Background:Resting hemodynamic assessment of suspected pulmonary hypertension (PH) in older adults with cardiovascular risk factors may not effectively discriminate pre-capillary from post-capillary disease. Exercise right-heart catheterization (RHC) can improve the ability to make this distinction, yet its clinical value remains unclear. We aimed to describe the challenges encountered in hemodynamic exercise phenotyping in this population and evaluate the relationships of exercise classifications to worsening clinical events, including mortality. Methods:We prospectively recruited patients aged > 50 years with ≥ 1 cardiovascular risk factor referred for hemodynamic assessment of suspected PH, to undergo cycle-ergometry during initial RHC. Resting hemodynamics were classified per the 2022 European Society of Cardiology/European Respiratory Society guidelines, and exercise pressure-flow relationships were analyzed but not disclosed to treating physicians. Win-ratio and Kaplan-Meier analyses evaluated associations between exercise hemodynamic phenotypes and worsening clinical events. Results:Among 43 patients (aged 72 ± 9 years, 47% female), 37 completed exercise. Resting classifications included the following: No-PH (19%), pulmonary arterial hypertension (PAH) (53%), and PH associated with left-heart disease (PH-LHD; 28%). Exercise hemodynamics revealed predominantly PH-LHD (62%), and 22% of patients demonstrated limited increases in cardiac output. The win-ratio was unfavourable for resting PH-LHD vs PAH (0.59; P = 0.035), but no differences in mortality incidence were present (P = 0.858). Conversely, the win-ratio was unfavourable for exercise PAH vs PH-LHD (0.59; P = 0.037), and exercise PAH demonstrated a higher mortality incidence (P = 0.031). Conclusions:In older patients with cardiovascular risk factors undergoing RHC to diagnose suspected incident PH, the upfront addition of exercise was challenging, yielding inconclusive results in approximately one-third of patients. Results also showed that time to death was more unfavourable for those with exercise PAH.

A footbath may be an accessible form of passive heat therapy (PHT) to improve cardiovascular health. As a localized PHT stimulus, it is unclear whether longer durations are superior for promoting adaptive hemodynamic and vascular adjustments. Fourteen older adults (7 females; means ± SD; age: 68 ± 6 yr) performed 30-, 45-, and 60-min lower-leg hot-water (42°C) immersions and a 60-min thermoneutral (36°C) sham immersion on 4 separate days. Superficial femoral artery blood flow and flow-mediated dilation (FMD) were assessed pre- and postimmersion, and the time course of recovery was characterized over the 60 min following immersion. Twenty-four-hour ambulatory blood pressure was monitored over each experimental day. Femoral artery blood flow increased following immersion in all PHT conditions (mean of all PHT conditions: +345 ± 211%; P < 0.001) but was unchanged in sham. The 30- and 45-min PHT conditions sustained a higher leg blood flow than sham for the full hour following immersion (all post hoc comparisons: P < 0.01), whereas the 60-min condition was not different from sham by 30 min into recovery. FMD was greater following 45-min PHT than sham over the hour of recovery (mean of recovery time points: 2.5 ± 0.9% FMD vs. 1.7 ± 1.0%; P = 0.002). Twenty-four hour mean arterial pressure was lower with 45-min and 60-min PHT compared with sham (both -4 ± 4 mmHg; P < 0.05). A 45-min footbath results in comparable hemodynamic adjustments as 60 min of immersion and leads to the largest acute improvement in vascular function. As such, a 45-min footbath may be the preferred dose of PHT to use in future interventions seeking to improve vascular health and blood pressure.NEW & NOTEWORTHY A longer duration footbath may not be better for cardiovascular benefits in older adults. Leg blood flow increases, and ambulatory blood pressure is reduced similarly with 30, 45, and 60 min of lower-leg hot-water immersion. However, only a 45-min footbath improves endothelial function compared with a thermoneutral sham immersion. Forty-five minutes is the most favorable acute dose of lower-leg hot-water immersion and may be the most suitable for chronic interventions seeking to improve cardiovascular health.

To conduct a systematic review and meta-analysis of the prevalence, diagnostic accuracy of natriuretic peptides, prognosis, treatment response, and pathophysiological mechanisms of heart failure with preserved ejection fraction (HFpEF) in patients with chronic obstructive pulmonary disease (COPD). Diastolic dysfunction was highly prevalent in COPD, with a pooled prevalence of 43.4

Clinical differentiation of pre- vs. postcapillary pulmonary hypertension can be challenging in older patients with risk factors for both pathophysiologies. The use of exercise pressure-flow relationships during hemodynamic assessment is now recommended when resting pulmonary artery wedge pressure is proximate to a threshold of 15 mmHg. In this study, we examined relationships between resting pulmonary artery wedge pressure and the balance of pre- and postcapillary contributions to exercise pulmonary hypertension. Patients > 45 yr suspected of precapillary pulmonary hypertension (n = 29, 72 ± 10 yr, 52% Female) with risk factors for left-heart disease were prospectively recruited to undergo semiupright cycle-ergometry at the time of diagnostic right-heart catheterization. Hemodynamic data, including pressure-flow slopes and contributions of transpulmonary gradient and pulmonary artery wedge pressure to mean pulmonary artery pressure, were analyzed to evaluate pre- and postcapillary contributions, respectively, at rest and during exercise. Exercise pressure-flow slopes indicated 62% with postcapillary contributions to pulmonary hypertension, and 31% with solely precapillary contributions. Of patients with pulmonary artery wedge pressure <12 mmHg, 67% had postcapillary contributions to exercise pulmonary hypertension. Conversely, 50% of patients with pulmonary artery wedge pressure >15 mmHg had precapillary contributions to exercise pulmonary hypertension. Exercise-associated increases in pulmonary artery pressures were more strongly associated with precapillary contributions, regardless of postcapillary contributions or the value of resting pulmonary artery wedge pressure. In conclusion, in this population, postcapillary contributions to exercise pulmonary hypertension were commonly disclosed over a range of resting pulmonary artery wedge pressure, including <12 mmHg. The severity of exercise pulmonary hypertension was determined by the precapillary contributions.NEW & NOTEWORTHY Exercise is recommended in patients with pulmonary artery wedge pressure (PAWP) between 12 and 15 mmHg and risk factors for left-heart disease to differentiate pre- versus postcapillary contributions to pulmonary hypertension (PH). However, our prospective experience shows resting PAWP does not reliably predict exercise postcapillary PH, which remains common even at lower PAWP ranges (<12 mmHg). Our findings suggest that exercise may retain utility to elicit postcapillary PH across a broad range of resting PAWP.

Intrathoracic pressure modulates cardiac loading conditions, which then influence left ventricular (LV) chamber function, and may occur with underlying myocardial mechanical alterations. We investigated the independent effects of inspiratory negative and expiratory positive intrathoracic pressure on septal geometry, LV chamber function, and rotation, twist, and strain indices. After baseline, 20 healthy adults (11M/9F, 23 ± 4 yr) performed resistive breathing to manipulate inspiratory (-30, -20, -10 cmH2O) or expiratory (+10, +20 cmH2O) intrathoracic pressure. Echocardiography was used to acquire LV-focused two-dimensional (2-D) images, and mitral Doppler inflow and annular tissue velocity spectra. Images were analyzed for LV chamber volumes, tissue velocities, transmitral filling velocities, and speckle tracking-derived LV longitudinal, radial, and circumferential strain and strain-rate, basal and apical rotation, and twist. Across negative pressure trials, most profoundly at -30 cmH2O, we observed progressive end-diastolic septal flattening (3.9 ± 0.4 vs. 3.2 ± 0.4 cm, P < 0.05) and decreases in LV end-diastolic volume (103 ± 23 vs. 115 ± 25 mL, P < 0.05) and stroke volume, whereas end-systolic volume was unchanged. However, LV apical and basal rotation, twist (13.3° ± 3.6° vs. 13.9° ± 3.7°, P = 0.890), and circumferential, radial, and longitudinal strain indices were largely unchanged. During positive pressure trials, we observed main effects for septal flattening (P = 0.014) confined to inspiration, and modestly reduced LV end-diastolic volume (P < 0.001), end-systolic volume (P = 0.033), and stroke volume. Again, myocardial mechanics parameters changed little. Collectively, our data suggest that both positive and negative intrathoracic pressures can exacerbate direct ventricular interaction through opposing mechanisms that attenuate LV end-diastolic volume and stroke volume, but without specific changes in myocardial mechanics or mitral inflow.NEW & NOTEWORTHY Incrementally more negative or positive intrathoracic pressures, relative to normal dynamic breathing, progressively attenuate left ventricular end-diastolic volume and stroke volume in healthy younger adults. Incrementally more negative or positive intrathoracic pressures were each associated with progressive septal flattening during inspiration, indicating direct ventricular interaction. However, left ventricular transmitral inflow velocities, and myocardial rotation, twist, and circumferential, longitudinal, and radial strain parameters changed little.

