AimsSeveral causes have been reported for coronary artery ectasia (CAE), mostly atherosclerosis and tunica media abnormalities. The main aim of the present study was to investigate if CAE extension differs in distinct clinical settings.MethodsThree hundred and forty-one patients with diagnosis of CAE were identified among 9659 coronary angiographies and divided into four groups according to the patient's admission diagnosis: stable or unstable angina (S-UA), myocardial infarction (MI), aortic disease, aortic valvular disease (AVD). S-UA and MI were subgrouped according to the presence of obstructive coronary artery disease (OCAD). Multivariable logistic regression was used to investigate the relationship between clinical diagnosis and CAE extension as expressed by Markis classification and number of coronary vessels affected by CAE.ResultsNo significant differences in CAE extension were found among the four groups, in terms of vessels affected by CAE (P = 0.37) or Markis class (P = 0.33). CAE was not related to the extension of OCAD as assessed by the Gensini score, which was higher in MI and S-UA groups (P < 0.01). However, when ischemic patients were sub-divided on the basis of the presence of OCAD, MI without obstructive coronary artery disease (MINOCA) was associated with a higher extension of CAE in terms of Markis class 1 (OR 5.08, 95% CI 1.61-16.04; P < 0.01).ConclusionThe extension of CAE is comparable in patients referred to coronary angiography for different clinical scenarios, including S-UA, MI, aortic disease, and AVD; however, patients with MINOCA were associated with a higher extension of CAE.Graphical abstract: Difference in coronary artery ectasia extension in terms of Markis class severity, respectively, stratified by clinical presentation and obstructive coronary artery disease presence, http://links.lww.com/JCM/A519.

Coronary ectasia in different scenarios, primarily in myocardial infarction with nonobstructive coronary artery disease

Ghetti G.;Chietera F.;Bendandi F.;Minnucci M.;Bruno A. G.;Orzalkiewicz M.;Nardi E.;Palmerini T.;Saia F.;Galie N.;Taglieri N.
2023

Abstract

AimsSeveral causes have been reported for coronary artery ectasia (CAE), mostly atherosclerosis and tunica media abnormalities. The main aim of the present study was to investigate if CAE extension differs in distinct clinical settings.MethodsThree hundred and forty-one patients with diagnosis of CAE were identified among 9659 coronary angiographies and divided into four groups according to the patient's admission diagnosis: stable or unstable angina (S-UA), myocardial infarction (MI), aortic disease, aortic valvular disease (AVD). S-UA and MI were subgrouped according to the presence of obstructive coronary artery disease (OCAD). Multivariable logistic regression was used to investigate the relationship between clinical diagnosis and CAE extension as expressed by Markis classification and number of coronary vessels affected by CAE.ResultsNo significant differences in CAE extension were found among the four groups, in terms of vessels affected by CAE (P = 0.37) or Markis class (P = 0.33). CAE was not related to the extension of OCAD as assessed by the Gensini score, which was higher in MI and S-UA groups (P < 0.01). However, when ischemic patients were sub-divided on the basis of the presence of OCAD, MI without obstructive coronary artery disease (MINOCA) was associated with a higher extension of CAE in terms of Markis class 1 (OR 5.08, 95% CI 1.61-16.04; P < 0.01).ConclusionThe extension of CAE is comparable in patients referred to coronary angiography for different clinical scenarios, including S-UA, MI, aortic disease, and AVD; however, patients with MINOCA were associated with a higher extension of CAE.Graphical abstract: Difference in coronary artery ectasia extension in terms of Markis class severity, respectively, stratified by clinical presentation and obstructive coronary artery disease presence, http://links.lww.com/JCM/A519.
2023
Ghetti G.; Chietera F.; Donati F.; Bendandi F.; Minnucci M.; Bruno A.G.; Orzalkiewicz M.; Nardi E.; Palmerini T.; Saia F.; Marrozzini C.; Galie N.; Taglieri N.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11585/922012
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