Coincidence of Cerebrovascular Accident and Silent Myocardial Infarction

Coincidence of Cerebrovascular Accidentand Silent Myocardial Infarction

Elias Badui, M.D., F.A.C.A.Bruno Estanol, M.D.

andDavid Garcia-Rubi, M.D.

MEXICO CITY. MEXICO

Abstract

Although it is well known that a myocardial and a cerebral infarction may becoincident, the nature of this association is not clear. The problem is furthercomplicated because the myocardial infarction may be silent. This is a report of3 patients with cerebral infarct in whom a silent recent myocardial infarctionwas found. All patients with cerebrovascular disease should be screened for apossible myocardial lesion.

Introduction

The coincidence of myocardial and cerebral infarction is well recognized.'The mechanisms of this association, however, are still controversial. It hasbeen postulated that the cerebral infarction may be a consequence of dislodg-ment of a mural thrombi of the heart.- In support of this thesis, it has beenshown that the larger the size of the myocardial infarct the greater the likeli-hood of suffering an embolic cerebral infarction.'' On the other hand, it has beenargued that both vascular territories have atherosclerotic lesions in these typesof patients, and therefore, simultaneous occlusions are liable to occur on achance basis."* It is also possible that hemodynamic disturbances such aspostural hypotension may cause infarctions simultaneously in both organs.''

This paper reports 3 patients with silent myocardial infarctions whose firstclinical manifestations were cerebrovascular accidents. It is important to keepin mind this possibility when dealing with patients with cerebrovascular dis-ease.

From the Departments of Cardiology and Neurology, General Hospital, Centro Medico NacionalInstituto Mexicano del Seguro Social, Mexico City. Mexico

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Badiu—Cerebrovascular Accident and Silent Myocardial Infarction 703

Pre.sentation of Cases

Case IA 56-year-old man in good health had an acute onset of transient left

hemiparesis which resolved in 45 minutes. Physical examination disclosed aleft homonymous hemianopia. Blood pressure was 150/90 mm Hg, regularheart rate was 70/minute, and there were palpable carotid pulses withoutbruits. Cardiac, pulmonary, and vascular examination did not reveal anyimportant findings. SMA 12, serum lipids, complete CBC, urinalysis, coagula-tion tests, serum enzymes, serum electrolytes, and lumbar cerebral spinal fluidstudies were within normal limits. Chest x-ray showed chronic bronchitis andleft ventricular hypertrophy. Electrocardiogram showed sinus rhythm at 70 perminute with an area of anteroseptal necrosis with injury and subepicardicischemia including the lateral wall (Figure 1). Cranial computerized axialtomography showed an area of infarction in the territory of the right posteriorcerebral artery (Figure 2). The following diagnosis was made: left homony-mous hemianopia due to right posterior cerebral artery occlusion secondary toembolic phenomenon from an anteroseptal myocardial infarction of indetermi-nate age. 1

FIG. 1. ECG showing regular sinus rhythm, right axis deviation, anteroseptal myocardial infarctionwith injury, and subepicardic ischemia in the same area of necrosis.

704 Angiology—Journal of Vascular Diseases November 1982

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FIG. 2. Cranial computerized axial tomography. An area of infarction in the territory ofthe rightposterior cerebral artery is observed.

Case 2A 39-year-old male athlete with a 7-year history of allopurinol controlled

hyperuricemia complained of an acute, intense, generalized throbbingheadache of several hours duration, associated with vomiting and a I-hourepisode of unconsciousness. He regained consciousness with dysarthria andright hemiparesis unassociated with chest pain or other cardiac symptoms.Physical examination showed blood pressure at 120/80 mm Hg and regularheart rate (72/minute). No cardiac or vascular abnormalities were present. Thelumbar cerebral spinal fluid studies were normal, and a cerebral angiogramshowed occlusion of the left middle cerebral artery. Cardiac series werenormal, and the ECG showed sinus rhythm with extensive anterior wallmyocardial infarction and complete right bundle branch block (Figure 3). SerialECG showed injury and subepicardic ischemia without serum enzymeschanges. We thought it to be a recent but not acute myocardial infarction.Cranial computerized axial tomography showed a decrease in size of thecerebral ventricles with collapse ofthe left frontal horn and an area of infarc-tion in the territory ofthe left middle cerebral artery (Figure 4). Hyperlipidemiatype IV was detected. Other laboratory tests were within normal limits. Thepatient has a residual right hemiparesis without cardiac symptoms.


Q.*.F.

FIG. 3. ECG with sinus rhythm 74/minute. right axis deviation, complete right bundle branch block,and extensive anterior wall myocardial infarction {VI-V6. 1. VL), with persistent elevation ofthe STsegment.

FIG. 4. Cranial computerized axial tomography showing collapse ofthe left frontal horn and an areaof infarction in the territory of the left middle cerebral artery.


K.O.P.

170-J2663

FIG, 5. ECG with regular sinus rhythm 85/minute, left ventricular hypertrophy, and inferior andlateral wall myocardial infarction with possible involvement ofthe posterior wall. A slight elevation oftheJ point in 11, ill, and AVF and left atrial enlargement can be observed.