Pulmonary hypertension (PH) is a highly prevalent hemodynamic condition that occurs as a complication of circulatory, pulmonary, and systemic disorders, increases right ventricular (RV) afterload, and confers adverse prognosis. For patients experiencing chronic dyspnea, echocardiographic screening may raise suspicion for PH. Untangling its cause(s) can then be challenging, as the circulatory and pulmonary systems are functionally interlinked and diseases in both often co-exist, but is essential to appropriately select therapies that may unload the RV. Here, we highlight advances in the hemodynamic assessment of PH, with a focus on using exercise to clarify the underlying pathophysiology to better individualize management.

Background: Diagnosing pulmonary arterial hypertension (PAH) versus pulmonary hypertension associated with left hear disease (PH-LHD) can be challenging in patients with risk factors for both conditions. When resting pulmonary artery wedge pressure (PAWP) is proximate to a threshold of 15mmHg, exercise has been recommended to differentiate pre- versus post-capillary contributions to PH. To improve our understanding of this practice recommendation, we studied relationships between resting PAWP and the balance of pre- and post-capillary contributions to exercise PH. Methods: Patients suspected of PAH (n=29, 72±2y, 52% F) with risk factors for LHD were prospectively recruited to undergo cycle ergometry at time of diagnostic right-heart catheterization. Hemodynamic data, including pressure-flow slopes and contributions of transpulmonary gradient (TPG) and PAWP to mPAP, were analyzed to evaluate pre- and post-capillary contributions, respectively, at rest and during exercise. Results: PAWP ranged from 0 to 20 mmHg. Exercise pressure-flow slopes demonstrated 62% with post-capillary PH, and 31% with pre-capillary PH only. The relationship between resting PAWP and the pre- versus post-capillary contributions to exercise PH was not straightforward. Of patients with PAWP<12mmHg, 67% had post-capillary contributions to exercise PH. Conversely, 50% of patients with PAWP>15mmHg had pre-capillary contributions to exercise PH. Exercise-associated increases in pulmonary artery pressures were more strongly associated with pre-capillary contributions regardless of post-capillary contributions or the value of resting PAWP. Conclusion: In this population, post-capillary contributions to exercise PH were commonly disclosed over a range of resting PAWP, including <12mmHg. The severity of exercise PH was determined by the pre-capillary contributions. ### Competing Interest Statement The authors have declared no competing interest. ### Funding Statement The study was funded by Heart and Stroke Foundation of Canada Grant in Aid (G-18-0022220). Conflict of interest: All other authors have no relevant financial disclosures. ### Author Declarations I confirm all relevant ethical guidelines have been followed, and any necessary IRB and/or ethics committee approvals have been obtained. Yes The details of the IRB/oversight body that provided approval or exemption for the research described are given below: Institutional research ethics boards at Mount Sinai Hospital (#18-0257-A) and the University Health Network (19-5069.0) approved this study. I confirm that all necessary patient/participant consent has been obtained and the appropriate institutional forms have been archived, and that any patient/participant/sample identifiers included were not known to anyone (e.g., hospital staff, patients or participants themselves) outside the research group so cannot be used to identify individuals. Yes I understand that all clinical trials and any other prospective interventional studies must be registered with an ICMJE-approved registry, such as ClinicalTrials.gov. I confirm that any such study reported in the manuscript has been registered and the trial registration ID is provided (note: if posting a prospective study registered retrospectively, please provide a statement in the trial ID field explaining why the study was not registered in advance). Yes I have followed all appropriate research reporting guidelines, such as any relevant EQUATOR Network research reporting checklist(s) and other pertinent material, if applicable. Yes The data supporting this study's findings are available from the corresponding author upon reasonable request.

BACKGROUND:Broadly speaking, right heart failure (RHF) can be defined as a clinical syndrome with signs and symptoms of heart failure resulting from right ventricular dysfunction, as evidenced by abnormal structure or function. The heterogeneity of conditions associated with RHF combined with the challenges of characterizing the structural and functional relationships of the right ventricle make a singular definition of RHF elusive. We performed a concise scoping review of the literature that provides knowledge synthesis of RHF in different clinical populations, and extracted the recommended criteria to define the syndrome. METHODS:Searches were conducted to identify reviews, guidelines, consensus statements, systematic reviews, meta-analyses, and consensus statements concerning right heart or right ventricular failure in well-described adult human disease populations from the previous 10 years. After removal of case reports and duplicates, publications describing syndromes in the context of left-sided heart disease were also removed. Data extracted from selected manuscripts included the patient population and quantitative criteria to define RHF, categorized based on diagnostic modalities. RESULTS:Of 9487 articles initially identified, 71 were selected for full text review. We found that the majority of the reviewed literature offered multifaceted diagnostic approaches, including clinical, echocardiographic, hemodynamic, and therapeutic characteristics, with unique additions or omissions depending on the clinical contexts. Nomenclature for RHF was variable, and only 40% of articles articulated a narrative definition. CONCLUSIONS:At this time, development of consistent criteria and a universal definition for RHF remains a work in process.

