Exercise and pulsatile pulmonary vascular loading in chronic thromboembolic pulmonary disease.

Chronic thromboembolic pulmonary disease (CTEPD) is characterized by organized nonresolving thrombi in pulmonary arteries (PA). In CTEPD with pulmonary hypertension (PH), chronic thromboembolic PH (CTEPH), early wave reflection results in abnormalities of pulsatile afterload and augmented PA pressures. We hypothesized that exercise during right heart catheterization (RHC) would elicit more frequent elevations of pulsatile vascular afterload than resistive elevations in patients with CTEPD without PH. The interdependent physiology of pulmonary venous and PA hemodynamics was also evaluated. Consecutive patients with CTEPD without PH (resting mean PA pressure ≤20 mmHg) undergoing an exercise RHC were identified. Latent resistive and pulsatile abnormalities of pulmonary vascular afterload were defined as an exercise mean PA pressure/cardiac output >3 WU, and PA pulse pressure to PA wedge pressure (PA PP/PAWP) ratio >2.5, respectively. Forty-five patients (29% female, 53 ± 14 years) with CTEPD without PH were analyzed. With exercise, 19 patients had no abnormalities (ExNOR), 26 patients had abnormalities (ExABN) of pulsatile (20), resistive (2), or both (4) elements of pulmonary vascular afterload. Exercise elicited elevations of pulsatile afterload (53%) more commonly than resistive afterload (13%) (p < 0.001). ExABN patients had lower PA compliance and higher pulmonary vascular resistance at rest and exercise and prolonged resistance-compliance time product at rest. The physiological relationship between changes in PA pressures relative to PAWP was disrupted in the ExABN group. In CTEPD without PH, exercise RHC revealed latent pulmonary vascular afterload elevations in 58% of patients with more frequent augmentation of pulsatile than resistive pulmonary vascular afterload.

Alterations of pulmonary vascular afterload in exercise-induced pre- and post-capillary pulmonary hypertension.

Exercise imposes increased pulmonary vascular afterload based on rises in pulmonary artery (PA) wedge pressure, declines in PA compliance, and resistance-compliance time. In health, afterload stress stabilizes during steady-state exercise. Our objective was to examine alterations of these exercise-associated stresses in states of pre- and post-capillary pulmonary hypertension (PH). PA hemodynamics were evaluated at rest, 2 and 7 min of steady-state exercise at moderate intensity in patients who exhibited Pre-capillary (n = 22) and post-capillary PH (n = 22). Patients with normal exercise hemodynamics (NOR-HD) (n = 32) were also studied. During exercise in all groups, PA wedge pressure increased at 2 min, with no further change at 7 min. In post-capillary PH and NOR-HD, increases in PA diastolic pressure and diastolic pressure gradient remained stable at 2 and 7 min of exercise, while in pre-capillary PH, both continued to increase at 7 min. The behavior of the diastolic pressure gradient was linearly related to the duration of resistance-compliance time at rest (r2  = 0.843) and exercise (r2  = 0.760). Exercise resistance-compliance time was longer in pre-capillary PH associated with larger increases in diastolic pressure gradient. Conversely, resistance-compliance time was shortest in post-capillary PH compared to pre-capillary PH and NOR-HD and associated with limited increases in exercise diastolic pressure gradient. During steady-state, modest-intensity exercise-specific patterns of pulmonary vascular afterload responses were observed in pre- and post-capillary PH relative to NOR-HD. Longer resistance-compliance time related to greater increases in PA diastolic pressure and diastolic pressure gradients in pre-capillary PH, while shorter resistance-compliance time appeared to limit these increases in post-capillary PH.

Body Habitus Considerations During Right Heart Catheterization.

BACKGROUND: Obese and overweight body habitus are common among patients undergoing right heart catheterization for suspected pulmonary hypertension, but previous studies have described only patients with severe obesity. This study examined the effect of body habitus on intracardiac pressures, thermodilution cardiac output (TDCO), indirect Fick (iFick) cardiac output (CO), and pulmonary vascular resistance (PVR) in subjects with normal cardiopulmonary hemodynamics. METHODS: A retrospective analysis was conducted on healthy volunteers and patients referred for right heart catheterization for dyspnea of unknown origin with normal hemodynamics. Of the 65 subjects (53 ± 14 years; 51% female), 31% were normal weight, 49% were overweight, and 20% had obesity, as defined by a body mass index of 30-39.9 kg/m2. Mixed venous oxygen saturations and intracardiac pressures were compared across body mass index categories. Agreement between iFick CO calculated by 3 formulae, and TDCO and PVR was examined. RESULTS: No differences in intracardiac pressures were observed, but mixed venous oxygen saturations were lower in the obese group. iFick CO underestimated TDCO, particularly with the LaFarge formula, with a systematic difference of 0.33 L/min for every 1 L/min increase in CO. This difference was largest in the obese group-on average by 23% ± 10%, translating to an overestimation of PVR by 34% ± 16% on average. CONCLUSIONS: In individuals without severe obesity, intracardiac pressures are not different, but mixed venous oxygen saturations are lower. Obesity confounds estimations of CO and PVR by iFick methods, which could result in inappropriate hemodynamic classification. These data can inform best practices in hemodynamic assessment of populations with obesity.

