Page 32 - Cardiac abnormalities after aneurysmal subarachnoid hemorrhage

Chapter 2
effect was due to decrease of heart rate or due to systemic or neuroprotective effects of the beta-blockade. In contrast, tachycardia was associated with higher risk of death. Tachycardia may be a sign of poor hemodynamic condition or inotropic stimulation. Additionally, the presence of a P mitrale, a sign of left atrial dilatation, was associated with death. This abnormality may also represent a poor hemodynamic condition.
We also found a relation between cardiac abnormalities and DCI after SAH. DCI is a complication that occurs in around 30% of patients with SAH, usually between four to 12 days after the SAH,21 and is an important contributor to poor outcome. In contrast to thrombo-embolic stroke, which has a sudden onset, is unifocal, and usually does not affect consciousness, DCI usually has a gradual onset with often waxing and waning focal deficits, a decreasing level of consciousness, or both, and often is multifocal. The pathogenesis of DCI has not been elucidated yet, but is often attributed to vasospasm of the intracranial arteries. However, vasospasm cannot be the only initiator of DCI, as one third of patients with severe vasospasm do not develop DCI, and one third of patients with DCI do not have vasospasm.22 Powerful and independent predictors are the duration of loss of consciousness at time of the ictus and the total amount of extravasated blood,23 and the occurrence of hypovolemia and hypotension.24 Because many patients with SAH have narrowed arteries and hypovolemia, and also because autoregulation of cerebral perfusion is disturbed after SAH,25, 26 left ventricular dysfunction may directly affect cerebral perfusion. This is a potential explanation for the finding that cardiac abnormalities are also related to DCI. With this respect, not only the presence but also the degree of the cardiac abnormality may influence outcome. This notion is supported by the finding of a linear relation between the BNP levels and vasospasm severity.12 Additionally, the degree of troponin elevation has been associated with poor outcome.13
Although an association has been established, it remains unclear whether a definite causal relation exists between cardiac abnormalities and outcome after SAH. Several studies have found an independent effect of cardiac abnormalities on outcome, adjusted for clinical variables,11, 15, 27 whereas others did not.14, 28-30
Caution should be perceived when interpreting these results due to shortcomings of the included studies. First, the included studies were published over a period of more than 40 years. During this period, diagnosis and treatment of SAH has improved with decreased case fatality rates,1 possibly affecting prevalence and consequence of cardiac complications on outcome.
Second, reference values of cardiac markers were not given in all studies. Abnormal BNP levels were differently defined in the three studies that used BNP as prognosticator.
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