Alveolar Air and O2 Uptake During Exercise in Patients With Heart Failure

Iterson, Erik H. Van; Smith, Joshua R.; Olson, Thomas P.

doi:10.1016/j.cardfail.2018.08.001

Cited by 6 publications

(10 citation statements)

References 43 publications

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“…Studies reporting on clinical exercise physiological testing continue to provide evidence highlighting that abnormal heart–lung interactions exert potent whole‐body circulatory effects resulting in limited aerobic exercise capacity in HFrEF 1,2,11,32–36 . This body of knowledge is extended with this study.…”

Section: Discussionmentioning

confidence: 75%

All‐cause mortality predicted by peak oxygen uptake differs depending on spirometry pattern in patients with heart failure and reduced ejection fraction

et al. 2021

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AimsIn patients with heart failure and reduced ejection fraction (HFrEF), it remains unclear how exacerbated impairments in peak exercise oxygen uptake (V O 2peak ) caused by coexistent obstructive or restrictive ventilatory defects affect mortality risk. We evaluated in patients with HFrEF, whether demonstrating either an obstructive or restrictive-patterned ventilatory defect on spirometry affects V O 2peak to yield all-cause mortality risk predicted by V O 2peak that is spirometry pattern specific. Methods and resultsWe retrospectively analysed resting spirometry and treadmill cardiopulmonary exercise testing data of patients with HFrEF (left ventricular ejection fraction ≤ 40%). The study sample (N = 329) was grouped by spirometry pattern: normal [Group 1: N = 101; forced expiratory volume in 1 s (FEV 1 )/forced vital capacity (FVC) ≥ 0.70; FVC ≥ 80% predicted], restrictive without airflow obstruction (Group 2: N = 104; FEV 1 /FVC ≥ 0.70; FVC < 80% predicted), or obstructive (Group 3: N = 124; FEV 1 /FVC < 0.70). Patients were followed up to 1 year for the endpoint of all-cause mortality. V O 2peak was higher in Group 1 versus Groups 2 and 3 (13.4 ± 4.0 vs. 12.1 ± 3.7 and 12.2 ± 3.3 mL/kg/min, respectively; P = 0.014). Over the 1 year follow-up, n = 9, n = 16, and n = 12 deaths occurred in Groups 1-3, respectively, with corresponding crude survival rates of 88%, 81%, and 92%, respectively (log-rank; P = 0.352). V O 2peak was associated with all-cause mortality (crude hazard ratio = 0.77; P < 0.001). In multivariate analyses, a significant V O 2peak -by-spirometry group interaction yielded 1.99 (95% confidence interval, 1.14-3.46) and 2.43 (95% confidence interval, 1.44-4.11) higher mortality risk associated with V O 2peak in Group 2 versus Groups 1 and 3, respectively. Conclusions Demonstrating a restrictive pattern on spirometry yields the severest mortality risk associated with V O 2peak . Using spirometry to screen patients with HFrEF for ventilatory defects has a potential role in improving risk stratification based on V O 2peak .

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Section: Discussionmentioning

confidence: 75%

All‐cause mortality predicted by peak oxygen uptake differs depending on spirometry pattern in patients with heart failure and reduced ejection fraction

et al. 2021

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“…1 8 together these features imply that demonstrating a large Á _ VO 2 AT-RCP is indeed overwhelmingly dependent on the integrative degree to which the smallest increases in _ V E and O 2 delivery are able to properly accommodate rapidly increasing oxidative metabolic demand. 4,5 Certainly, for such associations to persist beyond the AT, the need for acid-base regulation at both lung and skeletal muscle is synonymous with the appearance of ''isocapnic buffering.'' For post-AT exercise, the buffering of lactic acid…”

Section: Erik H Van Itersonmentioning

confidence: 99%

“…The polymorphic nature of CPET is real, and understanding the “sum of the parts” as much as the “parts of the sum” is needed to narrate the complete V·O 2 phenotype. 2–5 Measurements involved in CPET should not be recognized as static or so straightforward in surreptitiously meeting pre-specified nomenclature norms. 2,6,7 The quest for what makes measuring and understanding exercise capacity invaluable in the realm of heart failure has yet to completely embrace the notion that providing a layered phenotype of exercise V·O 2 beyond “peak” and oversimplification of Fick’s Principle is necessary.…”

