Number 24, 2004
Angina Pectoris

Neurogenic induced myocardial dysfunction

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Ivo A.C. van der Bilt, Frans C. Visser
Department of Cardiology, VU Medical Centre, Amsterdam, The Netherlands
Correspondence: Ivo van der Bilt, Department of Cardiology, VU Medical Center, Amsterdam, The Netherlands.
Tel: +31 204440123, fax: +31 20444, 2446, e-mail: Vanderbilt@vumc.nl

Introduction
ECG changes following central nervous system (CNS) events have been reported extensively [1–12]. Segmental wall motion abnormalities (SWMA), increases in cardiac-specific enzymes, and subendocardial infarctions or band necrosis may also occur in these patients [4,8,10,13–18]. These clinical signs might be interpreted as representing myocardial ischemia. Also, reversible SWMA and hemodynamic and ECG changes have been reported in patients with subarachnoid hemorrhage, Guillain–Barré syndrome [19], and subdural hematoma [20]. This may imply a neurogenic stunned myocardium, but insufficient evidence makes this diagnosis uncertain. Without appropriate tests, ischemic ECG changes and SWMA are difficult to differentiate from coronary insufficiency. Pulmonary edema has also been described in relation to subarachnoid hemorrhage [21], head injury, and status epilepticus. We describe a patient with myocardial dysfunction and pulmonary edema after a thalamic bleed.

Case report
A 59-year-old man, without medical history, presented to our First Heart Aid unit. He had collapsed suddenly while eating. On arrival, he responded when spoken to by moving his eyes and making unrecognizable noises.
On physical examination, communication was just possible by eye movement. He was sweating. Blood pressure was 200/110mm Hg, heart rate 60 beat/min, central venous pressure not increased. There were no heart and lung abnormalities or edema on the extremities, but right-sided hemiparesis and a right nystagmus were present. Glasgow Coma Score was: E4M6V1, isocoric pupils, normal light reflex.
The ECG at admission (Figure 1) showed a 60 beats/min sinus rhythm, left axis deviation, negative T-waves in leads I, II, AvL, V5-V6, and ST-segment elevations in leads AvR, V1-V5. QRS complex voltages suggested left ventricular hypertrophy. ECGs weeks later showed minimal changes. An echocardiogram on day 1 showed a dilated left atrium, no significant valve regurgitation, good left ventricular function without SWMA, and no signs of left ventricular hypertrophy. Computed tomography (Figure 2) revealed a thalamic bleed with breakthrough to the ventricles, and blood in the posterior horns, 3rd and 4th ventricles, and aqueductus. Chest X-ray (Figure 3) on admission showed an enlarged heart with enlarged pulmonary veins and minimal signs of pulmonary edema. The blood results showed normal cardiac-specific enzymes during admission.

Discussion
ECG changes occur with a frequency of 50% to 90% in association with subarachnoid hemorrhage [1,2,4,6–8,10,11]. Serial ECG monitoring reveals abnormalities in 100% of cases [2,9]. Common ECG changes in subarachnoid hemorrhage are sinus bradycardia (50%), ST-segment changes (50%), T-wave abnormalities (48%), prominent U-wave (44%), Q–T_c interval abnormalities (39%), signs of left ventricular hypertrophy (36%), sinus tachycardia (20%) [2,9,10]. Arrhythmias associated with increased isoenzyme concentration occur in 91% of patients [5]. Brouwers et al. [2] found that poor outcome in patients with subarachnoid hemorrhage was associated with fast rhythm disturbances and/or cardiac ischemia. Thus ECG changes indicate myocardial damage after subarachnoid hemorrhage, and may reflect severity of bleed and poor outcome.
ECG changes do not reflect purely electrical phenomenon: affected patients frequently show evidence of structural cardiac damage [10,13]. Mayer et al. [10] found that the presence of T-waves or Q–T_c segment prolongation on any ECG was associated with 100% sensitivity and 81% specificity for left ventricular dysfunction. Increased creatine kinase myocardial band (2%) was associated with 100% sensitivity and 94% specificity. Increased plasma myocardial enzymes and characteristic pathological lesions (contraction band necrosis or myofibrillar degeneration), and subendocardial infarctions are common in patients with subarachnoid hemorrhage [10], but pathological studies [10] and coronary angiography [15,17,22] have failed to demonstrate coronary disease, as confirmed in dogs: SWMA after subarachnoid hemorrhage occurred in the absence of myocardial hypoperfusion [12]. In catecholamine infusion in animals, and in patients with pheochromocytoma, identical cardiac lesions and focal and subendocardial myofibrillar degeneration were found. These lesions can be induced in adrenalectomized animals, so a neurogenic mechanism is plausible [13].
Increased release of catecholamines from local nerve endings in the heart may mediate these cardiac abnormalities. Transient severe coronary vasoconstriction leads to ischemia followed by postischemic ventricular failure and subendocardial myocardial damage. Also, a direct cardiotoxic effect of catecholamines may cause the development of subendocardial damage [13,15,18]. We describe ECG changes, SWMA, and signs of pulmonary edema in a patient with a thalamic bleed. The pulmonary edema might not be caused by left--sided heart failure. The blast injury theory [23] states that pulmonary edema after CNS events could be caused by a transient catecholamine burst in the pulmonary veins, the blast. The increased pulmonary vessel pressure caused by the increased sympathetic activity is of short duration, but of such extent that it leads to pulmonary capillary wall damage and acute pulmonary edema with pinky foamy sputum. After this initial stage the pulmonary arterial pressure normalizes, but pulmonary edema will not be restored for several days.▪

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REFERENCES

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