PURPOSE:Research on intermittent training has mainly focused on the effects of exercise intensity while overlooking the specific effect of the modulations associated with alternating exercise and recovery. This study investigated how the frequency of modulations during moderate-intensity exercise affects postexercise vagal reactivation. METHODS:Healthy, active females and males 18-39 yr old were recruited for the study. Participants completed three treadmill running sessions on separate days. Each moderate-intensity session accumulated 30 min at 90% of the intensity associated with the second ventilatory threshold and was performed as either high-frequency intermittent (HiFi; 15 × [2 min + 2 min recovery]), low-frequency intermittent (LoFi; 5 × [6 min + 2 min recovery]), or moderate-intensity continuous training (MICT; 1 × 30 min). Heart rate recovery (HR rec ) at 1 min and heart rate variability recovery (HRV rec ; lnRMSSD) were assessed in response to submaximal constant-speed tests performed before (CST1) and after (CST2) each of the exercise sessions. HR rec , HRV rec , blood lactate (BLa), and blood pressure were also collected during the exercise sessions. RESULTS:Twenty-one individuals (8 females, 13 males) participated in the study. HR rec from CST2 was faster in HiFi versus MICT ( P < 0.001), whereas HRV rec post-CST2 was higher after HiFi versus both LoFi ( P = 0.024) and MICT ( P < 0.001). BLa increased in all conditions ( P = 0.007) but remained lower during HiFi compared with LoFi and MICT (both P < 0.001). Diastolic blood pressure did not change during exercise with HiFi ( P = 0.939) but decreased during LoFi ( P = 0.006) and MICT ( P = 0.008). CONCLUSIONS:Exercise pattern influences the physiologic response to exercise. Higher frequencies of modulations can preserve vagal activity and expedite postexercise recovery, suggesting moderate-intensity intermittent exercise as a potential strategy to mitigate autonomic impact and acute physiological stress while maintaining total work performed.

Abstract 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.

Pulmonary arterial hypertension affects females more frequently than males, and there are known sex-related differences in the lungs. However, normal sex-related differences in pulmonary vascular structure remain incompletely described. We aimed to contrast computed tomography-derived pulmonary vascular volume and its distribution within the lungs of healthy adult females and males. From the CanCOLD Study, we retrospectively identified healthy never-smokers. We analyzed full-inspiration computed tomography images, using vessel and airway segmentation to generate pulmonary vessel volume, vessel counts, and airway counts. Vessels were classified by cross-sectional area >10, 5-10, and <5 mm2 into bins, with volume summed within each area bin and in total. We included 46 females and 36 males (62 ± 9 years old). Females had lower total lung volume, total airway counts, total vessel counts, and total vessel volume (117 ± 31 vs. 164 ± 28 mL) versus males (all p < 0.001). Females also had lower vessel volume >10 mm2 (14 ± 8 vs. 27 ± 9 mL), vessel volume 5-10 mm2 (35 ± 11 vs. 55 ± 10 mL), and vessel volume <5 mm2 (68 ± 18 vs. 82 ± 19 mL) (all p < 0.001). Normalized to total vessel volume, vessel volume >10 mm2 (11 ± 4 vs. 16 ± 4%, p < 0.001) and 5-10 mm2 (30 ± 6 vs. 34 ± 5%, p = 0.001) remained lower in females but vessel volume <5 mm2 relative to total volume was 18% higher (59 ± 8 vs. 50 ± 7%, p < 0.001). Among healthy older adults, pulmonary vessel volume is distributed into smaller vessels in females versus males.

Exercise training requires the careful application of training dose to maximize adaptation while minimizing the risk of illness and injury. High-intensity interval training (HIIT) is a potent method for improving health and fitness but generates substantial autonomic imbalance. Assuming a supine posture between intervals is a novel strategy that could enhance physiological readiness and training adaptations. This study aimed to establish the safety and feasibility of supine recovery within a HIIT session and explore its acute effects. Fifteen healthy, active males (18–34 years) underwent assessment of cardiopulmonary fitness. Participants completed two identical HIIT treadmill sessions (4 x [3 min at 95

We combined invasive estimates of left atrial pressure with noninvasive left atrial volume measurements made at rest and during exercise in healthy humans. Left atrial pressure and volume both increased with exercise, though the pressure increase was relatively greater, and calculated compliance decreased modestly while estimated peak wall stress nearly doubled. Our results demonstrate left atrial loading during exercise in healthy older adults and provide insight into how the left atrium mediates cardiopulmonary interactions.

