Abstract
nappropriate and excessive activation of the sympathetic nervous system has been invoked as a cause of coronary heart disease. This pathophysiological linkage can take 2 forms. The most direct and explicit is when acute sympathetic nervous activation triggers adverse cardiac events (myocar- dial infarction, atrial fibrillation, ventricular arrhythmias, and Takotsubo cardiomyopathy have all been documented) dur- ing acute severe mental stress. 1 Systematic evidence has been gathered at times of disasters, including war, missile attacks on civilians, and earthquakes, that strongly supports this proposition. The recently published and already celebrated analysis of coronary heart disease clinical presentations in German nationals in Munich during the 2006 Federation Internationale de Football Association World Cup provides a telling example in demonstrating a dose-response relationship of the level of acute mental stress (judged from the closeness of the contest and the particular relevance of the result to Germany), and presumably sympathetic nervous activation, to cardiac events.2 The case is no less strong that chronic sympathetic activa- tion is similarly adverse. In patients with heart failure, the cardiac sympathetic outflow is preferentially and often very highly activated. The level of this stimulation of the cardiac sympathetic outflow is directly related to reduced survival. 3 -Adrenergic blocking drugs break this link. Similarly, in patients with end-stage renal disease, the very high level of sympathetic activity, which is equal to that present in heart failure, almost certainly contributes directly to cardiovascular mortality.4 A similar claim has been made for depressive illness that the sympathetic activation present in the heart 5 underlies the increased cardiovascular mortality that exists, but here the case is less certain. In patients with essential hypertension, sympathetic acti- vation is also common, present in perhaps 50% of patients. 6 Recent evidence with endovascular radiofrequency ablation of the renal sympathetic nerves in patients with drug-resistant hypertension suggests that this activation of the sympathetic nervous system sustains the blood pressure elevation. 6 Per-
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