Page 12 - Cardiac abnormalities after aneurysmal subarachnoid hemorrhage

Chapter 1
In 1902, Harvey Cushing reported that increased intracranial pressure due to cerebral tumors leads to cardiopulmonary dysfunction.1 Since this early observation, it gradually became established that cardiac dysfunction may occur following several forms of physical,2-5 and emotional stress.6, 7 This dysfunction typically occurs in the absence of coronary artery disease, is mostly reversible and consists of myocardial wall motion abnormalities (WMA), electrocardiographic (ECG) changes, elevated serum markers for myocardial damage (troponin, CK-MB, BNP), and histopathological changes.8
The last few years, reported incidence of- and interest in this stress induced cardiomyopathy have significantly increased. Especially cases of Takotsubo cardiomyopathy (TC) have been reported rather frequently. TC is a transient stress induced myocardial dysfunction typically affecting the apex of the left ventricle, with hyperkinesia of the basal segments. This leads to dyskinesia or “ballooning” of the apex. The characteristic left ventricular angiographic or echocardiographic image has similarities with the shape of a Japanese octopus trap. In Japanese “Tako” means octopus and “Tsubo” means trap, hence the term: “Takotsubo cardiomyopathy”. Other commonly used terms are apical ballooning, stress cardiomyopathy and broken heart syndrome.6, 7 Furthermore, several authors have also reported stress induced wall motion abnormalities without the typical apical ballooning shape, but with diffuse WMA, midventricular ballooning, basal ballooning and other patterns. Typical ECG changes in stress cardiomyopathy are ST-segment changes, T wave changes, prominent U-waves and QTc prolongation.9, 10 Transient Q-waves have also been reported.11 In addition, arrhythmias consisting of ventricular tachycardia, ventricular fibrillation, atrial fibrillation, and atrial tachycardia have been described.12, 13 Serum Troponin, N-terminal portion of proBrain Natriuretic Peptide (NT-pro-BNP) and CK-MB may be elevated,14-16 as the result of cellular degradation.
Stress induced cardiomyopathy has also been reported quite frequently after aneurysmal subarachnoid hemorrhage (aSAH), a devastating neurological disease which carries a poor prognosis. An aSAH is caused by rupture of an intracranial aneurysm, causing acute sympathetic stress. Following this rupture, blood spurts into the subarachnoid space under arterial pressure, continuing until increased local or generalized intracranial pressure stops the bleeding. The annual incidence of aSAH adjusted for age and sex, is 7.8-23.0 per 100,000 population.17 In a systematic review case fatality after aSAH was reported between 32 and 67%,18 mainly caused by the
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