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thrombus secondary to heparin-induced thrombocytopenia. Can J Cardiol 1989;5:308-10. 7. Augarten A, Apter S, Theodor R. Right ventricular thrombus and pulmonary arteritis in Behget’s disease. Isr J Med Sci 1987;23:900-1. 8. Coppock MA, Safford RE, Danielson GK. Intracardiac thrombosis, phospholipid antibodies, and two-chambered right ventricle. Br Heart J 1988;60:455-8. 9. Paul V, Foster CJ, Brownlee WC. Cross-sectional echocardiographic demonstration of biventricular thrombus. Int J Cardiol 198&l&266-70. 10. Taupin JM, Laudinat JM, Metz D, Charpoutot L, PolIet E, Chabert JP, Bajolet A. Ultrasonic diagnosis of biventricular thrombus during the acute phase of myocardial infarction. Ann Cardiol Angeiol (Paris) 1989;38:54%7. 11. Leimbach WN. Wallin BG. Victor RG. Avlward PE. Sundlof G, Mark AL. I%rect evidence from in&an&al recordings for increased central sympathetic outflow in patients with heart failure. Circulation 1$86;73:913-9. 12. Fereuson DW. Bere WJ. Sanders JS. Clinical and hemodvna;ic correlates ofiympathetic nerve activity in normal h;mans and patients with heart failure: evidence from direct microneurographic recordings. J Am Co11 Cardiol 1990; l&1125-34. 13. Starkey IR, de Bono DP. Echocardiographic identification of right-sided cardiac intracavitary tbromboembolus in massive pulmonary embolism. Circulation 1982;66:1323-5. 14. Kumar A, Rose JS, Reid CL, Perera PFN, Michael TAD, Chandraratna PAN. Echocardiographic demonstration of pulmonary embolism as it evolves through the right heart chambers. Am J Med 1985;79:538-40. 15. Cameron J, Pohlner PG, Stafford EG, O’Brien MF, Bett JHN, Murphy AL. Right heart thrombus: recognition, diagnosis and management. J Am Co11Cardiol 1985;5:1239-43. 16. Reeder GS, Lengyel M, Tajik AJ, Seward JB, Smith HC, Danielson GK. Mural thrombus in left ventricular aneurysm: incidence, role of angiography, and relation between anticoagulation and embolization. Mayo Clin Proc 1981;56:7781. 17. Stratton JR, Ritchie JL, Hammermeister KE, Kennedy JW, Hamilton GW. Detection of left ventricular thrombi with radionuclide angiography. Am J Cardiol 1981;48:565-72. 18. Visser CA, Kan G, David GK, Lie KI, Durrer D. Two-dimensional echocardiography in the diagnosis of left ventricular thrombus: a prospective study of 67 patients with anatomic validation. Chest 1983:83:228-32. 19. Mugge A, Daniel WG, ‘Haverich A, Lichtlen PR. Diagnosis of noninfective cardiac mass lesions by two-dimensional echocardiography: comparison of the transthoracic and transesophageal approaches. Circulation 1991;83:70-8. 20. Fiegenbaum H. Echocardiography. Philadelphia: Lea & Febinger, 1986:157-8. 21. Reiter S, Rumberger J, Feiring A, Stanford W, Marcus M. Precision of measurementa of right and left ventricular volume by tine computed tomography. Circulation 1986;74:890900. 22. Hajduczok Z, Weiss RM, Stanford W, Marcus ML. Determination of right ventricular mass in humans and dogs with ultrafast computed tomography. Circulation 1990;82:202-12. 23. Marzullo P, Oren RM, Marcassa C, Stanford W, Marcus ML. Simultaneous noninvasive characterization of biventricdar systolic and diastolic function using fast computed tomography [Abstract]. Eur Heart J 1990;11:98A. 24. Stanford W, Rooholamini SA, Galvin JR. Assessment of intracardiac masses and extracardiac abnormalities by ultrafast computed tomography. In: Marcus ML, Schelbert HR, Skorton DJ, Wolf GL, eds. Cardiac imaging. Philadelphia: WB Saunders Co, 1991. 25. Wisenberg G. Evaluation of ischemic heart disease by nuclear magnetic resonance. In: Marcus ML, Schelbert HR, Skorton DJ, Wolf GL, eds. Cardiac imaging. Philadelphia: WB Saunders Co, 1991.

Brief Communications

Myocardial

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injury in electrocution

Nicholas Xenopoulos, MD,B Assad Movahed, MD, Page Hudson, MD,b and William C. Reeves, MD.* Greenville, N.C.

