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New onset ventricular tachycardia during pregnancy
International Journal of Cardiology, 33 (1991) 409-412 >Q1991 Elsevier Science Publishers B.V. All rights reserved
CARD10
409 0167-5273//$03.50
01355
New onset ventricular tachycardia during pregnancy Alan C. Braverman, Bryann S. Bromley and John D. Rutherford Cardiouxculur
Diclision. Department of Medicine, and the Department of Obstetrics and Gynecology, Brighum and Women LrHospital, Harvard Medical School, Boston, MA, U.S.A. (Received
Braverman AC, Bromley BS, Rutherford Cardiol 1991;33:409-412.
2 April 1991; accepted
7 June
1991)
JD. New onset ventricular tachycardia during pregnancy. Int J
A previously healthy young woman who developed the new onset of symptomatic sustained ventricular tachycardia during pregnancy is described. Evaluation revealed mitral valve prolapse with minimal mitral regurgitation, and normal left ventricular size and function. The arrhythmia resolved after delivery, but recurred nine months later in a nonsustained form. Electrophysiologic study revealed only nonsustained ventricular tachycardia, and she was treated with propafenone. It is suggested that the pregnant state may have been important in the pathogenesis of her arrhythmia. Key words: Ventricular
tachycardia;
Pregnancy; Mitral valve prolapse
Introduction
During normal pregnancy, complaints of palpitations are common. In 1917, Sir James Mackenzie reported “extrasystoles present in approximately one half of normal pregnancies [l]. An increased awareness and frequency of paroxysmal atria1 arrhythmias during pregnancy has been described [2], but ventricular tachycardia presenting during pregnancy has been rarely reported [3]. We describe a previously asymptomatic woman who developed the new onset of symptomatic sustained ventricular tachycardia during pregnancy.
Correspondence to; J.D. Rutherford, M.B., ChB., Cardiovascular Div., Brigham and Women’s Hospital, Boston, MA 02115, U.S.A.
Case Report
A 33-year-old female, without prior cardiac symptoms, noted the onset of palpitations at 10 weeks gestation. Over the next 12 weeks the frequency of palpitations increased, with the occurrence of multiple daily episodes, each several seconds in duration. Lightheadedness and dyspnea accompanied the palpitations, but there was no history of syncope. There was no history of prior cardiac disease, and her first pregnancy 2 years previously was uncomplicated. The patient drank 1 cup of coffee daily, and denied alcohol, tobacco, or cocaine use. There was no history of any recent febrile illness. Her vital signs and general physical examination were normal. On cardiovascular exam, a mid-systolic click without mitral regurgitation was heard. A resting electrocardiogram was normal (Fig. 1).
410
While in the cardiology office, she complained of palpitations. A rhythm strip revealed an irregular, wide-complex tachycardia at a rate of 120-150 beats/minute with AV dissociation and capture beats, consistent with ventricular tachycardia (Fig. 2). An echocardiogram revealed mitral valve prolapse with mild mitral regurgitation. The left ventricular size and systolic function were normal. Serum potassium, magnesium and thyroxine levels were normal. While hospitalized, she had frequent episodes of nonsustained ventricular tachycardia. Metoprolol 50 milligrams twice daily was begun with a marked reduction in ventricular ectopy. While on metoprolol, the patient exercised 7 minutes on a standard Bruce protocoI stopping secondary to fatigue. There was no significant ectopy during exercise, and a single 4-beat salvo of ventricular tachycardia occurred during recovery. A 24-hour Holter monitor revealed up to 30 ventricular couplets/ hour and three 4-beat salvos of ventricular tachycardia.
Fig. 1. Normal
twelve-lead
electrocardiogram
Over the next 4 weeks the patient noted recurrent palpitations with episodes lasting up to 30 minutes. On readmission, telemetry revealed sustained ventricular tachycardia at 130-160 beats/ minute lasting up to 45 minutes. Quinidine gluconate was added to the metoprolol. With a therapeutic quinidine level the high-grade ectopy resolved, and telemetry monitoring revealed only occasional unifocal premature ventricular beats. The patient’s obstetrical course was notable for the development of intrauterine growth retardation. Intensive fetal surveillance was reassuring, and the patient was delivered of a healthy 4 pound 15 ounce neonate at term. There were no significant arrhythmias during labor and delivery. Telemetry monitoring postpartum revealed only occasional premature beats with no couplets or salvos of ventricular tachycardia. She remained asymptomatic while taking metoprolol and quinidine gluconate. Six weeks postpartum, metoprolol and quinidine were discontinued. A 24-hour
at rest in the patient
described.
