J Neurosurg 75:308-311. 1991
Coronary vasospasrn following subarachnoid hemorrhage as a cause of stunned myocardium Case report KIYOSIII YUKI, M.D., YASUNORI KODAMA, M.D., JUN ONDA, M.D., KArSUVA EMOTO, M.D., TADAO MORIMOTO, M.D., AND Totmu UOZUM1, M.D.
Departments ~[ Neurosurger.t' and Internal MedMne, Kure National Hospital, Kure, and Department of Neurosurgery, Hiroshima University N:hool ( f Medicine, Hiroshima, Japan ~" A patient with subarachnoid hemorrhage was found to have electrocardiographicabnormalities resembling an acute myocardialinfarction as well as left ventriculographic findings of cardiac dysfunction. These cardiac abnormalities resolved followingsurgical clipping of the aneurysm and the patient recovered well from the operation. She died 2 mon'ths later from cancer and a postmortem examination at that time revealed no evidence of myocardial necrosis. In this report, the authors discuss coronary vasospasm and reversible postischemic "stunned myocardium," a condition that has not been considered previously in relation to subarachnoid hemorrhage. KEY WORDS 9 subarachnoid hemorrhage 9 myocardial infarction coronary vasospasm stunned myocardiam
LECTROCARDIOGRAPHIC(EKG) abnormalities, which are indistinguishable from those due to an acute myocardial infarction, have occasionally been reported in cases of subarachnoid hemorrhage (SAH). 2-~-7'sWe recently encountered a patient with an SAH who exhibited findings similar to an acute myocardial infarction on EKG examination, as well as findings of anterior wall akinesis on left ventriculography. These cardiac abnormalities recovered. The disorder in our patient seems to correspond to the condition of "stunned myocardium," which was defined by Braunwald and Kloner in 1982 as reversible postischemic myocardial dysfunction. The cause of the EKG changes resembling an acute myocardial infarction in patients with an SAH remains unknown. Coronary vasospasm is considered to have been the main etiology of the cardiac abnormalities in our patient and is discussed in this report as the possible cause for "stunned myocardium."
E
Case Report This 70-year-old woman was referred to our hospital because of disturbances of consciousness. A diagnosis 308
9
of maxillary cancer had been made 6 months earlier for which she received radiation therapy. Examination. Examination conducted 3 hours after onset of symptoms revealed the patient to be disoriented and complaining of severe headache and vomiting. Paraparesis and bilateral pathological Babinski reflexes were noted. Electrocardiography was normal except for a right bundle branch block. Computerized tomography (CT) revealed an SAH, and cerebral angiography showed two saccular aneurysms: one arising from the anterior communicating artery and the other at the basilar artery bifurcation. Surgery for the aneurysms was not performed because of the patient's age and poor general condition. She did well until the 26th day after presentation, when she suffered a generalized seizure. During the period of recovery from unconsciousness, she complained of chest pain and the electrocardiac monitor showed ST elevation. An EKG examination conducted after the pain had subsided showed ST-T changes suggestive of an acute myocardial infarction in the anterior leads (Fig. 1). Another EKG examination on the following day showed abnormal Q waves in leads V~, V4, and V>
J. Neurosurg, / Volume 75/August, 1991
Subarachnoid hemorrhage and stunned m y o c a r d i u m
FIG. 1. Electrocardiographic (EKG) tracings recorded during the patient's clinical course, kTr~t Row: Tracings obtained at the time of initial hospitalization. Second Row: Tracings obtained at the time of chest pain, showing elevation of the ST-T segmenl. Third Row: Tracings obtained when an acute myocardial infarction was suspected, showing abnormal Q waves in leads V~, V~, and Vs. Fourth Row."The latest followup EKG tracing obtained.