Our aim was to conduct a sex-disaggregated analysis of pulmonary and systemic vascular function in healthy individuals both at rest and during submaximal exercise. Healthy individuals underwent right-heart catheterization at rest and during submaximal cycling. Hemodynamic data were collected in a control state and with moderate exercise. Pulmonary and systemic vascular variables including: compliance, resistance, and elastance were calculated, indexed to body surface area (BSA), adjusted for age and compared between male and female sex. Thirty-six individuals (18M/18F; 54 ± 7 vs. 58 ± 6 years, p = 0.04) were included. When adjusted for age and indexed to BSA, total pulmonary resistance (TPulmR) (516 ± 73 vs. 424 ± 118 WU m−2, p = 0.03) and pulmonary arterial elastance (PEa) (0.41 ± 0.1 vs. 0.32 ± 0.1 mmHg ml−1 m2, p = 0.03) were higher in females vs. males. Both pulmonary (Cpa) and systemic compliance (Csa) were lower in females vs. males however lost significance with adjustment for age. Systemic arterial elastance (SEa) was higher in females (1.65 ± 0.29 vs. 1.31 ± 0.24 mmHg ml−1, p = 0.05). Secondary analyses demonstrated significant correlations between age and PVR (r = 0.33, p = 0.05), TPulmR (r = 0.35, p = 0.04), Cpa (r = −0.48, p < 0.01), and PEa (r = 0.37, p = 0.03). During exercise, there were greater increases in TPulmR (p = 0.02) and PEa (p = 0.01) in females vs. males. In conclusion, TPulmR and PEa are significantly higher at rest and exercise in females vs. males. Cpa and Csa were lower in females, however this may have been confounded by age. Our results are consistent with the notion that indices of pulmonary and systemic vascular load are higher, related to both older age and female sex, independent of heart failure.

In healthy younger adults, the Mueller maneuver transiently reduces left atrial filling and passive emptying during the reservoir and conduit phases, respectively. Corresponding reductions are seen in left atrial reservoir and conduit phase longitudinal myocardial strain and strain rate. However, left atrial pump phase active function and mechanics are largely preserved compared with baseline. Rapid changes in LA chamber volumes and myocardial strain with recurrent forceful inspiratory efforts and relaxation may reflect acute LA stress.

Abstract 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.

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BACKGROUND: Early right heart failure (RHF) remains a major source of morbidity and mortality after left ventricular assist device (LVAD) implantation, yet efforts to predict early RHF have proven only modestly successful. Pharmacologic unloading of the left ventricle may be a risk stratification approach allowing for assessment of right ventricular and hemodynamic reserve. METHODS: We performed a multicenter, retrospective analysis of patients who had undergone continuous-flow LVAD implantation from October 2011 to April 2020. Only those who underwent vasodilator testing with nitroprusside during their preimplant right heart catheterization were included (n = 70). Multivariable logistic regression was used to determine independent predictors of early RHF as defined by Mechanical Circulatory Support-Academic Research Consortium. RESULTS: Twenty-seven patients experienced post-LVAD early RHF (39%). Baseline clinical characteristics were similar between patients with and without RHF. Patients without RHF, however, achieved higher peak stroke volume index (SVI) (30.1 +/- 8.8 vs 21.7 +/- 7.4 mL/m(2); p < 0.001; AUC: 0.78; optimal cut-point: 22.1 mL/m2) during nitroprusside administration. Multivariable analysis revealed that peak SVI was significantly associated with early RHF, demonstrating a 16% increase in risk of early RHF per 1 ml/m2 decrease in SVI. A follow up cohort of 10 consecutive patients from July 2020 to October 2021 resulted in all patients being categorized appropriately in regards to early RHF versus no RHF according to peak SVI. CONCLUSION: Peak SVI with nitroprusside administration was independently associated with post-LVAD early RHF while resting hemodynamics were not. Vasodilator testing may prove to be a strong risk stratification tool when assessing LVAD candidacy though additional prospective validation is needed. J Heart Lung Transplant 2022;41:1716- 1726 (c) 2022 International Society for Heart and Lung Transplantation. All rights reserved.