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Myocardial stunning after cerebral infarction
International Journal of Cardiology 58 (1997) 308–311
Myocardial stunning after cerebral infarction Tzung-Dau Wang, Chau-Chung Wu, Yuan-Teh Lee* Department of Internal Medicine, National Taiwan University, Hospital, 7, Chung-Shan South Road, Taipei, 10016, Taiwan, ROC Received 23 August 1996; accepted 6 November 1996
Abstract Myocardial stunning has not been described in patients with cerebrovascular accidents. We present a patient in whom inferior wall hypokinesis, ST-segment elevations and Q waves developed after acute right hemisphere ischemic stroke. Total recovery ensued within 5 days. Coronary vasospasm induced by stroke-related sympathetic surge might be the cause of this cardiac event. Copyright 1997 Elsevier Science Ireland Ltd. Keywords: Cerebral infarction; Electrocardiography; Autonomic nervous system
1. Introduction
2. Case report
Myocardial stunning, a prolonged but reversible myocardial contractile dysfunction, has been demonstrated clearly in patients with coronary occlusion who underwent early reperfusion, either by thrombolysis or by operative treatment, and in patients with brief episodes of ischemia caused by coronary vasospasm [1]. However, myocardial stunning after cerebral infarction has never been described before. We herein present a patient in whom myocardial stunning and the electrocardiographic (ECG) changes of reversible pathologic Q waves developed after acute right hemisphere ischemic stroke.
A 65-year-old woman was admitted because of fever, cough, and dyspnea for 5 days. Two months prior to admission, she suffered from an episode of chest tightness and had then been treated with both isosorbide dinitrate (10 mg) and ticlopidine (100 mg) three times a day. There was no other history of cardiac disease. On admission, the patient was febrile, dyspneic, and drowsy. Blood pressure was 110 / 60 mmHg. Physical examination revealed nothing unusual except for a carbuncle on the right flank. The hemogram gave a leukocyte count of 400310 6 / l with 100% lymphocytes. A chest radiograph showed a pneumonic patch over the right upper lobe. The ECG on admission (Fig. 1A) showed sinus tachycardia and non-specific ST and T wave changes. Blood cultures were negative. Cultures of
*Corresponding author.
0167-5273 / 97 / $17.00 Copyright 1997 Elsevier Science Ireland Ltd. All rights reserved PII S0167-5273( 96 )02879-3
T.-D. Wang et al. / International Journal of Cardiology 58 (1997) 308 – 311
309
Fig. 1. Twelve-lead electrocardiogram taken on the day of admission showing sinus tachycardia and non-specific ST and T wave changes (A); several minutes after stroke showing sinus tachycardia and 2- to 4-mm ST-segment elevation in the inferior leads with reciprocal changes in the precordial and high lateral leads (B); 30 min after stroke showing deep Q waves in the inferior leads and evolutional ST and T wave changes (C); and 5 days after stroke showing only sinus tachycardia and nonspecific ST and T wave changes (D). Note the disappearance of the preexisting Q waves.
