Page 104 - Cardiac abnormalities after aneurysmal subarachnoid hemorrhage
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Chapter 7
Also, autopsy on hearts of cerebrally injured patients revealed massive infiltration of inflammatory cells and contraction band necrosis or coagulative myocytolysis, both signs of myofibrillar degeneration.40, 42 Identical cardiac lesions were found in animal models with catecholamine infusion and in patients with pheochromocytoma.53, 54 As these lesions may also be induced in adrenalectomized animals44, but not in brain dead sympathectomized baboons55, it is concluded that a neurogenic mechanism is plausible. Furthermore, in Chapter 6 we describe a study that suggests a myocarditis in patients with aSAH. Myocarditis would be a plausible explanation for the cardiac abnormalities that are observed after aSAH.
Another approach to neurogenic myocardial dysfunction may be constructed using purinergic signaling. This non-adrenergic, non-cholinergic neurotransmission was discovered by Burnstock et al. in the early 1960’s.56 The neurotransmitter appeared to be extracellular Adenosine-5’-triphosphate (ATP) and was found to be an indispensable co-transmitter for the sympathetic nervous system.57 Mammalian cells have large quantities of the ATP molecule stored in secretory and synaptic vesicles of the sympathetic nerve endings.58 ATP in the CNS triggers pro-inflammatory reactions, predominantly by activation of the P2X7 receptor, which results in production and release of pro-inflammatory cytokines. Concomitantly with massive sympathetic activation, ATP is secreted in high quantities before being converted into extracellular adenosine. In ischemic heart disease, adenosine is known to protect the myocardium from reperfusion damage and massive infarction.59 Adenosine acts by opening ATP dependent potassium (KATP) channels, leading to membrane hyperpolarization, shortening of the cardiac action potential, and reduction of contractility.60, 61
Conclusions, clinical implications and future perspectives
This thesis shows that cardiac abnormalities after aSAH occur often, that they are associated with prognosis, independently of other clinical variables, that they are transient, that they may occur days after the onset of the aSAH and disappear several days/weeks after the aSAH, and that their occurrence may be predicted using troponin. Most likely, cerebral perfusion is impaired because of cardiac dysfunction which is a possible pathway through which prognosis is influenced. Finally, catecholamine induced myocarditis seems to occur after aSAH and would be a plausible explanation for the observed cardiac abnormalities.
The observed cardiac abnormalities after aSAH show striking similarities with stress cardiomyopathy or Tako-tsubo syndrome and they are reversible. Clinical implications of this thesis are: first, it may help physicians that are confronted with
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