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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.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.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/mPeak 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.

New-onset heart failure is a frequent complication after orthotopic liver transplantation (OLT). Left atrial enlargement (LAE) may be a sign of occult left heart disease. Our primary objective was to determine invasive hemodynamic and clinical predictors of LAE and then investigate its effect on post-transplant outcomes. Of 609 subjects who received OLT between January 1, 2010, and October 1, 2018, 145 who underwent preoperative right-sided cardiac catheterization and transthoracic echocardiography were included. Seventy-eight subjects (54%) had pretransplant LAE. Those with LAE had significantly lower systemic vascular resistance with higher cardiac and stroke volume index (61.0 vs 51.7 ml/m

The use of exercise right heart catheterisation for the assessment of cardiovascular diseases has regained attention recently. Understanding physiologic haemodynamic exercise responses is key for the identification of abnormal haemodynamic patterns. Exercise total pulmonary resistance >3 Wood units identifies a deranged haemodynamic response and when total pulmonary resistance exceeds 3 Wood units, an exercise pulmonary artery wedge pressures/cardiac output slope >2 mmHg/l/min indicates the presence of underlying exercise-induced pulmonary hypertension related to left heart disease. In the evolving field of transcatheter interventions for valvular heart disease, exercise right heart catheterisation may objectively unmask symptoms and underlying haemodynamic abnormalities. Further studies are needed on the use of the procedure to inform the selection of patients who might receive the most benefit from transcatheter interventions for valvular heart diseases.

Augmented negative intrathoracic pressures (nITP) and dynamic hyperinflation (DH) are adverse breathing mechanics (ABM) associated with chronic obstructive pulmonary disease (COPD) that attenuate left ventricular (LV) preload and augment afterload. In COPD, hypertension (elevated systemic arterial load) commonly adds additional afterload to the LV. Combined ABM and hypertension may profoundly challenge ventricular-vascular coupling and attenuate stroke volume (SV), particularly if LV systolic reserve is limited. However, even in the healthy heart, the combined impact of ABM and systemic arterial loading on LV function and ventricular-vascular coupling has not been fully elucidated. Healthy volunteers (10 M/9 F, 24 ± 3 yr old) were challenged with mild (-10 cmH

With each heartbeat, the right ventricle (RV) inputs blood into the pulmonary vascular (PV) compartment, which conducts blood through the lungs at low pressure and concurrently fills the left atrium (LA) for output to the systemic circulation. This overall hemodynamic function of the integrated RV-PV-LA unit is determined by complex interactions between the components that vary over the cardiac cycle but are often assessed in terms of mean pressure and flow. Exercise challenges these hemodynamic interactions as cardiac filling increases, stroke volume augments, and cycle length decreases, with PV pressures ultimately increasing in association with cardiac output. Recent cardiopulmonary exercise hemodynamic studies have enriched the available data from healthy adults, yielded insight into the underlying mechanisms that modify the PV pressure-flow relationship, and better delineated the normal limits of healthy responses to exercise. This review will examine hemodynamic function of the RV-PV-LA unit using the two-element Windkessel model for the pulmonary circulation. It will focus on acute PV and LA responses that accommodate increased RV output during exercise, including PV recruitment and distension and LA reservoir expansion, and the integrated mean pressure-flow response to exercise in healthy adults. Finally, it will consider how these responses may be impacted by age-related remodeling and modified by sex-related cardiopulmonary differences. Studying the determinants and recognizing the normal limits of PV pressure-flow relations during exercise will improve our understanding of cardiopulmonary mechanisms that facilitate or limit exercise.

