Impact of Aging on Pulmonary Hemodynamics in the General Population

Abstract

Introduction: With the rapidly aging population referred for echocardiography, elevated pulmonary artery (PA) systolic pressure (PASP) in the elderly is increasingly observed. Yet the impact of aging on PASP remains unclear. Previous studies in highly selected groups have produced mixed results, highlighting the need for community-based data. Hypotheses: PASP increases with age, even without cardiopulmonary disease, and is related to: 1) increasing pulmonary capillary wedge pressure (PCWP) from age-related LV diastolic dysfunction; 2) increasing pulsatile PA load from pulmonary vascular stiffening in association with systemic arterial stiffening. Methods: Prospective population-based study of randomly sampled adults (N=1413; 63±11y; 43% male) from Olmsted County, MN. All underwent Doppler echo and spirometry. A subset without cardiopulmonary disease (N=430; EF>50%; FEV1>80%; FEV1/FVC>70%) was identified. PASP was derived from the tricuspid regurgitation velocity and PCWP from E/e'. Mean PA pressure (mPAP), previously shown to be closely related to invasively measured PCWP, was [1.44*PCWP+0.8]. Total PA load was reflected by effective pulmonary arterial elastance (Epa)[=mPAP*1.06/stroke volume] and non-pulsatile load by total pulmonary resistance (TPR)[=mPAP/cardiac output]. Brachial pulse pressure (PP) was used as an index of systemic arterial stiffening. Results: In the whole sample, median (25th,75th percentile) PASP was 26(24,30) mmHg. PASP increased with age (r=0.31; p<0.001) and correlated with PCWP and PP after adjusting for age (both p<0.001). Total PA load (Epa) increased with age (r=0.18; p<0.001) while non-pulsatile load (TPR) did not (p=0.13), suggesting that age-dependence of total load was primarily related to increased pulsatile loading (ie vascular stiffening). Without cardiopulmonary disease, PASP still increased with age (r=0.133; p=0.039) and with PP (p=0.022), but not PCWP, after adjusting for age. Adjusting for age and PCWP, PP remained an independent predictor of PASP (p=0.033). Conclusions: In these first population-based data on aging and pulmonary hemodynamics, PASP increased with age, even in the absence of cardiopulmonary disease. Increasing PASP was related to changes in left-sided filling pressures and right-sided pulsatile load. The association with systemic arterial stiffening (PP) suggests a common age-related vascular stiffening process involving the pulmonary circulation as well, contributing to increasing PASP. The implications for development of exercise intolerance and clinical events with aging merit further study. Introduction: With the rapidly aging population referred for echocardiography, elevated pulmonary artery (PA) systolic pressure (PASP) in the elderly is increasingly observed. Yet the impact of aging on PASP remains unclear. Previous studies in highly selected groups have produced mixed results, highlighting the need for community-based data. Hypotheses: PASP increases with age, even without cardiopulmonary disease, and is related to: 1) increasing pulmonary capillary wedge pressure (PCWP) from age-related LV diastolic dysfunction; 2) increasing pulsatile PA load from pulmonary vascular stiffening in association with systemic arterial stiffening. Methods: Prospective population-based study of randomly sampled adults (N=1413; 63±11y; 43% male) from Olmsted County, MN. All underwent Doppler echo and spirometry. A subset without cardiopulmonary disease (N=430; EF>50%; FEV1>80%; FEV1/FVC>70%) was identified. PASP was derived from the tricuspid regurgitation velocity and PCWP from E/e'. Mean PA pressure (mPAP), previously shown to be closely related to invasively measured PCWP, was [1.44*PCWP+0.8]. Total PA load was reflected by effective pulmonary arterial elastance (Epa)[=mPAP*1.06/stroke volume] and non-pulsatile load by total pulmonary resistance (TPR)[=mPAP/cardiac output]. Brachial pulse pressure (PP) was used as an index of systemic arterial stiffening. Results: In the whole sample, median (25th,75th percentile) PASP was 26(24,30) mmHg. PASP increased with age (r=0.31; p<0.001) and correlated with PCWP and PP after adjusting for age (both p<0.001). Total PA load (Epa) increased with age (r=0.18; p<0.001) while non-pulsatile load (TPR) did not (p=0.13), suggesting that age-dependence of total load was primarily related to increased pulsatile loading (ie vascular stiffening). Without cardiopulmonary disease, PASP still increased with age (r=0.133; p=0.039) and with PP (p=0.022), but not PCWP, after adjusting for age. Adjusting for age and PCWP, PP remained an independent predictor of PASP (p=0.033). Conclusions: In these first population-based data on aging and pulmonary hemodynamics, PASP increased with age, even in the absence of cardiopulmonary disease. Increasing PASP was related to changes in left-sided filling pressures and right-sided pulsatile load. The association with systemic arterial stiffening (PP) suggests a common age-related vascular stiffening process involving the pulmonary circulation as well, contributing to increasing PASP. The implications for development of exercise intolerance and clinical events with aging merit further study.