Deceleration capacity of heart rate as a predictor of mortality after myocardial infarction: cohort study

Summary

Background

Decreased vagal activity after myocardial infarction results in reduced heart-rate variability and increased risk of death. To distinguish between vagal and sympathetic factors that affect heart-rate variability, we used a signal-processing algorithm to separately characterise deceleration and acceleration of heart rate. We postulated that diminished deceleration-related modulation of heart rate is an important prognostic marker. Our prospective hypotheses were that deceleration capacity is a better predictor of risk than left-ventricular ejection fraction (LVEF) and standard deviation of normal-to-normal intervals (SDNN).

Methods

We quantified heart rate deceleration capacity by assessing 24-h Holter recordings from a post-infarction cohort in Munich (n=1455). We blindly validated the prognostic power of deceleration capacity in post-infarction populations in London, UK (n=656), and Oulu, Finland (n=600). We tested our hypotheses by assessment of the area under the receiver-operator characteristics curve (AUC).

Findings

During a median follow-up of 24 months, 70 people died in the Munich cohort and 66 in the London cohort. The Oulu cohort was followed-up for 38 months and 77 people died. In the London cohort, mean AUC of deceleration capacity was 0·80 (SD 0·03) compared with 0·67 (0·04) for LVEF and 0·69 (0·04) for SDNN. In the Oulu cohort, mean AUC of deceleration capacity was 0·74 (0·03) compared with 0·60 (0·04) for LVEF and 0·64 (0·03) for SDNN (p<0·0001 for all comparisons). Stratification by dichotomised deceleration capacity was especially powerful in patients with preserved LVEF (p<0·0001 in all cohorts).

Interpretation

Impaired heart rate deceleration capacity is a powerful predictor of mortality after myocardial infarction and is more accurate than LVEF and the conventional measures of heart-rate variability.

Introduction

Results of randomised trials1, 2 indicate that, in high-risk survivors of myocardial infarction, mortality can be greatly reduced by implantation of a cardioverter defibrillator. Extent of impairment of left-ventricular ejection fraction (LVEF) is generally used to predict risk.³ However, in unselected post-infarction populations undergoing modern treatment, particularly treatment involving acute revascularisation procedures,⁴ most deaths arise in patients with preserved LVEF. An alternative, more accurate method of risk prediction is, therefore, needed. One approach might be to measure LVEF—ie, a marker of myocardial viability—and a marker of cardiac autonomic responsiveness,⁵ such as heart-rate variability. However, although there is evidence that decreased heart-rate variability is associated with a poor prognosis, the clinical usefulness of established measures is low.⁵

Heart-rate variability is affected by both vagal and sympathetic modulation of the sinus node. Evidence from experimental and clinical studies6, 7, 8 indicates that a fall in vagal activity increases the risk of death. However, overall measures of heart-rate variability, such as the standard deviation of all normal-to-normal intervals (SDNN), do not distinguish between vagal and sympathetic effects.⁹ Without directly recording neural activity, which is impractical in a clinical setting, exact assessment of the effect of these separate limbs of the autonomic nervous system is not possible. However, an approximate distinction of the effects might be made possible by separate assessment of deceleration-related and acceleration-related heart-rate variability.

We propose a way to analyse heart-rate variability and use it to try to characterise rhythm modulations associated separately with deceleration and acceleration. We postulate that extent of deceleration-related heart-rate variability is, in terms of post-infarction risk prediction, better than the acceleration-related heart-rate variability, the established global heart-rate variability indices, and LVEF.