BackgroundResting right heart catheterization can assess both left heart filling and pulmonary artery (PA) pressures to identify and classify pulmonary hypertension. Although exercise may further elucidate hemodynamic abnormalities, current pulmonary hypertension classifications do not consider the expected interrelationship between PA and left heart filling pressures. This study explored the utility of this relationship to enhance the classification of exercise hemodynamic phenotypes in pulmonary hypertension.Methods and ResultsData from 36 healthy individuals (55, 50–60 years, 50% male) and 85 consecutive patients (60, 49–71 years, 48% male) with dyspnea and/or suspected pulmonary hypertension of uncertain etiology were analyzed. Right heart catheterization was performed at rest and during semiupright submaximal cycling. To classify exercise phenotypes in patients, upper 95% CIs were identified from the healthy individuals for the change from rest to exercise in mean PA pressure over cardiac output (ΔmPAP/ΔCO ≤3.2 Wood units [WU]), pulmonary artery wedge pressure over CO (ΔPAWP/ΔCO ≤2 mm Hg/L per minute), and exercise PA pulse pressure over PAWP (PP/PAWP ≤2.5). Among patients with a ΔmPAP/ΔCO ≤3.2 WU, the majority (84%) demonstrated a ΔPAWP/ΔCO ≤2 mm Hg/L per minute, yet 23% demonstrated an exercise PP/PAWP >2.5. Among patients with a ΔmPAP/ΔCO >3.2 WU, 37% had an exercise PP/PAWP >2.5 split between ΔPAWP/ΔCO groups. Patients with normal hemodynamic classification declined from 52% at rest to 36% with exercise.ConclusionsThe addition of PP/PAWP to classify exercise hemodynamics uncovers previously unrecognized abnormal phenotypes within each ΔmPAP/ΔCO group. Our study refines abnormal exercise hemodynamic phenotypes based on an understanding of the interrelationship between PA and left heart filling pressures.

AimsThe assumption of equivalence between right ventricular (RV) and pulmonary arterial systolic pressure is fundamental to several assessments of RV or pulmonary vascular haemodynamic function. Our aims were to (i) determine whether systolic pressure gradients develop across the RV outflow tract in healthy adults during exercise, (ii) examine the potential correlates of such gradients, and (iii) consider the effect of such gradients on calculated indices of RV function.Methods and resultsHealthy untrained and endurance-trained adult volunteers were studied using right-heart catheterization at rest and during submaximal cycle ergometry. RV and pulmonary artery (PA) pressures were simultaneously transduced, and the cardiac output was determined by thermodilution. Systolic pressures, peak and mean gradients, and indices of chamber, vascular, and valve function were analysed offline. Summary data are reported as mean ± standard deviation or median (interquartile range). No significant RV outflow tract gradients were observed at rest [mean gradient = 4 (3–5) mmHg], and the calculated effective orifice area was 3.6 ± 1.0 cm2. The increase in right ventricular systolic pressure during exercise was greater than the PA systolic pressure. Accordingly, mean gradients were developed during light exercise [8 (7–9) mmHg] and increased during moderate exercise [12 (9–14) mmHg, P ConclusionsIn healthy adults without pulmonic stenosis, systolic pressure gradients develop during exercise, and the magnitude is related to the blood flow rate.

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.

Non-invasive hemodynamic monitoring has the potential to be a valuable clinical tool for the screening and management of hypertensive disorders of pregnancy. The objective of this study was to validate the clinical utility of the non-invasive cardiac output monitoring (NICOM) system in pregnant women.Twenty healthy pregnant women with a singleton pregnancy at 22 to 26 weeks' gestation were enrolled in this study. Measures of heart rate, stroke volume, and cardiac output were obtained through NICOM and compared with Doppler echocardiography.NICOM significantly overestimated measures of both stroke volume and cardiac output compared with Doppler echocardiography (95 ± 4 vs. 73 ± 4 mL, P0.0001; and 7.4 ± 0.2 vs. 5.6 ± 0.2 L/min, P0.0001; respectively).There is no gold standard for the measurement of cardiac output in the setting of pregnancy. However, once normal values have been established, NICOM has the potential to be a useful clinical tool for monitoring maternal hemodynamics in pregnant women. Further investigation regarding the validity of NICOM is required in larger populations of healthy and hypertensive pregnant women to determine whether this device is appropriate for maternal hemodynamic assessment during pregnancy.

Purpose: An augmented pulmonary artery wedge pressure (PAWP) response may explain exercise intolerance in some humans. However, routine use of exercise hemodynamic testing is limited by a lack of data from normal older men and women. Our objective was to evaluate the exercise PAWP response and the potential for sexual dimorphism in healthy, nondyspneic older adults. Methods: Thirty-six healthy volunteers (18 men [54 ± 7 yr] and 18 women [58 ± 6 yr]) were studied at rest (control) and during two stages of semi-upright cycle ergometry, at heart rates of 100 bpm (light exercise) and 120 bpm (moderate exercise). Right heart catheterization was performed to measure pulmonary pressures. The PAWP response to exercise was assessed in context of exercise work rate and body size. Results: At control, PAWP was similar between men and women. Work rates were significantly smaller in women at comparable HR (P < 0.001). PAWP increased similarly at light exercise, with no further increase at moderate exercise. When indexed to work rate alone or work rate adjusted to body weight and height, the PAWP response at light and moderate exercise was significantly elevated in women compared with men (P < 0.05 condition–sex interaction). The change in PAWP relative to the increase in cardiac output did not exceed 2 mm Hg·L−1·min−1 in any volunteer at moderate exercise. Conclusions: The similar rise in the PAWP response to submaximal exercise occurs despite lower work rate in healthy older women compared with men, even when adjusted for smaller body size. It is important to consider sex in the development of normal reference ranges for exercise hemodynamic testing.

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.

KEY POINTS A consistent inverse hyperbolic relationship has been observed between pulmonary vascular resistance and compliance, although changes in pulmonary artery wedge pressure (PAWP) may modify this relationship. This relationship predicts that pulmonary artery systolic, diastolic and mean pressure maintain a consistent relationship relative to the PAWP. We show that, in healthy exercising human adults, both pulmonary vascular resistance and compliance decrease in relation to exercise-associated increases in PAWP. Pulmonary artery systolic, diastolic and mean pressures maintain a consistent relationship with one another, increasing linearly with increasing PAWP. Increases in PAWP in the setting of exercise are directly related to a decrease in pulmonary vascular compliance, despite small decreases in pulmonary vascular resistance, thereby increasing the pulsatile afterload to the right ventricle. ABSTRACT The resistive and pulsatile components of right ventricular afterload (pulmonary vascular resistance, Rp; compliance, Cp) are related by an inverse hyperbolic function, expressed as their product known as RpCp-time. The RpCp-time exhibits a narrow range, although it may be altered by the pulmonary artery wedge pressure (PAWP). Identifying the determinants of RpCp-time should improve our understanding of the physiological behaviour of pulmonary arterial systolic (PASP), diastolic (PADP) and mean (mPAP) pressures in response to perturbations. We examined the effect of exercise in 28 healthy non-athletic adults (55 ± 6 years) who underwent right heart catheterization to assess haemodynamics and calculate Rp and Cp. Measurements were made at rest and during two consecutive 8-10 min stages of cycle ergometry, at targeted heart-rates of 100 beats min(-1) (Light) and 120 beats min(-1) (Moderate). Cardiac output increased progressively during exercise. PASP, PADP, mPAP and PAWP increased for Light exercise, without any further rise for Moderate exercise. RpCp-time decreased for Light exercise (0.39 ± 0.08 to 0.25 ± 0.08, P

Objectives The clinical and prognostic significance of ‘exaggerated’ elevations in pulmonary artery wedge pressure (PAWP) during symptom-limited exercise testing is increasingly recognised. However, the paucity of normative data makes the identification of abnormal responses challenging. Our objectives was to describe haemodynamic responses that reflect normal adaptation to submaximal exercise in a group of community-dwelling, older, non-dyspnoeic adults. Methods Twenty-eight healthy volunteers (16 men/12 women; 55±6 years) were studied during rest and two consecutive stages of cycle ergometry, at targeted heart rates of 100 bpm (light exercise) and 120 bpm (moderate exercise). Right-heart catheterisation was performed to measure pulmonary artery pressures, both early (2 min) and after sustained (7 min) exercise at each intensity. Results End-expiratory PAWP at baseline was 11±3 mm Hg and increased to 22±5 mm Hg at early-light exercise (p Conclusions The range of PAWP responses to submaximal exercise is broad in health, but also time-variant. PAWP may routinely exceed 20 mm Hg early in exercise. Initial increases in PAWP and mean pulmonary artery pressures do not necessarily reflect abnormal cardiopulmonary physiology, as pressures may normalise within a period of minutes.

