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Mitral valve prolapse and systolic anterior motion: A dynamic spectrum
Volume
105
Number
4
Brief
Communications
685
I. Echocardiographic measurements*
arrhythmias during acute myocardial infarction. J Cardiovasc Pharmacol 1:43, 1979. 15. DiMarco JP, Garan H, Ruskin JN: Mexiletine for refractory ventricular arrhythmias: Results using serial electrophysiologic testing. Am J Cardiol 47:131, 1981. 16. Podrid PJ, Lown B: Mexiletine for ventricular arrhythmias. Am J Cardiol47:895, 1981. 17. Smirk FH, Ng J: Cardiac ballet: Repetition of complex electrocardiographic patterns. Br Heart J 31:426, 1969. 18. Allen JD, Ekue JM, Shanks RG, Zaidi SA: The effect of Kc 1173, a new anticonvulsant agent on experimental cardiac arrhythmias. Br J Pharmacol 45:561, 1972. 19. Weld FM, Bigger JT Jr, Swistel D, Bordiuk J: Effects of mexiletine (Kii 1173) on electrophysiological properties of sheep cardiac Purkinje fibers. Am J Cardiol 39:292, 1977.
Table
Mitral valve prolapse and systolic motion: A dynamic spectrum
particular note becausethese changes occurred in the absenceof hypertrophy. A 62-year-old woman was admitted with vomiting, abdominal fullness, and profound
anterior
J. Myerburg,
M.D. Miami,
Fla.
Mitral valve prolapse is a specific sign in Barlow’s syndrome’; it may represent a nonspecific echocardiographic finding (e.g., cardiomyopathy’) or may be artifactual (e.g., pericardial effusion or abnormal transducer positioning2). Similarly, systolic anterior motion of the mitral valve may be a characteristic finding in idiopathic hypertropic subaortic stenosis,3may be a nonspecific finding in hypovolemia*or in hypertrophic or hyperkinetic hearta,5v6or may be artifactual (e.g., pericardial effusion2). Both of these mitral motion abnormalities are closely related to the volume and contraction characteristics of the left ventricle.5s7rRAlthough described separately, anterior motion and posterior motion of the mitral apparatus are theoretically not mutually exclusive concepts in that the mitral apparatus potentially may undergo anterior and/or posterior motion in systole, depending on net hemodynamic forces. Such a synthesis of concepts has been forwarded by reports of simultaneous mitral valve prolapse (representing posterior mitral apparatus motion) and chordal buckling (representing anterior mitral apparatus motion).g However, an increase in buckling to the degree of being considered “obstructive” could not be induced in these patients even with amyl nitrite9 We present a patient who, during her clinical course, demonstrated both echocardiographically and clinically a spectrum of mitral valve motion patterns that were of From the Divisions of Cardiology Medicine and Radiology, University Received accepted
for publication Apr. 21, 1982.
Reprint requests: (D-39), Department P.O. Box 016960,
Dec.
and
Nuclear of Miami
7, 1981;
Kenneth M. Kessler, of Medicine, University Miami, FL 33101.
revision
Medicine, Departments School of Medicine. received
Mar.
of
9, 1982;
M.D., Division of Cardiology of Miami School of Medicine,
B
94.0
HR Own) LVIDd (cm) LVIDs (cm) SF (SO) Septal thickness (cm) Posterior wall (cm)
C
101.0
90.0
4.2
4.2
1.9
1.5
55.0
64.0
4.4
2.1 52.0
1.0 1.0
1.0 1.0
1.0 1.0
Abbreviations: HR = Heart rate; LVIDd = left ventricular internal dimension in diastole; LVIDs = left ventricular internal dimension in systole; SF = shortening fraction. *Dimensions recorded in initial echo (A), echo showing systolic anterior mitral motion (B), and follow-up normal echo (C).
weight
Kenneth M. Kessler, M.D., Edmund0 Anzola, M.D., Rafael Sequeira, M.D., Aldo N. Serafini, M.D., and Robert
A
loss for evaluation
of possible
malignancy.
