Right Ventricular Epicardial Vascularisation in Patients With Pulmonary Arterial Hypertension

Abstract

Pulmonary arterial hypertension (PAH) leads to a haemodynamic overload and ischaemia of the right ventricle (RV), which are important triggers of an arterial growth. Thus, we aimed to assess whether patients with PAH have altered epicardial vasculature of the RV, and how it corresponds to RV haemodynamic stress. We enrolled consecutive patients with PAH diagnosed in a single pulmonary hypertension centre, who underwent coronary angiography. The control group consisted of patients with normal coronary arteries. Artery branches from segments I-III of the right coronary artery (RCAB) and branches of the left coronary artery (LCAB) were assessed. The sum of the diameters of RCABs (RCAB_sum) was used as a marker of RV epicardial vascularisation. Linear regression models were used to investigate associations between the RCAB_sum and markers of RV dysfunction. We recruited 37 PAH patients (idiopathic, n=25; associated with connective tissue disease, n=12) and 37 control subjects of similar age (56±18 vs. 56±13 years, p=0.99) and sex (73% vs. 73% of women, p=0.99). Pulmonary arterial hypertension patients as compared with control subjects had more RCABs (7 [6-8] vs. 6 [5-7], p<0.001) and increased RCAB_sum (9.4 [8.2-10.5] vs. 7.3 [6.6-7.40] mm; p<0.001) although comparable LCAB count (4 [4-5] vs. 4 [4-5]; p=0.50). In a stepwise multivariable linear regression model, RA area (β=0.152 [0.062-0.242]; p=0.002) and diastolic wall stress (β=0.025 [0.005-0.045]; p=0.02) were significant predictors of RCAB_sum (model R2=0.65; p<0.0001). Right ventricular epicardial vasculature is more extensive in PAH patients as compared with control subjects, and it is in linear relation to potential markers of RV diastolic dysfunction.