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T.-D. Wang et al. / International Journal of Cardiology 58 (1997) 308 – 311
sputum and discharge of the carbuncle grew Staphylococcus aureus, which was sensitive to ticarcillin / clavulanate. Intravenous ticarcillin / clavulanate (12.4 g / day) and netilmicin (300 mg / day), together with subcutaneous filgrastim (150 mg / day), were given. The patient’s condition improved slowly thereafter. On the morning of the 25th hospital day, the patient became irritable and developed dense left hemiparesis. The brain stem reflexes were preserved. Blood pressure increased from 106 / 64 mmHg to 160 / 90 mmHg and heart rate from 70 / min to 120 / min at that time. Several minutes later, a significant ST-segment elevation in lead II was noted on the continuous ECG monitoring screen. The 12-lead ECG (Fig. 1B), taken at the same time, revealed sinus tachycardia and 2- to 4-mm ST-segment elevation in the inferior leads and reciprocal changes in the precordial and high lateral leads. An immediate echocardiogram showed severe hypokinesis of the inferior wall with an ejection fraction of 42%. There were no vegetations or intracardiac thrombi. The ECG taken 30 min after stroke (Fig. 1C) showed deep Q waves in the inferior leads and evolutional ST and T wave changes. Computed tomography of the head, directly after stroke, showed no evidence of intracranial hemorrhage. The patient was then started on intravenous heparin, nitroglycerin, and aspirin (300 mg / day). A repeated computed tomographic scan, 6 h after stroke, showed obliterated sulci over the right parietotemporal area, a finding consistent with acute ischemic stroke over the right middle cerebral artery territory. Cardiac enzyme levels remained normal. A technetium-99m pyrophosphate scan showed no evidence of abnormal uptake. The ECG and echocardiographic changes completely resolved 5 days later (Fig. 1D). The ejection fraction increased to 60%. Nevertheless, her neurologic status deteriorated in spite of excellent supportive therapy and she died on the 38th hospital day. Autopsy of the heart showed no histologic evidence of previous myocardial infarction. The coronary arteries were patent, with only mild atherosclerosis.
3. Discussion In the present case, ST-segment elevations and inferior wall hypokinesis occurred within several
minutes after the stroke symptoms, and evolved quickly with the development of Q waves. There was no elevation of cardiac enzymes. Over a period of 5 days, the improvement of wall motion abnormalities and disappearance of Q waves on the ECG revealed a simultaneous recovery of the wall motion and electric function of the ‘stunned myocardium’. The autopsy showed only mild atherosclerotic changes but no discrete coronary occlusions or myocardial infarction. We therefore speculated that the development of myocardial stunning was subsequent to brief episodes of ischemia caused by coronary vasospasm. The cardiac event was also possibly caused by coronary embolism or in situ thrombosis with rapid lysis, but this seems to be less likely since there were no suitable clinical situations (like active infective endocarditis, atrial fibrillation, left ventricular aneurysm, hematologic diseases, and so on) in which coronary embolism or in situ thrombosis might occur [2] in this patient. The temporal association of events in this case suggests a causal relationship between right hemisphere ischemic stroke and the cardiac event. Over the past half century, attention has repeatedly been drawn to the ECG changes accompanying acute stroke. The patients generally showed repolarization changes manifested by QT prolongation, large U waves, T wave anomalies, and ST segment elevation or depression [3]. Although one series found the occurrence of Q waves in 6% of 72 patients with cerebral infarction [4], to the best of our knowledge, only three cases of reversible Q waves have been reported [5]. However, coronary artery anatomy and left ventricular function were not assessed in these cases. Contrary to the exclusive relationship between myocardial necrosis and pathologic Q waves, transient Q waves have been observed in patients with intense but reversible myocardial ischemia [6]. Recent findings suggest that, not only the cardiac contractile function, the cardiac electrical system may also become stunned by intense myocardial ischemia [6]. The present case also demonstrated that transient pathologic Q waves and repolarization abnormalities might represent myocardial stunning. The mechanism underlying myocardial dysfunction after cerebral infarction is not clear. Recently, experimental and clinical evidence has implicated the insular cortex, which lies below the frontoparietal
T.-D. Wang et al. / International Journal of Cardiology 58 (1997) 308 – 311
and temporal opercula and is supplied by the middle cerebral artery, as a crucial site involved in strokeinduced cardiac effects [3]. Lateralization studies indicate that destruction of areas adjacent to the right insular cortex generates sympathetic phenomena (elevations of blood pressure and heart rate) whereas the opposite effects occur on stimulation of the left insula [3]. Besides, a recent study found a higher incidence of supraventricular tachycardias in patients with acute right vs. left hemisphere strokes [7]. They speculated that parasympathetic tone was diminished ipsilateral to the affected hemisphere associated with a reciprocal rise in sympathetic tone on that side. In the present case, we therefore postulated that the stroke in the right middle cerebral artery territory might have similarly influenced the cortical inhibitory effect on the insular cortex and resulted in a sympathetic surge, which could induce coronary artery vasospasm and subsequent myocardial dysfunction. Though we did not measure serum or urine catecholamine levels, increased sympathetic activity was obvious from the increase in blood pressure and the tachycardiac response immediately after the stroke. This case illustrated that primary cerebral mechanisms might be important in determining the cardiac
311
event of stroke patients. Simultaneous ECG and echocardiographic studies might bring us more insight into the brain–heart interaction.
