Deterioration of left ventricular performance in response to pulmonary hypertension, in patients with scleroderma versus patients with coronary artery disease |

Objective: We aimed to conduct a comparative analysis of indexes characterizing left ventricular systolic and diastolic function, in two etiological types of pulmo-nary hypertension involving different pathophysiologi-cal mechanisms: PH caused by systemic sclerosis and PH caused by myocardial ischemia.

Methods: We performed a prospective study on 83 pa-tients (36 patients with documented PAH with a systo-lic pulmonary arterial pressure – sPAP of >35 mmHg and 47 subjects with normal sPAP), out of which group 1 – with systemic sclerosis (n=48); group 2 – significant coronary artery disease – CAD (n=35). Patients of each group were divided in two subgroups based on the diagnosis of PH: group 1A – subjects with scleroderma and associated PH (n=20), group 1B – subjects with scleroderma without PH (n=28), group 2A – ischemic patients with associated PH (n=16) and subgroup 2B – patients with ischemic disease without PH (n=19).

Results: Patients in group 1 presented a significantly higher number of female subjects (p=0.001) and a hi-gher mean age (p=0.009) compared to group 2. Pati-ents with associated PH presented a significantly lower left ventricular ejection fraction (LVEF) compared to those without PH within the ischemic group (p=0.023). There was a significant inverse correlation between the sPAP and LVEF in ischemic patients (r=-0.52, p=0.001) as well as for scleroderma patients without PH (r=-0.51, p=0.04). Tissue Doppler analysis of the left ventricular function indicated a significant negative correlation between the septal E’ value versus the sPAP and lateral E’ value versus the sPAP (r=-0.49, p=0.0024; r=-0.43, p=0.0083).

Conclusions: Intrinsic myocardial damage plays an important role in left ventricular systolic function even in the absence of PH. Scleroderma patients present a less pronounced deterioration of the LVEF in respon-se to pulmonary hypertension, indicating that in this group, additional compensatory mechanisms could be involved in the complex response of myocardium to elevated pulmonary pressures.