Is In-Stent Restenosis After a Successful Coronary Stent Implantation Due to Stable Angina Associated With TG/HDL-C Ratio?

Kundi H., Korkmaz A., Balun A., Cicekcioglu H., Kiziltunc E., Gursel K., ...More

ANGIOLOGY, vol.68, no.9, pp.816-822, 2017 (SCI-Expanded) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 68 Issue: 9
  • Publication Date: 2017
  • Doi Number: 10.1177/0003319716689366
  • Journal Name: ANGIOLOGY
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Page Numbers: pp.816-822
  • Keywords: angina, lipoprotein ratios, stent restenosis, triglyceride to high-density lipoprotein cholesterol ratio, DENSITY-LIPOPROTEIN-CHOLESTEROL, HEART-DISEASE, INSULIN-RESISTANCE, CARDIOVASCULAR-DISEASE, METABOLIC SYNDROME, DIABETES-MELLITUS, CLINICAL-OUTCOMES, OXIDATIVE STRESS, RISK, TRIGLYCERIDES
  • Gazi University Affiliated: No

Abstract

We examined the impact of the preprocedural triglyceride (TG)/high-density lipoprotein cholesterol (HDL-C) ratio on risk of in-stent restenosis (ISR). Patients with typical anginal symptoms and/or positive treadmill or myocardial perfusion scintigraphy test results who underwent successful coronary stent implantation due to stable angina were examined; 1341 patients were enrolled. The hospital files of the patients were used to gather data. Cox regression analysis showed that the TG/HDL-C ratio was independently associated with the presence of ISR (P < .001). Moreover, diabetes mellitus (P = .007), smaller stent diameter (P = .046), and smoking status (P = .001) were also independently associated with the presence of ISR. Using a cutoff of 3.8, the TG/HDL-C ratio predicted the presence of ISR with a sensitivity of 71% and a specificity of 68%. Also, the highest quartile of TG/HDL-C ratio had the highest rate of ISR (P < .001). Measuring preprocedural TG/HDL-C ratio, in fasting or nonfasting samples, could be beneficial for the risk assessment of ISR. However, further large-scale prospective studies are required to establish the exact role of this simple, easily calculated, and reproducible parameter in the pathogenesis of ISR.