Past
medical history was unremarkable. She was mildly hypovolemic and cachectic, and she had a blood pressure of 120/88mm Hg and a heart rate of 90 bpm. The remainder of the physical examination was unremarkable but included a grade l-2/6 systolic ejection murmur best heard at the apex and left sternal border. Echocardiography performed to evaluate the murmur showedmild mid- and late-systolic mitral valve prolapse,as well as mitral apparatus buckling (Fig. 1; dimensionscharted in Table I). She continued to have inadequate fluid intake and became hypovolemic. When the echocardiogramwas repeated 3 days later, prominent systolic anterior motion of the mitral valve was noted without evidence of mitral valve prolapse (Fig. 2). At that time the carotid pulse contour had becomebisferious, and her murmur had increasedto grade 416 and was best heard at the left sternal border with poor radiation
to the carotid
arteries.
She had noted
dizziness, palpitations, and presyncope when standing. Following
rehydration
these symptoms
resolved.
Follow-
up 2 weeks later was remarkable for a lack of findings. Both M-mode and two-dimensionalechocardiogramswere within normal limits, the carotid pulsations were normal in contour, and the murmur had returned to grade l-216 in
intensity. A diagnosis of gastric carcinoma was made; however, her further hospital course was stable from a cardiovascular point of view. On admission, our patient had a small enough endsystolic dimension to allow for both mitral valve prolapse and mitral apparatus buckling. On further volume depletion the heart rate increased, the heart became more
hyperkinetic, and the end-systolic dimension decreased (Table I). At this point the hyperkinesis was associated with systolic anterior mitral motion, possibly secondary to a Venturi effect,6 and prolapse was no longer present.
Secondary left ventricular outflow tract “obstruction” was suggestedby the clinical symptoms, the degree of septal abutment
by the mitral
valve apparatus,
the change in the
contour of the carotid pulse, and the change in the intensity
and location
of the murmur.
Such systolic ante-
April.
686
Brief Communications
American
Heart
1993 Journal
Fig. 1. Panel a, Mitral valve echogramshowingmild mid- and late-systolic mitral valve prolapse (MVP) and “chordal” buckling (CB). Panel b, Two-dimensional long-axis echogram in end-systole showing “chordal” buckling (arrow). There is no abutment of the septum by the mitral apparatus. Panel c, Accompanying schematic representation showing mitral valve prolapse and mitral apparatus buckling (CB). Ao = Aorta; IVS = interventricular septum; LA = left atrium; PW = posterior left ventricular wall; and RV = right ventricle.
rior mitral motion in the absence of asymmetric or symmetric left ventricular hypertrophy is rare.” These findings prompted volume replacement, after which the clinical symptoms resolved and the echocardiographic (Table I) and clinical findings becamenormal. Since the patient was critically ill during this entire sequence, further provocative maneuverswere believed to be inappropriate. Although mitral valve prolapse is prevalent and the
finding of systolic anterior mitral motion in hyperkinetic and hypertrophic settings is well described, to our knowledgethe “spontaneous” sequential echocardiographicand clinical changes noted in this patient have not been reported, particularly in the absenceof hypertrophy. This instructive case supports a dynamic spectrum of mitral apparatus motion abnormalities and emphasizesthe clinical importance of understanding the hemodynamic determinants and consequencesof mitral valve motion.
Volume Number
105 4
Brief Communications
667
2. Panel a, Mitral valve echogramshowingprominent systolic anterior motion (SAM) of the mitral apparatus with abutment of the interventricular septum (IVS). Panel b, Two-dimensional long-axis echogram in end-systole, showing abutment of the mitral apparatus with the interventricular septum (arrow). Panel c, Schematic representation showingsystolic anterior motion of the mitral apparatus with septal abutment and the absenceof mitral valve prolapse. Ao = Aorta; LA = left atrium; PW = posterior left ventricular wall; and RV = right ventricle.
Fig.
REFERENCES
1. Barlow JB, Pocock WA: Mitral valve prolapse, the specific billowing mitral leaflet syndrome, or an insignificant nonejection systolic click. AM HEART J 97:277, 1979. 2. Feigenbaum H: Echocardiography, ed 3. Philadelphia, 1981, Lea & Febiger, pp 257, 452. 3. Maron BJ, Epstein SE: Hypertrophic cardiomyopathy. Am J Cardiol 45:141, 1980. 4. Levisman JA: Systolic anterior motion of the mitral valve due to hypovolemia and anemia. Chest 70:687, 1976. 5. Maron BJ, Gottdiener JS, Roberts WC, Henry WL, Savage DD, Epstein SE: Left ventricular outflow tract obstruction due to systolic anterior motion of the anterior mitral leaflet in
patients with concentric left ventricular hypertrophy. Circulation 57:527, 1978. 6. Come PC, Buckley BH, Goodman ZD, Hutchins GM, Pitt B, Fortuin NJ: Hypercontractile cardiac states simulating hypertrophic cardiomyopathy. Circulation 55:901, 1977. 7. Mintz GS, Kotler MN, Segal BL, Parry WR: Systolic anterior motion of the mitral valve in the absence of asymmetric septal hypertrophy. Circulation 57:256, 1978. 8. Mathey DG, Decoodt PR, Allen HN, Swan HJC: The determinants of onset of mitral valve prolapse in the systolic click-late systolic murmur syndrome. Circulation 53:872, 1976.
