Prolonged mean VO2 response time in systolic heart failure: an indicator of impaired right ventricular-pulmonary vascular function.
Prolonged mean VO2 response time in systolic heart failure: an indicator of impaired right ventricular-pulmonary vascular function.
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DOI:
10.1161/circheartfailure.112.000157
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发表时间:
2013-05
期刊:
影响因子:
--
通讯作者:
Lewis GD
中科院分区:
文献类型:
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作者:
Chatterjee NA;Murphy RM;Malhotra R;Dhakal BP;Baggish AL;Pappagianopoulos PP;Hough SS;Semigran MJ;Lewis GD
In patients with left ventricular systolic dysfunction (LVSD), the rate at which oxygen uptake (VO2) increases upon initiation of exercise is inadequate to match metabolic demands. To gain mechanistic insights into delayed VO2 kinetics in LVSD we simultaneously assessed hemodynamic measurements, ventilatory parameters, and peripheral oxygen utilization during exercise. 42 patients with symptomatic LVSD (age 59±2 years [mean±SEM], LV ejection fraction (LVEF) 30±1%) and 17 controls (LVEF 68±1%) underwent maximum upright cycle ergometry cardiopulmonary exercise testing (CPET). Hemodynamic monitoring and first-pass radionuclide ventriculography were performed at rest and during exercise. VO2 kinetics were quantified by mean response time (MRT), which was significantly longer in patients with LVSD compared to controls (64±3 vs. 45±5 seconds (s), p =0.004). In LVSD patients, MRT was associated with higher biventricular filling pressures and reduced cardiac output during early exercise. LVSD patients with MRT≥60s, compared to LVSD subjects with MRT<60s, demonstrated greater impairment in right ventricular-pulmonary vascular (RV-PV) function during exercise as evidenced by lower RVEF (35±2 vs. 45±2%, p=0.03), steeper increment in trans-pulmonary gradient relative to cardiac output (3.7 vs. 2.2, p<0.001), and increased ventilatory dead-space fraction (17±1 vs. 12±2%, p=0.03). In contrast, MRT was not associated with LVEF (rest, exercise), PaO2, hemoglobin, or resting pulmonary function test results. Delayed oxygen uptake upon initiation of exercise (i.e. MRT ≥60s) in LVSD is closely related to impaired RV-PV function and may represent an important surrogate for inability to augment RV performance during physical activity in patients with HF.