Original Title: Bioresorbable Vascular Scaffold Thrombosis. Multicenter Comprehensive Analysis of Clinical Presentation, Mechanisms, and Predictors. Reference: Puricel S et al. J Am Coll Cardiol 2016;67:921-31.
Courtesy of Dr. Guillermo Migliaro.
Bioresorbable scaffolds (BVS) were introduced in interventional cardiology to avoid late DES complications. However, recent reports suggest an elevated incidence of thrombosis with these new devices.
The referred article is a registry carried out in 4 centers including 1305 consecutive patients undergoing PCI with BVS in de novo lesions both for ACS and stable heart disease. Mean age was 64 and 78% were men. In this group of patients, thrombosis frequency and clinical and angiographic characteristics were analyzed to determine the possible mechanisms involved.
Thrombosis occurred in 42 patients. Probable/definite thrombosis incidence was 1.8% at 30 days and 3% at 12 months with no differences across centers (p=0.60).
In 52% of cases, thrombosis presented as ST elevation AMI and 17% as sudden death.
Multivariable analysis of ostial lesions (p=0.049) and depressed ejection fraction (p=0.019) were independently associated to thrombosis.
hrombosis presented in 21% of patients that had stopped dual antiaggregation therapy, mostly before the first year. As regards angiographic variables, post procedural lower reference vessel and minimum lumen diameters were independent predictors of thrombosis (p<0.001).
These finding strongly suggest that underexpansion or incomplete malapposition could be the underlying mechanisms of thrombosis.
When implementing an implantation strategy, considering aggressive pre and post dilation with non-compliant balloons up to 0.5 mm larger than the BVS, thrombosis incidence dropped to 1%, which equals a 70% reduction in thrombosis incidence, when comparing both groups (p=0.012)
Conclusion
Thrombosis incidence in BVS is 3% at 12 months, though it could significantly reduce when using the adequate implantation strategy. Other thrombosis predictors were ostial lesions and depressed ventricular function, post procedural lower vessel and minimum lumen diameters. These last two findings suggest that the mechanism involved could be stent underexpansion.
Editorial Comment
This registry is not randomized and has a small number of events, which is why the mechanisms involved should be interpreted with caution. This study does not contemplate the use of intracoronary images for stent collocation, such as OCT.
Courtesy of Dr. Guillermo Migliaro.
