The prognostic significance of heart rate recovery is not dependent upon maximal effort in patients with heart failure

Department of Physical Therapy, Leonard M. Miller School of Medicine, University of Miami, Miami, FL, United States. Electronic address: .
International journal of cardiology (Impact Factor: 4.04). 02/2013; 168(2). DOI: 10.1016/j.ijcard.2012.12.102
Source: PubMed


Heart rate recovery (HRR) has been observed to be a significant prognostic measure in patients with heart failure (HF). However, the prognostic value of HRR has not been examined in regard to the level of patient effort during exercise testing. Using the peak respiratory exchange ratio (RER) and a large multicenter HF database we examined the prognostic utility of HRR.

Cardiopulmonary exercise testing (CPX) was performed in 806 HF patients who then underwent an active cool-down of at least 1 min. Peak oxygen consumption (VO2), ventilatory efficiency (VE/VCO2 slope), and peak RER were determined with subjects categorized into subgroups according to peak RER (<1.00, 1.00-1.09, ≥ 1.10). HRR was defined as the difference between heart rate at peak exercise and 1 min following test termination. Patients were followed for major cardiac events for up to four years post-CPX.

There were 163 major cardiac events (115 deaths, 20 left ventricular assist device implantations, and 28 transplantations) during the four year tracking period. Univariate Cox regression analysis results identified HRR as a significant (p<0.05) univariate predictor of adverse events regardless of the RER achieved. Multivariate Cox regression analysis in the overall group revealed that the VE/VCO2 slope was the strongest predictor of adverse events (chi-square: 110.9, p<0.001) with both HRR (residual chi-square: 16.7, p<0.001) and peak VO2 (residual chi-square: 10.4, p<0.01) adding significant prognostic value.

HRR after symptom-limited exercise testing performed at sub-maximal efforts using RER to categorize level of effort is as predictive as HRR after maximal effort in HF patients.

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    • "For example, heart rate recovery between 1 and 5 min after a moderate intensity bout of dynamic exercise is an independent predictor of all-cause mortality (Johnson and Goldberger, 2012). Both heart rate and blood pressure recovery can provide non-invasive clinical indicators related to autonomic function, making these simple measurements highly informative (Terziotti et al., 2001; Buchheit et al., 2007; Cahalin et al., 2013). In fact, measurements in recovery can non-invasively be used to assess future clinical risks that would otherwise not be apparent in a typical health screening (Cole et al., 2000; Shetler et al., 2001). "
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    ABSTRACT: Why should we study the recovery from exercise as a discrete phenomenon from exercise itself? We identify three distinct (but not mutually exclusive) rationales that drive the need to investigate the physiology of recovery from exercise. (1) Some individuals are at a heightened risk of clinical outcomes in the immediate post-exercise period; thus the potential negative outcomes of this "vulnerable state" must be weighed against the numerous benefits of exercise training, and may be mitigated to reduce risk. (2) Many of the signaling mechanisms responsible for the beneficial effects of exercise training remain amplified during the exercise recovery period, and may present a "window of opportunity" that can be exploited by interventions to enhance the beneficial adaptations to exercise training, especially in clinical populations. (3) On an individual level, exercise recovery responses may provide investigators with a "crystal ball" ability to predict future clinical outcomes even in apparently healthy individuals. In short, the physiology of recovery is a multi-faceted and complex process, likely involving systems and pathways that are distinct from the physiology of exercise itself. For these reasons, it merits ongoing study.
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    ABSTRACT: It is unclear which exercise training protocol yields superior heart rate recovery (HRR) improvement in heart failure (HF) patients. Whether baseline HRR normality plays a role in the improvement is unknown. We hypothesized that an exercise training protocol and baseline HRR normality would be factors in altering HRR in HF patients. In this prospective, randomized, controlled and 3 group parallel study, 41 stable HF patients. Forty-one stable HF patients were randomly assigned to 3-times-weekly training sessions for 12 weeks, consisting of i) 30 minutes of interval training (IT) (n=17, 63.7±8.8 years old) versus ii) 30 minutes of continuous training (CT) (n=13, 59.6±6.8 years old) versus iii) no training (CON) (n=11, 60.6±9.9 years old). Each patient had cardiopulmonary exercise testing before and after the training program. Maximum heart rates attained during the test and heart rates at 1 and 2 min (HRR1 and HRR2) during the recovery phase were recorded. Paired samples t-test or Wilcoxon signed-rank test was used for comparisons before and after training. One-way ANOVA or Kruskal-Wallis variance analysis were used for comparisons among groups. HRR1 was unchanged after training. HRR2 improved in the IT group after training, and post-training HRR2 values were significantly faster in the IT group than in controls. Both HRR1 and HRR2 was significantly faster, irrespective of exercise protocol in patients with abnormal baseline values after training. HRR1 did not improve after training. HRR2 improved only in the IT group. Both HRRs in patients with abnormal baseline values improved after both exercise protocols. IT might be superior to CT in improving HRR2. Baseline HRR might play a role in its response to exercise.
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