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

Alberico Del Torto, Nicoletta Corrieri, Carlo Vignati, Piero Gentile, Gaia Cattadori, Stefania Paolillo, Piergiuseppe Agostoni

Research output: Contribution to journalArticle

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 languageEnglish
Pages (from-to)252-256
Number of pages5
JournalInternational Journal of Cardiology
Volume248
DOIs
Publication statusPublished - Dec 1 2017

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Cardiac Output
Heart Failure
Exercise
Noble Gases
Exercise Test
Oxygen Consumption
Oxygen
prednylidene

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 journalArticle

Del Torto, Alberico ; Corrieri, Nicoletta ; Vignati, Carlo ; Gentile, Piero ; Cattadori, Gaia ; Paolillo, Stefania ; Agostoni, Piergiuseppe. / Contribution of central and peripheral factors at peak exercise in heart failure patients with progressive severity of exercise limitation. In: International Journal of Cardiology. 2017 ; Vol. 248. pp. 252-256.
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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.",
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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

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