Contribution of central and peripheral factors at peak exercise in heart failure patients with progressive severity of exercise limitation

Abstract

Background: A reduced cardiac output (CO) response during exercise is a major limiting factor in heart failure (HF). Oxygen consumption (VO₂) is directly proportional to CO. Peripheral mechanisms via arteriovenous oxygen difference (Δ(a-v)O₂) play a pivotal role in chronic HF. We hypothesized a weak correlation between peak VO₂ and peak CO with a greater Δ(a-v)O₂ variability in most severe HF.

Methods: We analyzed 278 HF patients (NYHA II-III) who performed maximal cardiopulmonary exercise test with non-invasive CO measurement by inert gas rebreathing.

Results: Median peakVO₂, CO and Δ(a-v)O₂ were 0.96 (0.78-1.28) L/min, 6.3 (5.1-8.0) L/min and 16.0 (14.2-18.0) mL/100mL respectively, with a linear relationship between VO₂ and CO: CO=5.3×VO₂+1.13 (r²=0.705, p<0.001). Patients were grouped according to exercise limitation. Group 1 (101 patients) peakVO₂<50% pred: peakVO₂ 0.80 (0.67-0.94) L/min, peakCO 5.6 (4.7-6.5) L/min, peakΔ(a-v)O₂ 14.8 (12.9-17.1) mL/100mL. Group 2 (89 patients) peakVO₂≥50-<65% pred: peakVO₂ 1.02 (0.84-1.29) L/min, peakCO 6.4 (5.1-8.0) L/min, peakΔ(a-v)O₂ 16.7 (15.0-18.5) mL/100mL. Group 3 (88 patients) peakVO₂≥65% pred: peakVO₂ 1.28 (0.93-1.66) L/min, peakCO 8.0 (6.2-9.7) L/min, peakΔ(a-v)O₂ 16.8 (14.6-18.3) mL/100mL. A peakVO₂ and peakCO linear relationship was observed in Group 1 (r²=0.381, p<0.001), Group 2 (r²=0.756, p<0.001) and Group 3 (r²=0.744, p<0.001).

Conclusions: With worsening HF we observed a progressive reduction of peak CO and peak VO₂. However in most compromised patients also peripheral mechanisms play a role as indicated by reduced Δ(a-v)O₂.

Keywords: Heart failure; Peak exercise cardiac output; Peak exercise oxygen uptake.