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Transient myocardial injury after elective electrical cardioversion
ELSEVIER
International Journal of Cardiology 46 (1994) 283-285
Transient myocardial injury after elective electrical cardioversion Juan C. Garcia-Rubira*,
Dolores Romero, Juan T. Garcia, Josh M. Cruz
Victor L6pez,
Coronary Care Unit, University Hospital Virgen Macarena, Avenida Dr Fedriani 3. 41009, Sevilla, Spain
Received 28 March 1994; revision accepted 31 May 1994
Abstract A patient with recent myocardial infarction underwent elective direct current countershock because of atria1 tibrillation. After several shocks, the ST segments were strikingly raised throughout the precordial leads, which disappeared with the administration of a perfusion of nitroglycerin. This case is evidence that electrical cardioversion can cause myocardial damage. Keywords:
Atria1 fibrillation;
Cardioversion,
electrical;
1. Introduction
Electrical cardioversion is the preferred treatment when atria1 fibrillation results in acute heart failure [l]. However, it is not free of adverse effects, and it is controversial if electrical countershock can cause myocardial damage [2]. We describe a patient in whom electrical countershock produced severe ST segment elevation. 2. Case report A 74-year-old man was admitted to our Coronary Care Unit because of acute myocardial infarction of the anterior wall. He had a previous history of hypertension and was smoker of 5 cigarettes/day. On admission he had rales over the lung bases, and a soft diastolic murmur at the apex. The l
Corresponding author.
0167-5273/94/%07.00 0 1994 Elsevier Science SSDI 0167-5273(94)02105-R
Ireland
Myocardial
injury; ST segment
elevation
echocardiography revealed hypokinesis of the apex and anterior wall, and mild mitral stenosis. During the third day he developed atria1 fibrillation with a high ventricular rate (Fig. 1). The heart rate was poorly controlled by digoxin plus propafenone and amiodarone, and he developed signs of left ventricular failure, so that electrical countershock was planned. After sedation with thiopentone sodium, 6 consecutive synchronized shocks were delivered (50, 100, 150, 200, 300 and 300 J) without success. Five minutes after the last shock, blood pressure was 140/80 mmHg, and the electrocardiogram showed elevation of the ST segments over the precordial leads (Fig. 2a). A 50@min infusion of nitroglycerin was started, and the ST-segment elevation disappeared in 10 min (Fig. 2b). The serum creatine kinase levels were raised to 1430 (normal, < loo), with an MB fraction of 1%. Sinus rhythm reappeared 4 days later. The coronary arteriography showed severe
Ltd. All rights reserved
284
J.C. Cur&-Rubira
Fig. 1. Two days after presenting with an acute myocardial heart rate and left ventricular failure.
em ul. /hr.
infarction,
i. Cardiol. 46 (I994)
the patient
developed
283-285
atria1 ~briliation
which resulted in rapid
b
Fig. 2. (a) Immediately after unsuccessful electrical cardioversion. severe elevation leads. (b) After administration of nitroglycerin, ST segment elevation disappeared.
of the ST-segment
was noted over the anterior
_I.C. Garcia-Rubira
et al. /ht.
