Spontaneous subarachnoid hemorrhage simulating acute transmural myocardial infarction

Volume

105

Number

3

Brief

with Duchenne’s dystrophy is lower than in the erythrocytes of controls, suggesting that these calcium transport channels may be more sensitive to verapamil than are normal channels.8 Evidence thus supports the contention that verapamil may adversel:y affect skeletal muscle contraction, especially if the neuromuscular transmissionexcitation-contraction safety margin is compromised, as in Duchenne’s dyst,rophy. Certain drugs whose main action is at a site other than the neuromuscular junction have been associated with postoperative respiratory depression and with aggravation or unmasking of myasthenia gravis.6 Proposed mechanisms include depression of postsynaptic sensitivity (e.g., procainamide, tetracyclines) or combined depression at postsynaptic and presynaptic sites. The latter is due to interference with calcium ion fluxes at the nerve terminal, causing inhibition of neurotransmitter release (e.g., phenytoin).” Although verapamil might interfere with calcium fluxes in an analogous fashion, conclusive data are not available. Thus the above mechanisms are speculative. Our patient also received intravenous procainamide for 1 week following respiratory arrest,. Procainamideinduced muscle weakness has been reported not. only in patients with myasthenia gravis but in patients with other conditions in which the neuromuscular transmission safety margin is decreased? Procainamide might thus have contributed to the persistence of respiratory muscle dysfunction. Another factor that may have promoted respiratory muscle failure was direct-current cardioversionrespiratory muscle fatigue following vigorous contraction. However, the observed sequence of events implicates verapamil, not cardioversion, as the precipitating mechanism. Atria1 flutter and respiratory muscle weakness and failure are common complications of advanced Duchenne’s dystrophy. Intravenous verapamil can be used to slow the ventricular response to atria1 flutter, but it may precipitate respiratory muscle failure in Duchenne patients with marginal reserve. Procainamide can induce muscle weakness when the neuromuscular transmissionexcitation-contraction safety margin is diminished, and cardioversion, by stimulating vigorous contraction of injured respiratory muscles, may cause serious muscle fatigue. We especially call attention to sudden respiratory failure believed to have been precipitated by intravenous verapamil, and we discuss the theoretical basis for this effect. REFERENCES

Emery AE, Skinner

R, Howden LC, Matthews MB: Verapamil in Duchenne muscular dystrophy (Letter). Lancet 1:559, 1982. 2. Singh BH, Ellrodt G, Peter CT: Verapamil: A review of its pharmacological properties and therapeutic use. Drugs

1.

15:169,

1978.

3. Langer GA, Serena SD, Nudd LM: Localization of contractile-dependent CA: Comparison of Mn and verapamil in cardiac and skeletal muscle. Am J Physiol 229:1003, 1975. 4. Bondi AY: Effects of verapamil on excitation-contraction coupling in frog sartorius muscle. J Pharmacol Exp Ther 205x49, 1978. 5. Durant NN, Nguyen N, Briscoe JR, Katz RL: Potentiation of

Communications

511

pancuronium and succinylcholine by verapamil. Anesthesiology. (In press.) Argov Z, Mastaglia FL: Disorders of neuromuscular transmission caused by drugs. N Engl J Med 301:409, 1979. Balzer H: The effect of quinidine and drugs with quinidinelike action (propranolol, verapamil and tetracaine) on calcium transport system in isolated sarcoplasmic reticulum vesicles of rabbit skeletal muscle. Naunyn Schmiedehergs Arch Pharmacol 274:256, 1972. Mollman JE, Cardenas JC, Pleasure DE: Alteration of calcium transport in Duchenne erythrocytes. Neurology 30:1236, 1980. Niakan E, Bertorini ET, Acchiardo SR, Werner MF: Procainamide-induced myasthenia-like weakness in a patient with peripheral neuropathy. Arch Neurol 38:378, 1982.

Spontaneous subarachnoid hemorrhage simulating acute transmural myocardial infarction Pedro Gas&n, M.D., Ph.D., Timothy J. Ley, M.D., Robert J. Toltzis, M.D., and Robert 0. Bonow, M.D. Bethesda,

Md.

