In early CpcPH, impaired RV and right atrial strain plus increased ECV at the RV posterior insertion point were independently associated with normal RVEF before RV dysfunction.
Do CMR-derived markers (strain and ECV) identify early right ventricular maladaptation in patients with CpcPH before the onset of RV dysfunction?
Impaired RV and right atrial strain, along with increased extracellular volume at the RV posterior insertion point, serve as early CMR markers of right ventricular maladaptation in CpcPH patients before ejection fraction declines.
Absolute Event Rate: 0% vs 0%
Abstract Background Pulmonary hypertension (PH) associated with left heart disease is an increasingly prevalent condition associated with an unfavorable prognosis, especially when combined post-and pre-capillary PH (CpcPH) coexists with right ventricular (RV) failure. Since RV function is a relevant determinant of survival, early recognition of RV maladaptation in PH is critical. Purpose To identify cardiac magnetic resonance (CMR)-derived parameters affected in early stages of CpcPH before the onset of RV dysfunction. Methods We conducted a three-arm case-control study including patients with an invasive diagnosis of CpcPH, categorized into two groups based on RV ejection fraction (RVEF) by CMR: normal (RVEF≥53% in men, ≥55% in women) and reduced RVEF (53% and 55%, respectively). Both were compared to a control group of middle-aged healthy individuals. CMR studies included cine sequence and T1-mapping to quantify extracellular volume (ECV) at the RV insertion points as a surrogate of diffuse myocardial fibrosis. Both myocardial RV and biatrial strain were measured with feature tracking. Categorical variables were compared using the chi-square test, while quantitative variables were evaluated with the Kruskal-Wallis test, followed by Dunn’s post hoc analysis with Holm-Bonferroni correction. Results A total of 50 patients with CpcPH (14 with normal RVEF and 36 with reduced RVEF) and 10 controls were included. As expected, compared with healthy controls, CpcPH patients were older, had more cardiovascular risk factors and prevalent left heart disease. Patients with CpcPH and reduced RVEF exhibited worse hemodynamic profile (Table 1). In early stages, before deterioration of RVEF and significant dilatation of right chambers, patients with CpcPH showed a significant impairment of RV and right atrial strain and greater ECV at the posterior RV insertion point compared to healthy controls (Figure 1). After adjusting for sex and age, CpcPH despite normal RVEF remained independently associated with RV strain (β =8.6 3.6; 13.6, p=0.001), right atrial strain (β =-15.2 -21.7; -8.7, p 0.001), and ECV fraction (β =6.3 0.4; 12.3, p=0.038). In more advanced stages, RV-PA uncoupling was evident alongside RV dilatation and failure. Conclusions Impaired RV and atrial strain and increased ECV at the RV posterior insertion point emerge as early CMR markers of RV maladaptation in patients with CpcPH.Table Figure
Garcia et al. (Sat,) reported a other. In early CpcPH, impaired RV and right atrial strain plus increased ECV at the RV posterior insertion point were independently associated with normal RVEF before RV dysfunction.