Objectives To evaluate if diastolic pulmonary gradient (DPG) can predict survival in patients with pulmonary hypertension due to left heart disease (PH-LHD). Background Patients with combined post- and pre-capillary PH-LHD have worse prognosis than those with passive pulmonary hypertension. The transpulmonary gradient (TPG) and pulmonary vascular resistance (PVR) have commonly been used to identify high-risk patients. However, these parameters have significant shortcomings and do not always correlate with pulmonary vasculature remodeling. Recently, it has been suggested that DPG may be better marker, yet its prognostic ability in patients with cardiomyopathy has not been fully assessed. Methods A retrospective cohort of 1236 patients evaluated for unexplained cardiomyopathy at Johns Hopkins Hospital was studied. All patients underwent right heart catheterization and were followed until death, cardiac transplantation or the end of the study period (mean time 4.4 years). The relationships between DPG, TPG or PVR and survival in subjects with PH-LHD (n=469) were evaluated with Cox Proportional Hazards Regression and Kaplan Meier analyses. Results DPG was not significantly associated with mortality (HR 1.02; p=0.10) in PH-LHD whereas elevated TPG and PVR predicted death (HR 1.02, p=0.046 and HR 1.11, p=0.002, respectively). Similarly, DPG did not differentiate survivors from non-survivors at any selected cutpoints including a DPG of 7mmHg. Conclusions In this retrospective study of patients with cardiomyopathy and PH-LHD, an elevated DPG was not associated with worse survival.

Background Although the transpulmonary gradient (TPG) and pulmonary vascular resistance (PVR) are commonly used to differentiate heart failure patients with pulmonary vascular disease from those with passive pulmonary hypertension (PH), elevations in TPG and PVR may not always reflect pre-capillary PH. Recently, it has been suggested an elevated diastolic pulmonary artery pressure to pulmonary capillary wedge pressure gradient (DPG) may be better indicator of pulmonary vascular remodeling, and therefore, may be of added prognostic value in patients with PH being considered for cardiac transplantation. Methods Utilizing the United Network for Organ Sharing (UNOS) database, we retrospectively reviewed all primary adult (age >17 years) orthotropic heart transplant recipients between 1998–2011. All patients with available pre-transplant hemodynamic data and PH (mean pulmonary artery pressure ≥ 25mmHg were included (n=16,811). We assessed the prognostic value of DPG on post-transplant survival in patients with PH and an elevated TPG and PVR. Results In patients with PH and a TPG > 12mmHg (n=5,827), there was no difference in survival at up to 5 years post-transplant between high (defined as ≥3, ≥5, ≥7, or ≥10mmHg) and low DPG groups (<3, <5, <7, or <10mmHg). Similarly, there was no difference in survival between high and low DPG groups in those with a PVR > 3 wood units (n=6,270). Defining an elevated TPG as > 15mmHg (n=3,065) or an elevated PVR > 5 (n=1783) yielded similar results. Conclusions In the largest analysis to date investigating the prognostic value of DPG, an elevated DPG had no impact on post-transplant survival in patients with PH and an elevated TPG and PVR.

