Since the effects of bradycardia after cardiac transplantation are not known, we tested the hypothesis that perioperative bradycardia would lead to an increase in adverse outcomes after cardiac transplantation. We conducted a retrospective case control study with inclusion criterion of a heart rate (HR) less than 80 bpm during the 1st week after transplantation. Control patients were matched for gender, age and time since transplantation. We identified 34 patients as having perioperative bradycardia out of the 174 who underwent cardiac transplantation between 1994 and 1997. The results demonstrated no significant differences in donor ischemic times (180 vs. 183, p = 0.88), operative surgeon (p = 0.62) or pretransplant cardiac disease (p = 0.81) between groups. Bradycardic patients were more likely to be on pretransplant amiodarone (RR = 20.4, p < 0.001). Perioperative bradycardia did not lead to increases in cellular rejection (p = 0.72) or vasculopathy (p = 0.79). The patients prescribed pretransplant amiodarone (n = 14) had a trend toward delayed time to first rejection episode (31.0 vs. 15.5 days, median, p = 0.07). In conclusion, perioperative bradycardia does not increase adverse outcomes after cardiac transplantation and is associated with pretransplant use of amiodarone. Amiodarone may modify the recipients' immune response by delaying the occurrence of rejection.
BackgroundRegular risk assessment is recommended in pulmonary arterial hypertension (PAH) management to improve patient outcomes. The REVEAL risk score (RRS) predicts survival in patients with PAH, including those from the PATENT study, which assessed riociguat, a soluble guanylate cyclase stimulator approved for PAH treatment. An updated version, RRS 2.0, has been developed to further refine risk prediction.MethodsThis post hoc analysis of PATENT-1 and its open-label extension PATENT-2 (n = 396) assessed RRS 2.0 score and risk stratum and their association with survival and clinical worsening-free survival (CWFS).ResultsAt PATENT-1 Week 12, riociguat improved RRS 2.0 versus placebo (least-squares mean difference versus placebo: −1.0 [95% confidence interval − 1.4 to −0.6; p < 0.0001]) and more patients improved risk stratum with riociguat (57%) versus placebo (42%). These improvements were maintained at PATENT-2 Week 12. RRS 2.0 score and risk strata at PATENT-1 baseline and Week 12 were significantly associated with survival and CWFS in PATENT-2 (p < 0.0001); change in RRS 2.0 score from PATENT-1 baseline to Week 12 was also significantly associated with outcomes.ConclusionsThese data suggest that RRS 2.0 has clinical utility in predicting long-term outcomes and monitoring treatment response in patients with PAH.
Introduction: Measurements of RV function, such as RVEF and RV-measured ventricular-vascular coupling (VVC), maybe important in predicting survival in PAH, but are dependent on load and mathematical assumptions. However, independent measures, such as flow efficiency (FEI) within the main PA may be better predictors. FEI is dependent on the natural ratio between MPA area to pulsatile blood wavelength (λ), where λ is proportional to the product of λ velocity and the pulse time, but is difficult to measure directly. Hypothesis: We hypothesize pulmonary FEI will correlate with the VVC and RVEF. Methods: CMR was performed on 18 pts with PAH to assess RV function. Eight pts additionally underwent RV CMR during physiologic stressors: 1) inhaled NO 2) dobutamine (20μ/kg/min) and 3) volume challenge (500ml NaCl). MPA flow was measured via phase velocity mapping (PVM). The RVEF, VVC ratio and ejection time (ET) were calculated from CMR. The MPA area was measured from the PVM images along with avg velocity (Vel avg . Pulmonary FEI = (average Vel avg x ET) / MPA area. Results: A total of 38 unique measures of RVEF (52±12%), VVC (0.89±.3) and MPA flow conditions were measured: Vel avg (49±15cm/s), MPA area (51±11mm 2 ) and ET (295±61ms). The FEI correlated with RVEF and VVC via log term: RVEF = 11.5 log nat (FEI) + 37.2; and VVC = 0.34 log nat (FEI) + 1.17.Bland-Altman analysis of the measured RVEF vs. the FEI modeled RVEF (Fig 1) has an offset bias of 0, a four SD range of ±14.4; r=0. 0.8, while the measured VVC vs. modeled has a bias of 0 and a 4 SD range of ± 0.45; r = 0.74. Conclusions: The linear combination of average pulmonary blood velocity, ejection time and MPA area combine to form a pulmonary FEI that strongly correlates with RVEF and VVC. Importantly, it is devoid of the afterload/preload assumptions of RVEF and the multitude of assumptions of V 0 and RVEDP in VVC. As such, this index may provide additional clinical value since it reflects the directly measured intrinsic efficiency of integrated RV-PA conditions.
To develop a suite of quality indicators (QIs) for the evaluation of the care and outcomes for adults with pulmonary arterial hypertension (PAH). We followed the European Society of Cardiology (ESC) methodology for the development of QIs. This included (i) the identification of key domains of care for the management of PAH, (ii) the proposal of candidate QIs following systematic review of the literature, and (iii) the selection of a set of QIs using a modified Delphi method. The process was undertaken in parallel with the writing of the 2022 ESC/European Respiratory Society (ERS) guidelines for the diagnosis and treatment of pulmonary hypertension and involved the Task Force chairs, experts in PAH, Heart Failure Association (HFA) members and patient representatives. We identified five domains of care for patients with PAH: structural framework, diagnosis and risk stratification, initial treatment, follow-up, and outcomes. In total, 23 main and one secondary QIs for PAH were selected. This document presents the ESC QIs for PAH, describes their development process and offers scientific rationale for their selection. The indicators may be used to quantify and improve adherence to guideline-recommended clinical practice and improve patient outcomes.
Risk stratification has gained an increasing role in predicting outcomes and guiding the treatment of patients with pulmonary arterial hypertension (PAH). The most predictive prognostic factors are three noninvasive parameters (World Health Organization functional class, 6-min walk distance and natriuretic peptides) that are included in all currently validated risk stratification tools. However, suffering from limitations mainly related to reduced specificity of PAH severity, these variables may not always be adequate in isolation for guiding individualised treatment decisions. Moreover, with effective combination treatment regimens and emerging PAH therapies, markers associated with pulmonary vascular remodelling are expected to become of increasing relevance in guiding the treatment of patients with PAH. While reaching a low mortality risk, assessed with a validated risk tool, remains an important treatment goal, preliminary data suggest that invasive haemodynamics and cardiac imaging may add incremental value in guiding treatment decisions.
Pulmonary arterial hypertension (PAH) and novel coronavirus (SARS‐CoV‐2) disease COVID‐19 are characterized by extensive endothelial dysfunction and inflammation leading to vascular remodeling and severe microthrombi and microvascular obliterative disease. It is hypothesized that those patients with underlying lung disease, like PAH, represent a high‐risk cohort in this pandemic. However, reports of COVID‐19 in this cohort of patient have been scaring and an observational survey showed that the disease was relatively well tolerated. We postulate that specific PAH vasodilator may offer some protection and/or advantage in the case of concomitant COVID‐19. Here we review the literature describing mechanisms of action for each of the broad categories of PAH therapy, and offer potential hypothesis about why this therapy may impact outcomes in COVID‐19.
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