Abstract
Funding Acknowledgements
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Background
The relationship between the degree of pulmonary hypertension (PH) and left ventricular performance in patients with systemic sclerosis is still a controversial issue in the literature. We aimed to conduct a comparative analysis of indexes characterizing left ventricular systolic and diastolic function, in two etiological types of pulmonary hypertension involving different pathophysiological mechanisms: PH caused by systemic sclerosis and PH caused by myocardial ischemia.
Material and method
We performed a prospective study on 83 patients (36 patients with documented PAH with a systolic 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 higher mean age (p = 0.009) compared to group 2. Patients 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 = 0.002; r=-0.43, p = 0,008).
Conclusions
Intrinsic myocardial damage plays an important role in left ventricular systolic function even in the absence of PAH. Scleroderma patients present a less pronounced deterioration of the LVEF in response to pulmonary hypertension, indicating that in this group, additional compensatory mechanisms could be involved in the complex response of myocardium to elevated pulmonary pressures.
Effect of oral propranolol on rest, exercise and postexercise left ventricular performance in normal subjects and patients with coronary artery disease.
