@article{article_596933, title={The Relationship Between Serum Urotensin II Level and Contrast-Induced Nephropathy and One-year Clinical Follow-up Findings in Patients with Coronary Slow Phenomenon Undergoing Percutaneous Coronary Intervention}, journal={Sakarya Tıp Dergisi}, volume={9}, pages={442–454}, year={2019}, DOI={10.31832/smj.596933}, author={Huyut, Mustafa}, keywords={Urotensin II,Slow-Flow Phenomenon,Contrast-Induced Nephropathy,percutaneous coronary intervention,Major Adverse cardiovascular events}, abstract={<p class="MsoNormal" style="text-align:justify;line-height:150%;"> <b> <span style="font-size:10pt;line-height:150%;font-family:Arial, ’sans-serif’;">Background </span> </b> <span style="font-size:10pt;line-height:150%;font-family:Arial, ’sans-serif’;">:
Coronary slow-reflow phenomenon (CSFP) and </span> <span style="font-size:10pt;line-height:150%;font-family:Arial, ’sans-serif’;">Contrast-Induced
Nephropathy (CIN) are </span> <span style="font-size:10pt;line-height:150%;font-family:Arial, ’sans-serif’;"> associated with an increased risk of major
cardiovascular adverse events. </span> <span style="font-size:10pt;line-height:150%;font-family:Arial, ’sans-serif’;">
This study aimed to evaluate the relationship between serum </span> <span style="font-size:10pt;line-height:150%;font-family:Arial, ’sans-serif’;">Urotensin
II molecule (U-II </span> <span style="font-size:10pt;line-height:150%;font-family:Arial, ’sans-serif’;">)
levels and CIN in patients with CSFP undergoing percutaneous coronary
intervention (PCI). </span> </p> <p> </p> <p class="MsoNormal" style="text-align:justify;line-height:150%;"> <b> <span style="font-size:10pt;line-height:150%;font-family:Arial, ’sans-serif’;">Methods: </span> </b> <span style="font-size:10pt;line-height:150%;font-family:Arial, ’sans-serif’;"> We
enrolled  227  patients (161 male and 66 female; mean age:
61,44 ± 12,44 years) with angiographically diagnosed CSFP. The patients were
divided into two groups according to CIN development (Non-CIN (n=206) and CIN
group (n=21)). </span> </p> <p> </p> <p class="MsoNormal" style="text-align:justify;line-height:150%;"> <b> <span style="font-size:10pt;line-height:150%;font-family:Arial, ’sans-serif’;">Results: </span> </b> <span style="font-size:10pt;line-height:150%;font-family:Arial, ’sans-serif’;"> CIN
was observed in 9,25%(n=21) of the CSFP patients. Serum U-II level was
significantly higher in CIN group than in non-CIN group (6,79±2,2 vs. 3±1,29,
p<0.001). One year clinical follow-up findings including all-cause mortality
(7(33,3%) vs. 24(11,7%), p=0,013), cardiovascular death(7(33,3%) vs. 18(8,7%),
p=0,003) and </span> <span style="font-size:10pt;line-height:150%;font-family:Arial, ’sans-serif’;">Major Adverse
cardiovascular events </span> <span style="font-size:10pt;line-height:150%;font-family:Arial, ’sans-serif’;"> (MACE) (10(47,6%) vs. 46(22,4%), p: 0,011) were
significantly higher in CIN group. We also performed forward conditional
logistic regression analysis and found that U-II (Odds ratio (OR)= 3,983; 95%
confidence interval (CI): 2,25 to 7,052; p < 0.001) and Mehran score (OR=1,228,
95% CI: 1,083-1,393, p=0,001) were independently predicted CIN development in patients
with CSFP. </span> </p> <p> </p> <p> </p> <p class="MsoNormal" style="text-align:justify;line-height:150%;"> <b> <span style="font-size:10pt;line-height:150%;font-family:Arial, ’sans-serif’;">Conclusions: </span> </b> <span style="font-size:10pt;line-height:150%;font-family:Arial, ’sans-serif’;">
Baseline serum U-II concentrations and higher Mehran scores are independently
associated with CIN in CSFP patients. One year clinical follow-up findings
including all-cause mortality, cardiovascular death and MACE were significantly
higher in CIN group, but stroke and myocardial infarction rates were similar in
both groups. <b> </b> </span> </p> <p> <b> </b> </p> <b> </b>}, number={3}, publisher={Sakarya University}, organization={Bezmialem Vakıf Üniversitesi}