(Fig. 1). Serial determinations of creatine phosphokinase levels along with MB isoenzyme fractions, serum glutamic-pyruvic transaminase, and lactate dehydrogenase values were all within normal limits during the next 4 days. ACT scan obtained shortly after the seizure revealed SAH, mild hydrocephalus, and a hematoma in the fourth ventricle. Selective coronary arteriography performed 30 days after the SAH for preoperative evaluation purposes did not show any narrowing or spasm of the coronary, artery; however, left ventriculography revealed anterior wall akinesis although the overall cardiac function was not severely depressed. A decision was made to operate as an emergency measure regardless of the risks because of a gradual deterioration in the patient's level of consciousness.
pyrophosphate showed no localized or diffuse increase in tracer uptake by the myocardium. After a period of rehabilitation, the patient was discharged from the hospital, experiencing no neurological deficits at that time. She was readmitted 2 months later because of the recurrence of cancer and died of pneumonia. An autopsy showed no gross evidence of myocardial infarction and, although the coronary artery was mildly arteriosclerotic, no stenosis or thrombi of the artery could be detected. Microscopic examination of the anterior ventricular wall, which had shown akinesis, revealed no findings of individual myocyte drop-out, no myocytolysis, none of the characteristic changes of catecholamine overload, and no focal scarring.
Operation. On the 37th day after the onset of SAH, the neck of the aneurysm of the anterior communicating artery was clipped with placement of a ventricular drain. A transient ST elevation lasting a few minutes was observed several times, which was treated by nitroglycerin administration. After aneurysmal clipping, a ventriculoperitoneal shunt was placed, and excellent recovery was achieved. Postoperative Course. Postoperative EKG examination revealed negative T waves in leads V_~to V6; the abnormal Q wave and ST elevation had returned to normal (Fig. 1). Left ventriculography showed normal left ventricular wall motion, and a nuclear scan using
EKG Abnormalities Following SAH
J. Neurosurg. / Vohtme 75/August, 1991
Discussion Electrocardiographic abnormalities are often seen in association with central nervous system disorders, and have been reported with a 70% to 90% frequency in association with SAH. ~~~ The most common patterns noted are a broad or inverted T wave, a prolonged QT interval, an ST segment elevation or depression, a prominent U wave, and various rhythm abnormalities. 7-~J,~ Ischemic EKG changes simulating an acute myocardial infarction are, however, rare. 257'~Although reference has occasionally been made to the cause of the pathological Q wave, the etiology still remains unknown. 309
K. Yuki, el al. Several explanations have been suggested for EKG alterations in SAH, some relating the role of catccholanaines, hypercortisolism, or hypokalcnaia. Certain recent studies have unequivocally demonstrated that catecholamines play the principal role in EKG changes and furthermore that ischemic stimulation of the posterior hypothalamus following an SAH is responsible for an increase in sympathetic tone, L~'~"which has been implicated as the cause. Several reports-" have described a normal myocardium at autopsy, as was seen in our patient. Since the demonstration by Conno# that subtle areas of necrosis might be overlooked, careful postmortem examinations have shown focal myocytolysis in 8% to 12% of patients dying from acute cerebral lesions. Kolin and Norris ~e reported that transmurally scattered foci of damaged myocardial fibers are more common in patients with intraeranial lesions than in control subjects (p < 0.01 ). Norepinephrine may cause myocardial damage either by systemic hypertensive effects that lead to left ventricular strain or by direct tissue toxicity. ~a
Coronao' ~~l.s'o.~7~asm In view of the foregoing, the cardiac disorder associated with an SAH may be due not only to neurogenic factors but also to the myocardial damage itself. The cause for coronary vasospasm in patients with primary cardiovascular disease is unclear even now, and is still less clear in cases of SAH. Although the mechanisms of SAH were not given, some reports have suggested that coronary vasospasm may be responsible for the cardiac ischemic changes associated with SAH. ~ Toyarea, et at., '-r reported the occurrence of Prinzmetal's variant angina in a patient with SAH. Although coronary arteriography did not show vasospasm, the ischemic EKG changes and reduced contractility' in our patient are thought to be due to a coronary, spasm for the following reasons (even though ergonovine challenge was not performed): 1) no narrowing of the coronary artery was observed: 2) repeated sudden ST-T changes occurred which did not follow tachycardia or hypertension: and 3) there was good response to the use of nitroglycerin. Such factors as severity, duration, and frequency of coronary vasoconstriction may play an important role in coronary artery disturbances. Various factors involved in coronary, vasospasm following SAH can cause a wide spectrum of clinical syndromes ranging from transient ischemia, through "stunning" of the myocardium without necrosis or scattered myocytolysis to an irreversible infarction. Our patient's situation was intermediate between these extremes: she manifested reversible postischemic left ventricular dysfunction and a return of the EKG changes to normal. St un ned Myoca rdium Reduced contractile function and diastolic compliance following coronaD~ occlusion may persist for sev310
