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Cardiac output response to exercise in relation to metabolic demand in heart failure with preserved ejection fraction
Author(s) -
Abudiab Muaz M.,
Redfield Margaret M.,
Melenovsky Vojtech,
Olson Thomas P.,
Kass David A.,
Johnson Bruce D.,
Borlaug Barry A.
Publication year - 2013
Publication title -
european journal of heart failure
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.149
H-Index - 133
eISSN - 1879-0844
pISSN - 1388-9842
DOI - 10.1093/eurjhf/hft026
Subject(s) - medicine , cardiology , heart failure with preserved ejection fraction , stroke volume , supine position , heart failure , cardiac output , heart rate , ejection fraction , diastole , exercise intolerance , blood pressure , hemodynamics
Aims Exercise intolerance is a hallmark of heart failure with preserved ejection fraction (HFpEF), yet its mechanisms remain unclear. The current study sought to determine whether increases in cardiac output (CO) during exercise are appropriately matched to metabolic demands in HFpEF. Methods and results Patients with HFpEF ( n = 109) and controls ( n = 73) exercised to volitional fatigue with simultaneous invasive ( n = 96) or non‐invasive ( n = 86) haemodynamic assessment and expired gas analysis to determine oxygen consumption (VO 2 ) during upright or supine exercise. At rest, HFpEF patients had higher LV filling pressures but similar heart rate, stroke volume, EF, and CO. During supine and upright exercise, HFpEF patients displayed lower peak VO 2 coupled with blunted increases in heart rate, stroke volume, EF, and CO compared with controls. LV filling pressures increased dramatically in HFpEF patients, with secondary elevation in pulmonary artery pressures. Reduced peak VO 2 in HFpEF patients was predominantly attributable to CO limitation, as the slope of the increase in CO relative to VO 2 was 20% lower in HFpEF patients (5.9 ± 2.5 vs. 7.4 ± 2.6 L blood/L O 2 , P = 0.0005). While absolute increases in arterial–venous O 2 difference with exercise were similar in HFpEF patients and controls, augmentation in arterial–venous O 2 difference relative to VO 2 was greater in HFpEF patients (8.9 ± 3.4 vs. 5.5 ± 2.0 min/dL, P < 0.0001). These differences were observed in the total cohort and when upright and supine exercise modalities were examined individually. Conclusion While diastolic dysfunction promotes congestion and pulmonary hypertension with stress in HFpEF, reduction in exercise capacity is predominantly related to inadequate CO relative to metabolic needs.