Low frequency spectral component of heart rate variability and myocardial beta-adrenoceptor density after acute myocardial infarction.

OBJECTIVE

The low frequency spectral component (LF; 0.04-0.15 Hz) of heart rate variability (HRV) is considered to be an index of sympathetic modulation of sinus node activity under physiological conditions, although the relationship is less clearly defined in non-physiological conditions. Several cardiovascular diseases are characterized by an absent or blunted 24-h pattern of the LF spectral component. The aim of the present study was to investigate the relationship between chronically increased neural sympathetic efferent drive to the heart, quantified in terms of downregulation of myocardial beta-receptors, and the 24-h power of the LF spectral component in patients after acute myocardial infarction.

METHODS

In 24 patients, HRV was analyzed for a 24-h period, one month after an uncomplicated Q wave myocardial infarction. The following time domain measures and spectral components were calculated: mean RR, SDNN, SDANN, RMSSD, SDNN index, pNN50, and very low frequency (VLF), low frequency (LF) and high frequency (HF) spectral components. The density of beta-adrenoceptors was measured in vivo by positron emission tomography (PET) with 11-CGP-12177.

RESULTS

Post-AMI patients had normal plasma levels of adrenaline and noradrenaline (respectively 1.48 +/- 0.18 and 0.28 +/- 0.03 IU/L) but reduced myocardial beta-adrenoceptor density (6.86 +/- 0.24 pmol/g). Patients had similar heart rates but lower values of SDNN and SDANN compared with control subjects. The absolute and normalized power of the spectral components were similar in the two groups, but the usual day-night oscillation was blunted in patients. Moreover, the day-night change in the power of the LF spectral component was positively related (r = 0.51; p < 0.001) to the myocardial beta-adrenoceptor density.

CONCLUSIONS

The loss of the day-night oscillation of the LF spectral component appears to be a significant marker of sustained sympathetic over-activity in post-AMI patients.