Impact of Pulmonary Arterial Hypertension on Left Ventricular Function – a Comparative Study between Scleroderma and Coronary Artery Disease

Author:

Cucuruzac Roxana1,Marton Emese23,Hodas Roxana123,Blendea Ciprian123,Pirvu Mirela1,Benedek Annabella123,Benedek Theodora123

Affiliation:

1. University of Medicine and Pharmacy , Tîrgu Mureș , Romania

2. Center of Advanced Research in Multimodality Cardiac Imaging, Cardio Med Medical Center , Tîrgu Mureș , Romania

3. Cardiac Critical Care Unit, Clinic of Cardiology, County Clinical Emergency Hospital , Tîrgu Mureș , Romania

Abstract

Abstract Background: The impact of pulmonary arterial hypertension (PAH) on left ventricular performance in patients with scleroderma is still unknown. This study aims to perform a comparative echocardiographic analysis of left ventricular function between two different etiological varieties of PAH, namely PAH caused by systemic sclerosis as a representative of systemic inflammatory diseases and PAH caused by myocardial ischemia. Material and method: We conducted a prospective observational study on 82 patients, of which 36 were with documented PAH, with the systolic pressure in the pulmonary artery above 35 mmHg, and 46 were patients with normal pulmonary artery pressure. The study population was divided into two groups, based on the etiology of PAH: group 1 included patients diagnosed with scleroderma (n = 48); group 2 included patients with coronary artery disease (n = 35). Patients from each group were divided into two subgroups based on the diagnosis of PAH: subgroup 1A – subjects with scleroderma and associated PAH (n = 20); subgroup 1B – subjects with scleroderma without PAH (n = 28); subgroup 2A – ischemic patients with associated PAH (n = 16); and subgroup 2B – patients with ischemic disease without PAH (n = 19). Results: A significant difference between LVEF values in patients with PAH versus those without PAH in the ischemic group (p = 0.023) was recorded. Compared to scleroderma subjects, ischemic patients presented significantly lower values of LVEF in both PAH and non-PAH subgroups (p <0.0001 and p <0.0001, respectively). Linear regression analysis between sPAP and LVEF revealed a significant negative correlation only for the ischemia group (r = −0.52, p = 0.001) and the scleroderma 2B subgroup (r = −0.51, p = 0.04). Tissue Doppler analysis of left ventricular function revealed a significant impact of PAH on left ventricular diastolic performance in the ischemic group. Conclusions: Compared to patients with coronary artery disease, those with scleroderma present a less pronounced deterioration of LVEF in response to pulmonary arterial hypertension.

Publisher

Walter de Gruyter GmbH

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