Appearances Can Be Deceptive

Appearances Can Be Deceptive

ECG IMAGE OF THE MONTH Julia H. Indik, MD, PhD, Section Editor Appearances Can Be Deceptive Miguel Carrascosa Porras, MD,a Francisco Pascual Velasco,...

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ECG IMAGE OF THE MONTH Julia H. Indik, MD, PhD, Section Editor

Appearances Can Be Deceptive Miguel Carrascosa Porras, MD,a Francisco Pascual Velasco, MD,a Rubén Gómez Izquierdo, MDb a

Internal Medicine and bCardiology Sections, Internal Medicine Department, Hospital of Laredo, Laredo, Cantabria, Spain.

PRESENTATION A frightful ECG tracing suggested a serious cardiac event, but as it turned out, the abnormalities were not spurred by heart disease. A 60-year-old man was found on the floor at home, confused and with weakness of the right arm and leg. He was a heavy drinker and smoker, and he had undergone an aortobifemoral bypass many years earlier. However, he had no history of arterial hypertension or coronary artery disease, and he took no medications. Before this episode, the patient had been active without limited exercise tolerance.

ASSESSMENT On admission to the emergency department, the patient was dysarthric but fully oriented, and he denied other symptoms. His blood pressure was 176/86 mm Hg, and his heart rate was 64 beats per minute. He had hemiparesis involving the left arm, the left leg, and the left side of the face. His heart rhythm was regular, and there were no murmurs or rubs. The physical examination was otherwise unremarkable. A chest radiograph was normal, and noncontrast computed tomography imaging of the brain showed a right temporoparietal hypodensity. The ECG ordered on admission displayed a sinus rhythm of 58 beats per minute and extremely wide, deeply inverted, T waves. These were most noticeable in leads V3-V6 and, to a lesser extent, in leads II, III, and AVF (Figure 1). QT and QTc intervals were prolonged to 600 msec and 590 msec, respectively. Initially, the patient was diagnosed with acute infarction of the right middle cerebral-artery. The striking ECG abnormalities led the attending physician to hypothesize that inferior and lateral wall ischemia might be present as well. Yet, the patient’s serum troponin T concentration was repeatedly normal, and Doppler echocardiography revealed Conflicts of Interest: All of authors confirm that there are no conflicts of interest. The corresponding author is Miguel Carrascosa Porras, MD, Internal Medicine Section, Hospital of Laredo, Avda Derechos Humanos s/n, 39770 Laredo, Cantabria, Spain. E-mail address: [email protected]

0002-9343/$ -see front matter © 2009 Elsevier Inc. All rights reserved. doi:10.1016/j.amjmed.2008.06.015

no alterations; specifically, imaging showed a structurally normal heart and normal wall motion of the left ventricle.

DIAGNOSIS Our patient’s ECG abnormalities were induced by his cerebral infarction. This case emphasizes the autonomic nervous system’s effect on the heart; in particular, its capacity for injuring the heart.1 While ECG abnormalities like those seen in our patient have been described for decades, understanding the mechanisms of the aberrations has been difficult. In more recent years, takotsubo cardiomyopathy (so-called apical ballooning syndrome), a cardiac disorder with its roots in the autonomic nervous system and sympathetic-parasympathetic balance, has been studied more extensively.1,2 Several types of ECG changes are seen in the setting of neurological diseases, but arrhythmias and repolarization abnormalities are described most frequently.1,3 Of repolarization abnormalities, long QT intervals, abnormal T waves, and ST segment alterations have been reported, as have irregular Q waves and U waves.3,4 New T-wave abnormalities appear in about 15% of patients with acute stroke, even in the absence of primary ischemic heart disease.5 Although deeply symmetrical T-wave inversions are often called cerebral T waves, some authors have also applied the term to tall, peaked, T waves seen in some patients.6 Although cerebral T waves were originally described in patients with subarachnoid hemorrhage, later reports also detailed such findings in patients who had an ischemic stroke or transient ischemic attacks.7,8 Neurogenic repolarization abnormalities occur in patients with other neurologic diseases, as well, including neoplasms, infections, epilepsy, psychiatric disorders, and alcohol withdrawal syndrome.3,4 It seems likely that neurogenic repolarization abnormalities reflect centrally-mediated release of catecholamines due to hypothalamic hypoperfusion, and subsequent myocardial and subendocardial injury.1,9 In fact, cardiac myofibrillar degeneration or necrosis is usually observed in patients who died from stroke, and it is histologically identical to the cardiac lesions caused by catecholamine infusion, stress (human stress cardiomyopathy1), nervous sys-