References [1] Rutherford JD, Braunwald E. Chronic ischemic heart disease. In: Braunwald E, ed. Heart disease: a textbook of cardiovascular medicine. Philadelphia, PA: W.B. Saunders, 1992; 1292–1364. [2] Waller BF. Nonatherosclerotic coronary heart disease. In: Schlant RC, Alexander RW, eds. Hurst’s the heart: arteries and veins. New York: McGraw-Hill, 1994; 1239–1261. [3] Oppenheimer SM. Neurogenic cardiac effects of cerebrovascular disease. Curr Opin Neurol 1994; 7: 20–24. [4] Dimant J, Grob D. Electrocardiographic changes and myocardial damage in patients with acute cerebrovascular accidents. Stroke 1977; 8: 448–455. [5] Ramani A, Shetty U, Kundaje GN. Electrocardiographic abnormalities in cerebrovascular accidents. Angiology 1990; 41: 681–686. [6] Bateman TM, Czer LSC, Gray RJ, et al. Transient pathologic Q waves during acute ischemic events: An electrocardiographic correlate of stunned but viable myocardium. Am Heart J 1983; 6: 1421–1426. [7] Lane RD, Wallace JD, Petrosky PP, Schwartz GE, Gradman AH. Supraventricular tachycardia in patients with right hemisphere strokes. Stroke 1992; 23: 362–366.
Myocardial stunning after cerebral infarction Tzung-Dau Wang, Chau-Chung Wu, Yuan-Teh Lee* Department of Internal Medicine, National Taiwan University, Hospital, 7, Chung-Shan South Road, Taipei, 10016, Taiwan, ROC Received 23 August 1996; accepted 6 November 1996
Abstract Myocardial stunning has not been described in patients with cerebrovascular accidents. We present a patient in whom inferior wall hypokinesis, ST-segment elevations and Q waves developed after acute right hemisphere ischemic stroke. Total recovery ensued within 5 days. Coronary vasospasm induced by stroke-related sympathetic surge might be the cause of this cardiac event. Copyright 1997 Elsevier Science Ireland Ltd. Keywords: Cerebral infarction; Electrocardiography; Autonomic nervous system
1. Introduction
2. Case report
Myocardial stunning, a prolonged but reversible myocardial contractile dysfunction, has been demonstrated clearly in patients with coronary occlusion who underwent early reperfusion, either by thrombolysis or by operative treatment, and in patients with brief episodes of ischemia caused by coronary vasospasm [1]. However, myocardial stunning after cerebral infarction has never been described before. We herein present a patient in whom myocardial stunning and the electrocardiographic (ECG) changes of reversible pathologic Q waves developed after acute right hemisphere ischemic stroke.
A 65-year-old woman was admitted because of fever, cough, and dyspnea for 5 days. Two months prior to admission, she suffered from an episode of chest tightness and had then been treated with both isosorbide dinitrate (10 mg) and ticlopidine (100 mg) three times a day. There was no other history of cardiac disease. On admission, the patient was febrile, dyspneic, and drowsy. Blood pressure was 110 / 60 mmHg. Physical examination revealed nothing unusual except for a carbuncle on the right flank. The hemogram gave a leukocyte count of 400310 6 / l with 100% lymphocytes. A chest radiograph showed a pneumonic patch over the right upper lobe. The ECG on admission (Fig. 1A) showed sinus tachycardia and non-specific ST and T wave changes. Blood cultures were negative. Cultures of
*Corresponding author.
