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Sudden death during continuous holter monitoring out of hospital after nitroglycerin consumption
September 1, 1984
THE AMERICAN JOURNAL OF CARDIOLOGY
Volume 54
677
FIGURE 1. Electrocardiograms recorded at rest and during treadmill exercise. A, tracing at rest before exercise. Heart rate is 75 beats/min. B, during exercise, left bundle branch block and chest discomfort develop. Heart rate is 115 beats/min. C, 17 minutes after stopping exercise, left bundle branch block was still present at a heart rate of 72 beatsr’min. but chest discomfort was gone. The heart rate at this time is less than that in panel A. D, 19 minutes after exercise, conduction is normal. Heart rate is 68 beats/min.
exercise induced. Furthermore, extensive investigation did not reveal objective evidence of myocardial ischemia. We conclude that patients with rate-related left BBB need not have iscbemia in order to be symptomatic with exercise. The exact cause of the discomfort remains unclear. Although the patients of Virtanen et al had altered systolic motion on kinetocardiography, our patient had no discer:nible change in septal systolic motion, and thus, we cannot incriminate this as the mechanism.
Acknowledgment: We thank Dr. Brian Wagg, who referred this patient and Elizabeth Milliken for typing the manuscript.
SuddenDeath DuringContinuousHalter MonitoringOut of HospitalAfter NitroglycerinConsumption
systolic ejection murmur. Chest x-ray and an electrocardiogram at rest were normal. A maximal exercise test performed 3 months previously gave no evidence of myocardial ischemia or arrhythmia. His only medication was trinitroglycerin, which he took as needed. On 12129182, he underwent Holter monitoring with 2 modified bipolar leads (CM1 and CMh). Electrocardiographic monitoring began at lo:40 AM (Fig. 1A). At 12.35 PM, the patient began to ascend a flight of steps on his way home and at 12:41 PM, he had the same chest pain he had had previously. The heart rate was 150 beatshin; lead CM1 showed 1.5 mm of ST-segment elevation, lead CM5 showed tall, peaked, narrow T waves and 1 mm of ST-segment depression, junctional in shape (Fig. 1B). Coupled, bigeminal and multiform repetitive ventricular premature contractions (VPCs) appeared, none of which were “early cycle” (R-on-T) (Fig. 1C). On interrupting his’ walk, his chest pain diminished. At 12.45 PM he started walking again and reached home at 12:50 PM. During this period the ECG showed no arrhythmia, and ST-segment abnormalities in lead CM1 and CM5 remained unchanged. At home, his chest pain disappeared, but he nevertheless took trinitroglycerin (12:52 PM). After taking trinitroglycerin, ST elevation in lead CM1 diminished (1 mm) and no arrhythmia occurred; in lead CMc, ST-segment depression became horizontal in shape; the QTc interval was normal. At 12:55 PM, although the patient was asymptomatic, he suddenly lost consciousness; he was immediately taken to the hospital, but on arrival he was dead. On the electrocardiographic recording at 12:55 PM, a single VPC occurred
MASSIMO ZONI BERISSO, MD ALBERTO CAVALLINI, MD MARIO IANNETTI, MD
Sudden death is most often the result of ventricular fibrillation (VF) in patients with coronary heart disease.lg2 Numerous caseis of sudden death after VF have been recorded in the setting of acute myocardial infarction in the coronary care unit.2 However, only a few reported cases have been documented outside the hospital during the patient’s daily activity.ls Such a case is described herein. A 38-year-old manager underwent ambulatory electrocardiographic monitoring for recurrent chest pain at rest and during effort. Several relatives had died suddenly. He had had systemic hypertension, hyperdyslipidemia, and smoked more than 40 cigarettes per day. He had a l/6 aortic midthe Depdmnt of CardkMgy, University of Gmova, Gsnova, itaty. Manuscript received March 2a1.1984; revisedmanuscript received May 24.1984, accepted May 31.1984.
Fmn
References 1. Vktanen KS. Mkkiia J, Kata R, 8iltanm1P. chest painand raw tefttxndlebrsnchbk&inpstienKwithnormstcomnsryarterlogems.Chest 1982;81:326-331. 2. VBwqtWVK,8@donKC,A@utJ8,HagcmAD.Fts~leftbundB brsnchblodcwithanginspectalsandncrmslcomnsrysrWqrsrns.Chsst 1978;69:123-124.
676
BRIEF REPORTS
FIGURE 1. A, basal electracardbgram;
B, electrocatdiogramwhentha patient hsd chest pain;C, muttiformrepetitive prematureventricularcomplexesduring chest pain.
during the ventricular vulnerable period (RR’IQT = 0.63; coupling period 240 ms). This VPC triggered a ventricular flutter, which deteriorated into VF (Fig. 2). At 1:24 PM, a ventricular rhythm of 55 beatslmin was observed that lasted 30 seconds and was followed by ventricular standstill. Ne-
cropsy showed left ventricular hypertrophy; the heart weighed 475 g. An old myocardiat infarct that involved the superior ventricular septum was present. There was no evidence of coronary artery stenosis, fresh thrombosis of subepicardial coronaries or recent myocardial necrosis.