Electrical injury of the myocardium has been described in several settings. Lightning injury, one of the first forms ever encountered, is known to cause life-threatening arrhythmias, transient myocardial ischemia, and electrocardiographic plus enzymatic changes simulating myocardial infarcti0n.l High voltage electrical injury produces similar manifestations, and even direct-current cardioversion and electroconvulsive therapy have occasionally been associated with electrocardiographic changes and myocardial injury.l Low voltage 60 Hz alternating current (AC) has been increasingly reported to be the cause of various forms of myocardial injury. 2-4 Although the echocardiographic findings in patients with AC electrical injury have been described39 4 and the correlation of echocardiographic and angiographic findings has been attempted,2*3 there is no report correlating echocardiographic with autopsy findings. This latter omission is important because of the pathogenetic implications of our findings. A 19-year-old man was admitted to the hospital after sustaining an electrical injury (110 V AC) while he was installing a hoist. The patient was found on an aluminum ladder with his back on the sheet metal wall of a tobacco barn, in a tetanic contraction. He was discovered by a coworker who witnessed the electrocution. The electrical supply was disconnected and the patient was caught in the process of falling from the ladder. The rescue squad arrived within 5 minutes. While he was being transferred to the local primary care facility, he experienced cardiac arrest and basic life support was provided. Upon his arrival at the facility 10 minutes later, he was in ventricular fibrillation. He was intubated and received resuscitation including intravenous atropine, epinephrine, and three cycles of defibrillation of 200, 300, and 360 joules, respectively. His heart reverted to sinus rhythm with a palpable pulse 30 minutes after his cardiac arrest. A 12-lead electrocardiogram (ECG) recorded after resuscitation suggested massive hyperacute anterior myocardial injury (Fig. 1). He was transferred to the Intensive Care Unit under mechanical ventilation, and received lidocaine and dopamine intravenously. Peripheral pulses were present, pupillary reflexes were intact, but he did not respond to painful stimuli. During his stay in the unit, the patient had a generalized tonic-clonic seizure and was started on phenytoin. Dopamine infusion was tapered

From the Section

of Cardiology,B Department of Medicine; and Section of Forensic Pathology, b Department of Pathology and Laboratory Medicine, East Carolina University School of Medicine. Reprint requests: Assad Movahed, MD, Section of Cardiology, Department of Medicine, School of Medicine, East Carolina University, Greenville, NC 21850-4354. 414132456

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Fig.

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1. Serial electrocardiographic changesshowingrapid resolution of injury current in the precordial

leads.

and wasfinally discontinued within 8 hours. He wastransferred to our institution for further management. On admission,the patient had a heart rate of 116beats/ min and a systemic arterial pressureof 96/60 mm Hg. He was intubated and was diaphoretic and flaccid, and was unresponsiveto pain. His pupils were 2 to 3 mm and reactive. His heart examination did not reveal a gallop, rub, or murmur. There wasan obvious entry site of electrical current on the left shoulder and a smaller, probable exit site on the right foot. There were multiple defibrillation burns to the left upper chest. His abdomen was rigid with no bowel sounds.On admission,a 12-leadECG revealed sinus tachycardia with marked resolution of the ST segmentelevation comparedwith the ECG recorded 12 hours earlier (Fig. 1). Chemistry revealedserumpotassiumof 2.9 mEq/L, creatinine of 2 mg/dl, calcium of 7.6 mg/dl, lactate dehydrogenaseof 4340III/L (normal 100to 225IU/L), serum glutamic oxaloacetic transaminaseof 1547IU/L (normal 7 to 40 IU/L), and creatine phosphokinaseof 50,400 IU/L (normal 30 to 225 II-l/L) with 100% isoenzyme MM. A computed tomography (CT) scan of the head showeddiffuse cerebral edema; however, there was no evidence of herniation. A CT scanof the abdomenshowedileus with a large amount of air and fluid in multiple small bowelloops, colon, and stomach. Fluid was present in the abdominal cavity, particularly on the right side. (No fluid or organ injury waspresent at autopsy). A two-dimensional echocardiogram performed the following day showeda mildly dilated left ventricle with hypokinetic to akinetic regionsincluding the septum, anterior wall, and apex. The left ventricular ejection fraction wasan estimated 35%. (Fig. 2, A and B). No significant pericardial effusion was present. The patient remainedunresponsiveto stimuli. Pulmonary arterial pressures measured via a Swan-Ganz catheter (Baxter Healthcare Corp., Edwards Division, Santa Ana, Calif.) were 35/28 mm Hg, with pulmonary capillary wedge pressureof 28 mm Hg and a cardiac index of 2.2 L/min/m’. The chest x-ray film showedchangesinterpreted as pulmonary congestion. On the third day, the patient devel-

