Vascular closure devices in acute coronary syndromes: from arbitrary to a necessity?
Vascular closure devices (VCDs) were initially developed to improve access site hemostasis and allow for earlier ambulation in patients undergoing diagnostic catheterization and percutaneous coronary intervention (PCI). Though initially thought to be beneficial, large meta-analysis has shown conflicting data regarding whether VCDs alter access site bleeding in a variety of clinical settings. One area of particular interest for the adoption of VCDs has been in the setting of acute coronary syndromes (ACS) in which multiple antiplatelet strategies are often employed leading to a high risk of bleeding. Bleeding in ACS has been shown to be a powerful independent predictor of 30-day mortality. Recently, investigators have reported that VCDs reduce access site bleeding in the setting of ACS. In our review, we use several selected representative clinical trials to provide a historical account for the use of VCDs. We also provide for a review of data as it relates to access site bleeding in ACS along with analysis showing that VCDs may potentially provide for reductions in bleeding and vascular complications in patients with ACS undergoing PCI.
Department of Medicine, Division of Cardiology, Northshore University Healthsystem, University of Chicago Pritzker School of Medicine, Evanston, IL 60201, USA.
Jamil B
JB
Dihu
Amar R
AR
Chadaga
Timothy A
TA
Sanborn
D054058:Acute Coronary Syndrome / Q000000981:diagnostic imaging* / Q000628:therapy*; D015906:Angioplasty, Balloon, Coronary / Q000009:adverse effects; D006328:Cardiac Catheterization / Q000009:adverse effects; D017023:Coronary Angiography / Q000009:adverse effects; D004867:Equipment Design; D019317:Evidence-Based Medicine; D006470:Hemorrhage / Q000209:etiology / Q000517:prevention & control*; D006489:Hemostatic Techniques / Q000295:instrumentation*; D006801:Humans; D011677:Punctures; D018570:Risk Assessment; D012307:Risk Factors; D016896:Treatment Outcome; D057772:Vascular System Injuries / Q000209:etiology / Q000628:therapy*