oral days alter re-establishment of coronary perfusion. Even though this phenomenon was not a new find, it was termed "stunned myocardium" by Braunwald and Kloner.'The mechanism involved in the development of this condition is still unknown. Braunwald and Kloner attributed stunned myocardium to a delayed recovery of adenosine triphosphate (ATP) concentration because the process of a recovery of postischemic intracellular ATP depletion following the re-establishment of perfusion was found to occur in parallel with the recovery of myocardial contractility/' On the other hand, reduced myocardial contractility following the re-establishment of perfusion is alleviated by the administration of free radical scavengers, and electron paramagnetic resonance spectroscopy has shown that a burst of free radical production can occur in such reversible ischemie conditions. ~ These findings suggest that reversible cellular disturbances due to free radicals may be the cause of stunned myocardium. Because transient electrical instability may accompany coronary vasospasm, profound ischemia without cell death may cause a part of the myocardium to become electrically inert; consequently, electrically stunned myocardium may be associated with a transient Q wave.*-~ Therefore, coronary spasm is believed to have caused the EKG abnormalities and stunned myocardium in our patient. The manifestation of these various changes in association with SAH may be dependent upon the degree of a coronary vasospasm. ~s
Suggested Management To avoid unnecessary' delays in brain- and life-saving surgical intervention, it is very important for neurosurgeons and anesthesiologists to evaluate expeditiously whether these EKG abnormalities are electrical or ischemic. ~,,,22Echocardiography or radionuclide ventriculography is currently considered to be most useful and essential for such cardiac evaluations. In addition, coronary arleriography should be performed when there is any abnormal motion of the arterial wall; this study should assist in the differential diagnosis.
References
1. Akins CW, Pohost GM, Desanctis RW, et al: Selection of angina-free patients with severe left ventricular dysfunction for myocardial revascularization. Am J Cardiol 46: 695-700, 1980 2. Beard EF, Robertson JW, Robertson RCL: Spontaneous subarachnoid hemorrhage simulating acute myocardial infarction. Am Heart J 58:755-759, 1959 3. Braunwald E, Kloner RA: The stunned myocardium: prolonged, postischemic ventricular dysfunction. Circulation 66:l 146-1149, 1982 4. Connor RCR: Heart damage associated with intracranial lesions. Br Med J 3:29-31, 1968 5. Cropp G J, Manning GW: Electrocardiographic changes simulating myocardial ischemia and infarction associated with spontaneous intracranial hemorrhage, Circulation 22:25-38, 1960
J. Neur~zs'ur,~./ Volume 75 / August, t 991
Subarachnoid laemorrhageand stunned myocardium 6. DeBoer LWV, Ing~all JS, Kloner RA, cl al: Prolonged derangements of canine mvocardiaI purine metabolism after a brief coronary artcrx occlusion not associated with anatomic evidence of necrosis. Proc Natl Acad Sci USA 77:5471-5475, 1980 7. Gascon P, Ley T J, Toltzis RJ, el ah Spontaneous subarachnoid hemorrhage simulating acute transmural myocardial infraction. Am fteart .I 105:511-513. 1983 8. Hammermeister KE, Reichenbach DD: QRS changes, pulmonary edema, and myocardial necrosis associated with subarachnoid hemorrhage. Am ttearr J 78:94-100, 1969 9. Harries AD: Subarachnoid hemorrhage and the electrocardiogram, a review. Postgrad Med J 57:294-296, 1981 10. Hunt D, McRae C, Zapf P: Electrocardiographic and serum enzyme changes in subarachnoid hemorrhage. Am tleart J 77:479-488, 1969 11. Kerin NZ, Rubenfire M, Naini M, et al: Prinzmetal's variant angina. Electrocardiographic and angiographic correlations, a Electrocardiol 15:365-379, 1982 12. Kolin A, Norris JW: Myocardial damage from acute cerebral lesions. Stroke 15:990-993. 1984 13. Kubo S, Era O, Tagawa H, el al: [Electrocardiographic changes in 150 patients with cerebrovascular accidents.] J Jpn Soe Intern Med 72:1519-1526, 1983 (Jpn) 14. Marion DW, Segal R, Thompson ME: Subarachnoid hemorrhage and the heart. Neurosurgery 18:101-106, 1986 15. Mathias P, Kerin NZ, Blevins RD, el ah Coronary vasospasm as a cause of stunned myocardium. Am tleart J 113:383-385, 1987
J, Neurosurg. / Volume 75/August, 1991
19,
20. 21. 22.
