Pulmonary Vascular Pressures and Ventilatory Control during Exercise in Heart Failure with Preserved or Reduced Ejection Fraction

Abstract

IntroductionA disproportionate increase in ventilation relative to carbon dioxide output (VE/VCO2) slope is a strong prognostic indicator in heart failure with reduced (HFrEF) or preserved ejection fraction (HFpEF) patients. Similarly, secondary pulmonary hypertension also poses a profound mortality risk in these patients. Exaggerated ventilation and pulmonary pressures appear to parallel one another during exercise in HF. However, an underlying pathophysiologic mechanism relating these two outcomes remains incompletely understood. Thus, the aim of this study was to determine associations between anatomical and physiologic metrics of ventilatory control and pulmonary pressures during exercise in HFrEF and HFpEF.Methods32 HFpEF and 33 HFrEF (EF: 62±2 vs 22±1%; male: 17 and 31; age: 70±2 and 55±2 yrs; BMI: 34±1 and 28±1 kg/m2; weight: 98±4 and 86±3 (all P<0.05), respectively, participated in cardiopulmonary exercise testing during right heart catheterization. Measures of pulmonary pressures included: systolic (PASP); diastolic (PADP); mean (mPAP); wedge (PCWP); pulse (PP); transpulmonary gradient (TPG). Partial pressure of arterial oxygen (PaO2) and carbon dioxide (PaCO2) were measured via radial arterial catheterization. Ventilation was measured continuously using a breath by breath metabolic measurement system. We calculated dead space to tidal volume [Vd/Vt=(VE×PaCO2)‐(863×VCO2)/(VE×PaCO2)] and Alveolar‐arterial oxygen gradient (A‐a)=PAO2‐PaO2; VE/VCO2 slope=rest to peak exercise.ResultsAt rest, pulmonary pressures did not differ between groups (P>0.05); whereas Vd/Vt was lower in HFpEF vs HFrEF (0.42±0.02 vs 0.48±0.01, respectively, P=0.03). At peak exercise, HFpEF had higher PCWP (34.8±1.2 vs 30.2±1.5 mm Hg, P=0.02) and PADP (35.4±1.3 vs 29.8±1.6 mm Hg, P=0.02), but lower Vd/Vt (0.32±0.02 vs 0.38±0.01, P=0.03) and VE/VCO2 slope (35.3±1.6 vs 43.5±2.0, P<0.01) vs HFrEF. At peak in HFpEF, Vd/Vt was related to PASP (r=0.40, P=0.03), PP (r=0.44, P=0.01), and TPG (r=0.53, P<0.01), and A‐a was related to PASP (r=0.43, P=0.01), PP (r=0.44, P=0.01), and TPG (r=0.46, P<0.01). At peak in HFrEF, Vd/Vt was related to PADP (r=0.41, P=0.02), and A‐a was related to PASP (r=0.43, P<0.01), PADP (r=0.42, P=0.01), and mPAP (r=0.44, P<0.01). There were no significant relationships between measures of pulmonary pressures and PaCO2. Remaining correlations between pulmonary pressures and anatomical or physiologic metrics of ventilatory control were negligible in both groups (P>0.05).ConclusionThese data suggest pulmonary pressures play a role in dead space ventilation during exercise in HF. Moreover, as suggested by the A‐a gradient, augmented pulmonary pressures may contribute to an exacerbation of ventilation/perfusion mismatch during exercise in both HFrEF and HFpEF patients.Support or Funding InformationNone