Activated clotting time and outcomes of chronic total occlusion percutaneous coronary intervention: insights from the PROGRESS-CTO Registry.

activated clotting time bleeding chronic total occlusion ischemia net adverse cardiovascular events percutaneous coronary intervention

Journal

The Journal of invasive cardiology
ISSN: 1557-2501
Titre abrégé: J Invasive Cardiol
Pays: United States
ID NLM: 8917477

Informations de publication

Date de publication:
Dec 2023
Historique:
medline: 18 12 2023
pubmed: 18 12 2023
entrez: 18 12 2023
Statut: ppublish

Résumé

The optimal range of activated clotting time (ACT) in chronic total occlusion (CTO) percutaneous coronary intervention (PCI) has received limited study. We examined the association between ACT and in-hospital ischemic and bleeding outcomes in patients who underwent CTO PCI in the Prospective Global Registry for the Study of CTO Intervention. ACT values were available for 4377 patients who underwent CTO PCI between 2012 and 2023 at 29 centers. The mean ACT distribution was less than 250 seconds (19%), 250 to 349 seconds (50%), and greater than or equal to 350 seconds (31%). The incidence of ischemic events, bleeding events, and net adverse cardiovascular events (NACE) was 0.8%, 3.0%, and 3.8%, respectively. In multiple logistic regression analysis, increasing nadir ACT was associated with decreasing ischemic events (adjusted odds ratio [aOR] per 50-second increments: 0.69 [95% confidence interval (CI), 0.50-0.94; P=.017]; and increasing peak ACT was associated with increasing bleeding events (aOR per 50-second increments: 1.17 [95% CI ,1.01-1.36; P=.032]). A U-shaped association was seen between mean ACT and NACE, where restricted cubic spline analysis demonstrated that patients with a low ( less than 200 seconds) or high ( greater than 400 seconds) ACT had increasing NACE risk compared with an ACT of 200 to 400 seconds (aOR 2.06, 95% CI 1.18-3.62; P=.012). Among patients who underwent CTO PCI, mean ACT had a U-shaped relationship with NACE, where patients with a low ( less than 200 seconds) ACT (driven by ischemic events) or high ( greater than 400 seconds) ACT (driven by bleeding) had higher NACE compared with an ACT of 200 to 400 seconds.

Sections du résumé

BACKGROUND BACKGROUND
The optimal range of activated clotting time (ACT) in chronic total occlusion (CTO) percutaneous coronary intervention (PCI) has received limited study.
METHODS METHODS
We examined the association between ACT and in-hospital ischemic and bleeding outcomes in patients who underwent CTO PCI in the Prospective Global Registry for the Study of CTO Intervention.
RESULTS RESULTS
ACT values were available for 4377 patients who underwent CTO PCI between 2012 and 2023 at 29 centers. The mean ACT distribution was less than 250 seconds (19%), 250 to 349 seconds (50%), and greater than or equal to 350 seconds (31%). The incidence of ischemic events, bleeding events, and net adverse cardiovascular events (NACE) was 0.8%, 3.0%, and 3.8%, respectively. In multiple logistic regression analysis, increasing nadir ACT was associated with decreasing ischemic events (adjusted odds ratio [aOR] per 50-second increments: 0.69 [95% confidence interval (CI), 0.50-0.94; P=.017]; and increasing peak ACT was associated with increasing bleeding events (aOR per 50-second increments: 1.17 [95% CI ,1.01-1.36; P=.032]). A U-shaped association was seen between mean ACT and NACE, where restricted cubic spline analysis demonstrated that patients with a low ( less than 200 seconds) or high ( greater than 400 seconds) ACT had increasing NACE risk compared with an ACT of 200 to 400 seconds (aOR 2.06, 95% CI 1.18-3.62; P=.012).
CONCLUSIONS CONCLUSIONS
Among patients who underwent CTO PCI, mean ACT had a U-shaped relationship with NACE, where patients with a low ( less than 200 seconds) ACT (driven by ischemic events) or high ( greater than 400 seconds) ACT (driven by bleeding) had higher NACE compared with an ACT of 200 to 400 seconds.

