Key result
Blunted heart rate recovery is linked to ~34% lower peak VO2 in heart failure patients.
Why the study?
The determinants of altered heart rate recovery after exercise in heart failure patients are unknown.
What are the echocardiographic, neurohormonal, and hemodynamic correlates of blunted heart rate recovery in patients with heart failure?
Observational (n=98)
What are the echocardiographic, neurohormonal, and hemodynamic correlates of blunted heart rate recovery in patients with heart failure?
Absolute Event Rate: 14.6% vs 22.2%
p-value: p=<0.001
Blunted heart rate recovery in heart failure patients is associated with higher left ventricular filling pressures, elevated neurohormones, and worse exercise capacity.
Blunted HR recovery may flag HF patients with higher filling pressures and poorer capacity; leaves open its added value for risk stratification.
PURPOSE: Heart failure (HF) is associated with blunted HR recovery after exercise. The determinants of altered HR recovery in HF are unknown. The aim of this study was to investigate clinical correlates of HR recovery in HF patients. METHODS: Echocardiography, pulmonary function tests, exercise testing, and neurohormonal measurements were performed in 98 HF patients. HR recovery was calculated as the difference between heart rate at peak exercise and at 1 min into a recovery period. Study subjects were divided into three groups based on HR recovery tertiles: group 1 (HR recovery < or = 6 bpm), group 2 (7 < or = HR recovery < or = 12), and group 3 (HR recovery > or = 13). RESULTS: There were significant differences between the groups in multiple parameters. Compared with group 3, patients in group 1 had greater E/A ratios (1.81 +/- 0.26 vs 0.98 +/- 0.12, P = 0.011), shorter deceleration time (170 +/- 11 vs 223 +/- 11 ms, P = 0.016), and higher plasma atrial natriuretic peptide levels (207 +/- 32 vs 101 +/- 12 pg.mL, P = 0.008), indicating higher left ventricular filling pressures and elevated left atrial pressures. Pulmonary function tests were suggestive of greater restrictive changes in the lungs. Finally, subjects in group 1 had impaired exercise capacity, as evidenced by shorter exercise duration (5.2 +/- 0.2 vs 8.3 +/- 0.4 min, P < 0.001), lower peak VO2 (14.6 +/- 0.6 vs 22.2 +/- 1.0 mL.kg(-1).min(-1), P < 0.001), higher VE/VCO2 ratios (36.4 +/- 1.1 vs 31.1 +/- 0.9, P = 0.001), and reduced chronotropic responses to exercise (39 +/- 3 vs 69 +/- 4 bpm, P < 0.001). CONCLUSION: HR recovery may be a clinically useful index identifying HF patients with distinct echocardiographic, neurohormonal, and hemodynamic characteristics. This may have implications for our understanding of the pathophysiology of impaired HR recovery in HF as well as for the clinical evaluation of such patients.
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Wolk et al. (2006) conducted an observational in Heart failure (n=98). Blunted heart rate recovery (≤ 6 bpm) vs. Preserved heart rate recovery (≥ 13 bpm) was evaluated on Peak VO2 (mL.kg-1.min-1) (p=<0.001). Blunted heart rate recovery (≤6 bpm) in heart failure patients was associated with significantly lower peak VO2 (14.6 vs 22.2 mL/kg/min, P<0.001) compared to those with recovery ≥13 bpm.
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