Fig. 1. Continuous
rhythm strip (leads 1. II, 111) during an episode of ventricular
tachycardia.
Note the presence of a capture beat
(arrows).
Holter monitor revealed less than one unifocal premature ventricular beat/ hour with no higher grade ventricular ectopy. Nine months later the patient noted recurrent presyncopal episodes, especially with exertion. Electrocardiogram revealed a PR interval of 0.09 seconds but was otherwise normal. Telemetry monitoring revealed frequent episodes of a regular, wide-complex tachycardia at a rate of 220/minute, with the same morphology as her previous arrythmia. A repeat echocardiogram was unchanged. Because of the recurrent arrhythmia and short PR interval on electrocardiogram, an electrophysiologic study was performed. A maximal stimulation protocol using up to 3 consecutive extrastimuli from the right ventricular apex and outflow tract failed to provoke ventricular tachycardia. With isoproterenol infusion, nonsustained ventricular tachycardia was induced. No accessory pathway was found. Propafenone 150
milligrams twice daily was begun with resolution of the ventricular ectopy. On follow-up exercise testing the patient completed 10 minutes on a standard Bruce protocol with a maximal heart rate of lSO/minute and no ventricular ectopy. She has remained asymptomatic four months later with Holter monitor revealing only occasional unifocal ventricular premature beats. Discussion While an increased awareness of palpitations during pregnancy is common, the development of ventricular tachycardia during pregnancy is exceedingly rare [3]. Recognized causes of ventricular tachycardia which may manifest during pregnancy include cardiomyopathy, myocarditis, long QT syndrome, drugs (cocaine, ethanol) and electrolyte abnormalities. None of these were evident in our patient. Mitral valve prolapse is frequently
412
present in women of childbearing age, and its exact relationship to ventricular arrhythmias is unknown. Patients with mitral valve prolapse, severe mitral regurgitation and associated left ventricular dysfunction seem more likely to develop serious arrhythmias [4]. However, controlled studies of patients with mitral valve prolapse reveal no greater prevalence of ventricular arrhythmias than in normal subjects [4]. In the patient described, the absence of symptoms before pregnancy suggests that the pregnant state may have played an important role in the pathogenesis of this patient’s arrhythmias. Hemodynamic alterations during pregnancy include an increase in end-diastolic volume and cardiac output with a decrease in peripheral resistance. These changes can alter the physical findings in mitral valve prolapse. However, pregnancy has not been reported to precipitate arrhythmias in patients with mitral valve prolapse [5]. While we cannot exclude that the hemodynamic changes of pregnancy increased the patient’s awareness of preexisting ventricular tachycardia, when the ar-
rhythmia recurred 9 months postpartum the patient noted symptoms identical to those on initial presentation. Alternatively, ventricular tachycardia first presenting during pregnancy may have been coincidental in this patient. Because this is a highly unusual occurrence, it is suggested that the various neurohumoral changes associated with pregnancy may also have played a role in the development of this patient’s ventricular arrhythmias.
References Mackenzie J. Principles of diagnosis and treatment in heart affections. London: Oxford Medical Publications, 1917;26. Mendelson CL. Disorders of the heartbeat during pregnancy. Am J Obstet Gynecol 1956;72:1268-1301. Russell RO. Paroxysmal ventricular tachycardia associated with pregnancy. Ala J Med Sci 1969;6:11l-120. Devereux RB, Kramer-Fox R, Kligfield P. Mitral valve prolapse: causes, clinical manifestations, and management. Ann Intern Med 1989;111:305-317. Tang LCH, Chan SYW, Wong VCW, Ho-Kei MA. Pregnancy in patients with mitral valve prolapse. Int J Gynaecol Obstet 1985;23:217-221.
CARD10
409 0167-5273//$03.50
01355
New onset ventricular tachycardia during pregnancy Alan C. Braverman, Bryann S. Bromley and John D. Rutherford Cardiouxculur
Diclision. Department of Medicine, and the Department of Obstetrics and Gynecology, Brighum and Women LrHospital, Harvard Medical School, Boston, MA, U.S.A. (Received
Braverman AC, Bromley BS, Rutherford Cardiol 1991;33:409-412.
2 April 1991; accepted
7 June
1991)
JD. New onset ventricular tachycardia during pregnancy. Int J
A previously healthy young woman who developed the new onset of symptomatic sustained ventricular tachycardia during pregnancy is described. Evaluation revealed mitral valve prolapse with minimal mitral regurgitation, and normal left ventricular size and function. The arrhythmia resolved after delivery, but recurred nine months later in a nonsustained form. Electrophysiologic study revealed only nonsustained ventricular tachycardia, and she was treated with propafenone. It is suggested that the pregnant state may have been important in the pathogenesis of her arrhythmia. Key words: Ventricular
tachycardia;
Pregnancy; Mitral valve prolapse
Introduction
During normal pregnancy, complaints of palpitations are common. In 1917, Sir James Mackenzie reported “extrasystoles present in approximately one half of normal pregnancies [l]. An increased awareness and frequency of paroxysmal atria1 arrhythmias during pregnancy has been described [2], but ventricular tachycardia presenting during pregnancy has been rarely reported [3]. We describe a previously asymptomatic woman who developed the new onset of symptomatic sustained ventricular tachycardia during pregnancy.
Correspondence to; J.D. Rutherford, M.B., ChB., Cardiovascular Div., Brigham and Women’s Hospital, Boston, MA 02115, U.S.A.
Case Report
A 33-year-old female, without prior cardiac symptoms, noted the onset of palpitations at 10 weeks gestation. Over the next 12 weeks the frequency of palpitations increased, with the occurrence of multiple daily episodes, each several seconds in duration. Lightheadedness and dyspnea accompanied the palpitations, but there was no history of syncope. There was no history of prior cardiac disease, and her first pregnancy 2 years previously was uncomplicated. The patient drank 1 cup of coffee daily, and denied alcohol, tobacco, or cocaine use. There was no history of any recent febrile illness. Her vital signs and general physical examination were normal. On cardiovascular exam, a mid-systolic click without mitral regurgitation was heard. A resting electrocardiogram was normal (Fig. 1).
410
While in the cardiology office, she complained of palpitations. A rhythm strip revealed an irregular, wide-complex tachycardia at a rate of 120-150 beats/minute with AV dissociation and capture beats, consistent with ventricular tachycardia (Fig. 2). An echocardiogram revealed mitral valve prolapse with mild mitral regurgitation. The left ventricular size and systolic function were normal. Serum potassium, magnesium and thyroxine levels were normal. While hospitalized, she had frequent episodes of nonsustained ventricular tachycardia. Metoprolol 50 milligrams twice daily was begun with a marked reduction in ventricular ectopy. While on metoprolol, the patient exercised 7 minutes on a standard Bruce protocoI stopping secondary to fatigue. There was no significant ectopy during exercise, and a single 4-beat salvo of ventricular tachycardia occurred during recovery. A 24-hour Holter monitor revealed up to 30 ventricular couplets/ hour and three 4-beat salvos of ventricular tachycardia.
Fig. 1. Normal
twelve-lead
electrocardiogram
Over the next 4 weeks the patient noted recurrent palpitations with episodes lasting up to 30 minutes. On readmission, telemetry revealed sustained ventricular tachycardia at 130-160 beats/ minute lasting up to 45 minutes. Quinidine gluconate was added to the metoprolol. With a therapeutic quinidine level the high-grade ectopy resolved, and telemetry monitoring revealed only occasional unifocal premature ventricular beats. The patient’s obstetrical course was notable for the development of intrauterine growth retardation. Intensive fetal surveillance was reassuring, and the patient was delivered of a healthy 4 pound 15 ounce neonate at term. There were no significant arrhythmias during labor and delivery. Telemetry monitoring postpartum revealed only occasional premature beats with no couplets or salvos of ventricular tachycardia. She remained asymptomatic while taking metoprolol and quinidine gluconate. Six weeks postpartum, metoprolol and quinidine were discontinued. A 24-hour
at rest in the patient
described.
