P, et aL Le syndrome "aUongement de QT et syncopes per torsade de pointe" Laval Med 1971; 42:353. 6. Molle G, Coumel P, Abitol G, el al. Le syndrome QT long et syncopes par "torsade de pointe" Arch Med Coeur 1970; 6:831.
REPLY
TREATMENT OF TORSADE DE POINTES
Two recent articles 1,2in this Journal discuss torsade de pointes arrhythmias. In 1977, we described the occurrence of "torsade de pointes" arrhythmias in 8 patients selected from 1,100 patients treated in our coronary care unit. 3 We proposed to call the arrhythmia "ventricular fibrillo-flutter" in analogy with its atrial counterpart. For this selection we used the criteria described by Desertenne et al.4 Two patients died of the rhythm disturbance and the others were able to leave the hospital in good condition. They all showed a typical pattern of "torsade de pointes" episodes and all but one had greatly prolonged Q-Tc intervals (0.60 s or more) during sinus rhythm. The origin of this arrhythmia was attributed to severe coronary ischemia in three patients, acute myocardial infarction combined with digitalis intoxication in one patient, hypokalemia in two others, thioridazine treatment (300 mg/day) in one and subarachnoid hemorrhage in the eighth patient. All patients were treated with electric defibrillation during episodes of"torsade de pointes" and subsequently with lignocaine and aprindine infusions to prevent recurrences. One patient required electric pacing for severe sinus bradycardia. It is our impression, contrary to the view of the French authors, 5,6 that the particular form of arrhythmia can be prevented by the administration of these two drugs providing that the basic rhythm is not too slow. Otherwise, electric pacing at a rate of about 100 to 110 beats/min seems to be a good preventive measure. The appearance of severe ventricular arrhythmias due to disopyramide toxicity seems to be a very rare complication. We use disopyramide therapy for ventricular arrhythmias as a second choice drug after failure with lignocaine. To date we have not observed ventricular arrhythmias due to disopyramide toxicity. However, we have never used the large dosage regimens (1,200 to 2,400 rag/day) mentioned in Dr. Meltzer's article; our standard dosage is 600 rag/day. In conclusion, we make a plea for consideration of the "torsade de pointes" phenomenon as a distinct electrocardiographic and clinical entity for etiologic, morphologic and therapeutic reasons. G. Parizel, Prof Dr R. Ranquin, MD Service of Internal Medicine Middelheim General Hospital University of Antwerp Antwerp, Belgium
Although multiple nondrug-related conditions have been associated with atypical ventricular tachycardia, drug toxicity is a frequent cause. Because quinidine is perhaps the most prominent offender, and disopyramide has similar electrophysiologic effects, we were not surprised to note a slow "torsade de pointes" phenomenon with the disopyramide toxicity in our patient. As stated in our article, the overdose was inadvertent, probably a consequence of lack of familiarity with a newly introduced drug by the house staff and nurses. Indeed, the prescribed dosage of disopyramide in our hospital rarely exceeds 1,200 mg/day, even for patients with refractory ventricular arrhythmias. Whether atypical ventricular tachycardia will be noted in patients taking conventional therapeutic doses of disopyramide remains in question. We have no data on the incidence of atypical ventricular arrhythmias with disopyramide toxicity, but we agree with Parizel and Ranquin that they are not common. Richard Meltzer, MD Edward W. Robert, MD Stanford University School of Medicine Stanford, California
SPONTANEOUS RUPTURE OF ABDOMINAL ANEURYSM
Young et al. 1 point out that the spontaneous rupture of an abdominal aneurysm into the inferior vena cava may be predicted by certain clinical characteristics, but do not mention the electrocardiogram. Pertinent is the report by Dickson et al., 2 which pointed out that the sudden appearance of electrocardiographic changes consistent with right ventricular overload in patients suffering from an acute abdominal catastrophe should suggest the possibility of an aortocaval fistula, particularly in those with known abdominal aortic aneurysms. Irwin J. Schatz, MD, FACC John A. Burns School of Medicine Department of Medicine University of Hawaii at Manoa Honolulu, Hawaii References 1. Young JB, Roehm Jr JOF, Lawrle GM, et al. Fortuitous rupture of aortic aneurysm: a catastrophic event affording time for surgical cure. Am J Cardiol 1978; 42:862-7. 2. Dlckson ER, Schatz IJ, Marshall KG, Cain JC. Rupture of abdominal aortic aneurysm into vena cava. Arch Intern Med 1963; 112:29-31.
REPLY
References 1. Meltzer RS, Robert EW, McMorrow M, Martin RP. Atypicat ventricular tachycardia as a manifestation of disopyramide toxicity. Am J Cardlol 1978; 42:1049-53.
