Power spectral analysis of cardiovascular variability in patients at risk for sudden cardiac death

Abstract

The time series of successive heart periods present important variations around its mean value, determining the phenomenon of heart rate variability (HRV), assessed with both time and frequency domain approaches. A low standard deviation of the heart period (a time domain index of HRV) is a powerful prognostic indicator of sudden coronary death in patients recovering from acute myocardial infarction. Spectral analysis of HRV usually demonstrates two major components: indicated as LF (low frequency, approximately 0.1 Hz) and HF (high frequency, approximately 0.25 Hz). They are defined by center frequency and associated power, which is expressed in msec2 or normalized units. When assessed in normalized units, LF and HF provide quantitative indicators of neural control of the sinoatrial node. Numerous experimental and clinical studies have consistently indicated that the LF component is a marker of sympathetic modulation and HF a marker of vagal modulation; the LF/HF ratio is a synthetic index of sympathovagal balance. In the analysis of 24-hour Holter recordings of normal subjects, a circadian rhythmicity of spectral markers of sympathetic and vagal modulation is clearly present, with a sympathetic predominance during the day and a vagal predominance during the night. In patients recovering from an acute myocardial infarction, spectral analysis of HRV revealed an increased sympathetic and decreased vagal activity during early convalescence, and a return to their normal balance by 6 to 12 months. A clear increase of LF was also evident in patients studied within a few hours of the onset of symptoms related to an acute myocardial infarction, independent of its location. Similarly, LF increased during transient myocardial ischemia. An increase in markers of sympathetic activity has also been observed prior to episodes of malignant arrhythmias. Spectral analysis of HRV could help in the understanding of the role of abnormal neural mechanisms in sudden coronary death, thus contributing to its prevention.