Case 3A 56-year-old male with a 5-year history of a-methyl-dopa-controlled

hypertension was hospitalized with an acute onset of left hemiparesis. Therewas no history of angina pectoris, diabetes mellitus, or cardiovascular disease.On physical examination, he had a blood pressure of 115/80 mm Hg and aregular heart rate at 85 per minute. Right central facial paralysis, deviation ofthe eyes to the left, a right Babinski reflex, and right myotatic hyperreflexiawere present. The rest ofthe physical examination showed no remarkablefmdings. Lumbar cerebral spinal fluid studies were normal as well as all theroutine laboratory tests. ECG showed sinus rhythm, left ventricular hyper-trophy, and inferior wall myocardial infarction with involvement ofthe lateralwall and probably of the posterior wall (Figure 5). Serum enzymes were:lactate dehydrogenase, 850 units, CPK-MB 146 milli-units/ml, anda-hydroxybutyric acid 282 milliunits/ml. Both serial ECG and serum enzymesshowed evolutionary changes suggesting a recent myocardial infarction. Car-


FIG. 6. Cranial computerized axial tomography in which changes compatible with infarction oftheleft middle cerebral artery are seen.

diac x-ray showed chronic bronchitis and left ventricular hypertrophy. Cranialcomputerized axial tomography showed changes compatible with infarction ofthe left middle cerebral artery (Eigure 6). One year after the cerebral insult, hehas a residual right hemiparesis without cardiac symptoms.

Discussion

Pathologic studies show a high correlation between the degree of atheromain coronary, cerebral, and carotid arteries. On the other hand, in some clinicalstudies it has been confirmed that, in survivors of myocardial infarction, theprevalence of cerebrovascular disease is surprisingly low. The discrepancybetween the reported frequency of cerebrovascular episodes due to embolifrom the heart in pathologic and clinical studies remains unexplained.*'

According to Chin et al.," 13% of patients over the age of 60 who areadmitted to the hospital with a myocardial infarction develop a stroke.Thompson and Robinson' in 783 patients with myocardial infarction found thatabout 2% of them had brain infarctions. As the percentage varies greatly if oneuses myocardial infarction as the index, there is low incidence of stroke, but ifone uses stroke as an index, a higher incidence of myocardial infarction isdetected.^ Serum elevation of creatine phosphokinase and serum fibrinogenhas been used as an index to measure the size of myocardial infarction. Thegreater the myocardial damage, the greater the risk of experiencing cerebral


emboli. This has brought to light the necessity of anticoagulate prophylac-tically those patients with large-sized myocardial infarction.'' Once a strokeoccurs, little can be done. The only adequate treatment is prevention through asuitable management of the risk factors such as hypertension, hypercholes-terolemia, hyperlipidemia, heavy cigarette smoking, diabetes mellitus, ele-vated hematoerit, and generalized obesity.'* However, for some other authors,hypercholesterolemia and cigarette smoking, which increase the risk ofmyocardial infarction, have little effect on cerebral infarction risk.^ Also, it iswell known that diabetic patients are more prone to silent myocardial infarc-tions; however, this was not the case in our 3 patients. None of them haddiabetes mellitus, and the cerebral accident was the first manifestation of theirmyocardial infarction. The detection of this whole clinical setting is important,because patients experiencing myocardial infarction with stroke have twice themortality of patients experiencing a stroke alone within the next 5 years."*

It is possible that some patients with an acute stroke may develop amyocardial infarction, and this may be undetected due to an impaired state ofconsciousness.•'' It has also been postulated that the heart may be damaged bymassive sympathetic discharges from the brain and by an increased amount ofcirculating catecholamines." None ofthe patients had hemodynamic complica-tions, and neither serious hypertension nor hypotension were found. Also, wedid not observe cardiac arrhythmias in any ofthe cases. Although it is impossi-ble to be certain ofthe embolic nature ofthe cerebral infarction, the clinicalcourse characterized by sudden onset ofthe cerebral deficit seems to supportthis contention. The ECGs showed extensive myocardial necrosis. Thesecases support the idea that large-sized myocardial infarcts may be associatedwith cerebrovascular accidents and emphasize that a silent myocardial infarc-tion should be sought in each case of cerebral infarct.

Acknowledgement

The authors wish to acknowledge Adela Badui for her valuable help in thepreparation of this manuscript.

Ellas Badui, M.D., F.A.C.A.Bosque de Granados 521Bosque de las LomasMexico 11700, D.F.Mexico

Badiu—Cerebrovascular Accident and Silent Myocardial Infarction 709References

1. Angiotensin, myocardial infarction, andstrokes (editorial). Lancet 1:1273. 1972.

2. Hurst JW: The Heart. Fourth Edition. NewYork, McGraw Hill. p. 1130.

3. Thompson PL, Robinson JS: Stroke afteracute myocardial infarction: Relation to in-farct size. Br Med J 2:457. 1978.

4. Cerebral infarction, myocardial infarction: Asimilar etiology (editorial). Lancet 1:1239.1978,

5. Conomy JP: Stroke and disorders ofthe heart.Vol. 2. In: Special Courses of The AmericanAcademy of Neurology, Meeting, 1979. pp.32-100.

6. McAllen PM. Marshall J: Cerebrovascular in-cidence after myocardial infarction. J NeurotNeurosurg Psychiatry 40:951. 1977.

7. Chin PL. et al: Myocardial infarction: Coinci-dent with cerebrovascular accidents in the el-derly. Age and Aging 40:951, 1977.

8. Kagan AR: Atherosclerosis and myocardiallesions in subjects dying from fresh cere-brovascular disease. Bull WHO 53:697. 1976.

9. Dimant J. Grob D: Electrocardiographicchanges and myocardial damage in patientswith acute cerebrovascular accidents. Stroke8:448. 1977.

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Coincidence of Cerebrovascular Accident and Silent Myocardial Infarction