Heart rate variability in time domain after acute myocardial infarction

These results suggest that analysis of heart rate variability recorded even very early after acute myocardial infarction (1 to 2 days after onset of pain) is feasible in clinical routine and strongly related to subsequent arrhythmic events and cardiac mortality. Decreased HRV is considered not only a marker of impaired vagal activity of the heart but complete autonomic impairment, strongly associated with the degree of myocardial damage. HRV represents the integrated response of the cardiovascular system to a variety of different influences: the plasma level of catecholamines, the baroreflex activation and the direct sympathetic and vagal activity. The HRV profile is dynamic-HRV reduction caused by myocardial damage changes over time presenting a progressive increase up to normality over a 2-month follow-up. The observed early differences between anterior and inferior myocardial infarction disappear later in the healing phase. However, group analysis results of different HRV indices are stabile over time and highly reproducible, but presenting large individual variations. HRV parameters which are adjusted to heart rate (e. g. CV) seemed to be more stabile. The role of HRV analysis in risk stratification of patients after myocardial infarction is strongly related to the actual model of the genesis of ventricular arrhythmias. Multiple experimental and clinical studies described the development of life threatening ventricular arrhythmias as a multifactorial event which can not be described adequately using just one risk parameter for stratification. The arrhythmogenic substrate representing the underlying inhomogeneity of electrical behaviour of adjacent myocardial areas might be detectable by the analysis of ventricular late potentials or frequency disturbances from the signal averaged ECG. The autonomic modulation of this substrate is represented by an altered heart rate variability. Possible trigger factors to initiate arrhythmias in a modulated arrhythmogenic substrate like ventricular premature beats or transient myocardial ischemia can be detected by conventional arrhythmia and ST segment analysis from Holter tapes. The optimized combination of these non-invasive risk predictors together with well known evident clinical risk parameters, like left ventricular ejection fraction, may lead to a valid set of screening parameters for individual risk estimation after myocardial infarction.