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Pacemaker-induced sustained ventricular tachycardia
454
BRIEF REPORTS
is still not seen 5 cardiac cycles after injection
of contrast medium, and no increase in contrast appearance time is present during hyperemia (CFR = 1.00). After PTCA, the vessel is opacified in 2 cardiac cycles at baseline, and appearance time is faster during hyperemia (CFR = 1.48). The right coronary artery distribution CFR also improved from 1.42 before PTCA to 1.63 after PTCA (Fig. 2). The collateral perfusion distribution originating from the right coronary artery was seen before PTCA and had a CFR of 1.19, but disappeared after successful PTCA of the LAD.
This case demonstrates several important concepts about coronary flow and collateral function. First, it confirms that angiographically visible collateral channels disappear quickly after successful PTCA.3 In this case, a corresponding improvement in CFR of the stenotic vessel was measured. Second, the inability of collateral flow to maintain adequate perfusion during stress was documented by the exercise test results, which were normal after successful PTCA. This corresponds to the abnormal CFR in the LAD and collateral distributions before PTCA and the improved CFR in the LAD after PTCA. Finally, right coronary artery CFR improved after successful PTCA of the LAD. Schaper et al4 demonstrated in a dog model that vessels supplying collaterals to functionally jeopardized beds have decreased CFR and increased coronary vascular resistance. Schwartz et al5 showed an increase in basal
Pacemaker-InducedSustained VentricularTachycardia PAUL A. TIBBITS, MD MARY ELIZABETH O’BRIEN, ABT, RN, MSN STEPHEN J. BOCCUZZI, RN, MSN DONALD P. MESSERSMITH, MD WILLIAM P. BAKER, MD
Ventricular tachycardia (VT) induced by an implanted endocardial pacemaker has been described,l but the clinical context was usually not clear. Studies on programmed endocardial extrastimulation have shown that the specificity of VT induced by a single extrastimulus is 100% as a predictor of clinical sustained VT.zJ We present a case of pacemaker-induced ventricular tachycardia with syncope of unknown cause. This case emphasized the danger of pacemaker therapy in such a patient. T.L., an 87-year-old man, had had 8 episodes without prodromal or postictal manifestations tember 1981 until the time of the next permanent implantation in February 1981. Each episode
of syncope from Seppacemaker was 1 to 2
From the Cardiovascular Disease Division, Naval Hospital Bethesda, Naval Medical Command, National Capital Region, Bethesda, Maryland 20814. Manuscript received February 15, 1984; revised manuscript received March 28. 1984, accepted April 2, 1984. The opinions expressed herein are those of the authors and are not to be construed as reflecting the views of the Navy Department, of the Naval Service at large, or of the Department of Defense.
flow in normal coronary arteries following occlusion of a neighboring vessel. Because CFR is a relative measure of maximal to resting flow, either an increase in maximal flow or a decrease in resting flow will increase its value. Thus, the loss of collateral function in this case with concomitant improvement in the right coronary CFR could be due either to decreased right coronary basal flow or to decreased coronary vascular resistance which would allow for an increased hyperemic flow. The ability to study collateral function using digital radiographic techniques should provide a more comprehensive and physiologic assessment of this complex phenomenon.
1. Cohen YV. Tha functionalvalue of coronary collaterals in myocardtl ischemiaand therapeuticapproachto enhance collateral flow. Am Heart J 197895396-404. 2. Vo@ K,.LeFrea M, Sates E, O’Nelll W, Foster R, Klrlln P, Smith D, Pitt B. Applicabonof digital techniquesto selective coronaryarteriwraohv: use of rnyocardialcontrastappearancetima to maasue coronaryfl~w’resarve. Am heart J 1984;107:153-164, 3. GruentzfgA, Pyle R, Goebel N, SchtumpfM. Tha fate of collateralsafter percutaneoustransluminalcoronaryangioplasty(PTCA)(abstr).Circulation 1980;63:suppllll:1ll-161. 4. SchaperW, FtamengW, Wlnkler S, WustenB, TurscbmannW, Naugabauar 0, Carl M, Pasyk S. Quantificationof collateral resistance In acute and c&rto_~77experimantal coronary occlusion in the dog. Circ Res t976;39:
_...
