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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. Résumé: 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.

BACKGROUND Pulmonary hypertension (PH) is a state of high afterload to the right ventricle (RV), which is described as afterload sensitive. The purpose of this study was to examine the effect of exercise on the relationship between RV systolic performance [measured as end-systolic elastance (Ees)], and RV afterload [measured as pulmonary arterial (PA) elastance (Ea)] between 2 groups of patients with pulmonary arterial hypertension (PAH) or PH due to left heart disease (PH-LHD). METHODS AND RESULTS Patients with suspected PH underwent right heart catheterization with cycle-ergometry and classified by their exercise hemodynamic responses: 1) Normal 2) PAH and 3) PH-LHD. RV, right atrium (RA), and PA pressures were recorded continuously and analyzed offline. As our lab previously reported, RV Ees and PA Ea were calculated using the single-beat method, and Ees:Ea ratio expresses RV-PA coupling. Ees:Ea is defined as uncoupled if CONCLUSION During exercise, RV afterload increases in patients with PAH and PH-LHD. In both PH groups, the proportion of patients with Ees:Ea uncoupling was high, and the decline in Ees:Ea ratio reached statistical significance in PH-LHD. Uncoupling of the Ees:Ea ratio occurred with larger increases in Ea and was associated with evidence of impaired RV systolic and diastolic function with exercise. Limiting the increase in Ea with exercise and/or preservation of Ees:Ea coupling may optimize RV function in PH patients.

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 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 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.

Purpose In healthy humans, pulmonary artery pressures (PAP) increase modestly and equilibrate rapidly in response to constant intensity exercise. PAP increase markedly in pre- or post-capillary pulmonary hypertension (pre-cap or post-cap PH), but the time course is unclear. We studied pulse (PP) and diastolic (PADP) PAP as indices of pulsatile load and pulmonary vascular outflow pressure, respectively, and explored whether the magnitude and time course of their response to exercise differs in pre-cap or post-cap PH. Methods Patients underwent right heart catheterization with cycle-ergometry (25/40W, F/M), and were classified by their exercise hemodynamic responses: 1) Normal 2) pre-cap PH and 3) post-cap PH. PAP were recorded continuously and analyzed offline. Changes from Control, 2 min, and 7 min were examined. Results We studied 76 patients (47% F; 59±15 years); groups comprised 32 Normal, 22 pre-cap PH, and 22 post-cap PH. After exercise onset in the Normal group, PADP increased at 2 min (∆5±3mmHg). This increase was less than both pre-cap PH (∆9±4mmHg, p Conclusion During exercise, patients with pre-cap or post-cap PH demonstrate differences in both the magnitude and temporality of change in PAP. Despite constant work-rate, the pulmonary vascular load continues to increase in both pre-cap and post-cap PH.