Abrupt closure during coronary intervention

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Editor(s)-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Hardik Patel, M.D., Sapan Patel M.B.B.S

Overview

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.

Definition

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

Classification

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.

Causes

Abrupt closure occurs primarily as a result of acute coronary dissection, thrombosis, intracoronary spasm, embolization, intra-procedural stent thrombosis or, most often, a combination of all the above during coronary intervention.

Epidemiology and Demographics

It occurs during 3-5% of balloon angioplasty procedures. Its incidence has been markedly reduced with the availability of coronary stents.

Risk Factors

• 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
• Diabetes

Treatment

• Intracoronary imaging as necessary to evaluate the cause
• Intracoronary stent placement to treat dissection
• Intracoronary vasodilators to treat epicardial vessel and microvascular spasm
• Imaging, additional dilation, anticoagulation and antiplatelets to treat intraprocedural stent thrombosis