Page 65 - Cardiac abnormalities after aneurysmal subarachnoid hemorrhage

Time course and risk factors for myocardial dysfunction after aSAH
and using liberal inclusion criteria we are confident we minimized potential bias.
Another possible limitation of observational studies is the generalizability to large
population cohorts. By designing this study as a multicenter national project in which
the majority of the Dutch aSAH treatment centers participated, we are confident we
minimized this limitation. Finally, we have no information on coronary arteries in our
patients as coronary angiograms or cardiac CT scans were not routinely performed.
The potential clinical benefit of our study is that troponin T may allow us to early
identify patients with a risk of developing early and late WMA. As delayed cerebral ischemia(DCI), an important prognosticator for poor outcome, usually occurs 4-7
days after the aSAH,23 the occurrence of late WMA may play an important role in
the development of DCI. However, this needs further investigation. We suggest that
patients with troponin T elevation after an aSAH are closely monitored and that
cardiac evaluation is performed to evaluate presence of WMA. Our data suggest that
therapy aimed at restoring LV function if the troponins are increased but WMA
are not (yet) present may be beneficial. However, the present study does not answer 4 the pathophysiologic question why positive troponins are risk factors for early and
late WMA. We hypothesize that cardiac abnormalities may manifest as a spectrum with some patients having ECG changes, troponin release and a severe impaired left ventricular function. Others may present with only ECG changes and they may develop troponin release or WMA in a later phase of the disease. Furthermore, we cannot exclude that treatment such as triple H therapy, Nimodipine or vasopressors also plays a role. These questions warrant more research.
Indeed, some studies have suggested that the use of ß-sympaticomimetics, phosphodiesterase inhibitors or calcium sensitizers can improve LV function.24, 25 As calcium overload due to the sympathetic catecholamine surge is suggested to be the mechanism of the WMA,26 these drugs should be effective in recruiting inotropic reserve. However, a drop in blood pressure and left ventricular outflow tract obstruction is reported after the use of for example dobutamine which may be especially harmful in patients with aSAH as cerebral perfusion must be optimized. Furthermore, the cardiac effects of aSAH treatment, for example administration of nimodipine, a calcium antagonist to prevent cerebral vasospasm, are also unknown. Therefore, before implementing such strategies, it is critical that large randomized clinical trials are performed to evaluate any potential therapeutic consequence of our findings.
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