5. Schwartz JS, Cohn JNr Bacba RJ. Effectsof coronaryocclusionon flow in tha distributionof a nerghboringstenotic coronaryartery in the dog. Am J Cardiol 1983;52:189-195.
minutes in duration and occurred in the erect position, not related to exertion. The patient sustained facial abrasions with each episode. Neurologic evaluation, including electroencephalogram, was not revealing. Inpatient cardiac rhythm telemetry was performed continuously in October 1981 for 1 month, during which no syncope or dysrhythmias occurred, He was again hospitalized in February 1982 for cardiac monitoring because of recurrent syncope. Episodic sinus bradycardia (30 beatslmin) during waking hours was discovered, although there were no associated symptoms. A permanent demand ventricular pacemaker (VVZ) was implanted for the suspicion of symptomatic sinus bradycardia with an inadequate junctional escape mechanism. Blood pressure was 110160 mm Hg without orthostatic decline. An electrocardiogram showed left atria1 enlargement, right bundle branch block and old anterolateral and inferior wall myoeardial infarctions. The chest x-ray showed cardiomegaly. After pacemaker implantation the patient had syncope once. Soon after electrocardiography, the patient became pulseless and collapsed. Resuscitation efforts were successful within 2 minutes, with return of a strong regular pulse. The patient was transferred to the coronary care unit in normal sinus rhythm. No electrocardiographic leads were connected
FIGURE 1. The first complex is a normally conducted sinus beat followed by a pacemaker spike (negative deflection) occurring on the T wave initiating ventricular tachycardia.
August 1.1984
to the patient during the arrest. While in the coronary care unit, during cardiac monitoring, an attempt to check the adequacy of pacer funciion using a magnet to switch the pulse generator to the as,ynchronous mode produced an episode of VT from which the patient could not be resuscitated (Fig. 1).
We conclude that pacemaker therapy can be lethal for patients with syncope of unknown cause. Furthermore, in selected patients, syncope of undefined cause should be investigated with the programmed extra-
Absence of Mitral Valve Prolapsein Juvenile Iiyperthyroidism
THE AMERICAN JOURNAL OF CARDIOLOGY
Fourteen hyperthyroid patients, aged 9 to 20 years (mean 15), were studied. Physical and echocardiographic examinations were performed by a pediatric cardiologist. All 14 patients underwent M-mode and 2-dimensional (2-D) echocardiography (echo ). The biochemical data confirming the diagnosis are shown in Table I. The duration of hyperthyroidism ranged from 3 to 60 months (mean 23). Fourpatients had hyperthyroidism at the time of study. To establish the frequency of MVP in normal children of comparable age, 175 consecutive M-mode echocardiograms were taken as control. M-mode echocardiognxms were recorded on an Ekoline 20A Smith Kline apparatus coupled with a Cambridge fiberoptic recorder. The echocardiograms were performed with the transducer in the fourth or fifth intercostal space at the left sternal border and with )!he echo beam perpendicular to the chest wall. Only complexes in which both the anterior and posterior leaflets of the mitral valve could be visualized in diastole were chosen for the study. MVP was defined on the M-mode echo as a posterior displacement of the mitral leaflets in late ventricular systole.3 An image of holosystolic bowing of the leaflets was considered diagnostic only when confirmed by 2-D echo, which was performed using a ATL Mark IV echocardiograph in the supine position. Both apical 4-chamber and long-axis parasternal views were taken. MVP From the Cardiology and Endocrinology Sections, Departments of Pediatrics and Pediatric Research, Sainte-Justine Hospital and University of fvlontraal.Montreal, Quebec, Canada. Manuscript received November 5, 1983; revised manuscript received April 4, 1984, accepted April 8, 1984.
455
stimulus technique to exclude a diagnosis of sustained recurrent VT before pacemaker implantation. References 1. Furman S. Pacemaker emergencies. Med Clin North Am 1979;63:113126. 2. Fiehw JD, Dstrow E, Mechra R. Clinicalcorrelationsof ventricularvulner-
abilityto electrophysiologicstress. In: Mere C, ed. hoc Vlth World Syrnp Cardiac Pacing. Montreal:Pace Symposium,1979;L5.
3. Vandepol CJ, Farshldi A, Splelman SR, Greenspan AM, Horowftz LN, Josephson ME. Incidenceand clinical significanceof inducedventricular tachycsrdia.Am J Cardiol 1980;45:725-731.