OflL'rhaus J, van Gool J: Electrocardiographic changes and tissue catecholamines in experimental subarachnoid haenlorrhage. Cardiovasc Res 3:433-440, 1969 Reichenbach DD, Bcnditt EP: Catecholamines and cardiomyopathy: the pathogenesis and potential importance of myofibrillar degeneration. Hum Pathol 1:125-150, 1970 Roberto B: Oxygen-derived free radicals and postischemic myocardial dysfunction ("stunned myocardium"). J Am Coil Cardiol 12:239-249, 1988 Samra SK, Kroll DA: Subarachnoid hemorrhage and intraoperative electrocardiographic change simulating myocardial ischemia - - anesthesiologist's dilemma. Anesth Analg 64:86-89, 1985 Stober T, Kunze K: Electrocardiographic alterations in subarachnoid hemorrhage. J Neurol 227:99--13, 1982 Toyama T, Tanaka H. Nuruki K, et al: Prinzmetal's variant angina associated with subarachnoid hemorrhage: a case report. Angiology 30:211-218. 1979 White JC, Parker SD, Rogers MC: Preanesthetic evaluation of a patient with pathologic Q waves following subarachnoid hemorrhage. Anesthesiology 62:351-354, 1985
Manuscript received November 7. 1989. Accepted in final form December 19, 1990. Address reprint requests to: Kiyosh[ Yuki, M.D., Department of Neurosurgery, Kure National Hospital, 3-1 Aoyamacho, Kure, Hiroshima 737. Japan.
311
Coronary vasospasrn following subarachnoid hemorrhage as a cause of stunned myocardium Case report KIYOSIII YUKI, M.D., YASUNORI KODAMA, M.D., JUN ONDA, M.D., KArSUVA EMOTO, M.D., TADAO MORIMOTO, M.D., AND Totmu UOZUM1, M.D.
Departments ~[ Neurosurger.t' and Internal MedMne, Kure National Hospital, Kure, and Department of Neurosurgery, Hiroshima University N:hool ( f Medicine, Hiroshima, Japan ~" A patient with subarachnoid hemorrhage was found to have electrocardiographicabnormalities resembling an acute myocardialinfarction as well as left ventriculographic findings of cardiac dysfunction. These cardiac abnormalities resolved followingsurgical clipping of the aneurysm and the patient recovered well from the operation. She died 2 mon'ths later from cancer and a postmortem examination at that time revealed no evidence of myocardial necrosis. In this report, the authors discuss coronary vasospasm and reversible postischemic "stunned myocardium," a condition that has not been considered previously in relation to subarachnoid hemorrhage. KEY WORDS 9 subarachnoid hemorrhage 9 myocardial infarction coronary vasospasm stunned myocardiam
LECTROCARDIOGRAPHIC(EKG) abnormalities, which are indistinguishable from those due to an acute myocardial infarction, have occasionally been reported in cases of subarachnoid hemorrhage (SAH). 2-~-7'sWe recently encountered a patient with an SAH who exhibited findings similar to an acute myocardial infarction on EKG examination, as well as findings of anterior wall akinesis on left ventriculography. These cardiac abnormalities recovered. The disorder in our patient seems to correspond to the condition of "stunned myocardium," which was defined by Braunwald and Kloner in 1982 as reversible postischemic myocardial dysfunction. The cause of the EKG changes resembling an acute myocardial infarction in patients with an SAH remains unknown. Coronary vasospasm is considered to have been the main etiology of the cardiac abnormalities in our patient and is discussed in this report as the possible cause for "stunned myocardium."