ECG abnormalities have long been reported in patients with central nervous system disorders.‘-“In 1954Burch et al.* described an ECG pattern that they considered distinctive of cerebrovascular accidents: large and often inverted T waves, prolonged QT intervals, and large U waves. In this report we describea patient with the ECG changes of an evolving acute transmural inferior wall myocardial infarction occurring in association with a subarachnoid hemorrhage. These EGG changesreverted to normal within 24 hours. A 57-year-old white clergyman with no history of heart diseasewasfound comatose.He presentedno focal neurologic deficits. His blood pressurewas 110/70 mm Hg but later rose to 140-150/70-80mm Hg. His ECG revealed atria1 fibrillation, abnormal Q waves in leads II, III, and aVF, and ST segmentdepressionin leadsI, II, aV,, and V, to V, (Fig. 1). These findings were new compared with a normal ECG taken 4 years previously. One hour later his ECG showedlossof R wave voltage in the inferior leads. Five hours later the inferior Q waveshad deepened.After 12 hours, the ECG abnormalities had almost,disappeared except for a Q wave in lead III and lateral wall ischemic changes.The ECG reverted to normal after 24 hours. The patient’s first hours of hospitalization were remarkable for an episode of nonsustained ventricular tachycardia and several episodesof Mob&z type II atrioventricular block. A computed tomographic scan of the brain (Fig. 2) and a cerebral arteriography revealed a subarachnoidhemorrhage causedby a ruptured aneurysm of the left middle cerebral artery, which was later successfullyrepaired. At From the Cardiology National Institutes Received Reprint Institutes

for publication

Branch, of Health. May

requests: Pedro Gas&n, of Health, Bethesda,

National

Heart,

10, 1982;

accepted

M.D., Building MD 20205.

Lung May

and

Blood

Institute,

19, 1982.

10, Room

7D-19,

National

512

Brief

March,

Communications

American

Heart

1983 Journai

2. Computed tomographic scan of the brain reveals an area of increased uptake in the left temporal lobe causedby a subarachnoidhemorrhage,subsequently documented to be secondary to a bleeding middle cerebral artery aneurysm. Fig.

0

1

2

3

4

5

Fig. 1. Evolution of the ECG in the first 24 hours of hospitalization. In column 0, the ECG obtained 4 years prior to the acute event is shownfor comparison.LeadsV, to V, were normal then and during the event.

the time of admission,the creatine phosphokinase(CPK) level was693 mu/ml and the lactic dehydrogenase(LDH) ievel was348 U/ml. However, subsequentCPK and LDH levels were all within normal limits. Furthermore, CPK and LDH isoenzymedeterminations of the patient’s initial serum samplesrevealed normal myocardial components. Resting thallium-201 scintigrams of the heart revealed normal myocardial perfusion. Although several reports of “cerebral Q waves” resembling anterior wall myocardial infarction have been published, very few patients have been reported to have new inferior lead Q waves associated with intracranial disease,3,‘,”and only one has demonstrated reversion of the ECG to normal.’ These caseshave been less completely documented than this one, in which the ECGs rapidly evolved in a pattern consistent with transmural inferior wall myocardial infarction. In addition, several arrhythmias developed during the first 24 hours of our patient’s hospitalization, further mimicking the course of acute myocardial infarction. The causeof “pseudoinfarction” Q wavesthat accompany central nervous system disorders remains unknown. Most authors postulate that sympathetic overstimulation is of prime importance in their development.7 In most casesof new “cerebral Q waves,” postmortem studieshave revealed no evidence of recent infarction or myocardial necrosis.3In a few cases,5,’ myocytolysis hasbeenreported to be unrelated to vascular distribution but similar to that induced by exogenouscatecholamines.RNew and persis-

Volume Number

105 3

Brief

tent & wavescould be due to neurohumoral damageto the myocardial cells, caused either by focal ischemia from vasoconstriction of the myocardial microcirculation or by a direct toxic effect of catecholamines. In the case of reversible Q waves, however, this hypothesis is not fully satisfying. Although T wave abnormalities associatedwith acute central

nervous system events are widely

recognized,

stenotic

Communications

Stenotic bicuspid 8‘ :

aortic valve -from above

513

con@enttalty aorttc valve

the

“cerebral Q wave” phenomenonhas been lesscompletely described precordial

and until now was well documented only in the leads. Potentially catastrophic mismanagement

of such patients may be avoided by awarenessof this condition. REFERENCES

1.

