Page 89 - Cardiac abnormalities after aneurysmal subarachnoid hemorrhage

Myocarditis in patients with subarachnoid hemorrhage: a histopathological study
implications. As treatment with inotropics, or sometimes even immunosuppressives may be beneficial in infectious myocarditis, we speculate that these treatments can be beneficial in SAH patients as well. Additionally, the myocardial microthrombosis found in this study suggests that antithrombotic therapy is an interesting treatment option in SAH patients. This suggestion is further supported by the finding that intracranial microthrombosis probably plays a role in the pathogenesis of DCI after SAH.23 However, this is speculative and more research should be done to substantiate this.
Other conditions with acute catecholaminergic stress such as pheochromocytoma24 or pulmonary embolism25 have also been associated with myocarditis. Moreover, stress cardiomyopathy also known as Takotsubo cardiomyopathy, which is caused by acute sympathetic stress, has been linked to myocarditis using cardiac magnetic imaging that showed edema and late gadolinium enhancement indicating inflammation.26 However, whether the catecholamine myocarditis is a reaction to cell damage or that catecholamines trigger another pathway (e.g. apoptosis of endothelial cells) that attracts the inflammatory cells is unknown.
Although we feel our study sufficiently shows evidence of a myocarditis in patients
with SAH compared to controls, our study has shortcomings. Because we performed
a retrospective search of the pathology database, detailed clinical data were unavailable
to us. Because the reason of the clinician to request an autopsy was often unknown,
this includes the risk of bias. Thus, we cannot draw conclusions on the proportion
of SAH patients that have myocarditis. A prospective histopathology study is needed
to answer these questions. Another limitation is that autopsy did not confirm the
presence of an aneurysm in all patients. Brain autopsy was not performed in all 6 patients, because it requires additional consent, which is often not given by the
family if the cause of death obviously was an intracranial one. For these patients we had only information provided by the clinicians written on the autopsy form, which is often rather limited. However, if neurologists or neurosurgeons write SAH as clinical information, they usually mean SAH from an aneurysm and not traumatic SAH invariably. Given the fact that these patients had died from SAH, an aneurysm, or other arterial course of the SAH such as intracranial artery dissection is likely. Moreover, the sensitivity analysis excluding the patients without an aneurysm found similar results as in the main analysis.
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