Page 103 - Cardiac abnormalities after aneurysmal subarachnoid hemorrhage

It is known that stimulation of, epileptic seizures or stroke in particularly the insular cortex and amygdala may cause cardiac arrhythmias and other autonomic manifestations of cardiopulmonary dysfunction.47, 48
In addition to the cardiopulmonary control of the above described anatomical structures, the nucleus of the vagus nerve contains, among others, neurons that innervate the heart and the lungs. The preganglionic fibers of the right vagus nerve supply mostly the sinoatrial node, whereas the left vagus fibers are concentrated at the atrioventricular node. Consequently, stimulation of the right vagus influences the heart rate; the atrioventricular conduction is affected by the left vagus. Moreover, it was recently shown that parasympathetic nerve fibers innervate both atria and ventricles. The nerve density is higher on the ventricular endocardium, but nerve thickness is greater on the epicardium. The right ventricle (RV) is more densely innervated than the LV, whereas the LV endocardium is more densely innervated than the RV endocardium.49
The cardiac sympathetic nerves extend from the sympathetic neurons in stellate ganglia, which are located bilateral to the thoracic vertebra. Sympathetic nerve fibers project from the base of the heart into the myocardium, and are located predominantly in the subepicardium of the ventricle.
Sympathetic nervous activity is increased in patients with aSAH according to Naredi
et al.50 Plasma catecholamine concentrations are accepted as an index of sympathetic
nervous activity in cardiovascular and neurological disorders and they are caused
by a neurotransmitter spillover. Elrifai et al.44 found that plasma catecholamine
levels rose in their animal model with SAH and Sato et al.32 found elevated plasma
catecholamine levels in their study with patients suffering from aSAH. Increased local
release of catecholamines from the local nerve endings in the heart might mediate the
cardiac abnormalities following acute CNS stress. Rona et al.51 first provided evidence
that administration of high systemic doses of isoproterenol produced focal necrotic
lesions in normal rat hearts. A transient severe coronary vasoconstriction causing
ischemia, post ischemic left ventricle failure, and myocardial damage has been posed 7 to be a consequence of the catecholamine release. This might cause a “neurogenic
stunned myocardium”, referring to the post ischemic reperfusion injury. However, Zaroff et al.52 found no evidence of myocardial hypoperfusion in his experimental SAH study on dogs. A more plausible hypothesis is that a direct cardiotoxic effect of catecholamines leads to development of myofibrillar degeneration and subsequent myocardial dysfunction. Catecholamines may act on the ß-adrenoreceptor, inducing reversible injury through excessive cellular Ca2+-influx.
General Discussion
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