TABLE I
Biochemical Data of the Hyperthyroid Patients
Age W) Sex
ANA-MARIA CARCELLER, MD JEAN-CLAUDE FOURON, MD JACQUE.S LETARTE, MD GILLES DUCHARME, MSc NICOLAAS H. van DOESBURG, MD PIERRE: MAURAN, MD ANDRE DAVIGNON, MD
In a recent article, Channick et all reported that 43% of patients with hyperth!yroidism had echocardiographic signs of mitral valve prolapse (MVP). The mean age of their patients was 44 f 14 years. The frequency of MVP in hyperthyroid children is not known. The present study assesses the frequency of MVP in hyperthyroid persons aged 20 years or younger.
Volume 54
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Normal valuas2: T3 (plasma triiodothyronine): 70 to 220 pgldl; T4 (plasma thyroxine): 5 to 14 ng/dl, TSH (thyrotmpin-stimulatirtghormone): less than 10 @J/ml. AB = antibodies. l
was defined as displacement or bulging of the mitral leaflet into the left atrium in systole, below a line parallel to the plane of the atrioventricular ring or the mitral valve anulus. 3*4Findings from our hyperthyroid patients were compared with those from the control group and the hyperthyroid group of Channick et al. Statistical significance was assessed by the Fisher-Yates exact test (2-tailed). Physical examination of the hyperthyroid patients did not reveal signs of MVP (midsystolic click or late systolic murmur). One patient had an early diastolic murmur associated with a regurgitant bicuspid aortic valve and another had an innocent murmur. The frequency of echocardiographic signs of MVP in our control group of pediatric patients was 5%. No echocardiographic sign of MVP was found in the hyperthyroid group. By M-mode echo, holosystolic bowing of the mitral leaflets was observed in 1 patient. This patient and the other 13 patients had a normal mitral valve by 2-D echo. Statistical analysis showed that the frequency of MVP in our hyperthyroid population was significantly different @ = 0.004) from that observed by Channick et al. However, no statistical difference was found between our hyperthyroid and our control group for the same variable.
The frequency of MVP detected by M-mode echocardiography in the general population is variable.3 The possibility of overdiagnosis has been stressed and may be related to transducer angulation or variability in diagnostic criteria.3T5 This could be responsible for the difference between the frequency of MVP found by
BRIEF REPORTS
is still not seen 5 cardiac cycles after injection
of contrast medium, and no increase in contrast appearance time is present during hyperemia (CFR = 1.00). After PTCA, the vessel is opacified in 2 cardiac cycles at baseline, and appearance time is faster during hyperemia (CFR = 1.48). The right coronary artery distribution CFR also improved from 1.42 before PTCA to 1.63 after PTCA (Fig. 2). The collateral perfusion distribution originating from the right coronary artery was seen before PTCA and had a CFR of 1.19, but disappeared after successful PTCA of the LAD.
This case demonstrates several important concepts about coronary flow and collateral function. First, it confirms that angiographically visible collateral channels disappear quickly after successful PTCA.3 In this case, a corresponding improvement in CFR of the stenotic vessel was measured. Second, the inability of collateral flow to maintain adequate perfusion during stress was documented by the exercise test results, which were normal after successful PTCA. This corresponds to the abnormal CFR in the LAD and collateral distributions before PTCA and the improved CFR in the LAD after PTCA. Finally, right coronary artery CFR improved after successful PTCA of the LAD. Schaper et al4 demonstrated in a dog model that vessels supplying collaterals to functionally jeopardized beds have decreased CFR and increased coronary vascular resistance. Schwartz et al5 showed an increase in basal
Pacemaker-InducedSustained VentricularTachycardia PAUL A. TIBBITS, MD MARY ELIZABETH O’BRIEN, ABT, RN, MSN STEPHEN J. BOCCUZZI, RN, MSN DONALD P. MESSERSMITH, MD WILLIAM P. BAKER, MD
Ventricular tachycardia (VT) induced by an implanted endocardial pacemaker has been described,l but the clinical context was usually not clear. Studies on programmed endocardial extrastimulation have shown that the specificity of VT induced by a single extrastimulus is 100% as a predictor of clinical sustained VT.zJ We present a case of pacemaker-induced ventricular tachycardia with syncope of unknown cause. This case emphasized the danger of pacemaker therapy in such a patient. T.L., an 87-year-old man, had had 8 episodes without prodromal or postictal manifestations tember 1981 until the time of the next permanent implantation in February 1981. Each episode
of syncope from Seppacemaker was 1 to 2
From the Cardiovascular Disease Division, Naval Hospital Bethesda, Naval Medical Command, National Capital Region, Bethesda, Maryland 20814. Manuscript received February 15, 1984; revised manuscript received March 28. 1984, accepted April 2, 1984. The opinions expressed herein are those of the authors and are not to be construed as reflecting the views of the Navy Department, of the Naval Service at large, or of the Department of Defense.