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confidence: 99%

“…By assuming that V· E , true to its expected nature, rises quasi-exponentially relative to V·O 2 beyond the AT, and ramp-slope exercise forces V· E and V·CO 2 to maintain linearity up to the RCP, 8 together these features imply that demonstrating a large ΔV·O 2 AT-RCP is indeed overwhelmingly dependent on the integrative degree to which the smallest increases in V· E and O 2 delivery are able to properly accommodate rapidly increasing oxidative metabolic demand. 4,5 Certainly, for such associations to persist beyond the AT, the need for acid-base regulation at both lung and skeletal muscle is synonymous with the appearance of “isocapnic buffering.”…”

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confidence: 99%

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Isocapnic buffering: An inconvenient truth about cardiopulmonary exercise testing in heart failure

Iterson

2019

Eur J Prev Cardiolog

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“…The impaired rise in peak exercise oxygen uptake ( _ VO 2 ) accompanying cardiopulmonary exercise testing (CPET) is a feature universally associated with impaired oxidative metabolic capacity, exercise intolerance, and heart failure (HF). [1][2][3][4][5][6] Patients with the lowest _ VO 2peak also commonly demonstrate the worst prognosis. 2,3,5,6 Still, it has also been observed that for patients demonstrating a high body mass index (BMI), the favorable prognostic impact yielded by obesity does not include invariable benefits to _ VO 2peak .…”

Section: Introductionmentioning

confidence: 99%

Obesity and hemoglobin content impact peak oxygen uptake in human heart failure

Iterson

Kim

Uithoven

et al. 2018

Eur J Prev Cardiolog

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Background: Exercise intolerance, obesity, and low hemoglobin (hemoglobin<13 and <12 g/dl, men/women, respectively) are common features of heart failure. Despite serving as potent contributors to metabolic dysfunction, the impact of obesity and low hemoglobin on exercise intolerance is unknown. This study tested the hypotheses, compared with non-obese (NO) heart failure with normal hemoglobin, (a) counterparts with low hemoglobin and obesity or nonobesity will demonstrate reduced peak exercise oxygen uptake; (b) obese with normal hemoglobin will demonstrate decreased peak exercise oxygen uptake; (c) compared across stratifications, obese with low hemoglobin will demonstrate the sharpest decrement in peak exercise oxygen uptake. Methods: Adults with heart failure (n ¼ 315; left ventricular ejection fraction 40%; 77% men) (Group 1: normal hemoglobin and non-obese, n ¼ 137; Group 2: low hemoglobin and non-obese, n ¼ 51; Group 3: normal hemoglobinþobesity, n ¼ 89; Group 4, n ¼ 38: low hemoglobinþobesity; body mass index ¼ 26 AE 3, 26 AE 2, 34 AE 4, 34 AE 4 kg/m 2 , respectively) completed treadmill cardiopulmonary exercise testing as part of routine clinical management. Peak exercise oxygen uptake was measured via standard metabolic system. Results: There were no group-wise differences for heart failure class, gender, left ventricular ejection fraction, and resting cardiopulmonary function. Group 1 demonstrated increased peak exercise oxygen uptake versus Groups 2-4 (20 AE 6 versus 17 AE 6, 17 AE 5, 13 AE 4 ml/kg/min, respectively; all p < 0.001); whereas Group 4 peak exercise oxygen uptake was reduced versus all groups (p < 0.001). Additionally, both body mass index (R 2 ¼ 0.10) and hemoglobin (R 2 ¼ 0.12) were significant predictors of peak exercise oxygen uptake in Group 1; which were relationships not mirrored for Groups 2-4. Conclusion: These data suggest obesity together with low hemoglobin are potent contributors to impaired peak exercise oxygen uptake and, hence, oxidative metabolic capacity. In diverse populations of heart failure where obesity and/or low hemoglobin are present, it is important to consider these features together when interpreting peak exercise oxygen uptake and underlying exercise limitations.

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Alveolar Air and O2 Uptake During Exercise in Patients With Heart Failure

Abstract: These data suggest that alveolar airway function that is not exclusively related to effects caused by localized lung diffusivity affects exercise V̇O in moderate-to-severe HF.

Cited by 6 publications

References 43 publications

All‐cause mortality predicted by peak oxygen uptake differs depending on spirometry pattern in patients with heart failure and reduced ejection fraction

All‐cause mortality predicted by peak oxygen uptake differs depending on spirometry pattern in patients with heart failure and reduced ejection fraction

Isocapnic buffering: An inconvenient truth about cardiopulmonary exercise testing in heart failure

Obesity and hemoglobin content impact peak oxygen uptake in human heart failure

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