Relation of mean heart rate and heart rate variability in patients with left ventricular dysfunction.
The new finding was that mean heart rate and heart rate variability were more closely coupled in patients with more advanced LV dysfunction. Mean heart rate explained a larger portion of variance in heart rate variability in patients in the lowest LVEF quartile than in those in the highest one. These results support our hypothesis that sympathetic activation in patients with more severe LV dysfunction results in closer correlation between heart rate and heart rate variability. Generally, the correlation between mean heart rate and heart rate variability is weak because heart rate and heart rate variability represent different modalities of cardiovascular regulation. Mean heart rate is normally determined by the interactions of both the sympathetic and parasympathetic nervous systems, whereas modulation of these activities, with different gains, determines the magnitude of heart rate variability. This results in great complexity in control of the heart by the autonomic nervous system. However, heart rate is likely to be more dominantly regulated by the sympathetic nervous system because of vagal withdrawal in patients with more severe LV dysfunction. The effect of sympathetic cardiac modulation has been shown to be more sluggish than that of the parasympathetic nervous system in beat-to-beat regulation of heart rate. This may result in more blunted heart rate variability concomitantly with elevated mean heart rate. Thus, variation in heart rate variability in any given mean heart rate is likely to be lower than in patients with more preserved LV function, and hence with more complex cardiac autonomic regulation with involvement of the parasympathetic nervous system. Indeed, even the slopes of regression lines between mean heart rate and heart rate variability were similar in the first and fourth LVEF quartile; the intercept of the regression line was significantly higher in the fourth quartile than in the first one. This further supports our hypothesis.
Hedman
A E
AE
Department of Cardiological Sciences, St. George's Hospital Medical School, London, United Kingdom.
Poloniecki
J D
JD
Camm
A J
AJ
Malik
M
M
D000328:Adult; D000368:Aged; D000638:Amiodarone / Q000627:therapeutic use; D000704:Analysis of Variance; D000889:Anti-Arrhythmia Agents / Q000627:therapeutic use; D015716:Electrocardiography, Ambulatory; D005260:Female; D006321:Heart / Q000294:innervation; D006339:Heart Rate; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000150:complications / Q000188:drug therapy; D012984:Software; D013318:Stroke Volume; D018487:Ventricular Dysfunction, Left / Q000209:etiology / Q000503:physiopathology*
D000889:Anti-Arrhythmia Agents; D000638:Amiodarone