Impact of preprocedural anemia on in-hospital and follow-up outcomes of chronic total occlusion percutaneous coronary intervention.
anemia
chronic total occlusion
percutaneous coronary intervention
Journal
Catheterization and cardiovascular interventions : official journal of the Society for Cardiac Angiography & Interventions
ISSN: 1522-726X
Titre abrégé: Catheter Cardiovasc Interv
Pays: United States
ID NLM: 100884139
Informations de publication
Date de publication:
11 2023
11 2023
Historique:
revised:
17
07
2023
received:
11
05
2023
accepted:
15
08
2023
medline:
15
11
2023
pubmed:
8
9
2023
entrez:
8
9
2023
Statut:
ppublish
Résumé
The impact of preprocedural anemia on the outcomes of chronic total occlusion (CTO) percutaneous coronary intervention (PCI) has received limited study. We examined the clinical and angiographic characteristics and procedural outcomes of 8633 CTO PCIs performed at 39 US and non-US centers between 2012 and 2023. Anemia was defined as a hemoglobin level of <13 g/dL in men and <12 g/dL in women. Anemia was present in 1652 (19%) patients undergoing CTO PCI. Anemic patients had a higher incidence of comorbidities, such as diabetes mellitus, hypertension, dyslipidemia, heart failure, cerebrovascular disease, and peripheral arterial disease. CTOs in anemic patients were more likely to have complex angiographic characteristics, including smaller diameter, longer length, moderate to severe calcification, and moderate to severe proximal tortuosity. Anemic patients required longer procedure (119 vs. 107 min; p < 0.001) and fluoroscopy (45 vs. 40 min; p < 0.001) times but received similar contrast volumes. Technical success was similar between the two groups. In-hospital major adverse cardiac events (MACE) rates were higher in patients with anemia; however, this association was no longer significant after adjusting for confounding factors. Baseline anemia was independently associated with follow-up MACE (adjusted hazard ratio [HR]: 1.63; 95% confidence interval [CI]: 1.07-2.49; p = 0.023) and all-cause mortality (adjusted HR: 3.03; 95% CI: 1.41-6.49; p = 0.004). Preprocedural anemia is associated with more comorbidities, higher lesion complexity, longer procedure times, and higher follow-up MACE and mortality after CTO PCI.
Sections du résumé
BACKGROUND
The impact of preprocedural anemia on the outcomes of chronic total occlusion (CTO) percutaneous coronary intervention (PCI) has received limited study.
METHODS
We examined the clinical and angiographic characteristics and procedural outcomes of 8633 CTO PCIs performed at 39 US and non-US centers between 2012 and 2023. Anemia was defined as a hemoglobin level of <13 g/dL in men and <12 g/dL in women.
RESULTS
Anemia was present in 1652 (19%) patients undergoing CTO PCI. Anemic patients had a higher incidence of comorbidities, such as diabetes mellitus, hypertension, dyslipidemia, heart failure, cerebrovascular disease, and peripheral arterial disease. CTOs in anemic patients were more likely to have complex angiographic characteristics, including smaller diameter, longer length, moderate to severe calcification, and moderate to severe proximal tortuosity. Anemic patients required longer procedure (119 vs. 107 min; p < 0.001) and fluoroscopy (45 vs. 40 min; p < 0.001) times but received similar contrast volumes. Technical success was similar between the two groups. In-hospital major adverse cardiac events (MACE) rates were higher in patients with anemia; however, this association was no longer significant after adjusting for confounding factors. Baseline anemia was independently associated with follow-up MACE (adjusted hazard ratio [HR]: 1.63; 95% confidence interval [CI]: 1.07-2.49; p = 0.023) and all-cause mortality (adjusted HR: 3.03; 95% CI: 1.41-6.49; p = 0.004).
CONCLUSIONS
Preprocedural anemia is associated with more comorbidities, higher lesion complexity, longer procedure times, and higher follow-up MACE and mortality after CTO PCI.
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
857-863Subventions
Organisme : The authors are grateful for the philanthropic support of our generous anonymous donors, and the philanthropic support of Drs. Mary Ann and Donald A Sens; Mrs. Diane and Dr. Cline Hickok; Mrs. Wilma and Mr. Dale Johnson; Mrs. Charlotte and Mr. Jerry Golinvaux Family Fund; the Roehl Family Foundation; the Joseph Durda Foundation. The generous gifts of these donors to the Minneapolis Heart Institute Foundation's Science Center for Coronary Artery Disease (CCAD) helped support this research proje
Informations de copyright
© 2023 Wiley Periodicals LLC.
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