Central venous catheter integrity during mechanical power injection of iodinated contrast medium

PURPOSE: To evaluate a widely used nontunneled triple-lumen central venous catheter in order to determine whether the largest of the three lumina (16 gauge) can tolerate high flow rates, such as those required for computed tomographic angiography. MATERIALS AND METHODS: Forty-two catheters were tested in vitro, including 10 new and 32 used catheters (median indwelling time, 5 days). Injection pressures were continuously monitored at the site of the 16-gauge central venous catheter hub. Catheters were injected with 300 and 370 mg of iodine per milliliter of iopamidol by using a mechanical injector at increasing flow rates until the catheter failed. The infusion rate, hub pressure, and location were documented for each failure event. The catheter pressures generated during hand injection by five operators were also analyzed. Mean flow rates and pressures at failure were compared by means of two-tailed Student t test, with differences considered significant at P < .05. RESULTS: Injections of iopamidol with 370 mg of iodine per milliliter generate more pressure than injections of iopamidol with 300 mg of iodine per milliliter at the same injection rate. All catheters failed in the tubing external to the patient. The lowest flow rate at which catheter failure occurred was 9 mL/sec. The lowest hub pressure at failure was 262 pounds per square inch gauge (psig) for new and 213 psig for used catheters. Hand injection of iopamidol with 300 mg of iodine per milliliter generated peak hub pressures ranging from 35 to 72 psig, corresponding to flow rates ranging from 2.5 to 5.0 mL/sec. CONCLUSION: Indwelling use has an effect on catheter material property, but even for used catheters there is a substantial safety margin for power injection with the particular triple-lumen central venous catheter tested in this study, as the manufacturer's recommendation for maximum pressure is 15 psig

On the primary structure of polysilenes and polygermenes

Despite the long history and prominence of addition polymerizations in alkene chemistry, addition polymerizations of the heavier main group analogs of alkenes are in their infancy. Herein, the detailed structural and end group analyses of polysilenes (polycarbosilanes) and polygermenes (polycarbogermanes) derived from the anionic polymerization of kinetically-stabilized silenes and germenes, respectively, are reported. The end groups were identified using ESI-TOF mass spectrometry. Careful examination of the C- H HSQC NMR spectra of both polymers confirmed the regular, alternating structure consistent with an addition polymerization with no significant amount of intramolecular rearrangement or back-biting. These results are in contrast to what has been observed during the synthesis of the analogous polyphosphenes. 13

Thrombin-receptor antagonist vorapaxar in acute coronary syndromes

BACKGROUND Vorapaxar is a new oral protease-activated–receptor 1 (PAR-1) antagonist that inhibits thrombin-induced platelet activation. METHODS In this multinational, double-blind, randomized trial, we compared vorapaxar with placebo in 12,944 patients who had acute coronary syndromes without ST-segment elevation. The primary end point was a composite of death from cardiovascular causes, myocardial infarction, stroke, recurrent ischemia with rehospitalization, or urgent coronary revascularization. RESULTS Follow-up in the trial was terminated early after a safety review. After a median follow-up of 502 days (interquartile range, 349 to 667), the primary end point occurred in 1031 of 6473 patients receiving vorapaxar versus 1102 of 6471 patients receiving placebo (Kaplan–Meier 2-year rate, 18.5% vs. 19.9%; hazard ratio, 0.92; 95% confidence interval [CI], 0.85 to 1.01; P = 0.07). A composite of death from cardiovascular causes, myocardial infarction, or stroke occurred in 822 patients in the vorapaxar group versus 910 in the placebo group (14.7% and 16.4%, respectively; hazard ratio, 0.89; 95% CI, 0.81 to 0.98; P = 0.02). Rates of moderate and severe bleeding were 7.2% in the vorapaxar group and 5.2% in the placebo group (hazard ratio, 1.35; 95% CI, 1.16 to 1.58; P<0.001). Intracranial hemorrhage rates were 1.1% and 0.2%, respectively (hazard ratio, 3.39; 95% CI, 1.78 to 6.45; P<0.001). Rates of nonhemorrhagic adverse events were similar in the two groups. CONCLUSIONS In patients with acute coronary syndromes, the addition of vorapaxar to standard therapy did not significantly reduce the primary composite end point but significantly increased the risk of major bleeding, including intracranial hemorrhage