Porras et al

Appearances Can Be Deceptive

Figure 1


This ECG was obtained when the patient presented at the hospital.

tem stimulation, and myocardial reperfusion.4 This myofibrillar necrosis occurs near intracardiac nerve terminals, and it is not in the macrovascular distribution typically seen in coronary artery disease patients.4 Moreover, the lesion seen in stroke patients differs from the necrosis seen in coronary disease because it is detected within a few minutes of the onset of stroke symptoms.4

MANAGEMENT After intracranial hemorrhage was ruled out with computed tomography of the brain, treatment with aspirin, 300 mg per day, was started. However, it was discontinued 4 days later because hemorrhagic transformation of the infarct occurred. An ECG obtained on the 17th hospital day showed a sinus rhythm of 76 beats per minute and QT and QTc intervals of 420 msec and 473 msec, respectively (Figure 2). The patient

Figure 2

did not report dyspnea or pain of the chest or limbs at any point in his hospital stay. On the 18th hospital day, the patient was discharged with no significant motor deficits. At that time, when it was clear no further risk for bleeding existed, he was instructed to resume a regimen of aspirin, 300 mg per day. When last seen 3 months after discharge, the patient was well. None of the marked abnormalities seen on the original ECG were present. The follow-up ECG revealed a sinus rhythm of 75 beats per minute, the QT interval was 400 msec, and the QTc interval was 447 msec (Figure 3). A repeated Doppler echocardiographic study was also normal. In summary, clinicians should not forget the brain-heart connection and the potential of stroke and other neurological diseases to produce cardiac pathologies.1 Thus, patients

On the 17th hospital day, a second ECG was obtained.


The American Journal of Medicine, Vol 122, No 3, March 2009

Figure 3

Three months after discharge, no repolarization abnormalities were evident.

with stroke should have repeated ECGs and be monitored for repolarization abnormalities and arrhythmias.

References 1. Samuels MA. The brain-heart connection. Circulation. 2007;116:77-84. 2. Tsuchihashi K, Ueshima K, Uchida T, et al. Transient left ventricular apical ballooning without coronary artery stenosis: a novel heart syndrome mimicking acute myocardial infarction. Angina Pectoris-Myocardial Infarction Investigations in Japan. J Am Coll Cardiol. 2001;38: 11-18. 3. Strauss WE, Samuels MA. Electrocardiographic changes associated with neurologic events. Chest. 1994;106:1316-1317. 4. Samuels MA. Electrocardiographic manifestations of neurologic disease. Sem Neurol. 1984;4:453-458.

5. Lavy S, Yaar I, Melamed E, Stern S. The effect of acute stroke on cardiac functions as observed in an intensive stroke care unit. Stroke. 1974;5:775-780. 6. Burch GE, Meyers R, Abildskov JA. A new electrocardiographic pattern observed in cerebrovascular accidents. Circulation. 1954;9:719723. 7. Goldstein DS. The electrocardiogram in stroke: relationship to pathophysiological type and comparison with prior tracings. Stroke. 1979;10: 253-259. 8. Dimant J, Grob D. Electrocardiographic changes and myocardial damage in patients with acute cerebrovascular accidents. Stroke. 1977;8: 448-455. 9. Chalela JA, Smith TL. Cardiac complications of stroke. Available at:⫽cva_dise/ 18150. Accessed on May 27, 2008.