716
March 1980
New electrocardiographic evidence of right ventricular overload with a rightward shift of axis (usually manifested by the
The American Journal of CARDIOLOGY Volume45
Bennett for rescuing me from categorization as a false prophet by providing the first incontrovertible evidence to support the prediction made. Bennett's successful management of his case with propranolol should be noted by all who treat arrhythrajas. Charles E. Kossmann, MD, FACC University of Tennessee College of Medicine Memphis, Tennessee
2. Kossmann CE. Torsade de pointes: an addition to the nosography of ventricular taehy. oardia. 3. Ranquln R, Parizel G. Ventricular fibrillo-flutter ("torsade de pointe"): an established electrocardiographic and clinica) entity. Angiology 1977; 28:115-8. 4. Oessert'enne F. La tachycardie ventriculaire a deux foyers opposes variables. Arch Mal Coeur 1966; 59:263. 5. Slama R, Metre G, Coumel P, et aL Le syndrome "aUongement de QT et syncopes per torsade de pointe" Laval Med 1971; 42:353. 6. Molle G, Coumel P, Abitol G, el al. Le syndrome QT long et syncopes par "torsade de pointe" Arch Med Coeur 1970; 6:831.
REPLY
TREATMENT OF TORSADE DE POINTES
Two recent articles 1,2in this Journal discuss torsade de pointes arrhythmias. In 1977, we described the occurrence of "torsade de pointes" arrhythmias in 8 patients selected from 1,100 patients treated in our coronary care unit. 3 We proposed to call the arrhythmia "ventricular fibrillo-flutter" in analogy with its atrial counterpart. For this selection we used the criteria described by Desertenne et al.4 Two patients died of the rhythm disturbance and the others were able to leave the hospital in good condition. They all showed a typical pattern of "torsade de pointes" episodes and all but one had greatly prolonged Q-Tc intervals (0.60 s or more) during sinus rhythm. The origin of this arrhythmia was attributed to severe coronary ischemia in three patients, acute myocardial infarction combined with digitalis intoxication in one patient, hypokalemia in two others, thioridazine treatment (300 mg/day) in one and subarachnoid hemorrhage in the eighth patient. All patients were treated with electric defibrillation during episodes of"torsade de pointes" and subsequently with lignocaine and aprindine infusions to prevent recurrences. One patient required electric pacing for severe sinus bradycardia. It is our impression, contrary to the view of the French authors, 5,6 that the particular form of arrhythmia can be prevented by the administration of these two drugs providing that the basic rhythm is not too slow. Otherwise, electric pacing at a rate of about 100 to 110 beats/min seems to be a good preventive measure. The appearance of severe ventricular arrhythmias due to disopyramide toxicity seems to be a very rare complication. We use disopyramide therapy for ventricular arrhythmias as a second choice drug after failure with lignocaine. To date we have not observed ventricular arrhythmias due to disopyramide toxicity. However, we have never used the large dosage regimens (1,200 to 2,400 rag/day) mentioned in Dr. Meltzer's article; our standard dosage is 600 rag/day. In conclusion, we make a plea for consideration of the "torsade de pointes" phenomenon as a distinct electrocardiographic and clinical entity for etiologic, morphologic and therapeutic reasons. G. Parizel, Prof Dr R. Ranquin, MD Service of Internal Medicine Middelheim General Hospital University of Antwerp Antwerp, Belgium
Although multiple nondrug-related conditions have been associated with atypical ventricular tachycardia, drug toxicity is a frequent cause. Because quinidine is perhaps the most prominent offender, and disopyramide has similar electrophysiologic effects, we were not surprised to note a slow "torsade de pointes" phenomenon with the disopyramide toxicity in our patient. As stated in our article, the overdose was inadvertent, probably a consequence of lack of familiarity with a newly introduced drug by the house staff and nurses. Indeed, the prescribed dosage of disopyramide in our hospital rarely exceeds 1,200 mg/day, even for patients with refractory ventricular arrhythmias. Whether atypical ventricular tachycardia will be noted in patients taking conventional therapeutic doses of disopyramide remains in question. We have no data on the incidence of atypical ventricular arrhythmias with disopyramide toxicity, but we agree with Parizel and Ranquin that they are not common. Richard Meltzer, MD Edward W. Robert, MD Stanford University School of Medicine Stanford, California
SPONTANEOUS RUPTURE OF ABDOMINAL ANEURYSM
Young et al. 1 point out that the spontaneous rupture of an abdominal aneurysm into the inferior vena cava may be predicted by certain clinical characteristics, but do not mention the electrocardiogram. Pertinent is the report by Dickson et al., 2 which pointed out that the sudden appearance of electrocardiographic changes consistent with right ventricular overload in patients suffering from an acute abdominal catastrophe should suggest the possibility of an aortocaval fistula, particularly in those with known abdominal aortic aneurysms. Irwin J. Schatz, MD, FACC John A. Burns School of Medicine Department of Medicine University of Hawaii at Manoa Honolulu, Hawaii References 1. Young JB, Roehm Jr JOF, Lawrle GM, et al. Fortuitous rupture of aortic aneurysm: a catastrophic event affording time for surgical cure. Am J Cardiol 1978; 42:862-7. 2. Dlckson ER, Schatz IJ, Marshall KG, Cain JC. Rupture of abdominal aortic aneurysm into vena cava. Arch Intern Med 1963; 112:29-31.
REPLY
References 1. Meltzer RS, Robert EW, McMorrow M, Martin RP. Atypicat ventricular tachycardia as a manifestation of disopyramide toxicity. Am J Cardlol 1978; 42:1049-53.
716
March 1980
New electrocardiographic evidence of right ventricular overload with a rightward shift of axis (usually manifested by the
The American Journal of CARDIOLOGY Volume45