666
Brief
Communications
American
9. GardinJM, TalanoJV, Stephanides L, FizzanoJ, LeschM: Systolicanteriormotionin the absence of asymmetricseptal hypertrophy.Circulation63181, 1981. 10. Maron BJ, GottdienerJS, Perry LW: Specificityof systolic anterior motion of anterior mitral leaflet for hypertrophic cardiomyopathy.Br Heart J 45:206,1981.
Long-term efficacy of verapamil in the treatment of paroxysmal supraventricular tachycardias K. I. Lie, M.D., D. R. Diiren, M.D., V. Manger Cats, M.D., G. K. David, M.D., and D. Durrer, M.D. Amsterdam,
The Netherlands
Although the efficacy of verapamil in the treatment of paroxysmal supraventricular tachycardia is well established,1-4 most of these studiesrefer to intravenous administration or short-term oral therapy. Since follow-up data on long-term oral prophylaxis are lacking, we have undertaken a study to assess the long-term efficacy of verapamil in the prevention of paroxysmal supraventricular t,achycardias. We selected56 consecutive patients with chronic recurrent (more than once-daily attacks) paroxysmal supraventricular tachycardia, in whom pretreatment with drugs such as digitalis, beta blockers, quinidine, disopyramide, and other antiarrhythmics had to be discontinued because of ineffectiveness (42 patients) or undesirableside effects (14 patients). All 56 patients responded to short-term (4 weeks)oral therapy with verapamil, continued their longterm medication, and could be followed up for at least 1 year. Of those 56 patients, 20 had paroxysmal atrioventricular junctional tachycardia, 9 had circus movement tachycardias in association with the Wolff-ParkinsonWhite (WPW) syndrome, since programmed electrical stimulation revealed that an acessorypathway wasusedin a ventriculoatrial direction ,5 24 had paroxysmal atria1 fibrillation or flutter, and 3 had paroxysmal atrial tachycardia. Their ages varied from 10 to 83 years (mean 52 years). Organic heart diseasewas present in 14, with coronary artery disease being the most frequent (8 patients). The dosageof long-term oral treatment varied from 120 to 320 mg, and the follow-up period ranged from 12 to 48 months (mean 25.4 months). Twenty-five patients were asymptomatic, whereas Holter monitoring showed no episodesof supraventricular tachycardia. The remaining 31 patients noticed a marked reduction of symptoms to at From the Department of Cardiology and Clinical Physiology Interuniversity Cardiologic Institute. Received for publication Aug. 13, 1980; revision received Aug. accepted Nov. 10, 1981. Reprint requests: K. I. Lie, Department of Cardiology and Physiology, Wilhelmina Gasthuis, le Helmersstraat 104, 1054 EG dam, The Netherlands.