stenoses of left anterior descending artery and the right coronary artery, with an ejection fraction of 0.70. 3. Discussion Jakobsson et al. [3] have shown, in a series of 30 consecutive patients who underwent elective electrical cardioversion, that total creatine kinase elevation correlated positively with the cumulative delivered energy. Analysis of enzyme fractions indicated a skeletal muscle origin of the enzyme release. On the other hand, animal experiments have demonstrated myocardial damage by repetitive electrical shocks. Wilson et al. [4] applied one, five, or ten transthoracic shocks of 400 J to healthy adult greyhounds, and observed an increasing acute mortality related to the number of shocks: 0 out of 6,8 out of 18, and 12 out of 17. They found a significant correlation both between the amount of cardiac damage (in grams) and the ST segment elevation with the number of shocks. This study cannot be directly applied to the clinical situation because, as the authors pointed out, transthoracic impedance in the heart of these dogs was less, and the peak current greater than those attained in clinical practice. In the patient whose case we report here, the presence of severely stenosed coronary arteries is a factor that may predisposes the myocardium to suffer damage from electrical shocks. The relief of ST segment elevation with nitroglycerin, together with the absence of a raise of serum MB creatine kinase levels, suggest that the mechanism was
J. Card&l. 46 (1994) 283-285
285
coronary artery spasm. However, we cannot exclude another mechanism. Zhu et al. [5] have recently reported a patient with transient ST segment elevation and reversible left ventricular dysfunction after electroconvulsive therapy that could be prevented by labetalol but not by nitrates and diltiazem. Although electroconvulsive therapy is very different to electrical cardioversion, their report illustrates about how transient ST segment elevation after an electrical shock is not necessarily expression of coronary spasm. We think that this case is evidence that electrical cardioversion can be followed by ST-segment elevation (possibly by coronary artery spasm), and that the ST segment must be observed in the 12lead electrocardiogram when several shocks are needed, especially in patients with coronary artery disease. References 111 Zipes DP. Specific arrhythmias: 17-l
131
[41
t51
diagnosis and treatment. In: Braunwald, E., ed. Heart disease. Philadelphia: WB Saunders, 1992: 667-725. Ehsani A, Gordon AE. Sobel BE. Effects of electrical countershock on serum creatine phosphokinase (CKP) isoenzyme activity. Am J Cardiol 1976; 36: 12-18. Jakobsson J, C)dmansson I, Notdlander R. Enzyme release after elective cardioversion. Eur Heart J, 1990: 1I: 749-152. Wilson CM, Allen JD, Bridges JB, Adgey AAJ. Death and damage caused by multiple direct current shocks: studies in an animal model. Eur Heart J, 1988; 9: 1257-1265. Zhu WX, Olson DE, Karon BL, Tajik AJ. Myocardial stunning after electroconvulsive therapy. Ann Intern Med, 1992, 117: 914-915.
International Journal of Cardiology 46 (1994) 283-285
Transient myocardial injury after elective electrical cardioversion Juan C. Garcia-Rubira*,
Dolores Romero, Juan T. Garcia, Josh M. Cruz
Victor L6pez,
Coronary Care Unit, University Hospital Virgen Macarena, Avenida Dr Fedriani 3. 41009, Sevilla, Spain
Received 28 March 1994; revision accepted 31 May 1994
Abstract A patient with recent myocardial infarction underwent elective direct current countershock because of atria1 tibrillation. After several shocks, the ST segments were strikingly raised throughout the precordial leads, which disappeared with the administration of a perfusion of nitroglycerin. This case is evidence that electrical cardioversion can cause myocardial damage. Keywords:
Atria1 fibrillation;
Cardioversion,
electrical;
1. Introduction
Electrical cardioversion is the preferred treatment when atria1 fibrillation results in acute heart failure [l]. However, it is not free of adverse effects, and it is controversial if electrical countershock can cause myocardial damage [2]. We describe a patient in whom electrical countershock produced severe ST segment elevation. 2. Case report A 74-year-old man was admitted to our Coronary Care Unit because of acute myocardial infarction of the anterior wall. He had a previous history of hypertension and was smoker of 5 cigarettes/day. On admission he had rales over the lung bases, and a soft diastolic murmur at the apex. The l
Corresponding author.
