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a patient with aSAH and cardiac dysfunction to better understand it and to avoid invasive investigations such as coronary angiography and associated anticoagulation because of suspected myocardial infarction. Second: potential donor hearts in neurologically injured patients could be rejected, because structural heart disease cannot be excluded. However, as stress cardiomyopathy is reversible, these hearts could be used for transplantation although data is not available. Third: this thesis helps in understanding the cardiac dysfunction after aSAH and may guide clinicians in treatment as management of patients stress cardiomyopathy after aSAH has not been established. Because of the potential reversible nature, supportive management may be sufficient. Evidence for prophylaxis is not yet provided, although α- and β-receptor blockers have been suggested. Early studies have shown a possible beneficial effect on prevention of cardiac abnormalities after aSAH. In rabbits, an α-blocker prevented death and pulmonary edema after they had been infused with epinephrine.62 90 patients with aSAH received orally the non-selective α-receptor blocker Phentolamine and the non-selective β-blocker Propanolol. Of the 12 patients that underwent autopsy, no myocardial lesions were found in the group that received drugs when they died. In the placebo group all patients had necrotic myocardial lesions.63 Clinical use however, is still under discussion. Calcium antagonists, in particular nimodipine, have proven to have a beneficial effect on neurological outcome. The calcium channel blocker prevents delayed cerebral events (although incidence of vasospasm did not decrease) and improves clinical outcome, but may induce hypotension and the effect on cardiac dysfunction or myocarditis in aSAH is unclear. Furthermore, decreased cardiac output in the acute phase of aSAH may impair cerebral perfusion as is described in Chapter 5. Inotropic support, for example dobutamine and milrinone, has been effective in restoring cardiac function, although evidence is weak.64, 65
The SEASAH paper in Chapter 3 describes the results of a prospective multicenter
study in the Netherlands in third line referral university centers. Clinical meaning
of our study in other settings such as different healthcare logistics or hospitals with 7 other aSAH protocols should be interpreted with caution. Since SEASAH was an
observational study and although associations could be made, sound conclusions on pathophysiology or therapeutic options should be perceived with caution.
Future studies in patients with aSAH and cardiac dysfunction should be directed
towards therapeutic studies such as inotropic therapy or immunosuppressives to
improve outcome. Also, further understanding of the purinergic signaling is an
important topic of study. Inhibition of purinergic signaling by the administration
General Discussion
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