and the 27, 1981; Clinical Amster-
April, 1993 Heart Journal
least twice-weekly attacks. In the latter, Holter monitoring revealed sporadic episodes of atria1 fibrillation in three, short runs of atria1 premature beats in five, frequent atrial premature beatsin three, and sporadic atria1premature beats in 20 patients. The basic sinus rate in 8 of 56 patients was below 60 bpm, but none had symptoms caused by bradycardia. Of 56 patients, seven (12.5%) noticed possible minor side effects such as dizziness, headache, and/or tiredness. In 12 of 17 patients with paroxysmal atrioventricular junctional tachycardia, the use of intravenous verapamil resulted in termination of the tachycardia. This occurred in five of nine patients with circus movement tachycardia in association with the WPW syndrome. This confirms earlier suggestions6 that intravenous verapamil in paroxysmal atrioventricular junctional tachycardia can be used in the selection of patients who will receive long-term oral treatment. However, a prospective study of a large number of patients is needed for confirmation. Since the useof intravenous verapamil resulted in termination of tachycardia in only five of nine patients with circus movement tachycardia in associationwith the WPW syndrome, the efficacy of long-term oral verapamil in these patients may be partly due to its preventive effects on the initiation of atria1 premature beats rather than to the inability to initiate reentrant tachycardias. Other arguments favoring this mechanismare evident in our patients with paroxysmal atria1 fibrillation, flutter, or tachycardia who also benefited from long-term oral treatment. In these patients both the reduction of complaints and the data during Holter monitoring suggestthat the efficacy of verapamil in managingthesepatients is mainly due to its efficacy in reducing the incidence of atria1 premature beats. Although we believe that verapamil is the first drug of choice in the long-term treatment of paroxysmal supraventricular tachycardia, especially in patients without severeorganic cardiac disease,long-term data obtained from prospective studieswith verapamil are neededto confirm this statement. REFERENCES
1. Schamroth L, Krikler DM, Garret C: Immediate effects of intravenous verapamil in cardiac arrhythmias. Br Med J 1:660, 1972. o‘. Brichard G. Zimmermann PE: Veranamil in cardiac dvsrhythmias anaesthesia. Br J Anaesth ;2:1005, 1970. I 3. Krikler DM, Spurrell RAJ: Verapamil in the treatment of paroxysmal supraventricular tachycardia. Postgrad Med J 50:447, 1974. 4. Midtbii K: Isoptin, a prophylactic agent in paroxysmal supraventricular tachyarrhythmias. In Atterhiig JJ, Haakana A, Nording B, editors: Symposium on arrhythmias: Isoptin. Aulendorf, W. Germany, 1974, Edition Cantor, pp. 100-103. 5. Wellens HJJ, Durrer D: The role of an accessory pathwav in reciprocal tachycardia: Observations in patients with and without the Wolff-Parkinson-White syndrome. Circulation 52:58, 1978. 6. Wellens HJJ, Tan SL, Biir FWH, Diiren DR, Lie KI, Dohmen HH: Effect of verauamil studied bv Droerammed electrical stimulation of the-heart in patients w%h paroxysmal reentrant supraventricular tachycardia. Br Med J 39:1058, 1977.
105
Number
4
Brief
Communications
685
I. Echocardiographic measurements*
arrhythmias during acute myocardial infarction. J Cardiovasc Pharmacol 1:43, 1979. 15. DiMarco JP, Garan H, Ruskin JN: Mexiletine for refractory ventricular arrhythmias: Results using serial electrophysiologic testing. Am J Cardiol 47:131, 1981. 16. Podrid PJ, Lown B: Mexiletine for ventricular arrhythmias. Am J Cardiol47:895, 1981. 17. Smirk FH, Ng J: Cardiac ballet: Repetition of complex electrocardiographic patterns. Br Heart J 31:426, 1969. 18. Allen JD, Ekue JM, Shanks RG, Zaidi SA: The effect of Kc 1173, a new anticonvulsant agent on experimental cardiac arrhythmias. Br J Pharmacol 45:561, 1972. 19. Weld FM, Bigger JT Jr, Swistel D, Bordiuk J: Effects of mexiletine (Kii 1173) on electrophysiological properties of sheep cardiac Purkinje fibers. Am J Cardiol 39:292, 1977.
Table
Mitral valve prolapse and systolic motion: A dynamic spectrum
particular note becausethese changes occurred in the absenceof hypertrophy. A 62-year-old woman was admitted with vomiting, abdominal fullness, and profound
anterior
J. Myerburg,
M.D. Miami,
Fla.
Mitral valve prolapse is a specific sign in Barlow’s syndrome’; it may represent a nonspecific echocardiographic finding (e.g., cardiomyopathy’) or may be artifactual (e.g., pericardial effusion or abnormal transducer positioning2). Similarly, systolic anterior motion of the mitral valve may be a characteristic finding in idiopathic hypertropic subaortic stenosis,3may be a nonspecific finding in hypovolemia*or in hypertrophic or hyperkinetic hearta,5v6or may be artifactual (e.g., pericardial effusion2). Both of these mitral motion abnormalities are closely related to the volume and contraction characteristics of the left ventricle.5s7rRAlthough described separately, anterior motion and posterior motion of the mitral apparatus are theoretically not mutually exclusive concepts in that the mitral apparatus potentially may undergo anterior and/or posterior motion in systole, depending on net hemodynamic forces. Such a synthesis of concepts has been forwarded by reports of simultaneous mitral valve prolapse (representing posterior mitral apparatus motion) and chordal buckling (representing anterior mitral apparatus motion).g However, an increase in buckling to the degree of being considered “obstructive” could not be induced in these patients even with amyl nitrite9 We present a patient who, during her clinical course, demonstrated both echocardiographically and clinically a spectrum of mitral valve motion patterns that were of From the Divisions of Cardiology Medicine and Radiology, University Received accepted
for publication Apr. 21, 1982.