0167-5273/94/%07.00 0 1994 Elsevier Science SSDI 0167-5273(94)02105-R
Ireland
Myocardial
injury; ST segment
elevation
echocardiography revealed hypokinesis of the apex and anterior wall, and mild mitral stenosis. During the third day he developed atria1 fibrillation with a high ventricular rate (Fig. 1). The heart rate was poorly controlled by digoxin plus propafenone and amiodarone, and he developed signs of left ventricular failure, so that electrical countershock was planned. After sedation with thiopentone sodium, 6 consecutive synchronized shocks were delivered (50, 100, 150, 200, 300 and 300 J) without success. Five minutes after the last shock, blood pressure was 140/80 mmHg, and the electrocardiogram showed elevation of the ST segments over the precordial leads (Fig. 2a). A 50@min infusion of nitroglycerin was started, and the ST-segment elevation disappeared in 10 min (Fig. 2b). The serum creatine kinase levels were raised to 1430 (normal, < loo), with an MB fraction of 1%. Sinus rhythm reappeared 4 days later. The coronary arteriography showed severe
Ltd. All rights reserved
284
J.C. Cur&-Rubira
Fig. 1. Two days after presenting with an acute myocardial heart rate and left ventricular failure.
em ul. /hr.
infarction,
i. Cardiol. 46 (I994)
the patient
developed
283-285
atria1 ~briliation
which resulted in rapid
b
Fig. 2. (a) Immediately after unsuccessful electrical cardioversion. severe elevation leads. (b) After administration of nitroglycerin, ST segment elevation disappeared.
of the ST-segment
was noted over the anterior
_I.C. Garcia-Rubira
et al. /ht.
stenoses of left anterior descending artery and the right coronary artery, with an ejection fraction of 0.70. 3. Discussion Jakobsson et al. [3] have shown, in a series of 30 consecutive patients who underwent elective electrical cardioversion, that total creatine kinase elevation correlated positively with the cumulative delivered energy. Analysis of enzyme fractions indicated a skeletal muscle origin of the enzyme release. On the other hand, animal experiments have demonstrated myocardial damage by repetitive electrical shocks. Wilson et al. [4] applied one, five, or ten transthoracic shocks of 400 J to healthy adult greyhounds, and observed an increasing acute mortality related to the number of shocks: 0 out of 6,8 out of 18, and 12 out of 17. They found a significant correlation both between the amount of cardiac damage (in grams) and the ST segment elevation with the number of shocks. This study cannot be directly applied to the clinical situation because, as the authors pointed out, transthoracic impedance in the heart of these dogs was less, and the peak current greater than those attained in clinical practice. In the patient whose case we report here, the presence of severely stenosed coronary arteries is a factor that may predisposes the myocardium to suffer damage from electrical shocks. The relief of ST segment elevation with nitroglycerin, together with the absence of a raise of serum MB creatine kinase levels, suggest that the mechanism was
J. Card&l. 46 (1994) 283-285
285
coronary artery spasm. However, we cannot exclude another mechanism. Zhu et al. [5] have recently reported a patient with transient ST segment elevation and reversible left ventricular dysfunction after electroconvulsive therapy that could be prevented by labetalol but not by nitrates and diltiazem. Although electroconvulsive therapy is very different to electrical cardioversion, their report illustrates about how transient ST segment elevation after an electrical shock is not necessarily expression of coronary spasm. We think that this case is evidence that electrical cardioversion can be followed by ST-segment elevation (possibly by coronary artery spasm), and that the ST segment must be observed in the 12lead electrocardiogram when several shocks are needed, especially in patients with coronary artery disease. References 111 Zipes DP. Specific arrhythmias: 17-l
131
[41
t51
diagnosis and treatment. In: Braunwald, E., ed. Heart disease. Philadelphia: WB Saunders, 1992: 667-725. Ehsani A, Gordon AE. Sobel BE. Effects of electrical countershock on serum creatine phosphokinase (CKP) isoenzyme activity. Am J Cardiol 1976; 36: 12-18. Jakobsson J, C)dmansson I, Notdlander R. Enzyme release after elective cardioversion. Eur Heart J, 1990: 1I: 749-152. Wilson CM, Allen JD, Bridges JB, Adgey AAJ. Death and damage caused by multiple direct current shocks: studies in an animal model. Eur Heart J, 1988; 9: 1257-1265. Zhu WX, Olson DE, Karon BL, Tajik AJ. Myocardial stunning after electroconvulsive therapy. Ann Intern Med, 1992, 117: 914-915.