flow in normal coronary arteries following occlusion of a neighboring vessel. Because CFR is a relative measure of maximal to resting flow, either an increase in maximal flow or a decrease in resting flow will increase its value. Thus, the loss of collateral function in this case with concomitant improvement in the right coronary CFR could be due either to decreased right coronary basal flow or to decreased coronary vascular resistance which would allow for an increased hyperemic flow. The ability to study collateral function using digital radiographic techniques should provide a more comprehensive and physiologic assessment of this complex phenomenon.
1. Cohen YV. Tha functionalvalue of coronary collaterals in myocardtl ischemiaand therapeuticapproachto enhance collateral flow. Am Heart J 197895396-404. 2. Vo@ K,.LeFrea M, Sates E, O’Nelll W, Foster R, Klrlln P, Smith D, Pitt B. Applicabonof digital techniquesto selective coronaryarteriwraohv: use of rnyocardialcontrastappearancetima to maasue coronaryfl~w’resarve. Am heart J 1984;107:153-164, 3. GruentzfgA, Pyle R, Goebel N, SchtumpfM. Tha fate of collateralsafter percutaneoustransluminalcoronaryangioplasty(PTCA)(abstr).Circulation 1980;63:suppllll:1ll-161. 4. SchaperW, FtamengW, Wlnkler S, WustenB, TurscbmannW, Naugabauar 0, Carl M, Pasyk S. Quantificationof collateral resistance In acute and c&rto_~77experimantal coronary occlusion in the dog. Circ Res t976;39:
_...
5. Schwartz JS, Cohn JNr Bacba RJ. Effectsof coronaryocclusionon flow in tha distributionof a nerghboringstenotic coronaryartery in the dog. Am J Cardiol 1983;52:189-195.
minutes in duration and occurred in the erect position, not related to exertion. The patient sustained facial abrasions with each episode. Neurologic evaluation, including electroencephalogram, was not revealing. Inpatient cardiac rhythm telemetry was performed continuously in October 1981 for 1 month, during which no syncope or dysrhythmias occurred, He was again hospitalized in February 1982 for cardiac monitoring because of recurrent syncope. Episodic sinus bradycardia (30 beatslmin) during waking hours was discovered, although there were no associated symptoms. A permanent demand ventricular pacemaker (VVZ) was implanted for the suspicion of symptomatic sinus bradycardia with an inadequate junctional escape mechanism. Blood pressure was 110160 mm Hg without orthostatic decline. An electrocardiogram showed left atria1 enlargement, right bundle branch block and old anterolateral and inferior wall myoeardial infarctions. The chest x-ray showed cardiomegaly. After pacemaker implantation the patient had syncope once. Soon after electrocardiography, the patient became pulseless and collapsed. Resuscitation efforts were successful within 2 minutes, with return of a strong regular pulse. The patient was transferred to the coronary care unit in normal sinus rhythm. No electrocardiographic leads were connected
FIGURE 1. The first complex is a normally conducted sinus beat followed by a pacemaker spike (negative deflection) occurring on the T wave initiating ventricular tachycardia.
August 1.1984
to the patient during the arrest. While in the coronary care unit, during cardiac monitoring, an attempt to check the adequacy of pacer funciion using a magnet to switch the pulse generator to the as,ynchronous mode produced an episode of VT from which the patient could not be resuscitated (Fig. 1).
