The goal of this observational study is to learn about the acute (days) changes in right ventricular functions caused by initiation of pharmacological therapies in patients with precapillary pulmonary hypertension. The main question it aims to answer is: • Course of afterload and intrinsic contractility throughout the hospital stay Participants will be equipped with a device for continuous monitoring and recording of the right ventricular pressure signal.
Pulmonary hypertension (PH) arises as a result of a vascular pathology affecting the pulmonary vessels, leading to an increase in resistance within the pulmonary circulation. The ability of the right ventricle to adapt to the elevated pressures caused by increased afterload is crucial for the progression and symptoms of the disease. This adaptation of the right ventricle to its afterload is referred to as ventriculoarterial coupling or RV-PA coupling, described by the ratio of contractility to afterload. Invasive pressure-volume loops (PV loops) are the gold standard for assessing RV-PA coupling. The loss of RV-PA coupling is considered a crucial factor in the development of right heart failure, the leading cause of mortality in patients with pulmonary hypertension. Therefore, reliable assessment of right cardiac function is essential for physicians to make informed decisions regarding further invasive diagnostics or therapy adjustments. Approved medications for the treatment of pulmonary arterial hypertension primarily induce pulmonary vasodilation, leading to a reduction in right ventricular afterload. The effects on right ventricular contractility and function, as represented by RV-PA coupling, are currently poorly understood and may not be consistent. In this study, 100 patients with PH requiring an inpatient stay for right heart catheterization will be equipped with a mobile, wireless system for invasive measurement of right ventricular pressure - the CorLog system (emka MEDICAL, Aschaffenburg, Germany). By combining continuously recorded pressure profiles with 3D echocardiographic volumetry, we will be able to generate PV loops and assess RV-PA coupling at various time points. The continuous monitoring of right ventricular pressure profiles throughout the entire hospital stay will allow us to capture the effects of newly initiated or expanded pulmonary vascular therapy on RV-PA coupling not only immediately but over several days. Furthermore, the 3D echocardiographic datasets will be analyzed using specialized software (ReVISION®, Argus Cognitive, Inc, Lebanon, NH) to mechanistically quantify the right ventricular contraction pattern and capture the immediate impact of pulmonary vasoreactive therapy on it. Additionally, a data pool will be created to validate the calculation of ejection fraction and RV-PA coupling based solely on pressure signals.
Study Type
OBSERVATIONAL
Enrollment
100
Department of Internal Medicine, Justus Liebig University Giessen, Universities of Giessen and Marburg Lung Center (UGMLC), German Center for Lung Research (DZL)
Giessen, Hesse, Germany
RECRUITINGAfterload
Responce of afterload (calculated from PV loops \[Ea\]) afterload during hospitalization to the initiation or escalation of pulmonary vascular therapy
Time frame: 3-7days
Contractility
Response of contractility (calculated from PV loops \[Ees\]) during hospitalization to the initiation or escalation of pulmonary vascular therapy
Time frame: 3-7days
Coupling
Response of Coupling (calculated from PV loops \[Ees/Ea\]) during hospitalization to the initiation or escalation of pulmonary vascular therapy
Time frame: 3-7days
Validation of Echo/CorLog PV-Loops
Validation of Echo/Corlog-generated PV loops based on conductance catheter-generated PV loops
Time frame: On first day
Validation of pressure-only methods
Validation of methods for calculating ejection fraction and RV-PA coupling using ventricular pressure signals
Time frame: 3-7days
Contraction patterns
Analysis of volumetric datasets of the right ventricle using ReVISION software. Isolated quantification of right ventricular systolic shortening along the ventricular axes in 3-dimensional space.
Time frame: 3-7 days
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