A CASE OF SUBARACHNOID HEMORRHAGE WITH PERSISTENT SHOCK AND TRANSIENT ST ELEVATION SIMULATING ACUTE MYOCARDIAL INFARCTION

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1 A CASE OF SUBARACHNOID HEMORRHAGE WITH PERSISTENT SHOCK AND TRANSIENT ST ELEVATION SIMULATING ACUTE MYOCARDIAL INFARCTION Hsiang-Chun Lee, Hsueh-Wei Yen, Ye-Hsu Lu, Kun-Tai Lee, Wen-Chol Voon, Wen-Ter Lai, and Sheng-Hsiung Sheu Division of Cardiology, Department of Internal Medicine, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan. Electrocardiographic changes in neurovascular disease are not rare. Patients with subarachnoid hemorrhage have electrocardiographic (ECG) abnormalities that may mimic ischemic heart disease and acute myocardial infarction. Outflow of catecholamines in the early stage of subarachnoid hemorrhage contributes to elevated blood pressure in most patients. Hypotension is a rare presentation in subarachnoid hemorrhage. We report a case of subarachnoid hemorrhage with transient ST elevation and intractable shock simulating acute myocardial infarction, and review the mechanism of ECG changes in subarachnoid hemorrhage. Key Words: subarachnoid hemorrhage, ST elevation, shock, acute myocardial infarction (Kaohsiung J Med Sci 2004;20:452 6) Electrocardiographic (ECG) changes in neurovascular disease may mimic ischemic heart disease and even acute myocardial infarction (MI). Approximately 25% of patients with subarachnoid hemorrhage (SAH) have ECG abnormalities consistent with myocardial ischemia and MI, including transient ST-segment elevation or depression, T- wave inversion, QT prolongation, abnormal Q wave, and various arrhythmias. A variety of mechanisms have been proposed to explain the central nervous system (CNS)- mediated ECG abnormalities. Due to overflow of catecholamines in the early stage of disease, most patients with SAH may present with high blood pressure. Hypotension has been reported in fewer than 3% of cases. Here, we present a case of SAH with transient ST-segment elevation and intractable vasogenic shock marked by low peripheral resistance. Received: May 3, 2004 Accepted: June 30, 2004 Address correspondence and reprint requests to: Dr. Hsueh-Wei Yen, Division of Cardiology, Department of Internal Medicine, Kaohsiung Medical University Hospital, 100 Shih-Chuan 1 st Road, Kaohsiung 807, Taiwan. hweyen@cc.kmu.edu.tw 452 CASE PRESENTATION A 77-year-old female lost consciousness suddenly as she was having dinner with her husband. According to her husband, she had complained of dizziness and headache but there was no chest pain. Her history indicated that she had hypertension and had been receiving regular medication from a local community hospital for years. She was suspected but not proven to have angina pectoris 3 years previously. However, she did not take an anti-ischemic agent. She had been quite well before this catastrophic event. On the way to our hospital, she was found to be breathless and without pulse. Emergency services personnel performed chest compression in the ambulance. She arrived in the emergency room about 20 minutes after loss of consciousness. ECG monitoring showed cardiac arrest. The standard procedure for advanced cardiovascular life support was immediately instituted. A total of 10 mg epinephrine was administered during cardiopulmonary resuscitation. After about 10 minutes of resuscitation, her blood pressure reached 226/177 mmhg and her pulse rate was around 136 bpm. However, the blood pressure was not maintained. Dopamine infusion was set up and titrated quickly. Unfortu Elsevier. All rights reserved.