We conclude that pacemaker therapy can be lethal for patients with syncope of unknown cause. Furthermore, in selected patients, syncope of undefined cause should be investigated with the programmed extra-
Absence of Mitral Valve Prolapsein Juvenile Iiyperthyroidism
THE AMERICAN JOURNAL OF CARDIOLOGY
Fourteen hyperthyroid patients, aged 9 to 20 years (mean 15), were studied. Physical and echocardiographic examinations were performed by a pediatric cardiologist. All 14 patients underwent M-mode and 2-dimensional (2-D) echocardiography (echo ). The biochemical data confirming the diagnosis are shown in Table I. The duration of hyperthyroidism ranged from 3 to 60 months (mean 23). Fourpatients had hyperthyroidism at the time of study. To establish the frequency of MVP in normal children of comparable age, 175 consecutive M-mode echocardiograms were taken as control. M-mode echocardiognxms were recorded on an Ekoline 20A Smith Kline apparatus coupled with a Cambridge fiberoptic recorder. The echocardiograms were performed with the transducer in the fourth or fifth intercostal space at the left sternal border and with )!he echo beam perpendicular to the chest wall. Only complexes in which both the anterior and posterior leaflets of the mitral valve could be visualized in diastole were chosen for the study. MVP was defined on the M-mode echo as a posterior displacement of the mitral leaflets in late ventricular systole.3 An image of holosystolic bowing of the leaflets was considered diagnostic only when confirmed by 2-D echo, which was performed using a ATL Mark IV echocardiograph in the supine position. Both apical 4-chamber and long-axis parasternal views were taken. MVP From the Cardiology and Endocrinology Sections, Departments of Pediatrics and Pediatric Research, Sainte-Justine Hospital and University of fvlontraal.Montreal, Quebec, Canada. Manuscript received November 5, 1983; revised manuscript received April 4, 1984, accepted April 8, 1984.
455
stimulus technique to exclude a diagnosis of sustained recurrent VT before pacemaker implantation. References 1. Furman S. Pacemaker emergencies. Med Clin North Am 1979;63:113126. 2. Fiehw JD, Dstrow E, Mechra R. Clinicalcorrelationsof ventricularvulner-
abilityto electrophysiologicstress. In: Mere C, ed. hoc Vlth World Syrnp Cardiac Pacing. Montreal:Pace Symposium,1979;L5.
3. Vandepol CJ, Farshldi A, Splelman SR, Greenspan AM, Horowftz LN, Josephson ME. Incidenceand clinical significanceof inducedventricular tachycsrdia.Am J Cardiol 1980;45:725-731.
TABLE I
Biochemical Data of the Hyperthyroid Patients
Age W) Sex
ANA-MARIA CARCELLER, MD JEAN-CLAUDE FOURON, MD JACQUE.S LETARTE, MD GILLES DUCHARME, MSc NICOLAAS H. van DOESBURG, MD PIERRE: MAURAN, MD ANDRE DAVIGNON, MD
In a recent article, Channick et all reported that 43% of patients with hyperth!yroidism had echocardiographic signs of mitral valve prolapse (MVP). The mean age of their patients was 44 f 14 years. The frequency of MVP in hyperthyroid children is not known. The present study assesses the frequency of MVP in hyperthyroid persons aged 20 years or younger.
Volume 54
TSH’ &U/ml)
(;$I)
AB
...
+
...
0
27 z 18
::: “3:;
:: + +
3:
...
*. .
:.4
:
4 i.9’ 214 1.4
!
9M 10M
987 238
30 ...
11F 12F 13F 14F 14F 17M 17F
1063 900 802 208
... ...
17F 18F 19F 20F 20F
900 906 167 506 535
322 f0 27 :: 20
8 +
Normal valuas2: T3 (plasma triiodothyronine): 70 to 220 pgldl; T4 (plasma thyroxine): 5 to 14 ng/dl, TSH (thyrotmpin-stimulatirtghormone): less than 10 @J/ml. AB = antibodies. l
was defined as displacement or bulging of the mitral leaflet into the left atrium in systole, below a line parallel to the plane of the atrioventricular ring or the mitral valve anulus. 3*4Findings from our hyperthyroid patients were compared with those from the control group and the hyperthyroid group of Channick et al. Statistical significance was assessed by the Fisher-Yates exact test (2-tailed). Physical examination of the hyperthyroid patients did not reveal signs of MVP (midsystolic click or late systolic murmur). One patient had an early diastolic murmur associated with a regurgitant bicuspid aortic valve and another had an innocent murmur. The frequency of echocardiographic signs of MVP in our control group of pediatric patients was 5%. No echocardiographic sign of MVP was found in the hyperthyroid group. By M-mode echo, holosystolic bowing of the mitral leaflets was observed in 1 patient. This patient and the other 13 patients had a normal mitral valve by 2-D echo. Statistical analysis showed that the frequency of MVP in our hyperthyroid population was significantly different @ = 0.004) from that observed by Channick et al. However, no statistical difference was found between our hyperthyroid and our control group for the same variable.
The frequency of MVP detected by M-mode echocardiography in the general population is variable.3 The possibility of overdiagnosis has been stressed and may be related to transducer angulation or variability in diagnostic criteria.3T5 This could be responsible for the difference between the frequency of MVP found by