Background: Coronary slow flow (CSF) phenomenon is characterized by delayed opacification of coronary vessels in a normal coronary angiogram. Although clinical and pathological features have been previously described, the underlying pathophysiology has not been fully elucidated. In this study, we aimed to evaluate central aortic pressure, aortic stiffness and left ventricular (LV) function in patients with coronary slow flow. Method and Results: The study population consisted of 154 patients who underwent coronary angiography because of typical and quasi-typical symptoms of angina. 81 patients with angiographically proven CSF and 73 cases with normal coronary flow pattern with similar risk profiles were enrolled in the study. Aortic pressures and indexes of elastic properties were evaluated using invasive methods. Aortic pulse pressure (mm Hg) and pulsality index of patients with CSF were found to be significantly higher than those of controls (60.8 ± 13.8 vs. 53.7 ± 14.5, p = 0.002; 0.84 ± 0.22 vs. 0.67 ± 0.18, p = 0.0001, respectively). LV Doppler parameters were deteriorated in patients with CSF. Aortic fractional pulse pressure and pulsality index were significantly correlated with the mean TIMI frame count and LV diastolic parameters in correlation analysis. Conclusion: The present findings allow us to conclude that impaired aortic elasticity in patients with CSF may also be responsible for the impaired LV diastolic parameters.

Lung development is impaired in mice generated through transfer of in vitro-derived blastocysts. The main objective of the current study was to determine if the composition of epithelial cells in the fetal and adult lung tissue is altered in mice generated through transfer of in vitro-derived blastocysts. The study comprised of two experimental (EGs) and two control (CGs) groups. Fetuses (18.5 d.p.c.) and adult mice (8-week-old) of the EGs (EGfetus , n=18, EGadult, n=15) were produced by the transfer of day-5 F2 blastocysts to pseudo-pregnant females. F2 fetuses and adult mice derived from naturally-ovulating females served as the CGs (CGfetus, n=18, CGadult n=15). The expression of Tuba-1a (a marker of ciliated cells), Foxj-1 (a marker of motile ciliated cells), Uch-L1 (a marker of neuroendocrine cells), Cldn-10 (a marker of Club cells), Aqp-5 (a marker of Type I alveolar cells), and Sp-C (a marker of Type II alveolar cells) was determined using western blot, immunohistochemistry/immunofluorescence and qRT-PCR analyses. Weight of fetuses as well as adult mice is decreased in mice comprising the EGs. Impaired lung development observed in EGfetus was associated with altered expression of Tuba-1a, Foxj-1, Cldn10, Uch-L1, Sp-C and Aqp-5. Morphology of the adult lung tissue was similar between the groups except for a significant increase in the thickness of the epithelia in EGadult. The expression of Cldn-10 and Sp-C was also altered in EGadult. It remains to be determined whether altered expression of these genes has any long-term impact on epithelial cell functions in the adult lung tissue.

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