Fig. 1. Continuous
rhythm strip (leads 1. II, 111) during an episode of ventricular
tachycardia.
Note the presence of a capture beat
(arrows).
Holter monitor revealed less than one unifocal premature ventricular beat/ hour with no higher grade ventricular ectopy. Nine months later the patient noted recurrent presyncopal episodes, especially with exertion. Electrocardiogram revealed a PR interval of 0.09 seconds but was otherwise normal. Telemetry monitoring revealed frequent episodes of a regular, wide-complex tachycardia at a rate of 220/minute, with the same morphology as her previous arrythmia. A repeat echocardiogram was unchanged. Because of the recurrent arrhythmia and short PR interval on electrocardiogram, an electrophysiologic study was performed. A maximal stimulation protocol using up to 3 consecutive extrastimuli from the right ventricular apex and outflow tract failed to provoke ventricular tachycardia. With isoproterenol infusion, nonsustained ventricular tachycardia was induced. No accessory pathway was found. Propafenone 150
milligrams twice daily was begun with resolution of the ventricular ectopy. On follow-up exercise testing the patient completed 10 minutes on a standard Bruce protocol with a maximal heart rate of lSO/minute and no ventricular ectopy. She has remained asymptomatic four months later with Holter monitor revealing only occasional unifocal ventricular premature beats. Discussion While an increased awareness of palpitations during pregnancy is common, the development of ventricular tachycardia during pregnancy is exceedingly rare [3]. Recognized causes of ventricular tachycardia which may manifest during pregnancy include cardiomyopathy, myocarditis, long QT syndrome, drugs (cocaine, ethanol) and electrolyte abnormalities. None of these were evident in our patient. Mitral valve prolapse is frequently
412
present in women of childbearing age, and its exact relationship to ventricular arrhythmias is unknown. Patients with mitral valve prolapse, severe mitral regurgitation and associated left ventricular dysfunction seem more likely to develop serious arrhythmias [4]. However, controlled studies of patients with mitral valve prolapse reveal no greater prevalence of ventricular arrhythmias than in normal subjects [4]. In the patient described, the absence of symptoms before pregnancy suggests that the pregnant state may have played an important role in the pathogenesis of this patient’s arrhythmias. Hemodynamic alterations during pregnancy include an increase in end-diastolic volume and cardiac output with a decrease in peripheral resistance. These changes can alter the physical findings in mitral valve prolapse. However, pregnancy has not been reported to precipitate arrhythmias in patients with mitral valve prolapse [5]. While we cannot exclude that the hemodynamic changes of pregnancy increased the patient’s awareness of preexisting ventricular tachycardia, when the ar-
rhythmia recurred 9 months postpartum the patient noted symptoms identical to those on initial presentation. Alternatively, ventricular tachycardia first presenting during pregnancy may have been coincidental in this patient. Because this is a highly unusual occurrence, it is suggested that the various neurohumoral changes associated with pregnancy may also have played a role in the development of this patient’s ventricular arrhythmias.
References Mackenzie J. Principles of diagnosis and treatment in heart affections. London: Oxford Medical Publications, 1917;26. Mendelson CL. Disorders of the heartbeat during pregnancy. Am J Obstet Gynecol 1956;72:1268-1301. Russell RO. Paroxysmal ventricular tachycardia associated with pregnancy. Ala J Med Sci 1969;6:11l-120. Devereux RB, Kramer-Fox R, Kligfield P. Mitral valve prolapse: causes, clinical manifestations, and management. Ann Intern Med 1989;111:305-317. Tang LCH, Chan SYW, Wong VCW, Ho-Kei MA. Pregnancy in patients with mitral valve prolapse. Int J Gynaecol Obstet 1985;23:217-221.