Association of radial versus femoral access with contrast-induced acute kidney injury in patients undergoing primary percutaneous coronary intervention for ST-elevation myocardial infarction.

BACKGROUND: Patients with ST-elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PCI) are at an increased risk of developing contrast-induced acute kidney injury (CI-AKI). Data on the association between transradial (TRA) vs. transfemoral (TFA) access and the risk of CI-AKI in this setting are limited. METHODS: We analyzed data on 1162 patients undergoing primary PCI for STEMI at two tertiary care centers between 2010 and 2014. Primary outcome was CI-AKI, defined as a relative rise in serum creatinine of ≥25%, or an absolute increase of ≥0.5mg/dL, within 48h of primary PCI. We used multivariable logistic regression and propensity analysis to determine the association between vascular access site and CI-AKI. RESULTS: Of 1162 patients who underwent primary PCI for STEMI, TFA was used in 857 (73.8%), and TRA in 305 (26.2%) patients. In the unmatched cohort, TRA was associated with numerically lower rates of CI-AKI as compared with TFA; however, this difference did not reach statistical significance (5.9% vs. 7.0%; unadjusted OR 0.83, 95%CI 0.48-1.44, p=0.510; adjusted OR 0.84, 95%CI 0.44-1.62, p=0.610). Similar results were seen in a propensity matched cohort of 508 patients (254 TRA and 254 TFA; CI-AKI 5.5% vs. 8.3%, OR 0.65, 95% CI 0.32-1.30, p=0.220). CONCLUSIONS: In patients with STEMI undergoing primary PCI, TRA was not associated with a lower risk of CI-AKI, as compared with TFA. Randomized controlled trials are needed to definitely assess the role of vascular access site in reducing the risk of CI-AKI in patients undergoing primary PCI for STEMI. SUMMARY: In patients with STEMI undergoing primary PCI, the overall incidence of contrast-induced acute kidney injury (CI-AKI) was low (6.7%). Transradial access was not associated with a lower risk of CI-AKI as compared with transfemoral access.

Appropriate timing of nitroglycerin prior to intravascular ultrasound.

OBJECTIVES: To determine the time to maximal coronary dilation following intracoronary (IC) nitroglycerin (NTG) and whether the decrease in aortic pressure (AoP) is a surrogate marker for coronary vasodilatation. BACKGROUND: Intravascular ultrasound (IVUS) facilitates assessment of coronary plaque severity and morphology and aids in stent sizing. NTG is often administered prior to IVUS to prevent catheter-induced spasm and to facilitate standardized and accurate vessel size measurements. The impact of dose, timing, and route of delivering NTG on vessel size remains undefined. METHODS: Twelve patients undergoing IVUS-guided stent placement were studied. An IVUS catheter was positioned proximal to the target lesion and the following measurements made at baseline and 30 second (sec) intervals for 180 sec following 200 mcg IC NTG: AoP, IVUS-derived lumen diameter (Ld), lumen cross-sectional area (La), external elastic membrane diameter (EEMd) and EEM area (EEMa). Lumen and EEM measurements were compared at different time intervals and the relationship between time to max Ld and nadir AoP was analyzed. RESULTS: All patients had a vasodilatory response to IC NTG. Increase from baseline to max Ld following IC NTG was statistically significant (mean change 0.31 ± 0.18 mm, P=.0001). Mean time to max Ld following IC NTG was 117 sec (range, 60-180 sec). No correlation between time to max Ld and AoP nadir was observed (r = 0.19). CONCLUSIONS: Our study suggests that administration of 200 mcg IC NTG results in a significant change in lumen diameter and area with maximal vasodilation occurring on average approximately 2 minutes following IC NTG administration. There was no significant correlation between AoP change and maximal NTG-induced coronary vasodilation.