Heart rate variability and functional severity of congestive heart failure secondary to coronary artery disease.

To investigate the behaviour of heart rate variability (HRV) with the advancing severity of heart failure (CHF) we studied 20 normal subjects and 80 coronary artery disease (CAD) patients in sinus rhythm. CAD patients were selected consecutively in order to form four equal groups of 20 subjects with different degrees of CHF according to the New York Heart Association (NYHA) functional classification. In each subject a 24 h ECG Holter tape was recorded and subsequently analysed to obtain measures of heart rate and HRV. We used several measures of HR and both spectral and non-spectral measures of HRV. Among these we employed the width of the R-R interval distribution over 24 h at three different heights (TV, 10%Var, 50%Var). The CAD group showed significantly lower HRV counts and smaller spectral components than controls. However, these differences were due to the presence of CHF rather than to CAD. Indeed, a progressive and significant increase in heart rate and a contemporary decrease in HRV was observed with the advancing severity of CHF. Class IV patients had the smallest HR variation; the spectral composition in this group was barely detectable. The decrease in time domain measures of HRV followed the increase in NYHA Class in a progressive and regular pattern, while the low frequency and high frequency spectral power showed the largest reduction from NYHA Class I to NYHA Class II patients. No significant change was demonstrated in NYHA Class I patients as compared to Controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Heart rate variability during the acute phase of myocardial infarction.

BACKGROUND: After acute myocardial infarction (AMI), several abnormalities of the autonomic control to the heart have been described. Heart rate (HR) variability has been used to explore the neural control to the heart. A low HR variability count measured 7-13 days after AMI is significantly related to a poor outcome. Little information is available on HR variability early after AMI and its relation to clinical and hemodynamic data. METHODS AND RESULTS: We studied 54 consecutive patients (42 men and 12 women; mean age, 60.4 +/- 11 years) with evidence of AMI by collecting the 24-hour HR SD from Holter tapes recorded on day 2 or 3. We also measured HR variability in 15 patients with unstable angina and in 35 age-matched normal subjects. HR variability was lower in AMI than in unstable angina patients (57.6 +/- 21.3 versus 92 +/- 19 msec; p less than 0.001) and controls (105 +/- 12 msec; p less than 0.001). Also, HR variability was greater in non-Q-wave than in Q-wave AMI (p less than 0.0001) and in recombinant tissue-type plasminogen activator-treated patients with respect to the rest of the group (p less than 0.02). No difference was found for infarct site. HR variability was significantly related to mean 24-hour HR, peak creatine kinase-MB, and left ventricular ejection fraction (all p less than 0.0001). Patients belonging to Killip class greater than I or who required the use of diuretics or digitalis had lower counts (p less than 0.004, p less than 0.001, and p less than 0.024, respectively). Six patients died within 20 days after admission to the hospital. In these patients, HR variability was lower than in survivors (31.2 +/- 12 versus 60.9 +/- 20 msec; p less than 0.001), and a value less than 50 msec was significantly associated with mortality (p less than 0.025). CONCLUSIONS: HR variability during the early phase of AMI is decreased and is significantly related to clinical and hemodynamic indexes of severity. The causes for the observed changes in HR variability during AMI may be reduced vagal and/or increased sympathetic outflow to the heart. It is suggested that early measurements of HR variability during AMI may offer important clinical information and contribute to the early risk stratification of patients.