Reviewer Critique of the Sympathetic Drive After Acute Myocardial Infarction in Hypertensive Patients

An abnormal sympathetic neural drive to the heart as well as to peripheral vessels characterizes a consistent number of cardiovascular as well as noncardiovascular diseases, such as hypertension, congestive heart failure, acute myocardial infarction (MI), thromboembolic stroke, obesity, metabolic syndrome, renal failure, respiratory failure, and hepatic cirrhosis.1 In some of these conditions (ie, heart failure, MI, stroke, renal failure, and liver cirrhosis), the sympathetic overactivity displays a clear prognostic relevance, higher circulating plasma levels of norepinephrine being associated with a worse prognosis, or life-threatening complications.1 In the present issue of the Journal, Hogarth and co-workers2 provide new data on the patterns of the adrenergic circulatory dysfunction characterizing a clinical state with an elevated cardiovascular risk (ie, an acute coronary event complicating an established hypertensive state). The main findings of the study can be summarized as follows. First, the degree of sympathetic activation in the acute post-MI phases is greater in magnitude in patients with than in those without high blood pressure (BP). Second, an analysis of the time course of the MI-related neuroadrenergic abnormalities shows that not only in the acute post-MI phases but also several weeks or months after the coronary event the magnitude of the hyperadrenergic state remains much greater in hypertensive than in normotensive patients. Finally, the reported sympathetic alterations appear to be almost completely reversible, no adrenergic overdrive being detected at the latest examination planned by the study’s investigators (9 months after MI).