Evidence of functional alterations in sympathetic activity after myocardial infarction

Abstract

To assess whether the presence of areas of efferent sympathetic denervation might contribute to alterations in sympathetic and vagal neural regulatory activities observed after myocardial infarction, we attempted to correlate the changes in the spectral components of RR variability with the I-123 MIBG and Thallium-201 uptake defects. Ten patients with first and uncomplicated myocardial infarction were studied. Thallium-201 and I-123 MIBG scintigraphy as well as spectral analysis of heart rate variability were performed 7 days, 4, 12 and 30 months after the acute event. Regional abnormalities in I-123 MIBG uptake were more extensive than the perfusion defects indicated by Thallium-201 images and remained constant throughout the entire period of observation. In the early post-infarction period, spectral analysis of RR variability was characterized by a predominant LF (74 +/- 6 nu) and a smaller HF (16 +/- 3 nu) component indicating a sympathetic predominance. Thereafter, we observed a progressive reduction in LF and a gradual increase in HF which were consistent with a normalization of sympatho-vagal balance. These data indicate that after a myocardial infarction, the presence and persistence of areas of sympathetic functional denervation do not seem to play a major role in determining the changes in sympathetic and vagal neural regulatory activities directed to the heart.

Early Time Course of Heart Rate Variability after Thrombolytic and Delayed Interventional Therapy for Acute Myocardial Infarction

“…Lombardi et al [16], who studied 33 patients with acute MI 3 h after the onset of symptoms and 1 week after hospital admission for HRV in time and frequency domain, found a lower HRV in patients with anterior MI during the acute phase and a significant increase in the low frequency component 1 week after the acute event in inferior MI reaching the values of patients with anterior MI. According to these findings, it can be hypothesized that the initial vagal hyperactivity [5]of an inferior MI is short-lasting, but capable of reducing sympathetic excitation, and is rapidly followed by sympathetic activation still detectable 4 weeks and several months after acute MI [17, 30]. After 1 year Lombardi et al [30]could detect a recovery of vagal tone and normalization of sympathovagal interaction in their infarct patients as compared to the control subjects.…”

“…To date, little data are available on the determinants of the cardiac autonomic tone represented by HRV in the acute phase of MI [8, 9, 14]and the time course during the first weeks after MI [15, 16, 17]. There is some information available on HRV analysis in postinfarction patients treated with thrombolysis [13, 18, 19, 20], but none on HRV in patients with both thrombolytic treatment and early interventional therapy for MI.…”

Cardiac adrenergic innervation within the first 3 months after acute myocardial infarction

“…However, any decisive conclusion cannot be drawn from their study, because only five patients underwent a 6‐month follow‐up. Correspondingly, in the study of Spinnler et al . (1993), no changes in the extent of MIBG defect were found between imagings obtained from 10 patients at 7 days and 30 months after a myocardial infarction.…”

Assessment of cardiovascular autonomic dysfunction in multiple system atrophy

“…The current study provided autonomic abnormalities in patients with MSA characterized by a decrease in sympathetic and parasympathetic activities. Previous studies [22,[30][31][32] reported that a diminished HRV, suggesting reduced sympathetic or parasympathetic activities, is associated with an increased risk of sudden cardiac death.…”