E
Case Report This 70-year-old woman was referred to our hospital because of disturbances of consciousness. A diagnosis 308
9
of maxillary cancer had been made 6 months earlier for which she received radiation therapy. Examination. Examination conducted 3 hours after onset of symptoms revealed the patient to be disoriented and complaining of severe headache and vomiting. Paraparesis and bilateral pathological Babinski reflexes were noted. Electrocardiography was normal except for a right bundle branch block. Computerized tomography (CT) revealed an SAH, and cerebral angiography showed two saccular aneurysms: one arising from the anterior communicating artery and the other at the basilar artery bifurcation. Surgery for the aneurysms was not performed because of the patient's age and poor general condition. She did well until the 26th day after presentation, when she suffered a generalized seizure. During the period of recovery from unconsciousness, she complained of chest pain and the electrocardiac monitor showed ST elevation. An EKG examination conducted after the pain had subsided showed ST-T changes suggestive of an acute myocardial infarction in the anterior leads (Fig. 1). Another EKG examination on the following day showed abnormal Q waves in leads V~, V4, and V>
J. Neurosurg, / Volume 75/August, 1991
Subarachnoid hemorrhage and stunned m y o c a r d i u m
FIG. 1. Electrocardiographic (EKG) tracings recorded during the patient's clinical course, kTr~t Row: Tracings obtained at the time of initial hospitalization. Second Row: Tracings obtained at the time of chest pain, showing elevation of the ST-T segmenl. Third Row: Tracings obtained when an acute myocardial infarction was suspected, showing abnormal Q waves in leads V~, V~, and Vs. Fourth Row."The latest followup EKG tracing obtained.
(Fig. 1). Serial determinations of creatine phosphokinase levels along with MB isoenzyme fractions, serum glutamic-pyruvic transaminase, and lactate dehydrogenase values were all within normal limits during the next 4 days. ACT scan obtained shortly after the seizure revealed SAH, mild hydrocephalus, and a hematoma in the fourth ventricle. Selective coronary arteriography performed 30 days after the SAH for preoperative evaluation purposes did not show any narrowing or spasm of the coronary, artery; however, left ventriculography revealed anterior wall akinesis although the overall cardiac function was not severely depressed. A decision was made to operate as an emergency measure regardless of the risks because of a gradual deterioration in the patient's level of consciousness.
pyrophosphate showed no localized or diffuse increase in tracer uptake by the myocardium. After a period of rehabilitation, the patient was discharged from the hospital, experiencing no neurological deficits at that time. She was readmitted 2 months later because of the recurrence of cancer and died of pneumonia. An autopsy showed no gross evidence of myocardial infarction and, although the coronary artery was mildly arteriosclerotic, no stenosis or thrombi of the artery could be detected. Microscopic examination of the anterior ventricular wall, which had shown akinesis, revealed no findings of individual myocyte drop-out, no myocytolysis, none of the characteristic changes of catecholamine overload, and no focal scarring.
Operation. On the 37th day after the onset of SAH, the neck of the aneurysm of the anterior communicating artery was clipped with placement of a ventricular drain. A transient ST elevation lasting a few minutes was observed several times, which was treated by nitroglycerin administration. After aneurysmal clipping, a ventriculoperitoneal shunt was placed, and excellent recovery was achieved. Postoperative Course. Postoperative EKG examination revealed negative T waves in leads V_~to V6; the abnormal Q wave and ST elevation had returned to normal (Fig. 1). Left ventriculography showed normal left ventricular wall motion, and a nuclear scan using
EKG Abnormalities Following SAH
J. Neurosurg. / Vohtme 75/August, 1991
Discussion Electrocardiographic abnormalities are often seen in association with central nervous system disorders, and have been reported with a 70% to 90% frequency in association with SAH. ~~~ The most common patterns noted are a broad or inverted T wave, a prolonged QT interval, an ST segment elevation or depression, a prominent U wave, and various rhythm abnormalities. 7-~J,~ Ischemic EKG changes simulating an acute myocardial infarction are, however, rare. 257'~Although reference has occasionally been made to the cause of the pathological Q wave, the etiology still remains unknown. 309