Rationale: Survivors of septic shock have impaired functional status. Volume overload is associated with poor outcomes in patients with septic shock, but the impact of volume overload on functional outcome and discharge destination of survivors is unknown.Objectives: This study describes patterns of fluid management both during and after septic shock. We examined factors associated with volume overload upon intensive care unit (ICU) discharge. We then examined associations between volume overload upon ICU discharge, mobility limitation, and discharge to a healthcare facility in septic shock survivors, with the hypothesis that volume overload is associated with increased odds of these outcomes. Methods:We retrospectively reviewed the medical records of 247 patients admitted with septic shock to an academic county hospital between June 2009 and April 2012 who survived to ICU discharge. We defined volume overload as a fluid balance expected to increase the subject's admission weight by 10%. Statistical methods included unadjusted analyses and multivariable logistic regression.Measurements and Main Results: Eighty-six percent of patients had a positive fluid balance, and 35% had volume overload upon ICU discharge. Factors associated with volume overload in unadjusted analyses included more severe illness, cirrhosis, blood transfusion during shock, and higher volumes of fluid administration both during and after shock. Blood transfusion during shock was independently associated with increased odds of volume overload (odds ratio [OR], 2.65; 95% confidence interval [CI], 1.33-5.27; P = 0.01) after adjusting for preexisting conditions and severity of illness. Only 42% of patients received at least one dose of a diuretic during their hospitalization. Volume overload upon ICU discharge was independently associated with inability to ambulate upon hospital discharge (OR, 2.29; 95% CI, 1.24-4.25; P = 0.01) and, in patients admitted from home, upon discharge to a healthcare facility (OR, 2.34; 95% CI, 1.1-4.98; P = 0.03).Conclusions: Volume overload is independently associated with impaired mobility and discharge to a healthcare facility in survivors of septic shock. Prevention and treatment of volume overload in patients with septic shock warrants further investigation.

Rationale: Patients with pulmonary arterial hypertension (PAH) and chronic thromboembolic pulmonary hypertension (CTEPH) typically undergo frequent clinical evaluation. The incidence and outcomes of COVID-19 and its impact on routine management for patients with pulmonary vascular disease is currently unknown. Objectives: For patients with PAH/CTEPH followed at accredited pulmonary hypertension centers, assess the cumulative incidence and outcomes of recognized COVID-19. Evaluate the pandemic's impact on clinic operations at these centers. Methods: A survey was emailed to program directors of centers accredited by the Pulmonary Hypertension Association. Descriptive analyses and linear regression were used to analyze results. Results: Seventy-seven center directors were successfully emailed a survey, 58 responded (75%). The cumulative incidence of COVID-19 recognized in individuals with PAH/CTEPH was 2.1 cases per 1,000 patients, similar to the general United States population. In patients with PAH/CTEPH and recognized COVID-19 30% were hospitalized and 12% died. These outcomes appear worse than the general population. A large impact on clinic operations was observed including fewer clinic visits and substantially increased use of telehealth. A majority of centers curtailed diagnostic testing and a minority limited new starts of medical therapy. Most centers did not use experimental therapies in PAH/CTEPH patients diagnosed with COVID-19. Conclusions: The cumulative incidence of COVID-19 recognized in patients with PAH/CTEPH appears similar to the broader population, although outcomes may be worse. While the total

Background Right ventricular (RV) failure is a source of morbidity and mortality after left ventricular assist device (LVAD) implantation. We sought to define hemodynamic changes in afterload and RV adaption to afterload both early after implantation and with prolonged LVAD support. Methods We reviewed right heart catheterization (RHC) data from participants who underwent continuous-flow LVAD implantation at our institutions (n=244), excluding those on inotropic or vasopressor agents, pulmonary vasodilators, or additional mechanical support at any RHC. Hemodynamic data was assessed at five time intervals: 1) pre-LVAD (within 6 months), 2) early post-LVAD (0–6 months), 3) 7–12 months, 4) 13–18 months and 3) very-late post-LVAD (18–36 months). Results Sixty participants met the inclusion criteria. All measures of right ventricular load (effective arterial elastance, pulmonary vascular compliance and pulmonary vascular resistance) improved between the pre- and early post-LVAD time periods. Despite decreasing load and pulmonary capillary artery pressure (PAWP), RAP remained unchanged and the RAP:PAWP ratio worsened early post-LVAD (0.44 [0.38, 0.63] versus 0.77 [0.59, 1.0], p<0.001), suggesting a worsening of RV adaptation to load. With continued LVAD support, both RV load and RAP:PAWP decreased in a steep, linear and dependent manner. Conclusion Despite reducing RV load, LVAD implantation leads to worsened RV adaptation. With continued LVAD support, both RV afterload and RV adaptation improve, and their relationship remains constant over time post-LVAD. These findings suggest the RV afterload sensitivity increases after LVAD implantation, which has important clinical implications for patients struggling with RV failure.