Systematic hemodynamic and clinical assessments for heart failure with reduced ejection fraction and pulmonary hypertension

Abstract

Acute decompensated heart failure (ADHF) and pulmonary arterial hypertension (PAH)—both characterized by high mortality and re-hospitalization rates and poor prognosis—are frequently caused by the response of the amount of high pressure-overload and increased peripheral vascular resistance in patients hospitalized with heart failure. Previous work provides insufficient evidence related to cardiovascular hemodynamic risk factors with comprehensive criteria systematic assessment to guide clinical management. This thesis describes a series of prospective, single-center observational studies from June 2018 to January 2020 involving a consecutive cohort of 56 patients upon hospital discharge after hospitalization for ADHF. The patients were monitored serially three times to examine alterations in functional hemodynamics and fluid response by a passive leg-raising maneuver upon discharge to predict the impact of clinical outcomes within 30 days. In relation to PAH, 80 PAH patients as historical controls from 2010 to 2017 were compared with 12 patients with newly diagnosed PAH enrolment from 2018 to 2019 under the new systematic management method to assess the impacts of implementation of regular comprehensive risk on clinical management and outcomes at 6-month intervals. In the ADHF study, we explored the characteristics of hospitalized patients at baseline, compared the changes of several cardiovascular indices, and found that the change of LVOT-VTI (ΔLVOT-VTI) was the most significant difference. The changes of ΔThe mean and median LVOT-VTI with the preload augmentation by passive leg elevation were 0.5 ± 3.1 and 0.4 cm (IQR: -1.1–2.2 cm), 0.52 ± 2.96 cm and 0.35 cm (IQR: -1.40–2.43 cm) respectively, which resulted in an increase in 30 patients (53.4%) and a reduction in 26 patients (46.6%) under the preload augmentation with the change of LVOT-VTI. Moreover, 9 patients (16.1%) had worse outcomes, especially in terms of the prevalence of patients at the higher quartiles of LVOT-VTI at 6 minutes (36.4% vs. 11.1%, p=0.041*). At last, in multivariate analysis, several cardiovascular indices associated with the body fluid status act as risk factors to predict fluid responsiveness. In the PAH assessment study, aside from depicting the clinical symptomatology at baseline, the patients with the new comprehensive management method had higher efficiency utilized on target medicines with a much lower incidence of PAH- related adverse events (0.0% vs. 35.0%, p=0.015*). In addition, compared with the control evaluation, several cardiovascular indices, exercise capacity, and biomedical markers were measured were shown to have improved after 12 months followed-up: there was a series of significant reductions among mPAP (42.9 ± 9.3 mmHg to 33.5 ± 9.7 mmHg (p=0.001*), PVR (from 9.3 ± 4.8 WU to 4.7 ± 4.1 WU (p<0.001*), and the median NT-proBNP (741 pg/ml to 166 pg/ml (p=0.010*), and strengthen the six-minute walk distance. In conclusion, we identified related hemodynamic parameters—such as the LVOT-VTI, CI, SV, and TPR—to be powerful correlation markers to assess fluid responsiveness, and we determined the factors to predict the short-term outcomes after discharge. In addition, implementation of regular PAH risk assessment at 6- month intervals is associated with higher utilization of PAH-specific medication and lower PAH-related outcome events.