In health, the aortic valve facilitates unidirectional forward flow from the left ventricle (LV) to the systemic circulation. This article is protected by copyright. All rights reserved

Purpose Exercise during right heart catheterization (RHC) can demonstrate cardiopulmonary hemodynamic abnormalities not evident at rest. The relationships of pulmonary artery pressure (PAP) or pulmonary artery wedge pressure (PAWP) to cardiac output (CO) do not fully consider that PAP and PAWP should also be closely related. Therefore, we sought to expand our understanding of cardiopulmonary hemodynamic abnormalities by calculating the ratio of PA pulse pressure to PAWP during exercise in health and in patients with dyspnea and uncertain mechanisms of pulmonary hypertension (PH). Methods Data from 36 healthy individuals (median, Q1-Q3; 55, 50-60 yr, 50% male) and 85 consecutive patients (60, 49-71 yr, 48% male) referred for RHC and exercise (semi-upright submaximal cycling) were analysed. Results In our healthy control population, the upper 95% confidence intervals were determined for the change from rest to exercise in mean PAP over CO (ΔmPAP/ΔCO; 3.2 WU), PAWP over CO (ΔPAWP/ΔCO; 2 mmHg/L/min), and exercise PA pulse pressure over PAWP (PP/PAWP; 2.5). In the dyspneic population, ΔmPAP/ΔCO 3.2 WU identified patients on the vertical and horizontal limbs of the pulmonary resistance-pulmonary compliance relationship respectively. While patients with a ΔmPAP/ΔCO 3.2 WU exhibited a broad ΔPAWP/ΔCO both below and above 2 mmHg/L/min. Exercise PP/PAWP >2.5 revealed subpopulations within each ΔmPAP/ΔCO group with inappropriate PP/PAWP responses (Figure 1). Conclusion Among dyspneic patients, we identified abnormal exercise phenotypes based upon ΔmPAP/ΔCO, ΔPAWP/ΔCO, and PP/PAWP responses. Our study refines quantitative classification of abnormal exercise hemodynamic phenotypes based on an improved understanding of the interrelationship between left heart filling pressure and pulmonary vascular behaviour.

Right ventricular (RV) function is closely coupled to pulmonary arterial (PA) hemodynamics and is believed to decline with prolonged exercise. A linear pressure-flow relationship is thought to exist between PA pressures and increasing exercise intensity in athletes, yet a paucity of directly measured pulmonary hemodynamic data exists supporting this contention. We sought to describe the PA pressure, PA wedge pressure (PAWP), and RV functional responses to brief and prolonged exercise in endurance-trained athletes. Twenty-one healthy athletes (54 ± 5 yr) underwent right heart catheterization to assess pulmonary hemodynamics during graded, submaximal exercise. Measurements were made at rest and during three stages of steady-state, semiupright cycle ergometry at heart rates of 100 beats/min (EX1), 130 beats/min (EX2), and 150 beats/min (EX3). Five athletes completed an additional 34 min at 130 beats/min for a total exercise time of 60 min [prolonged exercise (PLG)]. PA pressures and PAWP increased significantly at EX1 without a further rise at EX2, EX3, or PLG. PAWP adjusted for absolute work rate demonstrated a significant decline as exercise intensity increased from EX1 to EX2. The resistance compliance time constant decreased at EX1 without further changes at EX2, EX3, and prolonged exercise. RV function did not decline during PLG. After an initial rise in PA pressure and PAWP during early, nonsteady-state exercise, values remained constant despite increases in exercise intensity and duration. These data indicate that in healthy, middle-aged endurance-trained athletes, the PA and pulmonary venous/left atrial compartments rapidly accommodate high conduit flows produced during intensive and prolonged exercise while maintaining RV function. NEW & NOTEWORTHY The right ventricular (RV)-pulmonary arterial (PA) circulatory unit has not been well studied during prolonged exercise, and this study provides an ecological approach that reflects a typical bout of endurance training integrating a transition from rest to exercise with successive increases in intensity, progressing to steady-state, sustained exercise. We demonstrated a remarkably constant response of the PA and PA wedge pressure during incremental, steady-state exercise and that no changes occur in pulmonary pressures throughout prolonged exercise, concomitant to a preservation of RV performance.