Reprint requests: (D-39), Department P.O. Box 016960,
Dec.
and
Nuclear of Miami
7, 1981;
Kenneth M. Kessler, of Medicine, University Miami, FL 33101.
revision
Medicine, Departments School of Medicine. received
Mar.
of
9, 1982;
M.D., Division of Cardiology of Miami School of Medicine,
B
94.0
HR Own) LVIDd (cm) LVIDs (cm) SF (SO) Septal thickness (cm) Posterior wall (cm)
C
101.0
90.0
4.2
4.2
1.9
1.5
55.0
64.0
4.4
2.1 52.0
1.0 1.0
1.0 1.0
1.0 1.0
Abbreviations: HR = Heart rate; LVIDd = left ventricular internal dimension in diastole; LVIDs = left ventricular internal dimension in systole; SF = shortening fraction. *Dimensions recorded in initial echo (A), echo showing systolic anterior mitral motion (B), and follow-up normal echo (C).
weight
Kenneth M. Kessler, M.D., Edmund0 Anzola, M.D., Rafael Sequeira, M.D., Aldo N. Serafini, M.D., and Robert
A
loss for evaluation
of possible
malignancy.
Past
medical history was unremarkable. She was mildly hypovolemic and cachectic, and she had a blood pressure of 120/88mm Hg and a heart rate of 90 bpm. The remainder of the physical examination was unremarkable but included a grade l-2/6 systolic ejection murmur best heard at the apex and left sternal border. Echocardiography performed to evaluate the murmur showedmild mid- and late-systolic mitral valve prolapse,as well as mitral apparatus buckling (Fig. 1; dimensionscharted in Table I). She continued to have inadequate fluid intake and became hypovolemic. When the echocardiogramwas repeated 3 days later, prominent systolic anterior motion of the mitral valve was noted without evidence of mitral valve prolapse (Fig. 2). At that time the carotid pulse contour had becomebisferious, and her murmur had increasedto grade 416 and was best heard at the left sternal border with poor radiation
to the carotid
arteries.
She had noted
dizziness, palpitations, and presyncope when standing. Following
rehydration
these symptoms
resolved.
Follow-
up 2 weeks later was remarkable for a lack of findings. Both M-mode and two-dimensionalechocardiogramswere within normal limits, the carotid pulsations were normal in contour, and the murmur had returned to grade l-216 in
intensity. A diagnosis of gastric carcinoma was made; however, her further hospital course was stable from a cardiovascular point of view. On admission, our patient had a small enough endsystolic dimension to allow for both mitral valve prolapse and mitral apparatus buckling. On further volume depletion the heart rate increased, the heart became more
hyperkinetic, and the end-systolic dimension decreased (Table I). At this point the hyperkinesis was associated with systolic anterior mitral motion, possibly secondary to a Venturi effect,6 and prolapse was no longer present.
Secondary left ventricular outflow tract “obstruction” was suggestedby the clinical symptoms, the degree of septal abutment
by the mitral
valve apparatus,
the change in the
contour of the carotid pulse, and the change in the intensity
and location
of the murmur.
Such systolic ante-
April.