0167-5273 / 97 / $17.00 Copyright 1997 Elsevier Science Ireland Ltd. All rights reserved PII S0167-5273( 96 )02879-3
T.-D. Wang et al. / International Journal of Cardiology 58 (1997) 308 – 311
309
Fig. 1. Twelve-lead electrocardiogram taken on the day of admission showing sinus tachycardia and non-specific ST and T wave changes (A); several minutes after stroke showing sinus tachycardia and 2- to 4-mm ST-segment elevation in the inferior leads with reciprocal changes in the precordial and high lateral leads (B); 30 min after stroke showing deep Q waves in the inferior leads and evolutional ST and T wave changes (C); and 5 days after stroke showing only sinus tachycardia and nonspecific ST and T wave changes (D). Note the disappearance of the preexisting Q waves.
310
T.-D. Wang et al. / International Journal of Cardiology 58 (1997) 308 – 311
sputum and discharge of the carbuncle grew Staphylococcus aureus, which was sensitive to ticarcillin / clavulanate. Intravenous ticarcillin / clavulanate (12.4 g / day) and netilmicin (300 mg / day), together with subcutaneous filgrastim (150 mg / day), were given. The patient’s condition improved slowly thereafter. On the morning of the 25th hospital day, the patient became irritable and developed dense left hemiparesis. The brain stem reflexes were preserved. Blood pressure increased from 106 / 64 mmHg to 160 / 90 mmHg and heart rate from 70 / min to 120 / min at that time. Several minutes later, a significant ST-segment elevation in lead II was noted on the continuous ECG monitoring screen. The 12-lead ECG (Fig. 1B), taken at the same time, revealed sinus tachycardia and 2- to 4-mm ST-segment elevation in the inferior leads and reciprocal changes in the precordial and high lateral leads. An immediate echocardiogram showed severe hypokinesis of the inferior wall with an ejection fraction of 42%. There were no vegetations or intracardiac thrombi. The ECG taken 30 min after stroke (Fig. 1C) showed deep Q waves in the inferior leads and evolutional ST and T wave changes. Computed tomography of the head, directly after stroke, showed no evidence of intracranial hemorrhage. The patient was then started on intravenous heparin, nitroglycerin, and aspirin (300 mg / day). A repeated computed tomographic scan, 6 h after stroke, showed obliterated sulci over the right parietotemporal area, a finding consistent with acute ischemic stroke over the right middle cerebral artery territory. Cardiac enzyme levels remained normal. A technetium-99m pyrophosphate scan showed no evidence of abnormal uptake. The ECG and echocardiographic changes completely resolved 5 days later (Fig. 1D). The ejection fraction increased to 60%. Nevertheless, her neurologic status deteriorated in spite of excellent supportive therapy and she died on the 38th hospital day. Autopsy of the heart showed no histologic evidence of previous myocardial infarction. The coronary arteries were patent, with only mild atherosclerosis.
