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Supports SNS modulation as CVD target; leaves open confirmation via prospective trials.
The sympathetic nervous system has been viewed as the critical mechanism for cardiovascular response to increased circulatory needs during acute stress, augmenting cardiac rate and contractility and changing peripheral vascular tone. These physiologic responses, however, are increasingly thought to cause long-term adverse effects‒such as altered myocardial function; renal, systemic, and coronary vasoconstriction; ventricular arrhythmias; and left ventricular hypertrophy‒for some patients with cardiovascular disease. How the sympathetic nervous system affects the pathophysiology of cardiovascular diseases is not fully understood, although new techniques for assessing plasma catecholamines and for quantitating sympathetic activity are adding to our knowledge. Nevertheless, a review of the physiologic responses to sympathetic nervous system stimulation reveals much about their possible role in the cardiovascular disease process. Am J Hypertens 1989;2:353S–356S
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Joseph L. Izzo (1989) studied this question.
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