686
Brief Communications
American
Heart
1993 Journal
Fig. 1. Panel a, Mitral valve echogramshowingmild mid- and late-systolic mitral valve prolapse (MVP) and “chordal” buckling (CB). Panel b, Two-dimensional long-axis echogram in end-systole showing “chordal” buckling (arrow). There is no abutment of the septum by the mitral apparatus. Panel c, Accompanying schematic representation showing mitral valve prolapse and mitral apparatus buckling (CB). Ao = Aorta; IVS = interventricular septum; LA = left atrium; PW = posterior left ventricular wall; and RV = right ventricle.
rior mitral motion in the absence of asymmetric or symmetric left ventricular hypertrophy is rare.” These findings prompted volume replacement, after which the clinical symptoms resolved and the echocardiographic (Table I) and clinical findings becamenormal. Since the patient was critically ill during this entire sequence, further provocative maneuverswere believed to be inappropriate. Although mitral valve prolapse is prevalent and the
finding of systolic anterior mitral motion in hyperkinetic and hypertrophic settings is well described, to our knowledgethe “spontaneous” sequential echocardiographicand clinical changes noted in this patient have not been reported, particularly in the absenceof hypertrophy. This instructive case supports a dynamic spectrum of mitral apparatus motion abnormalities and emphasizesthe clinical importance of understanding the hemodynamic determinants and consequencesof mitral valve motion.
Volume Number
105 4
Brief Communications
667
2. Panel a, Mitral valve echogramshowingprominent systolic anterior motion (SAM) of the mitral apparatus with abutment of the interventricular septum (IVS). Panel b, Two-dimensional long-axis echogram in end-systole, showing abutment of the mitral apparatus with the interventricular septum (arrow). Panel c, Schematic representation showingsystolic anterior motion of the mitral apparatus with septal abutment and the absenceof mitral valve prolapse. Ao = Aorta; LA = left atrium; PW = posterior left ventricular wall; and RV = right ventricle.
Fig.
REFERENCES
1. Barlow JB, Pocock WA: Mitral valve prolapse, the specific billowing mitral leaflet syndrome, or an insignificant nonejection systolic click. AM HEART J 97:277, 1979. 2. Feigenbaum H: Echocardiography, ed 3. Philadelphia, 1981, Lea & Febiger, pp 257, 452. 3. Maron BJ, Epstein SE: Hypertrophic cardiomyopathy. Am J Cardiol 45:141, 1980. 4. Levisman JA: Systolic anterior motion of the mitral valve due to hypovolemia and anemia. Chest 70:687, 1976. 5. Maron BJ, Gottdiener JS, Roberts WC, Henry WL, Savage DD, Epstein SE: Left ventricular outflow tract obstruction due to systolic anterior motion of the anterior mitral leaflet in
patients with concentric left ventricular hypertrophy. Circulation 57:527, 1978. 6. Come PC, Buckley BH, Goodman ZD, Hutchins GM, Pitt B, Fortuin NJ: Hypercontractile cardiac states simulating hypertrophic cardiomyopathy. Circulation 55:901, 1977. 7. Mintz GS, Kotler MN, Segal BL, Parry WR: Systolic anterior motion of the mitral valve in the absence of asymmetric septal hypertrophy. Circulation 57:256, 1978. 8. Mathey DG, Decoodt PR, Allen HN, Swan HJC: The determinants of onset of mitral valve prolapse in the systolic click-late systolic murmur syndrome. Circulation 53:872, 1976.
666
Brief
Communications
American
9. GardinJM, TalanoJV, Stephanides L, FizzanoJ, LeschM: Systolicanteriormotionin the absence of asymmetricseptal hypertrophy.Circulation63181, 1981. 10. Maron BJ, GottdienerJS, Perry LW: Specificityof systolic anterior motion of anterior mitral leaflet for hypertrophic cardiomyopathy.Br Heart J 45:206,1981.
