Proper understanding of the mechanisms involved in heart rate turbulence (HRT) may offer an explanation of why it is such a potent postinfarction risk stratifier. This article reviews the physiological background of ventriculophasic sinus arrhythmia-a phenomenon which shares some underlying physiological features with HRT including cardiac autonomic regulation. It is now believed that HRT is principally triggered by a transient loss of vagal efferent activity in response to the missed baroreflex afferent input due to ventricular premature beat-induced haemodynamically inefficient ventricular contraction. Studies are summarized which support more or less directly this hypothesis. The physiology of early acceleration and late deceleration of heart rate after a ventricular premature beat is discussed. Qualitatively different but otherwise quantitatively uniform postectopic dynamics of systolic blood pressure after ventricular premature beats is demonstrated in subjects with normal and abnormal left ventricular function. It is concluded that the slope of late deceleration of heart rate after ventricular premature beats can serve as a reasonable surrogate for baroreflex sensitivity.