September 1, 1984
FIGURE 2. Terminal graphic B
THE AMERICAN JOURNAL OF CARDIOLOGY
Volume 54
679
electrocardic-
Few cases of sudden death during electrocardiographic recording out of hospital have been reported.193 Several studies show a close relation between sudden death and coronary heart diiease.Q However, a few rare cases have been described in apparently healthy subjects.* In our patient, necropsy showed an old myocardial septal infarction, left ventricular hypertrophy that had not been detected with routine tests, and normal coronary arteries. The presence of chest pain and ST-segment elevation during Holter monitoring associated with 11ormal coronary arteries suggest that sudden death resulted from a fatal arrhythmia after an ischemic attack, wh:ich in turn was probably a result of effort-induced coronary vasospasm.5 Moreover, VF occurred suddenly wh.en the chest pain had already disappeared, 3 minutes after taking trinitroglycerin, without previous VP& (except for the single “earlycycle” R-on-T, which began it). These findings suggest that VF could have been induced by coronary reperfusion,6 although it did occur without the ST-segment returning to baseline in lead CMI.~ The arrest appeared
3 minutes after taking trinitroglycerin. Could trinitroglycerin have produced it? It is well known that nitrates can remove coronary vasospasm during ergonovine tests or coronary angiography.6 Nevertheless, there do not appear to be any specific reports during life-threatening arrhythmias associated with reperfusion of an ischemic myocardial area after a patient has taken nitrates. We think that our case report could corroborate this hypothesis. References 1. pk4Ik QpB&%L2tpJ2m
deathmAed
dulng Halter man-
Ins MR, Godman MJ, Oliver MF, Julian W, Donald KW. 2. I.a DM, H Ventricular fibri ‘gf latlon complicating acute myocardial infarction. Lancet lQMk2r253-280. .___,_.--- ---. 3. PallldmI,mkgamulJ.HolterIntmitor&igdvingsuddellcaIdiacdeath:chms to its etblogy and prevention. Clrculatlcn 1982;68:suppl kll-25. oln 0, Hal H. Basis for 4. Lown B, Temte JV. R&h P. Gau@am C, R ‘p”coronary heart disease and recwring ventricular fibrillation In the absence o Its management. N E I J Med 1976:294:623-630. ‘di coronary artery 8 . demonstration definition, 5. M-1 & CMb Cardv i5%8225+39-196 dlagnosls and consequences. 6. Foldman RL, Pqine CJ, Cod ?!R . Coronaryerterik rkponee~ to graded dosesof nitroglycerin. Am J Cardiol 1979:49:91-103.
THE AMERICAN JOURNAL OF CARDIOLOGY
Volume 54
677
FIGURE 1. Electrocardiograms recorded at rest and during treadmill exercise. A, tracing at rest before exercise. Heart rate is 75 beats/min. B, during exercise, left bundle branch block and chest discomfort develop. Heart rate is 115 beats/min. C, 17 minutes after stopping exercise, left bundle branch block was still present at a heart rate of 72 beatsr’min. but chest discomfort was gone. The heart rate at this time is less than that in panel A. D, 19 minutes after exercise, conduction is normal. Heart rate is 68 beats/min.
exercise induced. Furthermore, extensive investigation did not reveal objective evidence of myocardial ischemia. We conclude that patients with rate-related left BBB need not have iscbemia in order to be symptomatic with exercise. The exact cause of the discomfort remains unclear. Although the patients of Virtanen et al had altered systolic motion on kinetocardiography, our patient had no discer:nible change in septal systolic motion, and thus, we cannot incriminate this as the mechanism.
Acknowledgment: We thank Dr. Brian Wagg, who referred this patient and Elizabeth Milliken for typing the manuscript.
SuddenDeath DuringContinuousHalter MonitoringOut of HospitalAfter NitroglycerinConsumption
systolic ejection murmur. Chest x-ray and an electrocardiogram at rest were normal. A maximal exercise test performed 3 months previously gave no evidence of myocardial ischemia or arrhythmia. His only medication was trinitroglycerin, which he took as needed. On 12129182, he underwent Holter monitoring with 2 modified bipolar leads (CM1 and CMh). Electrocardiographic monitoring began at lo:40 AM (Fig. 1A). At 12.35 PM, the patient began to ascend a flight of steps on his way home and at 12:41 PM, he had the same chest pain he had had previously. The heart rate was 150 beatshin; lead CM1 showed 1.5 mm of ST-segment elevation, lead CM5 showed tall, peaked, narrow T waves and 1 mm of ST-segment depression, junctional in shape (Fig. 1B). Coupled, bigeminal and multiform repetitive ventricular premature contractions (VPCs) appeared, none of which were “early cycle” (R-on-T) (Fig. 1C). On interrupting his’ walk, his chest pain diminished. At 12.45 PM he started walking again and reached home at 12:50 PM. During this period the ECG showed no arrhythmia, and ST-segment abnormalities in lead CM1 and CM5 remained unchanged. At home, his chest pain disappeared, but he nevertheless took trinitroglycerin (12:52 PM). After taking trinitroglycerin, ST elevation in lead CM1 diminished (1 mm) and no arrhythmia occurred; in lead CMc, ST-segment depression became horizontal in shape; the QTc interval was normal. At 12:55 PM, although the patient was asymptomatic, he suddenly lost consciousness; he was immediately taken to the hospital, but on arrival he was dead. On the electrocardiographic recording at 12:55 PM, a single VPC occurred
MASSIMO ZONI BERISSO, MD ALBERTO CAVALLINI, MD MARIO IANNETTI, MD
Sudden death is most often the result of ventricular fibrillation (VF) in patients with coronary heart disease.lg2 Numerous caseis of sudden death after VF have been recorded in the setting of acute myocardial infarction in the coronary care unit.2 However, only a few reported cases have been documented outside the hospital during the patient’s daily activity.ls Such a case is described herein. A 38-year-old manager underwent ambulatory electrocardiographic monitoring for recurrent chest pain at rest and during effort. Several relatives had died suddenly. He had had systemic hypertension, hyperdyslipidemia, and smoked more than 40 cigarettes per day. He had a l/6 aortic midthe Depdmnt of CardkMgy, University of Gmova, Gsnova, itaty. Manuscript received March 2a1.1984; revisedmanuscript received May 24.1984, accepted May 31.1984.