Long-term efficacy of verapamil in the treatment of paroxysmal supraventricular tachycardias K. I. Lie, M.D., D. R. Diiren, M.D., V. Manger Cats, M.D., G. K. David, M.D., and D. Durrer, M.D. Amsterdam,
The Netherlands
Although the efficacy of verapamil in the treatment of paroxysmal supraventricular tachycardia is well established,1-4 most of these studiesrefer to intravenous administration or short-term oral therapy. Since follow-up data on long-term oral prophylaxis are lacking, we have undertaken a study to assess the long-term efficacy of verapamil in the prevention of paroxysmal supraventricular t,achycardias. We selected56 consecutive patients with chronic recurrent (more than once-daily attacks) paroxysmal supraventricular tachycardia, in whom pretreatment with drugs such as digitalis, beta blockers, quinidine, disopyramide, and other antiarrhythmics had to be discontinued because of ineffectiveness (42 patients) or undesirableside effects (14 patients). All 56 patients responded to short-term (4 weeks)oral therapy with verapamil, continued their longterm medication, and could be followed up for at least 1 year. Of those 56 patients, 20 had paroxysmal atrioventricular junctional tachycardia, 9 had circus movement tachycardias in association with the Wolff-ParkinsonWhite (WPW) syndrome, since programmed electrical stimulation revealed that an acessorypathway wasusedin a ventriculoatrial direction ,5 24 had paroxysmal atria1 fibrillation or flutter, and 3 had paroxysmal atrial tachycardia. Their ages varied from 10 to 83 years (mean 52 years). Organic heart diseasewas present in 14, with coronary artery disease being the most frequent (8 patients). The dosageof long-term oral treatment varied from 120 to 320 mg, and the follow-up period ranged from 12 to 48 months (mean 25.4 months). Twenty-five patients were asymptomatic, whereas Holter monitoring showed no episodesof supraventricular tachycardia. The remaining 31 patients noticed a marked reduction of symptoms to at From the Department of Cardiology and Clinical Physiology Interuniversity Cardiologic Institute. Received for publication Aug. 13, 1980; revision received Aug. accepted Nov. 10, 1981. Reprint requests: K. I. Lie, Department of Cardiology and Physiology, Wilhelmina Gasthuis, le Helmersstraat 104, 1054 EG dam, The Netherlands.
and the 27, 1981; Clinical Amster-
April, 1993 Heart Journal
least twice-weekly attacks. In the latter, Holter monitoring revealed sporadic episodes of atria1 fibrillation in three, short runs of atria1 premature beats in five, frequent atrial premature beatsin three, and sporadic atria1premature beats in 20 patients. The basic sinus rate in 8 of 56 patients was below 60 bpm, but none had symptoms caused by bradycardia. Of 56 patients, seven (12.5%) noticed possible minor side effects such as dizziness, headache, and/or tiredness. In 12 of 17 patients with paroxysmal atrioventricular junctional tachycardia, the use of intravenous verapamil resulted in termination of the tachycardia. This occurred in five of nine patients with circus movement tachycardia in association with the WPW syndrome. This confirms earlier suggestions6 that intravenous verapamil in paroxysmal atrioventricular junctional tachycardia can be used in the selection of patients who will receive long-term oral treatment. However, a prospective study of a large number of patients is needed for confirmation. Since the useof intravenous verapamil resulted in termination of tachycardia in only five of nine patients with circus movement tachycardia in associationwith the WPW syndrome, the efficacy of long-term oral verapamil in these patients may be partly due to its preventive effects on the initiation of atria1 premature beats rather than to the inability to initiate reentrant tachycardias. Other arguments favoring this mechanismare evident in our patients with paroxysmal atria1 fibrillation, flutter, or tachycardia who also benefited from long-term oral treatment. In these patients both the reduction of complaints and the data during Holter monitoring suggestthat the efficacy of verapamil in managingthesepatients is mainly due to its efficacy in reducing the incidence of atria1 premature beats. Although we believe that verapamil is the first drug of choice in the long-term treatment of paroxysmal supraventricular tachycardia, especially in patients without severeorganic cardiac disease,long-term data obtained from prospective studieswith verapamil are neededto confirm this statement. REFERENCES
1. Schamroth L, Krikler DM, Garret C: Immediate effects of intravenous verapamil in cardiac arrhythmias. Br Med J 1:660, 1972. o‘. Brichard G. Zimmermann PE: Veranamil in cardiac dvsrhythmias anaesthesia. Br J Anaesth ;2:1005, 1970. I 3. Krikler DM, Spurrell RAJ: Verapamil in the treatment of paroxysmal supraventricular tachycardia. Postgrad Med J 50:447, 1974. 4. Midtbii K: Isoptin, a prophylactic agent in paroxysmal supraventricular tachyarrhythmias. In Atterhiig JJ, Haakana A, Nording B, editors: Symposium on arrhythmias: Isoptin. Aulendorf, W. Germany, 1974, Edition Cantor, pp. 100-103. 5. Wellens HJJ, Durrer D: The role of an accessory pathwav in reciprocal tachycardia: Observations in patients with and without the Wolff-Parkinson-White syndrome. Circulation 52:58, 1978. 6. Wellens HJJ, Tan SL, Biir FWH, Diiren DR, Lie KI, Dohmen HH: Effect of verauamil studied bv Droerammed electrical stimulation of the-heart in patients w%h paroxysmal reentrant supraventricular tachycardia. Br Med J 39:1058, 1977.