Species having experienced rapid range expansion represent unique opportunities to evaluate the dynamics of adaptation during colonization of new environments. We investigated the consequences of range expansion on local adaptation of a successful worldwide colonizer, the shepherd’s purseCapsella bursa-pastoris. This species is an annual weed that originated recently in Eurasia and has now broadly colonized both temperate and subtropical areas. We assessed the performance, genetic diversity, and phenology of field-collected accessions belonging to three distinct genetic clusters of decreasing age (Middle East, Europe and Asia) in three common gardens in Europe, Asia and North America. To understand the genetic basis of local adaptation in this species, we also tested for correlation between SNP allele frequencies and environmental factors in Europe and Asia. Overall, we showed that patterns of local adaptation depended on population history: some older populations were weakly adapted to local conditions while those closer to the front of the colonization wave, far from the origin of the species, were maladapted whatever the common gardens. Altogether, our results have important consequences for the understanding of the evolution and adaptation of self-fertilizing plant during range expansion.

Purpose Exercise during right heart catheterization (RHC) is employed in select centers to demonstrate the extent to which pulmonary artery (PA) hemodynamics and/or left heart filling pressures may be abnormal. We examined right ventricular (RV) end-systolic elastance (Ees), effective PA elastance (Ea), and their coupling (Ees:Ea) at rest and during exercise in patients with dyspnea and/or suspected pulmonary hypertension. Methods Patients referred for an exercise hemodynamic study performed submaximal cycle-ergometry during RHC. We transduced RV and PA pressures simultaneously, and measured thermodilution cardiac output. We determined Ees using the single-beat method and calculated Ea from the ratio of PA pressure to stroke volume. Exercise hemodynamic classifications defined a priori include: 1) left heart disease ( Ex-LHD ) based on an increased slope of the PA wedge pressure/cardiac output relationship; 2) pulmonary vascular disease ( Ex-PVD ) based on an elevated end-diastolic pressure gradient; 3) combined ( Ex-CPH) if both criteria are met; 4) hemodynamically Ex-Normal if neither criteria are met. Results Preliminary data were available for 54 patients (50% male; Age = 59 ± 14); exercise hemodynamic classifications comprised 23 Ex-Normal, 14 Ex-LHD, 12 Ex-PVD, and 5 Ex-CPH. At rest, Ees was similar in Ex-Normal, Ex-LHD, and Ex-PVD; Ea was higher in Ex-LHD and Ex-PVD compared to Ex-Normal (p Conclusion In patients with pulmonary vascular and/or left heart disease, ventricular-vascular coupling is less favorable than in patients with normal hemodynamics, and abnormalities persist during exercise.

