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/100 mL 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/100 mL. 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/100 mL. 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/100 mL. 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.
| Original language | English |
|---|---|
| Pages (from-to) | 252-256 |
| Number of pages | 5 |
| Journal | International Journal of Cardiology |
| Volume | 248 |
| DOIs | |
| Publication status | Published - Dec 1 2017 |
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Keywords
- Heart failure
- Peak exercise cardiac output
- Peak exercise oxygen uptake
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine
Cite this
Contribution of central and peripheral factors at peak exercise in heart failure patients with progressive severity of exercise limitation. / Del Torto, Alberico; Corrieri, Nicoletta; Vignati, Carlo; Gentile, Piero; Cattadori, Gaia; Paolillo, Stefania; Agostoni, Piergiuseppe.
In: International Journal of Cardiology, Vol. 248, 01.12.2017, p. 252-256.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Contribution of central and peripheral factors at peak exercise in heart failure patients with progressive severity of exercise limitation
AU - Del Torto, Alberico
AU - Corrieri, Nicoletta
AU - Vignati, Carlo
AU - Gentile, Piero
AU - Cattadori, Gaia
AU - Paolillo, Stefania
AU - Agostoni, Piergiuseppe
PY - 2017/12/1
Y1 - 2017/12/1
N2 - 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/100 mL 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/100 mL. 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/100 mL. 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/100 mL. 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.
AB - 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/100 mL 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/100 mL. 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/100 mL. 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/100 mL. 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.
KW - Heart failure
KW - Peak exercise cardiac output
KW - Peak exercise oxygen uptake
UR - http://www.scopus.com/inward/record.url?scp=85029716065&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85029716065&partnerID=8YFLogxK
U2 - 10.1016/j.ijcard.2017.07.071
DO - 10.1016/j.ijcard.2017.07.071
M3 - Article
AN - SCOPUS:85029716065
VL - 248
SP - 252
EP - 256
JO - International Journal of Cardiology
JF - International Journal of Cardiology
SN - 0167-5273
ER -