2 Subarachnoid hemorrhage simulating acute MI nately, both pupils remained dilated and fixed. The patient was in a comatose state. The first 12-lead ECG revealed atrial tachycardia and ST-segment elevation in leads I, avl, and V2 V6 with reciprocal ST-segment depression in leads II, III, avf, and V1 (Figure 1A). Subsequent biochemical tests showed serum creatinine µmol/l, sodium 141 mmol/l, potassium 3.3 mmol/l, aspartate aminotransferase 43 U/L, alanine aminotransferase 21 U/L, creatine phosphokinase (CPK) 46 U/L, and troponin-t (TnT) less than 0.01 µg/l. On admission to the cardiac care unit, the patient s blood pressure was around 80/50 mmhg and pulse rate was 120 bpm, even with 15 µg/kg/minute of dopamine infusion. Eighteen hours after the onset of symptoms, ECG showed deep T-wave inversion in leads I, II, III, avf, and V3 V6 (Figure 1B). Serial measurements of serum cardiac enzymes were elevated, peaking at 6 hours after onset: CPK 205 U/L, creatinine kinase, myocardial bound (CK- MB) 21.2 U/L, and TnT 1.68 µg/l. Owing to persistent hypotension, a Swan-Ganz catheter was inserted to monitor the patient s hemodynamic parameters. Cardiac output was 5.90 L/minute, cardiac index was 3.66 L/minute/m 2, pulmonary artery wedge pressure was 12 mmhg, and systemic vascular resistance index was 1,560 dyne.sec.cm 5 /m 2. A The systemic vascular resistance index decreased to 769 dyne.sec.cm 5 /m 2 13 hours later. Since no evidence of systemic infection or sepsis was found, vasogenic shock was most likely. Computerized tomography (CT) scan of the brain showed SAH with intraventricular extension and diffuse brain edema (Figure 2). Although norepinephrine was administered, shock persisted. Due to her poor general condition, no surgical intervention was possible. Three days after the onset of symptoms, the patient was pronounced dead due to persistent shock and irreversible brainstem death. DISCUSSION ECG abnormalities in patients with SAH are variable, including ST-segment elevation or depression, T-wave inversion, pathologic Q wave, QT prolongation, and variable arrhythmias [1 5]. The cause of transient ST-segment elevation accompanying SAH remains unclear. Stimulation of the anterior hypothalamus produces ST-segment elevation and deepening of T waves [2]. Ischemic stimulation of the posterior hypothalamus after SAH seems to be responsible for an abrupt increase in sympathetic tone. In experiments in animals and humans, increased serum catecholamine levels have been associated with ECG changes similar to those induced by SAH. B Figure 1. (A) First electrocardiogram (ECG) obtained after successful resuscitation: atrial tachycardia and ST-segment elevation in leads I, avl, and V2 V6 with reciprocal ST-segment depression in leads II, III, avf, and V1. (B) Follow-up ECG 18 hours after the onset of symptoms: deep T-wave inversion in leads I, II, III, avf and V3 V6. Figure 2. Computerized tomography scan of the brain: subarachnoid hemorrhage with intraventricular extension and diffuse brain edema. 453

