Time Course of Sympathetic Neural Hyperactivity After Uncomplicated Acute Myocardial Infarction

Abstract

Background-Little information is available on sympathetic activity after acute myocardial infarction (AMI), despite the belief that sympathetic drive is important in relation to morbidity and mortality. Indirect indices such as plasma catecholamines are transiently elevated after uncomplicated AMI, whereas other prognostically important autonomic indices may be affected longer. We planned to quantify central sympathetic output to the periphery after uncomplicated AMI and to investigate its progress over time. Methods and Results-After uncomplicated AMI, 13 patients had muscle sympathetic nerve activity (MSNA) assessed from multiunit discharges and from single units with defined vasoconstrictor properties (s-MSNA). Measurements were obtained 2 to 4 days after AMI and were repeated after 3 and 6 months. We also examined 3 matched control groups comprising normal subjects, patients with coronary artery disease, and hospitalized patients without AMI. MSNA and s-MSNA after AMI (84Ϯ4.6 bursts/100 beats and 95Ϯ5.8 impulses/100 beats) were unchanged at 3 months but decreased (PϽ0.01 and PϽ0.001) after 6 months (75Ϯ4.0 bursts/100 beats and 80Ϯ4.4 impulses/100 beats). These were still greater (at least PϽ0.01) than values in normal subjects, patients with coronary artery disease, and hospitalized patients without AMI (51Ϯ3.9 bursts/100 beats, 58Ϯ4.7 impulses/100 beats; 56Ϯ2.2 bursts/100 beats, 61Ϯ2.2 impulses/100 beats; and 55Ϯ3.6 bursts/100 beats, 61Ϯ3.3 impulses/100 beats, respectively). This sympathetic hyperactivity was inversely correlated to left ventricular ejection fraction but not to changes in blood pressure. Conclusions-A protracted state of sympathetic hyperactivity was shown to occur after uncomplicated AMI. It is suggested that this hyperactivity may explain delayed cardiovascular morbidity and mortality and that it arises because of an impairment of reflexes from cardiac receptors.

Sympathetic Drive in Anterior and Inferior Uncomplicated Acute Myocardial Infarction

“…The same protocol was performed between the hours of 9:00 AM and 12:00 noon for all groups as previously reported. 4 Subjects were asked to have a light breakfast and to empty their bladder before commencing the study and were requested to avoid alcohol, nicotine, and caffeine products for 12 hours before investigation.…”

“…ympathetic hyperactivity has been shown to occur early after acute myocardial infarction (AMI), [1][2][3][4] although very little is known about whether its magnitude differs between anterior wall (ant-AMI) and inferior wall (inf-AMI) infarction. This information is important because it may be relevant to the prognosis after AMI and to the mechanisms of associated sympathetic activation.…”

Improving Myocardial Perfusion by Percutaneous Coronary Intervention Reduces Central Sympathetic Activity in Stable Angina

“…2 This state of increased sympathetic tone seems to persist beyond the ischemic event. 1 To our knowledge, there are no studies that have shown that reversal of ischemia by PCI reduces central sympathetic tone. In our patient group, sympathetic nervous system activity was indeed clearly increased.…”

“…1,2 The most likely explanation is stimulation of sympathetic afferents in the myocardial wall due to ischemia-induced release of a number of afferentstimulating substances. 3,4 If the ischemic stimulus is strong enough, a reflex increase in central sympathetic output occurs, despite current pharmacological interventions.…”

“…2 -5 In myocardial infarction, as well as in unstable angina, this state of sympathetic hyperactivity appears to be protracted for several months after the occurrence of the ischemic event, suggesting a persistent change in central autonomic balance. 1 Patients with documented coronary artery disease (CAD) and exercise-provoked angina (stable angina) show a similar state of sympathetic hyperactivity, although the persistence of this effect in time is less well established. 6 As myocardial ischemia seems to be the trigger of this state of sympathetic hyperactivity, removing this trigger would be expected to reduce sympathetic overactivity.…”