Assessment of pulmonary arterial stiffness in patients with systemic sclerosis without overt pulmonary hypertension.

Pulmonary hypertension (PH) is a pathophysiological disorder that may involve multiple clinical conditions and complicate most systemic diseases. Systemic sclerosis (SSc), represents the leading cause of connective tissue disease (CTD) associated with PAH. Although SSc is a rare disease, it is associated with higher morbidity and early mortality than other rheumatological diseases due to developing SSc-associated interstitial pulmonary disease (ILD) and/or pulmonary arterial hypertension (PAH). The impact of the early diagnosis on the prognosis is evident. In this context, in our study, we aimed to investigate the early changes in pulmonary vascular bed by measuring pulmonary arterial stiffness (PAS) in SSc patients without overt PAH. Sixty-two SSc patients and fifty-eight gender and age-matched, healthy subjects enrolled in this cross-sectional observational study. SSc patients were evaluated in terms of disease duration and severity. Modified rodnan skin score (mRSS) was calculated as disease severity index. Echocardiographic parameters were assessed and compared to the control group. Right ventricular (RV) diameters, systolic pulmonary artery pressure (sPAP), and right ventricle myocardial performance index (RV-MPI) were significantly higher in the SSc group compared to the control group (p < 0.05). Tricuspid annular plane systolic excursion (TAPSE) and right ventricular fractional area change (RVFAC) were significantly lower in the SSc group compared to the control group (p < 0.05). PAS value (25.5 ± 9.2 kHz/ms vs. 18.1 ± 7.4 kHz/ms, p < 0.001) was significantly higher in the SSc group than in the control group. A statistically significant positive correlation relationship was detected between the PAS value and CRP, ESR, disease duration, mRSS. According to these results, in SSc patients, PAS as an inexpensive and easily applicable echocardiographic method might serve as a marker of early detection of PAH.

Echocardiographic assessment of pulmonary arterial stiffness in human immunodeficiency virus-infected patients.

BACKGROUND: Pulmonary hypertension (PH) is one of the complications of human immunodeficiency virus (HIV) infection. Despite the emergence of effective therapies, pulmonary arterial hypertension is commonly seen, especially at advanced stages. At the time of diagnosis, a majority of patients are at New York Heart Association-Functional Class III or IV. Many of the current screening modalities are dependent on detecting a rise in pulmonary arterial pressure (PAP). However, high capacitance of the pulmonary circulation implies that early microcirculation loss is not accompanied by a change in resting PAP. Therefore, we aimed to demonstrate early changes in pulmonary vascular disease in HIV-infected patients with a new echocardiographic parameter, called as pulmonary arterial stiffness (PAS). METHODS AND RESULTS: Thirty-six HIV-infected patients and 36 age- and sex-matched healthy control subjects were enrolled in this study. PAS was calculated echocardiographically by using maximal frequency shift and acceleration time of the pulmonary artery flow trace. There was no significant difference in diastolic functions, right ventricular diameters, systolic PAP, inferior vena cava widths, right atrial area, and tricuspid annular plane systolic excursion values between the two groups. However, PAS was calculated as 24.3 ± 6.4 Hz/msn in HIV-infected patients and 19.3 ± 3.1 Hz/msn in healthy control group (P < 0.001). Increase in PAS was correlated with duration of HIV infection (P < 0.05). CONCLUSION: Our results suggest that HIV infection affects pulmonary vascular bed starting early onset of disease and this can be demonstrated by an easy-to-measure echocardiographic parameter.