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Torsade de pointes complicating atrioventricular block: report of two cases
235
References 1 Freedom R, Wham G, Rowe R, et al. The criss cross and supero-inferior ventricular heart. An angiographic study. Am J Cardiol 1978;42:620-627. 2 Van Praagh S, La Coste M. Fellows KE, et al. Superoinferior ventricles. anatomic and angiocardiographic finding in ten post mortem cases. In: Van Praagh R, Takao A, eds. Etiology and morphogenesis of congenital heart disease. Mount Kisco, New York: Futura Publishing, 1980. 3 Attie F, Muiioz-Castellanos L. Ovseyevitz J. et al. Crossed atrioventricular connections. Am Heart J 1980;99:163-172. 4 Santos MA, Mall JN, Neto CD, et al. Ventriculo superoinferior: malforma@o cardiaca cspecifica ou uma nova terminologia? Arq Bras Cardiol 1981;37(suppl 1):123.
IJC 0494E
Torsade de pointes complicating atrioventricular block: report of two cases Naphtali
Maor, Dov Weiss, Avraham
intensitw Cardiac Cure Unit. L&y Duuis Camel (Received
16 June 1986: revision accepted
Lorber
Hosprtol, Hoifu. Israel 1 September
1986)
One patient with complete atrioventricular heart block and another with high-degree atrioventricular block, complicated by “torsade de pointes” are presented. Both patients were symptomatic. One had a syncopal episode and the other presented with signs and symptoms of congestive heart failure. The electrocardiographic phenomena of torsade de pointes was repeatedly recorded. No other known predisposing factors for torsade de pointes were identified. The use of right ventricular endocatdial pacing suppressed the paroxysms in both patients. (Key words:
Torsade
de pointes;
Atrioventricular
block)
Introduction Torsade de pointes refers to the characteristic ondulation of the QRS axis during paroxysms of ventricular tachycardia in the presence of a prolonged Q-T interval [I]. Although bradycardia and complete atrioventricular heart block are known to cause torsade de pointes, a limited number of cases has been described. Two cases of torsade de pointes. one associated with complete atrioventricular heart block and another with high-degree atrioventricular block are presented.
Correspondeme 10: A. Palant, 7222, Haifa 34362, Israel.
M.D.. Intensive
Cardiac
Internarronul Journal of Cardiologv, 14 (1987) 235-238 ,B Elsevier Science Publishers B.V. (Biomedical Division)
Care Unit, Lady Davis Carmel
Hospital.
P.0.B
236
Case Reports Case I. An 80-year-old woman was admitted to the coronary care unit following an episode of syncope, from which she had recovered spontaneously after several minutes. Medications on admission included furosemide only. Complete atrioventricular block was known for four years. The initial electrocardiogram (Fig. la) showed complete atrioventricular block and ventricular rate of 40 beats/min, few ventricular ectopic beats. The Q-T interval was 0.70 sec. On the second day there were ventricular ectopic beats giving rise to paroxysms of ventricular
V,
a
Fig. 1. a. Electrocardiogram on admission showing complete atrioventricular block with a ventricular rate of 40 beats/min. Q-T interval of 0.70 sec. b. Torsade de pointes complicating complete atrioventricular block.
231
tachycardia, with the typical morphological appearance of torsade de pointes (Fig. lb). The concentrations of potassium, magnesium and calcium in the serum were normal. Serial determinations of creatine phosphokinase, serum glutamine oxaloacetic and lactic dehydrogenase were within normal Limits. A temporary (and later permanent) transvenous demand pacemaker was inserted. This procedure completely eradicated the ventricular ectopic beats and the paroxysms of torsade de pointes. The Q-T interval was shortened to 0.36 sec. Case 2. A 64-year-old woman was admitted to the hospital because of dyspnea. Her medical history included hypertension and diabetes mellitus, insulin dependent. The serum potassium, calcium and magnesium values were normal. Serial determinations of creatine phosphokinase, serum glutamine oxaloacetic and lactic dehydrogenase were within normal limits. The electrocardiogram revealed high-degree atrioventricular block with a ventricular rate of 36 beats/min. There were frequent ventricular extrasystoles and bursts of ventricular
I
I
b Fig. 2. a. Monitor electrocardiographic strip on admission block with a ventricular rate of 36 beats/min. b. Torsade ventricular block.
demonstrating high-degree atrioventricular de pointes complicating high-degree atrio-
I
238
tachycardia with the typical morphological temporary (and later permanent) pacemaker the arrhythmia.