3 ECG abnormalities induced by SAH may reflect damage to the myocardium. Sakamoto et al reported a case of lethal SAH with postmortem histologic examination revealing multiple foci of myocytolysis with loss of myocardial cells and collapse of stroma, and a scant mononuclear cellular infiltrate [6]. There was no significant coronary artery stenosis or MI. Coronary artery stenosis is not necessarily found in patients with SAH [6,7]. Coronary artery spasm is thought to correlate with the clinical course [8,9]. Moreover, myocardial dysfunction is found in patients with SAH without evidence of coronary artery stenosis [6,7,8]. Myocardial changes with disruption of the cell architecture and disappearance of cross striations are exhibited on electron microscopic examinations in experimental SAH animals [10]. The change in cardiac function should be related to myocardial cell injuries induced by SAH. Regional left ventricular wall motion abnormalities have also been identified in an experimental SAH model, but no evidence suggested significant myocardial hypoperfusion or coronary artery disease [11]. The case presented here shows extensive ECG changes mimicking the hyperacute phase of MI with transient STsegment elevation followed by deep T-wave inversion. However, we do not consider that the patient had suffered a massive MI. First, no chest discomfort was stated to her family before her loss of consciousness. Second, cardiac enzymes rose atypically and were incompatible with extensive myocardial necrosis. Third, cardiac enzymes increased after prolonged resuscitation. Therefore, acute MI was least likely to be the cause of this event. The prominent ECG abnormalities could be secondary to CNS disease. Elevation of myocardial isoenzymes after SAH provides further evidence of myocardial damage. Elevated levels of CK-MB are found in about 43% of patients with SAH [12] and are correlated with typical ECG changes [13]. The brain isoenzyme of CPK is frequently found in severe head trauma, cerebral infarct, or meningitis, but is rarely found in SAH [14]. A typical rise and fall in serum cardiac markers with clinical symptoms or ECG change is important in the diagnosis of acute MI. Cardiac marker measurements may also be useful for a rough quantification of infarct size [15]. This patient had mild elevations of CPK, CK-MB, and cardiac-specific TnT, which could be caused by SAH-induced myocardial injury but not by massive acute MI. Most patients with SAH present with hypertension due to increased sympathetic tone and a sudden surge of 454 catecholamines. Hypotension is rarely seen in SAH [16]. Such hypotension may result from cardiac dysfunction or ominous complications of brainstem damage. Impaired adrenal blood flow after prolonged massive sympathetic discharge has been reported in SAH [17]. In one case of amphetamine abuse, the patient suffered from SAH and unusual hypotension [18]. Our patient did not have a record of drug abuse. Although adrenal insufficiency or failure was not checked, it could not have been the major cause of persistent hypotension. Invasive hemodynamic data revealed normal cardiac output and normal pulmonary artery wedge pressure that excluded severe myocardial damage. Interestingly, this patient did not have clinical evidence of sepsis, anaphylaxis, or any adverse drug reaction. Hemodynamic monitoring data showed a persistently low systemic vascular resistance index, despite treatment with high doses of sympathomimetic agents. As such, we conclude that abnormal vascular motor tone due to vasomotor center dysfunction may be the rationale for her hypotension. CONCLUSION SAH can induce ECG changes simulating acute MI and also present with uncommon complications such as refractory shock. If patients with ST-segment elevation have altered consciousness or any new neurologic deficit, it is recommended that a brain CT should be performed prior to administration of thrombolytic therapy, an essential therapeutic regimen for acute MI. REFERENCES 1. Zaroff JG, Rordorf GA, Newell JB, et al. Cardiac outcome in patients with subarachnoid hemorrhage and electrocardiographic abnormalities. Neurosurgery 1999;44: Davis TP, Alexander J, Lesch M. Electrocardiographic changes associated with acute cerebrovascular disease: a clinical review. Prog Cardiovasc Dis 1993;36: Brouwers PJ, Wijdicks EF, Hasan D, et al. Serial electrocardiographic recordings in aneurysmal subarachnoid hemorrhage. Stroke 1989;20: Melin J, Fogelholm R. Electrocardiographic findings in subarachnoid hemorrhage. Acta Med Scand 1983;213: Carruth JE, Silverman ME. Torsade de pointe atypical ventricular tachycardia complicating subarachnoid hemorrhage. Chest 1980;78: Sakamoto H, Nishimura H, Imataka K, et al. Abnormal Q wave, ST-segment elevation, T-wave inversion, and widespread focal myocytolysis associated with subarachnoid hemorrhage. Jpn Circ J 1996;60:254 7.

4 Subarachnoid hemorrhage simulating acute MI 7. Nakamura Y, Kaseno K, Kubo T. Transient ST-segment elevation in subarachnoid hemorrhage. J Electrocardiol 1989;22: Dominguez H, Torp-Pedersen C. Subarachnoid hemorrhage with transient myocardial injury and normal coronary arteries. Scand Cardiovasc J 1999;33: Yuki K, Konama Y, Onda J, et al. Coronary vasospasm following subarachnoid hemorrhage as a case of stunned myocardium. J Neurosurg 1991;75: Elrifia AM, Bailes JE, Shih SR, et al. Characterization of cardiac effects of acute subarachnoid hemorrhage in dogs. Stroke 1996;27: Zaroff JG, Rordorf GA, Titus JS, et al. Regional myocardial perfusion after experimental subarachnoid hemorrhage. Stroke 2000;31: Fabinyi G, Hunt D, McKinley L. Myocardial creatine kinase isoenzyme in serum after subarachnoid hemorrhage. J Neurol Neurosurg Psychiatry 1977;40: Kettunen P. Subarachnoid hemorrhage and acute heart injury. Clin Chim Acta 1983;134: Rudehill A, Gordon E, Sundqvist K, et al. A study of ECG abnormalities and myocardial specific enzymes in patients with subarachnoid hemorrhage. Acta Anaesth Scand 1982;26: Murray C, Alpert JS. Diagnosis of acute myocardial infarction. Curr Opin Cardiol 1994;9: Kassell NF, Torner JC, Haley EC Jr, et al. The International Cooperative Study on the Timing of Aneurysm Surgery. Part 1: Overall management results. J Neurosurg 1990;73: Shigeno T, Fritschka E, Shigeno S, et al. Neurogenic shock syndrome after experimental subarachnoid hemorrhage in cats. Adv Shock Res 1982;8: Gipe B, McFarland D. Subarachnoid hemorrhage: an unusual presentation of shock. Ann Emerg Med 1995;26:

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