INTRODUCTION: Les habitus corporels liés à l'obésité et à l'embonpoint sont fréquents chez les patients qui subissent un cathétérisme du cœur droit en raison d'une suspicion d'hypertension pulmonaire, mais les études antérieures n'ont porté que sur les patients atteints d'une obésité sérieuse. La présente étude portait sur les répercussions des habitus corporels sur les pressions intracardiaques, le débit cardiaque obtenu par thermodilution (DCTD), le débit cardiaque (DC) calculé selon le principe indirect de Fick (iFick) et la résistance vasculaire pulmonaire (RVP) chez les sujets ayant une hémodynamie cardiopulmonaire normale. MÉTHODES: Nous avons mené une analyse rétrospective auprès de volontaires en bonne santé et de patients orientés pour un cathétérisme cardiaque droit en raison de dyspnée d'origine inconnue, mais qui avaient une hémodynamie normale. Au sein de 65 sujets (53 ± 14 ans; 51 % de femmes), 31 % avaient un poids normal, 49 % faisaient de l'embonpoint et 20 % souffraient d'obésité d'après l'indice de masse corporelle entre 30-39,9 kg/m2. Nous avons comparé les saturations veineuses mixtes en oxygène et les pressions intracardiaques de toutes les catégories d'indice de masse corporelle. Nous avons examiné la concordance entre le calcul du DC selon le principe iFick au moyen de 3 formules, ainsi que le DCTD et la RVP. RÉSULTATS: Les pressions intracardiaques n'ont montré aucune différence, mais les saturations veineuses mixtes en oxygène étaient plus faibles chez les sujets obèses. Le DC calculé selon le principe iFick a démontré une sous-estimation du DCTD, particulièrement lors du calcul au moyen de la formule LaFarge, qui a révélé une différence systématique de 0,33 L/min à chaque augmentation du DC de 1 L/min. Cette différence qui était plus importante chez les sujets obèses (en moyenne de 23 % ± 10 %, se traduisait en moyenne par une surestimation de la RVP de 34 % ± 16 %). CONCLUSIONS: Chez les individus non atteints d'une obésité sérieuse, les pressions intracardiaques ne sont pas différentes, mais les saturations veineuses mixtes en oxygène sont plus faibles. L'obésité fait remettre en cause les estimations du DC et de la RVP par les méthodes iFick, lesquelles pourraient donner lieu à une classification hémodynamique erronée. Ces données peuvent permettre d'établir des pratiques exemplaires lors de l'évaluation hémodynamique des populations atteintes d'obésité.

Elevated pulmonary arterial elastance and right ventricular uncoupling are associated with greater mortality in advanced heart failure.

BACKGROUND: The objectives of this study were to describe right ventricular-pulmonary arterial elastance coupling hemodynamic phenotypes and their frequency in patients with advanced heart failure and to evaluate the association of elastance-based indices with all-cause mortality, cardiac transplantation, and left ventricular assist device therapy. METHODS: This study included 175 patients with heart failure undergoing right heart catheterization to evaluate candidacy for advanced therapies and 21 healthy controls. We modified a single-beat approach to elastance to account for the magnitude of pulmonary arterial pressure and estimated right ventricular end-systolic elastance (Ees), pulmonary arterial elastance (Ea), and the Ees:Ea ratio. We defined elevated pulmonary arterial load as an Ea > 0.5 mm Hg/ml, and ventriculo-arterial uncoupling as an Ees:Ea < 0.8. We evaluated associations between Ees, Ea, and Ees:Ea with all-cause mortality and composite event-free survival using multivariable Cox proportional-hazard models, adjusted for age and sex. RESULTS: All 21 controls had Ea ≤ 0.5 mm Hg/ml and Ees:Ea ≥ 0.8. Of 175 patients with heart failure, 63% had Ea > 0.5 mm Hg/ml. Ees:Ea was lower in patients than in controls (p < 0.001), and 47% of the patients demonstrated Ees:Ea < 0.8, including 8% with normal Ea. In median follow-up of 2.2 (0.8-4.6) years, 53 died, 37 received cardiac transplantation, and 33 received a left ventricular assist device. By multivariable analysis, Ea (hazard ratios [HR]: 2.01, 95% CI 1.18-3.41) and Ees:Ea (HR: 0.46, 95% CI: 0.26-0.82) were independently associated with mortality, whereas Ees was not. CONCLUSIONS: Right ventricular-pulmonary vascular coupling is frequently impaired in heart failure and associated with greater mortality. Elevated pulmonary arterial elastance is associated with greater mortality even when coupling is preserved.