The right ventricle systolic force ratio could predict the severity of the tricuspid regurgitation-RIVIERA ratio.

PURPOSE: For assessing the severity of tricuspid regurgitation (TR), there is no gold standard. We developed a parameter, the right ventricular systolic force ratio-RIVIERA, using the continious wave Doppler analysis of TR and pulsed-wave analysis of the right ventricle outflow tract. We hypothesized that the RIVIERA would facilitate the ability to identify severe TR in clinical settings. MATERIALS AND METHODS: We obtained data from routine transthoracic echocardiograms. All records reporting no or mild TR (n = 732), moderate TR (n = 584), and severe TR (n = 519) TR were reanalyzed to measure vena contracta (VC) width, TR jet area, effective regurgitant orifice (EROA) derived with the proximal isovelocity surface area method, the RIVIERA, and right-sided chamber volumes. RESULTS: Significant linear trends were demonstrated for right atrial volume index, end-diastolic volume index, RVOT velocity time integral, TR jet area, TR-Vmax, TR-VTI, TR acceleration, VC width, EROA with increasing TR severity. Independent predictors of severe RT included RIVIERA <4.8, VC width ≥0.7 cm, TR jet area > 10 cm2 , and EROA ≥0.4 cm2 . CONCLUSION: The RIVIERA is a feasible, effective, and independent predictor of severe TR that enhances established techniques for estimating TR severity. For clinical decision-making and management, accurate measurement and classification of TR severity are essential. Therefore, it should be thought about include the RIVIERA in the integrative method to assessing TR severity.

Increased circulating soluble urokinase-type plasminogen activator receptor (suPAR) levels in patients with slow coronary flow.

INTRODUCTION: Slow coronary flow (SCF) is an angiographic phenomenon characterized by delayed opacification of epicardial coronary arteries without an obstructive coronary disease. Serum soluble urokinase-type plasminogen activator receptor (suPAR) levels seem closely related to atherosclerosis due to increased inflammation and prothrombotic state. We studied whether circulating suPAR is related to SCF. MATERIAL AND METHODS: The present study was cross-sectional and observational. It included 75 individuals who underwent coronary angiography with suspected CAD and had angiographically normal coronary arteries of varying coronary flow rates. The relationship between suPAR, C-reactive protein (CRP) and SCF was investigated. Forty patients with isolated SCF (mean age: 46.0 ±4.14 years) and 35 age- and gender-matched control participants with normal coronary flow (NCF) and normal coronary arteries (NCA) (mean age: 46.0 ±5.7 years) were included in the study. We used logistic regression analysis to determine the predictors of SCF. RESULTS: The clinical characteristics were not statistically significantly different between SCF and NCA groups. Serum suPAR level was significantly higher in the SCF group than the control group (2.5-5.4 ng/ml vs. 0.1-1.4 ng/ml; p < 0.001). Also the serum CRP level was higher in the CSF group than the control group (1.57 ±0.43 mg/l vs. 0.53 ±0.23 mg/l; p < 0.001). CONCLUSIONS: This study revealed significantly increased serum suPAR levels in patients with SCF. Although we cannot draw conclusions on the underlying pathological process of SCF, we believe that these findings may be pioneering for further studies investigating the specific roles of circulating suPAR in the SCF phenomenon in the coronary vasculature.