Identifiants

pubmed: 38108868
doi: 10.25270/jic/23.00170
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Auteurs

Bahadir Simsek (B)

Minneapolis Heart Institute and Minneapolis Heart Institute Foundation, Minneapolis, Minnesota, USA.

Athanasios Rempakos (A)

Minneapolis Heart Institute and Minneapolis Heart Institute Foundation, Minneapolis, Minnesota, USA.

Spyridon Kostantinis (S)

Minneapolis Heart Institute and Minneapolis Heart Institute Foundation, Minneapolis, Minnesota, USA.

Michaella Alexandrou (M)

Minneapolis Heart Institute and Minneapolis Heart Institute Foundation, Minneapolis, Minnesota, USA.

Sevket Gorgulu (S)

Department of Cardiology, Biruni University, Istanbul, Turkey.

Khaldoon Alaswad (K)

Division of Cardiology, Henry Ford Hospital, Detroit, Michigan, USA.

Jarrod D Frizzell (JD)

Department of Cardiology, The Christ Hospital, Cincinnati, Ohio, USA.

Ufuk Yildirim (U)

Department of Cardiology, Ondokuz Mayis University, Samsun, Turkey.

Paul Poommipanit (P)

University Hospitals, Case Western Reserve University, Cleveland, Ohio, USA.

Nazif Aygul (N)

Department of Cardiology, Selcuk University, Konya, Turkey.

Nidal Abi Rafeh (N)

North Oaks Healthcare System, Hammond, Louisiana, USA.

Rodrigo Bagur (R)

Department of Cardiology, London Health Sciences Center, Western University, London, Ontario, Canada.

Rhian Davies (R)

Department of Cardiology, Wellspan York Hospital, York, Pennsylvania, USA.

Omer Goktekin (O)

Memorial Bahçelievler Hospital, Istanbul, Turkey.

James W Choi (JW)

Department of Cardiology, Texas Health Presbyterian Hospital, Dallas, Texas, USA.

Niranjan Reddy (N)

Department of Cardiology, Kettering Health Medical Group, Dayton, Ohio, USA.

Philip Dattilo (P)

UC Health Medical Center of the Rockies, Loveland, Colorado, USA.

Jimmy Kerrigan (J)

Ascension Saint Thomas Heart Hospital, Nashville, Tennessee, USA.

Elias V Haddad (EV)

Ascension Saint Thomas Heart Hospital, Nashville, Tennessee, USA.

Olga C Mastrodemos (OC)

Minneapolis Heart Institute and Minneapolis Heart Institute Foundation, Minneapolis, Minnesota, USA.

Bavana V Rangan (BV)

Minneapolis Heart Institute and Minneapolis Heart Institute Foundation, Minneapolis, Minnesota, USA.

Judit Karacsonyi (J)

Minneapolis Heart Institute and Minneapolis Heart Institute Foundation, Minneapolis, Minnesota, USA.

Salman S Allana (SS)

Minneapolis Heart Institute and Minneapolis Heart Institute Foundation, Minneapolis, Minnesota, USA.

Kathleen E Kearney (KE)

Division of Cardiology, Department of Medicine, University of Washington, Seattle, Washington, USA.

Yader Sandoval (Y)

Minneapolis Heart Institute and Minneapolis Heart Institute Foundation, Minneapolis, Minnesota, USA.

M Nicholas Burke (MN)

Minneapolis Heart Institute and Minneapolis Heart Institute Foundation, Minneapolis, Minnesota, USA.

Emmanouil S Brilakis (ES)

Minneapolis Heart Institute and Minneapolis Heart Institute Foundation, Minneapolis, Minnesota, USA.

Lorenzo Azzalini (L)

Division of Cardiology, Department of Medicine, University of Washington Medical Center, Seattle, WA 98195, USA. Email: azzalini@uw.edu.

Classifications MeSH