Abrupt closure during coronary intervention
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Abrupt closure during coronary intervention is defined as an abrupt cessation of coronary flow to TIMI grade 0 or 1 flow before or at ≤5 mm distal to the lesion in an artery in which PTCA was attempted where there had previously been TIMI grade 2 or 3 flow prior to the procedure. It occurs primarily due to acute coronary dissection, thrombosis, or, most often, a combination of both during coronary intervention.
Abrupt closure during coronary intervention is defined as an abrupt cessation of coronary flow to TIMI grade 0 or 1 flow before or at ≤5 mm distal to the lesion in an artery in which PTCA was attempted where there had previously been TIMI grade 2 or 3 flow prior to the procedure. If TIMI flow grade 1 was present prior to dilation, then the development of TIMI flow grade 0 will constitute abrupt closure. In cases in which the artery being dilated had TIMI flow grade 0 prior to the procedure, if TIMI flow grade 2 or 3 is achieved during the procedure, and if the procedure is completed with TIMI flow grade 0, then this will also constitute abrupt closure. The table below outlines the possible scenarios that would be classified as abrupt closure:
|Pre-PTCA Flow||Post-PTCA Flow|
|TIMI flow grade 0 with vessel patency established (TIMI flow grade 2 or 3) during the procedure||TIMI flow grade 0|
|TIMI flow grade 1||TIMI flow grade 0|
|TIMI flow grade 2||TIMI flow grade 0 or 1|
|TIMI flow grade 3||TIMI flow grade 0 or 1|
Abrupt closure can be classified as sustained or transient:
- Sustained abrupt closure: Abrupt closure that has been present when the patient left the cardiac catheterization laboratory.
- Transient abrupt closure: Abrupt closure that has been treated with restoration of coronary blood flow to TIMI flow grade 2 or 3 before the patient left the cardiac catheterization laboratory.
Abrupt closure occurs primarily as a result of acute coronary dissection, thrombosis, or, most often, a combination of both during coronary intervention. It may also occur as a result of embolization.
Epidemiology and Demographics
- Clinical: unstable angina, female, AMI, chronic renal failure
- Angiographic: Intraluminal thrombus, ACC/AHA score, multivessel disease, long lesions, >45 degree angulation, branch points, proximal tortuosity, ostial RCA, degenerated SVGs, prestenosis >90%, intimal dissections
Natural History, Complications and Prognosis
Factors predicting mortality after abrupt closure are as follows:
- % myocardium at risk
- LM and multivessel disease
- CHF, UAP
- Target vessels supplies collaterals
- > age 65 years
- Chronic renal failure
- Female gender
Stent Use in Abrupt Closure
- Gianturco-Roubin stent improves lumen size and reduced MACE
- PS stent improves outcome: mortality 1.3%, MI 4%, 1% CABG
- ACS Multi-Link: mortality 1.4%, MI 2.9%
- Mostly associated with subacute stent thrombosis
- Treatment: Maintain flow, complete coverage.
Abrupt Closure Examples
- Suh WW, Grill DE, Rihal CS, Bell MR, Holmes DR, Garratt KN (2002). "Unrestricted availability of intracoronary stents is associated with decreased abrupt vascular closure rates and improved early clinical outcomes". Catheter Cardiovasc Interv. 55 (3): 294–302. PMID 11870931.