oped ventricular tachycardia followed by ventricular fibrillation. Prolonged cardiopulmonary resuscitation lasted 30 minutes and was unsuccessful.The patient received 3 cycles of defibrillation of 360joules each. An autopsy was subsequentlyperformed. The macroscopicexamination of the heart showeda small amount of clear fluid in the pericardial sac.The epicardial surfaceswere clean and glistening. Coronary arteries pursuedtheir usualcoursesand had patent lumens. Only minimal traces of atheroma were encountered. The valves appeared intact, and the leaflets were unremarkable except that the tricuspid and mitral leaflets seemedslightly edematous, particularly at their distal margins. There were no intracardiac shunts. The muscle thicknesseswere well within normal limits. The openedheart revealed distinct hemorrhagein the myocardium, in the anterior septal and anterior free wall area.This changeincluded an apical patch approximately 3 cm in diameter. There wasslight sparing beneath the epicardium. The papillary musclesopened longitudinally showedextensive diffuse hemorrhagein the distal third. The basilar posterior left ventricular wall in the primary distribution of the right coronary artery was similarly affected. Widespread contraction band necrosis, myolysis, coagulative changes,lossof striations, and nuclear disappearancewere microscopicfeatures. The areasthat appeared mottled or dark to the naked eyeshowedabundant diffuse free blood in the interstitium. Occasionally this changewasbordered by polymorphonuclear leukocytes. Muscle injury and slight hemorrhagewerenoted in the areaof the conduction track. The right ventricular wall wasessentiallyspared.The malfunctioning areas as demonstrated via echocardiogram correspondedclosely with reperfusion changesrevealed at autopsy. Several cross sections of the coronary arteries were examined microscopically. There wasslight vacuolation between the endothelial layer and above the internal elastic membrane. No denudation of endothelium was seen,and the changesnoted were not above baselineconditions. The nature of electrical myocardial injury is intriguing.

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Fig. 2. Two-dimensional echocardiograms(A) and diagrammatic representation (6) of parasternal longaxis views in end diastole (left panels) and end systole (right panel) showingdilated left ventricle with hypokinetic to kinetic septum and apex.

The rarity of the event and the paucity of relevant experimental data make the task of revealing the pathogenetic mechanismsof electrical myocardial injury difficult. Careful examination and correlation of clinical and pathologic data may provide useful information, however. The most likely possiblefactor of myocardial injury in our patient appearsto be the AC electrical injury and lesslikely the initial cardiopulmonary resuscitation and DC cardioversion. Prolonged resuscitation in adults can produce myocardial injury, characterized by focal hemorrhage,contraction band necrosis, and coagulation necrosis.5However, thesechangesare concentrated in the subepicardium, the arearelatively sparedin our patient. ST segmentelevation’ and modest left ventricular dysfunction in animals61 7have been described, but DC shock has only minor functional consequenceswhen applied to normal hearts.’ The pathophysiologic mechanismof electrical myocardial injury is uncertain. Myocardial injury may be caused directly by conversion of electrical energy into heart, or indirectly by compromisingmyocardial perfusion. Changesof intramyocardial temperature during direct application of DC

countershock to the heart of anesthetized dogshave been described6;however, this theory doesnot explain the sparing of the right ventricular wall and subepicardiumin our patient. Typical thermal injury tissue changeswere not present elsewherein the body except at the entrance and exit sites, and to a lesserdegree,in the pectoral skin and superficial pectoral musculature at the defibrillation sites. The subepicardiumand right ventricle8 are more resistant to ischemiathan are the deeper and subendocardial layers of the left ventricle. It is tempting to speculatethat the underlying pathophysiology of injury in our patient was AC electric injury that induced transient ischemiaof the myocardium. This is further supported by the striking resemblanceof the naked eye and microscopic findings to those found in myocardial reperfusion injury. Indeed, microvascular hemorrhage, contraction band necrosis, and loss of striations are recognized pathology in reperfused myocardium after transient obstruction of the coronary circulation.g Contraction band necrosisis not pathognomanic of reperfusion injury. It has been described in patients who received cardiac resuscitation, and is most

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prominent in the subepicardial myocardium.5 Examination of the coronariesat autopsy excluded the presenceof thrombus in our patient and no overt endothelial damage or intimal denudation wasfound on light microscopy. Thus the possibility of a thrombus transiently occluding a coronary artery is remote. This is in agreementwith the finding of normal angiographicresults in two previous reports of patients who sustainedelectrical injury.2v 3 The resemblance between catecholamine-induced and reperfusion myocardial injury is striking.lO However, the distribution of catecholamine-mediatedinjury is random and patchy throughout the myocardium5and is not consistentwith the sparing of the right ventricular wall and epicardium seen in our patient. Therefore although possiblecatecholaminemediated injury can not be excluded, it was most likely minor. It seemsthat an electrogenic membrane mechanismof humancoronary smoothmuscleactivation exists.” Thus it could be theorized that electrical injury perceived as an electrical stimulus may produce coronary spasmand myocardial ischemia.Alternatively, prolonged electrical stimulation may result in inhibition of endothelium-dependent relaxation through the generation of oxygen radicals.i2 Our patient succumbedafter the development of irreversible ventricular fibrillation. There are similar reports about the delayed onset of lethal ventricular arrhythmias in the setting of electrical injury.’ Jensen et al1 detected increasednumbersof Na, K-pumps in endomyocardial biopsy specimensin two of three patients with ventricular tachycardia after electrical injury. An increased Na, Kpump concentration may be associated with transient localized changesof the transmembranepotential and thus could be important for the development of arrhythmias. The heterogeneity of necrotic and viable cells with reperfusion may make these patients more prone to the development of complex ventricular arrhythmias. In conclusion, the similarity of the myocardial injury in our patient to reperfusion injury as well as the absence of coronary thrombus or significant atherosclerosison autopsy makes coronary spasma likely causeof myocardial necrosis in electrocution. REFERENCES