appearance of torsade de pointes (Fig. 2). A was inserted, which resulted in abolishment of
Torsade de pointes has been reported at all ages, in association with many underlying conditions [l]. French authors have emphasized the frequent occurrence of torsade de pointes in the setting of marked bradycardia or complete heart block [1,2]. Schwartz et al. [3] were the first to point out the importance of this arrhythmia as a cause of syncope in patients with complete heart block. The electrophysiological mechanism underlying torsade de pointes is poorly understood. Dessertenne postulated the presence of several arrhythmic foci. Other authors favor a reentry mechanism [4]. From experimental work, it is known that temporal dispersion of the ventricular refractory periods is a direct function of the basic cycle length. In complete atrioventricular block when the basic idioventricular rate is slow, the range of refractory periods and action potential duration is greater, and it may account for the generation of reentrant arrhythmias [l]. Although temporal dispersion of refractoriness is the basis for reentrant mechanism with bradycardia, another mechanism is required for the initial ectopic beats. Recently, it has been proposed that after-depolarizations might play a role in arrhythmias of the long Q-T syndrome [l]. Based on an experimental model, Brachmann et al. [5] proposed a mechanism of bradycardia-dependent-triggered activity caused by early after-depolarizations. Whether this mechanism may account for torsade de pointes complicating complete atrioventricular block and bradycardia is not known. Further studies are required to understand this point.
References 1 Smith WM. Gallagher JJ. “Les torsade de pointes”: an unusual ventricular arrhythmia. Ann Intern Med 1980;93:578-584. 2 Motte G. Coumel PH, Abitol G, Dessertenne F, Slama R. Le syndrome QT long et syncopes par “torsade de pointe”. Arch Mal Coeur 1970;63:831-853. 3 Schwartz SP, Hallinger LN. Transient ventricular fibrillation. VI. Observation on peripheral arterial pulse pressures in the course of transient ventricular fibrillation during established auriculoventricular dissociation. Am Heart J 1954;48:390-404. 4 Horowitz LN, Greenspan AM, Spielman SR, Josephson ME. Torsade de pointes: electrophysiologic studies in patients without transient pharmacologic or metabolic abnormalities. Circulation 1981;63:1120-1128. 5 Brachmann J, Scherlag BJ, Rosenstraukh LV, Lazzara R. Bradycardia-dependent triggered activity relevance to drug-induced multiform ventricular tachycardia. Circulation 1983;68:846-856.
References 1 Freedom R, Wham G, Rowe R, et al. The criss cross and supero-inferior ventricular heart. An angiographic study. Am J Cardiol 1978;42:620-627. 2 Van Praagh S, La Coste M. Fellows KE, et al. Superoinferior ventricles. anatomic and angiocardiographic finding in ten post mortem cases. In: Van Praagh R, Takao A, eds. Etiology and morphogenesis of congenital heart disease. Mount Kisco, New York: Futura Publishing, 1980. 3 Attie F, Muiioz-Castellanos L. Ovseyevitz J. et al. Crossed atrioventricular connections. Am Heart J 1980;99:163-172. 4 Santos MA, Mall JN, Neto CD, et al. Ventriculo superoinferior: malforma@o cardiaca cspecifica ou uma nova terminologia? Arq Bras Cardiol 1981;37(suppl 1):123.
IJC 0494E
Torsade de pointes complicating atrioventricular block: report of two cases Naphtali
Maor, Dov Weiss, Avraham
intensitw Cardiac Cure Unit. L&y Duuis Camel (Received
16 June 1986: revision accepted
Lorber
Hosprtol, Hoifu. Israel 1 September
1986)
One patient with complete atrioventricular heart block and another with high-degree atrioventricular block, complicated by “torsade de pointes” are presented. Both patients were symptomatic. One had a syncopal episode and the other presented with signs and symptoms of congestive heart failure. The electrocardiographic phenomena of torsade de pointes was repeatedly recorded. No other known predisposing factors for torsade de pointes were identified. The use of right ventricular endocatdial pacing suppressed the paroxysms in both patients. (Key words:
Torsade
de pointes;
Atrioventricular
block)
Introduction Torsade de pointes refers to the characteristic ondulation of the QRS axis during paroxysms of ventricular tachycardia in the presence of a prolonged Q-T interval [I]. Although bradycardia and complete atrioventricular heart block are known to cause torsade de pointes, a limited number of cases has been described. Two cases of torsade de pointes. one associated with complete atrioventricular heart block and another with high-degree atrioventricular block are presented.
Correspondeme 10: A. Palant, 7222, Haifa 34362, Israel.
