Neurogenic heart disease: a unifying hypothesis

Electrocardiographic abnormalities have been known to occur in the context of neurologic disease for a long time. These changes fall into 2 categories: arrhythmias and repolarization abnormalities. However, until relatively recently these changes were believed to represent purely electrophysiologic alterations and not real heart disease. It is now clear that some patients with neurogenic electrocardiographic changes show cardiac enzyme release and myofibrillar degeneration at autopsy. There are 4 major methods for producing myofibrillar degeneration (i.e., contraction band necrosis or coagulative myocytolysis): catecholamine infusion, stress-steroid, nervous system stimulation and reperfusion. The common thread connecting these 4 methods is the opening of receptor-operated calcium channels, resulting in intense contraction of cardiac muscle. Thus, neurogenic influence over cardiac function may represent a continuum. In the mild reversible circumstance, only the electrocardiographic change will be seen, whereas in the severe, irreversible situation, myofibrillar degeneration will ensue with release of cardiac enzymes. Cardiac cell death may be caused by oxygen free radicals produced by metabolism of catecholamines or reperfusion or both, after variable periods of ischemia. This concept represents a unifying hypothesis, tying together the clinical, physiologic, biochemical and pathologic findings in neurogenic heart disease.