K. Yuki, el al. Several explanations have been suggested for EKG alterations in SAH, some relating the role of catccholanaines, hypercortisolism, or hypokalcnaia. Certain recent studies have unequivocally demonstrated that catecholamines play the principal role in EKG changes and furthermore that ischemic stimulation of the posterior hypothalamus following an SAH is responsible for an increase in sympathetic tone, L~'~"which has been implicated as the cause. Several reports-" have described a normal myocardium at autopsy, as was seen in our patient. Since the demonstration by Conno# that subtle areas of necrosis might be overlooked, careful postmortem examinations have shown focal myocytolysis in 8% to 12% of patients dying from acute cerebral lesions. Kolin and Norris ~e reported that transmurally scattered foci of damaged myocardial fibers are more common in patients with intraeranial lesions than in control subjects (p < 0.01 ). Norepinephrine may cause myocardial damage either by systemic hypertensive effects that lead to left ventricular strain or by direct tissue toxicity. ~a
Coronao' ~~l.s'o.~7~asm In view of the foregoing, the cardiac disorder associated with an SAH may be due not only to neurogenic factors but also to the myocardial damage itself. The cause for coronary vasospasm in patients with primary cardiovascular disease is unclear even now, and is still less clear in cases of SAH. Although the mechanisms of SAH were not given, some reports have suggested that coronary vasospasm may be responsible for the cardiac ischemic changes associated with SAH. ~ Toyarea, et at., '-r reported the occurrence of Prinzmetal's variant angina in a patient with SAH. Although coronary arteriography did not show vasospasm, the ischemic EKG changes and reduced contractility' in our patient are thought to be due to a coronary, spasm for the following reasons (even though ergonovine challenge was not performed): 1) no narrowing of the coronary artery was observed: 2) repeated sudden ST-T changes occurred which did not follow tachycardia or hypertension: and 3) there was good response to the use of nitroglycerin. Such factors as severity, duration, and frequency of coronary vasoconstriction may play an important role in coronary artery disturbances. Various factors involved in coronary, vasospasm following SAH can cause a wide spectrum of clinical syndromes ranging from transient ischemia, through "stunning" of the myocardium without necrosis or scattered myocytolysis to an irreversible infarction. Our patient's situation was intermediate between these extremes: she manifested reversible postischemic left ventricular dysfunction and a return of the EKG changes to normal. St un ned Myoca rdium Reduced contractile function and diastolic compliance following coronaD~ occlusion may persist for sev310
oral days alter re-establishment of coronary perfusion. Even though this phenomenon was not a new find, it was termed "stunned myocardium" by Braunwald and Kloner.'The mechanism involved in the development of this condition is still unknown. Braunwald and Kloner attributed stunned myocardium to a delayed recovery of adenosine triphosphate (ATP) concentration because the process of a recovery of postischemic intracellular ATP depletion following the re-establishment of perfusion was found to occur in parallel with the recovery of myocardial contractility/' On the other hand, reduced myocardial contractility following the re-establishment of perfusion is alleviated by the administration of free radical scavengers, and electron paramagnetic resonance spectroscopy has shown that a burst of free radical production can occur in such reversible ischemie conditions. ~ These findings suggest that reversible cellular disturbances due to free radicals may be the cause of stunned myocardium. Because transient electrical instability may accompany coronary vasospasm, profound ischemia without cell death may cause a part of the myocardium to become electrically inert; consequently, electrically stunned myocardium may be associated with a transient Q wave.*-~ Therefore, coronary spasm is believed to have caused the EKG abnormalities and stunned myocardium in our patient. The manifestation of these various changes in association with SAH may be dependent upon the degree of a coronary vasospasm. ~s
Suggested Management To avoid unnecessary' delays in brain- and life-saving surgical intervention, it is very important for neurosurgeons and anesthesiologists to evaluate expeditiously whether these EKG abnormalities are electrical or ischemic. ~,,,22Echocardiography or radionuclide ventriculography is currently considered to be most useful and essential for such cardiac evaluations. In addition, coronary arleriography should be performed when there is any abnormal motion of the arterial wall; this study should assist in the differential diagnosis.
