Transradial Approach for Cardiac Catheterization in Patients With Negative Allen's Test.

AIMS: To assess the efficacy and safety of transradial approach regardless of the Allen's test results for coronary angiography and angioplasty. METHODS AND RESULTS: Prospective data collection of 1035 consecutive patients who underwent coronary angiography with or without ad hoc angioplasty through the radial approach was conducted. Baseline demographic and procedural data were recorded. Allen's test was evaluated in all subjects before the procedure and catheterization was performed from the radial approach irrespective of the results. Radial artery patency was evaluated at discharge clinically, or by Doppler examination if pulse was not palpable. A total of 256 patients (24.7%) were found to have a negative Allen's test and 779 patients (75.3%) had a positive test. The baseline and procedural characteristics were similar in both groups. No significant differences in complications were reported. Radial artery thrombosis was observed in 6.2% of the negative Allen's test group and 4.8% of the positive Allen's test group (P=.85), but this was clinically silent even in the negative Allen's test group. CONCLUSION: Transradial approach for coronary angiography and ad hoc angioplasty can be performed with similar efficacy and safety regardless of the Allen's test results before the procedure.

Myocardial protection provided by chronic skeletal muscle ischemia is not further enhanced by ischemic pre- or postconditioning: comparative effects on intracellular signaling.

Chronic skeletal muscle ischemia protects the ischemic heart by preserving coronary flow and inducing arterioangiogenesis. We sought to determine the effect and the underlying molecular mechanisms of preconditioning (PreC) and postconditioning (PostC), applied in a model of chronic skeletal muscle ischemia. Male rabbits were divided into 3 series. In each series, the animals were subjected either to severe hind limb (HL) ischemia, by excision of the femoral artery, or to sham operation (SHO). After 4 weeks, all the animals underwent 30 minutes of regional heart ischemia and 3 hours reperfusion. The animals of the first series received no further intervention (HL and SHO groups), those of the second series underwent PreC (HL + PreC and SHO + PreC), and of the third series PostC (HL + PostC and SHO + PostC). Infarct size (I) and risk zones (R) were determined, and their ratio was calculated in percentage. Three additional series of experiments were performed with respective interventions up to the 10th minute of reperfusion, where sample tissue was obtained for assessment of protein kinase B (Akt), endothelial nitric oxide synthase (eNOS), glycogen synthase kinase 3ß (GSK3ß), p44/42, signal transducer and activator of transcription (STAT) 3, and STAT5. All groups demonstrated significantly smaller percentage of I/R compared with the SHO group (HL: 14.4% ± 3.7%, HL + PreC: 13.1% ± 1.0%, SHO + PreC: 21.3% ± 1.6%, HL + PostC: 18.0% ± 1.1%, and SHO + PostC: 24.3% ± 1.7%, P < .05 vs 35.7% ± 4.4% in SHO). The PreC and PostC did not further reduce the infarct size in HL groups. The Akt, eNOS, GSK3ß, p44/42, and STAT3 were activated in all PreC or PostC groups regardless of the infarct size reduction. The STAT5 was activated only in the HL groups compared with the SHO groups. In conclusion, chronic skeletal muscle ischemia results in effective cardioprotection, which is not further enhanced with application of PreC or PostC. The Akt, eNOS, GSK3ß, p44/42, and STAT3 may only be considered as indicators of the intracellular changes taking place during protection. Activation of STAT5 is possibly the end effector, which is responsible for infarct size reduction provided by chronic skeletal muscle ischemia.