Purpose Acute and chronic right ventricular (RV) dysfunction are common complications experienced by patients with advanced heart failure, particularly after receiving mechanical circulatory support. An elevated right atrial pressure to pulmonary artery wedge pressure ratio (RAP:PAWP) or a reduced pulmonary artery (PA) pulsatility index (PAPI) may identify patients at risk of RV dysfunction. We examined the relationship of these markers to RV end-systolic elastance (Ees), effective PA elastance (Ea), and their coupling ratio (Ees:Ea). Methods We studied patients with advanced heart failure undergoing right heart catheterization to assess cardiac transplant candidacy. We analyzed hemodynamics offline, and calculated both RAP:PAWP and PAPI. We determined RV Ees using the single-beat method and calculated PA Ea from the ratio of PA pressure to stroke volume. We considered cases with either RAP:PAWP >0.63 or PAPI Results Of 165 patients (age = 57 (53-60) years), 42 (25%) met either criteria for RV dysfunction; 33 (20%) had an elevated RAP:PAWP, 24 (15%) had a reduced PAPI, and 15 (9%) had both markers. There were no systematic differences between patients with (n = 42) or without (n = 123) RV dysfunction in terms of age, body mass index, heart rate, or mean arterial pressure. Cardiac index was lower among patients with RV dysfunction (1.8 (1.6-2.0) vs. 2.0 (1.7-2.2) L/min/m2, p = 0.025), as was RV stroke work index (4.6 (3.6-6.0) vs. 8.6 (6.6-11.0) g•m/m2, p Conclusion In patients with systolic heart failure being evaluated for advanced therapies, proposed markers of RV dysfunction are modestly associated with load-independent systolic RV performance, but not RV-PA coupling.

Background:The diastolic pressure difference (DPD) is recommended to differentiate between isolated postcapillary and combined pre-/postcapillary pulmonary hypertension (Cpc-PH) in left heart disease (PH-LHD). However, in usual practice, negative DPD values are commonly calculated, potentially related to the use of mean pulmonary artery wedge pressure (PAWP). We used the ECG to gate late-diastolic PAWP measurements. We examined the method’s impact on calculated DPD, PH-LHD subclassification, hemodynamic profiles, and mortality.Methods and Results:We studied patients with advanced heart failure undergoing right heart catheterization to assess cardiac transplantation candidacy (N=141). Pressure tracings were analyzed offline over 8 to 10 beat intervals. Diastolic pulmonary artery pressure and mean PAWP were measured to calculate the DPD as per usual practice (diastolic pulmonary artery pressure–mean PAWP). Within the same intervals, PAWP was measured gated to the ECG QRS complex to calculate the QRS-gated DPD (diastolic pulmonary artery pressure–QRS-gated PAWP). Outcomes occurring within 1 year were collected retrospectively from chart review. Overall, 72 of 141 cases demonstrated PH-LHD. Within PH-LHD, the QRS-gated DPD yielded higher calculated DPD values (3 [−1 to 6] versus 0 [−4 to 3] mm Hg;PPPConclusions:The DPD calculated in usual practice is underestimated in PH-LHD, which may classify Cpc-PH patients as isolated postcapillary pulmonary hypertension. The QRS-gated DPD reclassifies a subset of PH-LHD patients from isolated postcapillary pulmonary hypertension to Cpc-PH, which is characterized by an adverse hemodynamic profile.

A sedentary lifestyle and lack of physical activity are well-established risk factors for chronic disease and adverse health outcomes. Thus, there is enormous interest in measuring physical activity in biomedical research. Many consumer physical activity monitors, including Basis Health Tracker, BodyMedia Fit, DirectLife, Fitbit Flex, Fitbit One, Fitbit Zip, Garmin Vivofit, Jawbone UP, MisFit Shine, Nike FuelBand, Polar Loop, Withings Pulse O2, and others have accuracies similar to that of research-grade physical activity monitors for measuring steps. This review focuses on the unprecedented opportunities that consumer physical activity monitors offer for human physiology and pathophysiology research because of their ability to measure activity continuously under real-life conditions and because they are already widely used by consumers. We examine current and potential uses of consumer physical activity monitors as a measuring or monitoring device, or as an intervention in strategies to change behavior and predict health outcomes. The accuracy, reliability, reproducibility, and validity of consumer physical activity monitors are reviewed, as are limitations and challenges associated with using these devices in research. Other topics covered include how smartphone apps and platforms, such as the Apple ResearchKit, can be used in conjunction with consumer physical activity monitors for research. Lastly, the future of consumer physical activity monitors and related technology is considered: pattern recognition, integration of sleep monitors, and other biosensors in combination with new forms of information processing.