Details

Autor(en) / Beteiligte

• Tang, Yi-Da, MD, PhD
• Dewland, Thomas A., MD
• Wencker, Detlef, MD
• Katz, Stuart D., MD

Titel

Post-Exercise Heart Rate Recovery Independently Predicts Mortality Risk in Patients With Chronic Heart Failure

Ist Teil von

• Journal of cardiac failure, 2009-12, Vol.15 (10), p.850-855

Ort / Verlag

United States: Elsevier Inc

Erscheinungsjahr

2009

Quelle

MEDLINE

Beschreibungen/Notizen

• Abstract Background Post-exercise heart rate recovery (HRR) is an index of parasympathetic function associated with clinical outcomes in populations with and without documented coronary heart disease. Decreased parasympathetic activity is thought to be associated with disease progression in chronic heart failure (HF), but an independent association between post-exercise HRR and clinical outcomes among such patients has not been established. Methods and Results We measured HRR (calculated as the difference between heart rate at peak exercise and after 1 minute of recovery) in 202 HF subjects and recorded 17 mortality and 15 urgent transplantation outcome events over 624 days of follow-up. Reduced post-exercise HRR was independently associated with increased event risk after adjusting for other exercise-derived variables (peak oxygen uptake and change in minute ventilation per change in carbon dioxide production slope), for the Heart Failure Survival Score (adjusted HR 1.09 for 1 beat/min reduction, 95% CI 1.05-1.13, P < .0001), and the Seattle Heart Failure Model score (adjusted HR 1.08 for one beat/min reduction, 95% CI 1.05-1.12, P < .0001). Subjects in the lowest risk tertile based on post-exercise HRR (≥30 beats/min) had low risk of events irrespective of the risk predicted by the survival scores. In a subgroup of 15 subjects, reduced post-exercise HRR was associated with increased serum markers of inflammation (interleukin-6, r = 0.58, P = .024; high-sensitivity C-reactive protein, r = 0.66, P = .007). Conclusions Post-exercise HRR predicts mortality risk in patients with HF and provides prognostic information independent of previously described survival models. Pathophysiologic links between autonomic function and inflammation may be mediators of this association.