References
1. Akins CW, Pohost GM, Desanctis RW, et al: Selection of angina-free patients with severe left ventricular dysfunction for myocardial revascularization. Am J Cardiol 46: 695-700, 1980 2. Beard EF, Robertson JW, Robertson RCL: Spontaneous subarachnoid hemorrhage simulating acute myocardial infarction. Am Heart J 58:755-759, 1959 3. Braunwald E, Kloner RA: The stunned myocardium: prolonged, postischemic ventricular dysfunction. Circulation 66:l 146-1149, 1982 4. Connor RCR: Heart damage associated with intracranial lesions. Br Med J 3:29-31, 1968 5. Cropp G J, Manning GW: Electrocardiographic changes simulating myocardial ischemia and infarction associated with spontaneous intracranial hemorrhage, Circulation 22:25-38, 1960
J. Neur~zs'ur,~./ Volume 75 / August, t 991
Subarachnoid laemorrhageand stunned myocardium 6. DeBoer LWV, Ing~all JS, Kloner RA, cl al: Prolonged derangements of canine mvocardiaI purine metabolism after a brief coronary artcrx occlusion not associated with anatomic evidence of necrosis. Proc Natl Acad Sci USA 77:5471-5475, 1980 7. Gascon P, Ley T J, Toltzis RJ, el ah Spontaneous subarachnoid hemorrhage simulating acute transmural myocardial infraction. Am fteart .I 105:511-513. 1983 8. Hammermeister KE, Reichenbach DD: QRS changes, pulmonary edema, and myocardial necrosis associated with subarachnoid hemorrhage. Am ttearr J 78:94-100, 1969 9. Harries AD: Subarachnoid hemorrhage and the electrocardiogram, a review. Postgrad Med J 57:294-296, 1981 10. Hunt D, McRae C, Zapf P: Electrocardiographic and serum enzyme changes in subarachnoid hemorrhage. Am tleart J 77:479-488, 1969 11. Kerin NZ, Rubenfire M, Naini M, et al: Prinzmetal's variant angina. Electrocardiographic and angiographic correlations, a Electrocardiol 15:365-379, 1982 12. Kolin A, Norris JW: Myocardial damage from acute cerebral lesions. Stroke 15:990-993. 1984 13. Kubo S, Era O, Tagawa H, el al: [Electrocardiographic changes in 150 patients with cerebrovascular accidents.] J Jpn Soe Intern Med 72:1519-1526, 1983 (Jpn) 14. Marion DW, Segal R, Thompson ME: Subarachnoid hemorrhage and the heart. Neurosurgery 18:101-106, 1986 15. Mathias P, Kerin NZ, Blevins RD, el ah Coronary vasospasm as a cause of stunned myocardium. Am tleart J 113:383-385, 1987
J, Neurosurg. / Volume 75/August, 1991
19,
20. 21. 22.
OflL'rhaus J, van Gool J: Electrocardiographic changes and tissue catecholamines in experimental subarachnoid haenlorrhage. Cardiovasc Res 3:433-440, 1969 Reichenbach DD, Bcnditt EP: Catecholamines and cardiomyopathy: the pathogenesis and potential importance of myofibrillar degeneration. Hum Pathol 1:125-150, 1970 Roberto B: Oxygen-derived free radicals and postischemic myocardial dysfunction ("stunned myocardium"). J Am Coil Cardiol 12:239-249, 1988 Samra SK, Kroll DA: Subarachnoid hemorrhage and intraoperative electrocardiographic change simulating myocardial ischemia - - anesthesiologist's dilemma. Anesth Analg 64:86-89, 1985 Stober T, Kunze K: Electrocardiographic alterations in subarachnoid hemorrhage. J Neurol 227:99--13, 1982 Toyama T, Tanaka H. Nuruki K, et al: Prinzmetal's variant angina associated with subarachnoid hemorrhage: a case report. Angiology 30:211-218. 1979 White JC, Parker SD, Rogers MC: Preanesthetic evaluation of a patient with pathologic Q waves following subarachnoid hemorrhage. Anesthesiology 62:351-354, 1985
Manuscript received November 7. 1989. Accepted in final form December 19, 1990. Address reprint requests to: Kiyosh[ Yuki, M.D., Department of Neurosurgery, Kure National Hospital, 3-1 Aoyamacho, Kure, Hiroshima 737. Japan.
311
