Hemodynamic correlates of exercise function in patients with primary pulmonary hypertension

Abstract

The purpose of this investigation was to study the hemodynamic correlates of exercise function in patients with primary pulmonary hypertension and to further define the role of exercise testing in the evaluation of these individuals. Data from the progressive exercise tests and subsequent cardiac catheterization in 16 consecutive patients, aged 16.9 +/- 10.4 years (range 6 to 35), with primary pulmonary hypertension were prospectively collected and analyzed. Exercise capacity averaged 40 +/- 36% (range 0 to 117%) of that predicted for age, height and gender. Statistically significant correlations existed between exercise capacity and 10 invasively measured hemodynamic variables. Mean right atrial pressure, a variable previously noted to be one of the best predictors of survival in patients with primary pulmonary hypertension, correlated best with exercise capacity (r = -0.83, p less than 0.0001). Exercise capacity greater than 75% of the predicted value identified the two patients who had a positive response to acute pulmonary vasodilator drug testing. Poor exercise capacity (less than 10% of the predicted value) identified the three patients who died during or soon after cardiac catheterization. The ability of exercise testing to identify patients at high risk for cardiac catheterization was superior to that of other noninvasive variables. Results of exercise testing may help guide decisions regarding the optimal timing of heart-lung or single lung transplantation.

Exercise testing in pulmonary arterial hypertension and in chronic heart failure

“…Previous studies have shown that advanced PAH and CHF are both characterised by decreased peak work-rate, peak V9O 2 , V9O 2 at the anaerobic threshold and peak oxygen pulse, and increased ventilatory equivalents [2][3][4][5][6][7][9][10][11][12][13]. In the present patients, the anaerobic threshold occurred at a higher percentage of peak V9O 2 than in normal subjects.…”

“…Increased ventilatory equivalents at exercise in CHF have been explained by a combination of increased dead space related to low cardiac output, early lactic acidosis [9] and increased chemosensitivity in the context of increased sympathetic nervous system tone [26]. Additional factors in PAH could include a greater increase in physiological dead space because of pulmonary vascular obliteration, and hypoxaemia on right-to-left shunting through a patent foramen ovale [2][3][4][5]27]. The present PAH patients exhibited a slightly lower Sp,O 2 at rest, and presented with exercise-induced hypoxaemia, which probably contributed to increase ventilatory equivalents and dyspnoea score.…”

“…The condition evolves over years, with prominent exercise-induced symptoms, due to the inability of the overloaded right ventricle to perfuse the lungs and to adapt systemic oxygen delivery to peripheral tissue oxygen demand. Accordingly, PPH patients present with reductions in peak oxygen uptake, anaerobic threshold, oxygen pulse, ventilatory efficiency and 6-min walking distance [2][3][4][5][6][7], which have been found to be correlated with New York Heart Association Functional Class (NYHAFC) and survival better than with resting pulmonary haemodynamic measurements [6,7]. These concepts probably apply to pulmonary arterial hypertension (PAH) defined as PPH with identifiable associated conditions [8].…”

Application of exercise testing in the diagnosis, prognosis, and treatment of patients with Pulmonary Hypertension

“…CPET has been proven superior to other noninvasive testing to identify patients at high risk for heart catheterization (Rhodes, Barst, Garofano, Thoele, & Gersony, 1991). Poor exercise capacity (as a percent predicted of VO₂ max) in patients with primary PH put them at risk for RHC.…”

“…In the future it is suggested that these compromised patients are trained under professional supervision (Grunig et al, 2011;Grunig, et al, 2012). Training would help patients with IPAH increase VO₂ and 6MWD which would translate into increase of quality of life and life expectancy (H. Groepenhoff, et al, 2008;Miyamoto, et al, 2000;Rhodes, et al, 1991;Wensel, et al, 2002). Increasing pVO₂ by training would translate into using less percentage of pVO₂ during a 6MWT.…”