3. Discussion In the present case, ST-segment elevations and inferior wall hypokinesis occurred within several
minutes after the stroke symptoms, and evolved quickly with the development of Q waves. There was no elevation of cardiac enzymes. Over a period of 5 days, the improvement of wall motion abnormalities and disappearance of Q waves on the ECG revealed a simultaneous recovery of the wall motion and electric function of the ‘stunned myocardium’. The autopsy showed only mild atherosclerotic changes but no discrete coronary occlusions or myocardial infarction. We therefore speculated that the development of myocardial stunning was subsequent to brief episodes of ischemia caused by coronary vasospasm. The cardiac event was also possibly caused by coronary embolism or in situ thrombosis with rapid lysis, but this seems to be less likely since there were no suitable clinical situations (like active infective endocarditis, atrial fibrillation, left ventricular aneurysm, hematologic diseases, and so on) in which coronary embolism or in situ thrombosis might occur [2] in this patient. The temporal association of events in this case suggests a causal relationship between right hemisphere ischemic stroke and the cardiac event. Over the past half century, attention has repeatedly been drawn to the ECG changes accompanying acute stroke. The patients generally showed repolarization changes manifested by QT prolongation, large U waves, T wave anomalies, and ST segment elevation or depression [3]. Although one series found the occurrence of Q waves in 6% of 72 patients with cerebral infarction [4], to the best of our knowledge, only three cases of reversible Q waves have been reported [5]. However, coronary artery anatomy and left ventricular function were not assessed in these cases. Contrary to the exclusive relationship between myocardial necrosis and pathologic Q waves, transient Q waves have been observed in patients with intense but reversible myocardial ischemia [6]. Recent findings suggest that, not only the cardiac contractile function, the cardiac electrical system may also become stunned by intense myocardial ischemia [6]. The present case also demonstrated that transient pathologic Q waves and repolarization abnormalities might represent myocardial stunning. The mechanism underlying myocardial dysfunction after cerebral infarction is not clear. Recently, experimental and clinical evidence has implicated the insular cortex, which lies below the frontoparietal
T.-D. Wang et al. / International Journal of Cardiology 58 (1997) 308 – 311
and temporal opercula and is supplied by the middle cerebral artery, as a crucial site involved in strokeinduced cardiac effects [3]. Lateralization studies indicate that destruction of areas adjacent to the right insular cortex generates sympathetic phenomena (elevations of blood pressure and heart rate) whereas the opposite effects occur on stimulation of the left insula [3]. Besides, a recent study found a higher incidence of supraventricular tachycardias in patients with acute right vs. left hemisphere strokes [7]. They speculated that parasympathetic tone was diminished ipsilateral to the affected hemisphere associated with a reciprocal rise in sympathetic tone on that side. In the present case, we therefore postulated that the stroke in the right middle cerebral artery territory might have similarly influenced the cortical inhibitory effect on the insular cortex and resulted in a sympathetic surge, which could induce coronary artery vasospasm and subsequent myocardial dysfunction. Though we did not measure serum or urine catecholamine levels, increased sympathetic activity was obvious from the increase in blood pressure and the tachycardiac response immediately after the stroke. This case illustrated that primary cerebral mechanisms might be important in determining the cardiac
311
event of stroke patients. Simultaneous ECG and echocardiographic studies might bring us more insight into the brain–heart interaction.
References [1] Rutherford JD, Braunwald E. Chronic ischemic heart disease. In: Braunwald E, ed. Heart disease: a textbook of cardiovascular medicine. Philadelphia, PA: W.B. Saunders, 1992; 1292–1364. [2] Waller BF. Nonatherosclerotic coronary heart disease. In: Schlant RC, Alexander RW, eds. Hurst’s the heart: arteries and veins. New York: McGraw-Hill, 1994; 1239–1261. [3] Oppenheimer SM. Neurogenic cardiac effects of cerebrovascular disease. Curr Opin Neurol 1994; 7: 20–24. [4] Dimant J, Grob D. Electrocardiographic changes and myocardial damage in patients with acute cerebrovascular accidents. Stroke 1977; 8: 448–455. [5] Ramani A, Shetty U, Kundaje GN. Electrocardiographic abnormalities in cerebrovascular accidents. Angiology 1990; 41: 681–686. [6] Bateman TM, Czer LSC, Gray RJ, et al. Transient pathologic Q waves during acute ischemic events: An electrocardiographic correlate of stunned but viable myocardium. Am Heart J 1983; 6: 1421–1426. [7] Lane RD, Wallace JD, Petrosky PP, Schwartz GE, Gradman AH. Supraventricular tachycardia in patients with right hemisphere strokes. Stroke 1992; 23: 362–366.