Byer E, Ashman R, Toth LA: Electrocardiograms with large, upright T waves and long Q-T intervals. AM HEART J 33:796, 1947.

Burch GE, Myers R, Abildskov JA: A new electrocardiographic pattern observed in cerebrovascular accidents. Circulation 9:719, 1954. 3. Srivastava SC, Robson AO: Electrocardiographic abnormalities associated with subarachnoid hemorrhage. Lancet 2:431, 1964. 4. Yamour BJ, Sridharan MR, Rice JF, Flowers NC: Electrocardiographic changes in cerebrovascular hemorrhage. AM 2.

HEART J 99:294,

Aneurysm

’

/’

,I’ Cal&urn

Thr&bus

1980.

Duren DR, Becker AE: Focal myocytolysis mimicking the electrocardiographic pattern of transmural anteroseptal myocardial infarction. Chest 69:506, 1976. 6. Hammermeister KE, Reichenbach DD: QRS changes, pulmonary edema, and myocardial necrosis associated with subarachnoid hemorrhage. AM HEART J 76:94, 1969. Cruickshank JM, Neil-Dwyer G, Scott AW: Possible role of catecholamines, corticosteroids and potassium in production of electrocardiographic abnormalities associated with subarachnoid hemorrhage. Br Heart J 36:697, 1974. Alpert LI, Soo Hwan P, Zak FG, Werthamer S: Cardiomyopathy associated with a pheochromocytoma: Report of a case with ultrastructural examination of the myocardial lesions. Arch Path01 93:544, 1972. 5.

Fig. 1. Drawing of heart (upper panel) showing the healed left ventricular apical aneurysm and the congenitally bicuspid, stenotic aortic valve; and a photograph the valve (lower panel).

of

ventricular (LV) pressuregenerally returns to or toward normal

Aortic valve stenosis and left ventricular apical aneurysm and/or rupture: Real or potential complications of persistent left ventricular systolic hypertension after acute myocardial infarction William C. Roberts, M.D., Ernest N. Arnett, M.D., SeenaC. Aisner, M.D., and Paul Techlenberg, M.D. Bethesda

and Baltimore,

Md.

When acute myocardial infarction (MI) occursin patients with systemic hypertension,

the systemic arterial

end left

From the Pathology Branch, National Heart, Lung and Blood Institute, National Institutes of Health; and the Departments of Cardiology and Pathology, Franklin Square Hospii.al. Received for publication July 8, 1982; accepted July 27, 1982. Reprint requests:William C. Roberts, M.D., National Institutes of Health, Bldg. lOA, Room 3E-30, Bethesda, MD 20205.

if the MI was fairly large. When acute MI occurs in

patients with significant aortic valve stenosis(AS), however, the LV systolic pressure remains elevated and the continuation

of this pressure

elevation

increases

the like-

lihood of LV rupture or aneurysmalformation, particularly when the MI involves the LV apical wall which normally is several times thinner than the LV basal wa11.‘,2 Such

wasthe casein a 67-year-old man, who died of progressive congestiveheart failure after healing of more than one (by history) acute MI in the previous 5 years. At necropsy he had a severely stenotic congenitally bicuspid aortic valve and a large apical aneurysm at the site of a healed LV MI (Fig. 1). The heart weighed 630 gm. Both the left anterior descending and left circumflex coronary arteries were narrowed 76% to 100% in cross-sectionalarea by atherosclerotic plaques.The occurrenceof LV free wall rupture and/or aneurysmalformation hasnot beenreported previously in a patient with severeAS. This fact is surprising in view of the elderly age of many patients with AS. REFERENCES

1. Roberts WC, Ronan ventricular free wall

JA Jr, Harvey WP: Rupture of the left (LVFW) or the ventricular septum (VS)