Effects of the hypoxic test on left and right ventricular contractility in progressive systemic sclerosis with pulmonary arterial hypertension |
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Authors: | Talantbek A. Batyraliev M.D. Zarcma A. Niyazova M.D. Ferit Akgül M.D. Gülmira Z. Kudaiberdieva M.D. Kairgeldy S. Aikimbaev M.D. Kayipbek K. Kadiraliev M.D. Ahmet Birand M.D. |
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Affiliation: | (1) Kyrgyz Scientific Institute of Cardiology, Bishkek, Republic of Kyrgyzstan;(2) Medical School, Department of Cardiology, Balcali Hospital, Balcali, Çukurova University, 01330 Adana, Turkey |
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Abstract: | The purpose of this investigation was to assess hypoxic test effects on left and right ventricular contractility in patients with progressive systemic sclerosis (PSS) and pulmonary arterial hypertension (PAH). Ten patients (mean age 48.8±13.2 years) who were diagnosed with PSS and PAH were included in the study. All the patients underwent left and right heart catheterization. Right ventricular (RV) contractility was measured according to the method of Ferlinz [1] and left ventricular (LV) contractility according to the method of Kennedy et al. [2] using indirect digital substraction angiography. The mean pulmonary artery pressures (PA) and oxygen saturation of the pulmonary artery (SaO2) were registered at each stage of graded hypoxic exposure 14%, 12%, and 10% of O2. Right atrial pressures (PRA,syst, PRA,diast,RA), right ventricular pressures (PRV,syst, PRV,diast,RV, PRV,end-diast), right and left ventricular end-diastolic volume index (EDVI), end-systolic volume index (ESVI), stroke volume index (SVI), cardiac index (CI), ejection fraction (EF), and heart rate (HR) were calculated before and after breathing a hypoxic mixture of 10% of O2 for 30 minutes. The hypoxic test induced significant elevation (p<0.05) ofPA, PRA,syst, PRA,diast,RA, PRV,syst, PRV,end-diast, RV EDVI, LV, EDVI, CI, and HR, whereas, SaO2 decreased significantly after the hypoxic test. These findings suggest that patients with PSS and PAH are characterized by hyperreactivity of pulmonary artery to hypoxia and the preservation of compensatory mechanism of RV and LV contractility. |
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