Radial artery flow-mediated dilation predicts arterial spasm during transradial coronary interventions.

BACKGROUND: Transradial coronary catheterization has emerged over the last years as a favorable catheterization practice, based on evidence that it is associated with less vascular complications and shorter hospital stays. However, access site crossover appears to be more frequent when the initial route is the transradial one, one of the main reasons being arterial spasm. We hypothesized that radial flow-mediated dilation (FMD) measurements could be used as a preprocedural method to assess the likelihood of arterial spasm. METHODS: The study population consisted of patients scheduled for transradial diagnostic catheterization in whom ad hoc percutaneous coronary intervention (PCI) was performed. FMD was measured 1-2 days before PCI. The primary endpoint of the study was operator-defined (operators were blinded as to the FMD results) radial artery spasm. RESULTS: A total of 172 patients (110 male, age 65.3 ± 9) were included. Radial artery spasm was recorded in 13 patients (7.6%). FMD showed a very significant univariate association with the occurrence of spasm (P < 0.001) and was the most important predictor of spasm in the multivariate logistic regression analysis (beta -3.15; P < 0.001), followed by baseline radial artery diameter (P = 0.04), the number of catheters used (P = 0.049) and the administered volume of contrast medium (P = 0.017). CONCLUSION: Preprocedural FMD is a significant predictor of arterial spasm before elective transradial PCI. It is a low cost, safe, and feasible noninvasive modality, whose results might be taken into account when deciding on the vascular access route for an elective procedure, the size of sheaths or catheters to be used or the intensity of antispasm medication.

Effect of quinapril on in-stent restenosis and relation to plasma apoptosis signaling molecules.

Angiotensin-converting enzyme inhibitors have been reported to inhibit in-stent restenosis. To assess the effect of angiotensin-converting enzyme inhibition on in-stent restenosis and its relation to apoptosis, 86 patients with chronic coronary artery disease who required stent implantation in the left anterior descending coronary artery or a major diagonal branch were studied. Patients were randomized to receive quinapril 40 mg/day orally (n = 43) or a placebo (n = 43). Drug therapy was initiated 1 week before initial stenting and continued for 6 months. Plasma levels of the apoptotic signaling molecules soluble Fas and soluble Fas ligand obtained from blood drawn from the left anterior descending coronary artery were measured just before initial stenting and 6 months later, at the time of repeat coronary angiography. In-stent restenosis was present in 9.3% of patients in the quinapril group and 25.6% of patients in the placebo group (p = 0.047). Mean late luminal loss was 0.56 +/- 0.51 mm in the quinapril group and 0.95 +/- 0.95 mm in the placebo group (p = 0.003). There were no significant differences in plasma soluble Fas or soluble Fas ligand levels at baseline. At 6 months, the change in plasma soluble Fas level was significantly higher in the quinapril group (0.72 +/- 1.24 ng/ml) than in the placebo group (0.28 +/- 0.72 ng/ml) (p = 0.024). The change in plasma soluble Fas ligand levels at 6 months was significantly higher in the quinapril group (7.43 +/- 12.2 pg/ml) than in the placebo group (0.06 +/- 6.8 pg/ml) (p = 0.002). In conclusion, the angiotensin-converting enzyme inhibitor quinapril inhibits in-stent restenosis by stimulating apoptosis after percutaneous intervention.