Fmn
References 1. Vktanen KS. Mkkiia J, Kata R, 8iltanm1P. chest painand raw tefttxndlebrsnchbk&inpstienKwithnormstcomnsryarterlogems.Chest 1982;81:326-331. 2. VBwqtWVK,8@donKC,A@utJ8,HagcmAD.Fts~leftbundB brsnchblodcwithanginspectalsandncrmslcomnsrysrWqrsrns.Chsst 1978;69:123-124.
676
BRIEF REPORTS
FIGURE 1. A, basal electracardbgram;
B, electrocatdiogramwhentha patient hsd chest pain;C, muttiformrepetitive prematureventricularcomplexesduring chest pain.
during the ventricular vulnerable period (RR’IQT = 0.63; coupling period 240 ms). This VPC triggered a ventricular flutter, which deteriorated into VF (Fig. 2). At 1:24 PM, a ventricular rhythm of 55 beatslmin was observed that lasted 30 seconds and was followed by ventricular standstill. Ne-
cropsy showed left ventricular hypertrophy; the heart weighed 475 g. An old myocardiat infarct that involved the superior ventricular septum was present. There was no evidence of coronary artery stenosis, fresh thrombosis of subepicardial coronaries or recent myocardial necrosis.
September 1, 1984
FIGURE 2. Terminal graphic B
THE AMERICAN JOURNAL OF CARDIOLOGY
Volume 54
679
electrocardic-
Few cases of sudden death during electrocardiographic recording out of hospital have been reported.193 Several studies show a close relation between sudden death and coronary heart diiease.Q However, a few rare cases have been described in apparently healthy subjects.* In our patient, necropsy showed an old myocardial septal infarction, left ventricular hypertrophy that had not been detected with routine tests, and normal coronary arteries. The presence of chest pain and ST-segment elevation during Holter monitoring associated with 11ormal coronary arteries suggest that sudden death resulted from a fatal arrhythmia after an ischemic attack, wh:ich in turn was probably a result of effort-induced coronary vasospasm.5 Moreover, VF occurred suddenly wh.en the chest pain had already disappeared, 3 minutes after taking trinitroglycerin, without previous VP& (except for the single “earlycycle” R-on-T, which began it). These findings suggest that VF could have been induced by coronary reperfusion,6 although it did occur without the ST-segment returning to baseline in lead CMI.~ The arrest appeared
3 minutes after taking trinitroglycerin. Could trinitroglycerin have produced it? It is well known that nitrates can remove coronary vasospasm during ergonovine tests or coronary angiography.6 Nevertheless, there do not appear to be any specific reports during life-threatening arrhythmias associated with reperfusion of an ischemic myocardial area after a patient has taken nitrates. We think that our case report could corroborate this hypothesis. References 1. pk4Ik QpB&%L2tpJ2m
deathmAed
dulng Halter man-
Ins MR, Godman MJ, Oliver MF, Julian W, Donald KW. 2. I.a DM, H Ventricular fibri ‘gf latlon complicating acute myocardial infarction. Lancet lQMk2r253-280. .___,_.--- ---. 3. PallldmI,mkgamulJ.HolterIntmitor&igdvingsuddellcaIdiacdeath:chms to its etblogy and prevention. Clrculatlcn 1982;68:suppl kll-25. oln 0, Hal H. Basis for 4. Lown B, Temte JV. R&h P. Gau@am C, R ‘p”coronary heart disease and recwring ventricular fibrillation In the absence o Its management. N E I J Med 1976:294:623-630. ‘di coronary artery 8 . demonstration definition, 5. M-1 & CMb Cardv i5%8225+39-196 dlagnosls and consequences. 6. Foldman RL, Pqine CJ, Cod ?!R . Coronaryerterik rkponee~ to graded dosesof nitroglycerin. Am J Cardiol 1979:49:91-103.