Why the study?
The study aimed to investigate the clinical, structural, and hemodynamic characteristics of patients with pulmonary arterial hypertension in relation to mean left atrial pressure.
In severe precapillary PAH, elevated mean LA pressure identifies a distinct phenotype with significant LA myopathy and worse exercise tolerance despite lower NT-proBNP levels.
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Elevated LA pressure may mark a distinct precapillary PAH phenotype with myopathy and reduced exercise capacity; leaves open targeted assessment or management implications.
Objectives The study aimed to investigate the clinical, structural, and hemodynamic characteristics of patients with pulmonary arterial hypertension (PAH) in relation to mean left atrial (LA) pressure. Methods 58 patients with precapillary PAH were prospectively enrolled and stratified into two groups based on mean LA pressure assessed by transthoracic echocardiography: Group 1 (<8 mmHg) and Group 2 (>8 mmHg). All patients underwent clinical evaluation, right heart catheterization, echocardiography including LA strain and stiffness analysis. Results Patients in Group 2 were older (55.96±2.52 vs 41.4±2.53 years, p<0,001), had a higher burden of left heart comorbidities, and demonstrated more advanced LA myopathy with significantly impaired reservoir (20.03±2.37 vs 31.42±2.21%, p=0.0014), conduit (13.91±1.78 vs. 18.52±1.48%, p=0.053), and contractile strain (7.96±1.26 vs. 16.41±1.56%, p<0.001). Despite more favorable markers of heart failure compensation (NT-proBNP levels: 888.81±216.06 vs 2187.34±707.11 pg/mL, p=0.050), they exhibited worse exercise tolerance on the 6MWT (294.39±18.80 vs 349.68±19.05 m, p =0.047). Hemodynamically, RV dysfunction in Group 1 was predominantly driven by the resistive component of afterload, while in Group 2 both resistive and pulsatile components were involved. Conclusions Patients with severe precapillary PAH and elevated mean LA pressure represent a distinct clinical phenotype characterized by significant LA dysfunction and a combined hemodynamic burden. These findings underscore the need for personalized diagnostic approaches that account for the complex interactions between pulmonary vascular disease and left-heart pathology.
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Kalashnykova et al. (2025) studied this question.
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