Why the study?
The effect of chronic thromboembolic pulmonary hypertension lesion location on right ventricular load and function was unknown.
Does the location of chronic thromboembolic pulmonary hypertension lesions (proximal vs distal) influence right ventricular afterload and function?
Does the location of chronic thromboembolic pulmonary hypertension lesions (proximal vs distal) influence right ventricular afterload and function?
This study aims to evaluate whether the anatomical location of CTEPH lesions (proximal vs. distal) differentially impacts right ventricular load and function using multimodality imaging and hemodynamics.
Proximal CTEPH lesions were associated with worse RV function; leaves open whether location should guide therapy selection.
To the Editor:The clinical presentation of chronic thromboembolic pulmonary hypertension (CTEPH) ranges from central pulmonary obstruction to more peripheral obstruction and small vessel vasculopathy.Location of CTEPH lesions does not seem to influence pulmonary artery pressures (1, 2), but its effect on right ventricular (RV) load and function is currently unknown.In this retrospective analysis, we aimed to determine the influence of proximal and distal vascular lesions on RV afterload and function, integrating static and pulsatile components of afterload and RV function parameters. MethodsSeventy-five patients from our clinical registry were selected on the basis of the presence of high-quality computed tomographypulmonary angiography, right heart catheterization (RHC), and cardiac magnetic resonance (CMR) imaging before initiation of treatment (maximum interval between investigations was 6 mo).According to computed tomography-pulmonary angiography, CTEPH was classified as either proximal (level I/II disease: lesions starting in the main or lobar arteries) or distal (level III-IV disease: lesions starting in the segmental and subsegmental) (3) for each side separately.Twenty-nine patients with asymmetrical lesions (proximal on one side and distal on the other side) were not included in the final analysis.RHC and CMR were performed and analyzed as previously described (4): d Pulmonary artery (PA) pulse pressure (mm Hg) = systolic pulmonary artery pressure (PAP) 2 diastolic PAP d PA compliance (ml/mm Hg) = ( _ Q/heart rate)/pulse pressure d Resistance-compliance (RC) time (s) = 0.75 $ 10 23 $ pulmonary vascular resistance (PVR, dyn s cm 25 ) $ compliance
No takes yet. Share an insight, caveat, or question.
Ruigrok et al. (2019) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: