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(Circulation. 2007;116:2655.)
© 2007 American Heart Association, Inc.

Issue Highlights

An extract of the first 250 words of the full text is provided, because this article has no abstract.

	TIME TO CORONARY ANGIOGRAPHY AND OUTCOMES AMONG PATIENTS WITH HIGH-RISK NON–ST-SEGMENT–ELEVATION ACUTE CORONARY SYNDROMES: RESULTS FROM THE SYNERGY TRIAL, by Tricoci et al.

 
In this issue, Tricoci et al evaluated the relationship between time from hospital admission to coronary angiography and outcomes in high-risk patients with non–ST-segment–elevation acute coronary syndromes. Data from 10 027 patients enrolled in the SYNERGY trial were analyzed, and patients were grouped by 6-hour time from hospital admission–to–coronary angiography intervals. Primary outcomes were 30-day death or myocardial infarction, in-hospital TIMI and GUSTO major bleeding, and blood transfusion. Overall, 9216 (92%) patients underwent angiography, with 6352 (64%) within 48 hours. Unadjusted and adjusted rates of death/myocardial infarction increased with increasing time to angiography. The adjusted odds ratio for death/myocardial infarction in patients receiving angiography in <6 hours was 0.56 (95% confidence interval 0.41–0.74), whereas after 30 hours, there was no significant benefit compared with further delayed angiography. Major bleeding and transfusion did not significantly vary across time-to-angiography intervals. In addition, the analyses showed that 2 variables, admission to US hospitals and day of admission, were the most powerful predictors of time to angiography and suggest that randomized clinical trials are needed to provide definitive evidence on optimal timing of coronary angiography. See p 2669 (editorial p 2656).

	FIRST-IN-HUMAN EVALUATION OF ANTI–VON WILLEBRAND FACTOR THERAPEUTIC APTAMER ARC1779 IN HEALTHY VOLUNTEERS, by Gilbert et al.

 
Although antithrombotic therapies that alter platelet–platelet interactions are commonly used in primary and secondary prevention of cardiovascular disease, much less is known about the utility of inhibiting platelet binding to the blood vessel wall. In this study, Gilbert and colleagues report the results of a novel inhibitor (ARC1779) of platelet-vessel wall binding. This inhibitor is an aptamer that binds to activated von . . . [Full Text of this Article]

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