A Simple Risk Score to Differentiate Between Coronary Artery Obstruction and Coronary Artery Spasm of Patients With Acute Coronary Syndrome Without Persistent ST-Segment Elevation.


Journal

Circulation journal : official journal of the Japanese Circulation Society
ISSN: 1347-4820
Titre abrégé: Circ J
Pays: Japan
ID NLM: 101137683

Informations de publication

Date de publication:
22 09 2022
Historique:
pubmed: 23 5 2022
medline: 24 9 2022
entrez: 22 5 2022
Statut: ppublish

Résumé

The aim of this study was to create a risk scoring model to differentiate obstructive coronary artery (CA) from CA spasm in the etioology of acute coronary syndrome (ACS).Methods and Results: We included 753 consecutive patients with ACS without persistent ST-segment elevation (p-STE). The exclusion criteria were: (1) out-of-hospital cardiac arrest; (2) cardiogenic shock; (3) hemodialysis; (4) atrial fibrillation/flutter; (5) severe valvular disease; (6) no coronary angiography; (7) non-obstructive coronary artery without "definite" vasospastic angina definition; and/or (8) missing data. From the multivariate logistic regression analysis for prediction of obstructive CA, an integer score of 2 to each 0.5 increment in odds ratio was given, and values were divided into quartiles according to the total score. The scores were as follows: age >70 years (6 points), non-STE myocardial infarction (9 points), diabetes mellitus (5 points), B-type natriuretic peptide >90 pg/mL (7 points), neutrophil to lymphocyte ratio >2 (5 points), and high-density lipoprotein cholesterol <50 mg/dL (5 points). CA spasm-induced ACS occurred in 50.0% in Quartile 1 (total score: 0-13), 20.5% in Quartile 2 (total score: 14-19), 4.9% in Quartile 3 (total score: 20-26), and 2.2% in Quartile 4 (total score: 27-37) (P<0.001), indicating that a total score of <20 was a potential clinical indicator of CA spasm-induced ACS. CA spasm-induced ACS should be suspected if a total score of <20, and a spasm provocation test was being considered.

Sections du résumé

BACKGROUND
The aim of this study was to create a risk scoring model to differentiate obstructive coronary artery (CA) from CA spasm in the etioology of acute coronary syndrome (ACS).Methods and Results: We included 753 consecutive patients with ACS without persistent ST-segment elevation (p-STE). The exclusion criteria were: (1) out-of-hospital cardiac arrest; (2) cardiogenic shock; (3) hemodialysis; (4) atrial fibrillation/flutter; (5) severe valvular disease; (6) no coronary angiography; (7) non-obstructive coronary artery without "definite" vasospastic angina definition; and/or (8) missing data. From the multivariate logistic regression analysis for prediction of obstructive CA, an integer score of 2 to each 0.5 increment in odds ratio was given, and values were divided into quartiles according to the total score. The scores were as follows: age >70 years (6 points), non-STE myocardial infarction (9 points), diabetes mellitus (5 points), B-type natriuretic peptide >90 pg/mL (7 points), neutrophil to lymphocyte ratio >2 (5 points), and high-density lipoprotein cholesterol <50 mg/dL (5 points). CA spasm-induced ACS occurred in 50.0% in Quartile 1 (total score: 0-13), 20.5% in Quartile 2 (total score: 14-19), 4.9% in Quartile 3 (total score: 20-26), and 2.2% in Quartile 4 (total score: 27-37) (P<0.001), indicating that a total score of <20 was a potential clinical indicator of CA spasm-induced ACS.
CONCLUSIONS
CA spasm-induced ACS should be suspected if a total score of <20, and a spasm provocation test was being considered.

Identifiants

pubmed: 35599005
doi: 10.1253/circj.CJ-22-0096
doi:

Substances chimiques

Lipoproteins, HDL 0
Natriuretic Peptide, Brain 114471-18-0
Cholesterol 97C5T2UQ7J

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

1509-1518

Auteurs

Masaomi Gohbara (M)

Department of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine.
Division of Cardiology, Yokohama City University Medical Center.

Noriaki Iwahashi (N)

Division of Cardiology, Yokohama City University Medical Center.

Kozo Okada (K)

Division of Cardiology, Yokohama City University Medical Center.

Yutaka Ogino (Y)

Department of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine.
Division of Cardiology, Yokohama City University Medical Center.

Yohei Hanajima (Y)

Division of Cardiology, Yokohama City University Medical Center.

Jin Kirigaya (J)

Division of Cardiology, Yokohama City University Medical Center.

Yugo Minamimoto (Y)

Division of Cardiology, Yokohama City University Medical Center.

Yasushi Matsuzawa (Y)

Division of Cardiology, Yokohama City University Medical Center.

Manabu Nitta (M)

Department of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine.

Masaaki Konishi (M)

Department of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine.
Division of Cardiology, Yokohama City University Medical Center.

Kiyoshi Hibi (K)

Division of Cardiology, Yokohama City University Medical Center.

Masami Kosuge (M)

Division of Cardiology, Yokohama City University Medical Center.

Toshiaki Ebina (T)

Division of Cardiology, Yokohama City University Medical Center.
Department of Laboratory Medicine and Clinical Investigation, Yokohama City University Medical Center.

Teruyasu Sugano (T)

Department of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine.

Toshiyuki Ishikawa (T)

Department of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine.

Kouichi Tamura (K)

Department of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine.

Kazuo Kimura (K)

Department of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine.
Division of Cardiology, Yokohama City University Medical Center.

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