1. Jensen PJ, Thomsen PEB, Bagger JP, et al. Electrical injury causing ventricular arrhythmias. Br Heart J 1987;57:279-83. 2. Walton AS, Harper RW, Coggins GL. Myocardial infarction after electrocution. Med J Aust 1988;148:365-7. 3. Ku CS, Lin SL, Hsia TL, et al. Myocardial damage associated with electrical injury. AM HEART J 1989;118:621-3. 4. Homma S, Gillam LD, Weyman AE. Echocardiographic observations in survivors of acute electrical injury. Chest 1990; 97:103-5. 5. Karch SB. Resuscitation-induced myocardial necrosis. Am J Med Path01 1987;8:3-8. 6. Doherty PW, McLaughlin PR, Billingham M, et al. Cardiac damage produced by DC countershock applied to the heart. Am J Cardiol 1979;43:225-32. 7. Ditchey RV, LeWinter MM. Effects of direct-current electrical shocks on systolicanddiastolicLV function in dogs.AM HEART J 1983;105:727-31. 8. Kloner RA, Ellis SG, Carlson NV, Braunwald E. Coronary reperfusion for the treatment of acute myocardial infarction:

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postischemic ventricular dysfunction. Cardiology 1983;70:23346.

9. Malsuda M, Fujiwara H, Onodera T, et al. Quantitative analysis of infarct size, contraction band necrosis, and coagulation necrosis in human autopsied hearts with acute myocardial infarction after treatment with selective intracoronary thrombolysis. Circulation 1987;76:981-90. 10. Rona G. Catecholamine cardiotoxicity. J Mol Cell Cardiol 1985;17:291-306. 11. Vedernikov YP. Mechanisms of coronary snasm of isolated

humanepicardialcoronarysegments excised3 to 5 hoursaf12.

ter sudden death. J Am Co11 Cardiol 1986;8:42A-SA. Marshall JJ, Kontos HA. Endothelium-derived relaxing factors a perspective from in vivo data. Hypertension 1990;16:37186.

Cardiac rhabdomyomas causing supraventricular and lethal ventricular arrhythmias in an infant Christopher L. Case,MD, Paul C. Gillette, MD, and Fred A. Crawford, MD. Charleston, S.C.

The clinical spectrum of cardiac rhabdomyomas in children is diverse. The tumors may be asymptomatic or may causeseriousclinical symptoms as a result of myocardial depression,inflow or outflow obstruction of cardiac output, or arrhythmias.lp2 Rhythm disturbances secondary to these tumors include ventricular preexcitation syndrome, supraventricular tachycardia (SVT), ventricular tachycardia (VT), and atrioventricular b1ock.t 4 Since these rhabdomyomas may be multiple, there is a potential for complex and/or multiple cardiac arrhythmias5 We herein report a caseof a g-month-old white female infant with multiple cardiac rhabdomyomaswho originally presented with ventricular preexcitation with SVT and subsequently developedmalignant ventricular arrhythmias. Despite aggressive pharmacologic and nonpharmacologic management of these rhythm disturbances,this child had a sudden cardiac death, illustrating the potential lethal nature of this condition. The patient wasborn to a 23-year-old gravida 3 para 1 white woman. The infant’s prenatal history was complicated by a fetal bradycardia that was assessed by a fetal echocardiogramat 37 weeks.This examination revealed a normal cardiac structure with a slight cardiomegaly, and a small pericardial effusion. The infant wasdelivered by cesareansection at 40 weekswith a birth weight of 3655gm. Apgar scoreswere 7 and 9. An echocardiogramat that time showeda tumor-like structure on the anterior mitral leaflet and ventricular preactivation on the surfaceelectrocardiogram (Fig. 1). The child had no cardiac symptomsasa neFrom South Carolina Children’s Heart Center, Medical University Carolina. Reprint requests: Christopher L. Case, MD, Pediatric Cardiology, ley Ave., Charleston, SC 29425. 414/32457

of South 171 Ash-