M.D.. Intensive
Cardiac
Internarronul Journal of Cardiologv, 14 (1987) 235-238 ,B Elsevier Science Publishers B.V. (Biomedical Division)
Care Unit, Lady Davis Carmel
Hospital.
P.0.B
236
Case Reports Case I. An 80-year-old woman was admitted to the coronary care unit following an episode of syncope, from which she had recovered spontaneously after several minutes. Medications on admission included furosemide only. Complete atrioventricular block was known for four years. The initial electrocardiogram (Fig. la) showed complete atrioventricular block and ventricular rate of 40 beats/min, few ventricular ectopic beats. The Q-T interval was 0.70 sec. On the second day there were ventricular ectopic beats giving rise to paroxysms of ventricular
V,
a
Fig. 1. a. Electrocardiogram on admission showing complete atrioventricular block with a ventricular rate of 40 beats/min. Q-T interval of 0.70 sec. b. Torsade de pointes complicating complete atrioventricular block.
231
tachycardia, with the typical morphological appearance of torsade de pointes (Fig. lb). The concentrations of potassium, magnesium and calcium in the serum were normal. Serial determinations of creatine phosphokinase, serum glutamine oxaloacetic and lactic dehydrogenase were within normal Limits. A temporary (and later permanent) transvenous demand pacemaker was inserted. This procedure completely eradicated the ventricular ectopic beats and the paroxysms of torsade de pointes. The Q-T interval was shortened to 0.36 sec. Case 2. A 64-year-old woman was admitted to the hospital because of dyspnea. Her medical history included hypertension and diabetes mellitus, insulin dependent. The serum potassium, calcium and magnesium values were normal. Serial determinations of creatine phosphokinase, serum glutamine oxaloacetic and lactic dehydrogenase were within normal limits. The electrocardiogram revealed high-degree atrioventricular block with a ventricular rate of 36 beats/min. There were frequent ventricular extrasystoles and bursts of ventricular
I
I
b Fig. 2. a. Monitor electrocardiographic strip on admission block with a ventricular rate of 36 beats/min. b. Torsade ventricular block.
demonstrating high-degree atrioventricular de pointes complicating high-degree atrio-
I
238
tachycardia with the typical morphological temporary (and later permanent) pacemaker the arrhythmia.
appearance of torsade de pointes (Fig. 2). A was inserted, which resulted in abolishment of
Torsade de pointes has been reported at all ages, in association with many underlying conditions [l]. French authors have emphasized the frequent occurrence of torsade de pointes in the setting of marked bradycardia or complete heart block [1,2]. Schwartz et al. [3] were the first to point out the importance of this arrhythmia as a cause of syncope in patients with complete heart block. The electrophysiological mechanism underlying torsade de pointes is poorly understood. Dessertenne postulated the presence of several arrhythmic foci. Other authors favor a reentry mechanism [4]. From experimental work, it is known that temporal dispersion of the ventricular refractory periods is a direct function of the basic cycle length. In complete atrioventricular block when the basic idioventricular rate is slow, the range of refractory periods and action potential duration is greater, and it may account for the generation of reentrant arrhythmias [l]. Although temporal dispersion of refractoriness is the basis for reentrant mechanism with bradycardia, another mechanism is required for the initial ectopic beats. Recently, it has been proposed that after-depolarizations might play a role in arrhythmias of the long Q-T syndrome [l]. Based on an experimental model, Brachmann et al. [5] proposed a mechanism of bradycardia-dependent-triggered activity caused by early after-depolarizations. Whether this mechanism may account for torsade de pointes complicating complete atrioventricular block and bradycardia is not known. Further studies are required to understand this point.
References 1 Smith WM. Gallagher JJ. “Les torsade de pointes”: an unusual ventricular arrhythmia. Ann Intern Med 1980;93:578-584. 2 Motte G. Coumel PH, Abitol G, Dessertenne F, Slama R. Le syndrome QT long et syncopes par “torsade de pointe”. Arch Mal Coeur 1970;63:831-853. 3 Schwartz SP, Hallinger LN. Transient ventricular fibrillation. VI. Observation on peripheral arterial pulse pressures in the course of transient ventricular fibrillation during established auriculoventricular dissociation. Am Heart J 1954;48:390-404. 4 Horowitz LN, Greenspan AM, Spielman SR, Josephson ME. Torsade de pointes: electrophysiologic studies in patients without transient pharmacologic or metabolic abnormalities. Circulation 1981;63:1120-1128. 5 Brachmann J, Scherlag BJ, Rosenstraukh LV, Lazzara R. Bradycardia-dependent triggered activity relevance to drug-induced multiform ventricular tachycardia. Circulation 1983;68:846-856.