{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,25]],"date-time":"2026-02-25T20:30:16Z","timestamp":1772051416079,"version":"3.50.1"},"reference-count":38,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2021,11,12]],"date-time":"2021-11-12T00:00:00Z","timestamp":1636675200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Clin Physio Funct Imaging"],"published-print":{"date-parts":[[2022,1]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background and Aim<\/jats:title><jats:p>The aim of this study was to assess the nature of myocardial dysfunction in the cardiac syndrome X (CSX) and insignificant coronary artery disease (ICAD) using dobutamine stress echocardiography (DSE) and coronary calcium scoring (CAC).<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>We prospectively studied 35 consecutive patients who complained of exertional angina, had \u22651\u00a0mm ST shift on exercise stress test but normal or no obstructive CAD (&lt;50%) on angiography. Patients were divided into CSX (<jats:italic>n<\/jats:italic>\u00a0=\u00a027) with normal arteries and ICAD (<jats:italic>n<\/jats:italic>\u00a0=\u00a08) with insignificant stenosis.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>CSX patients had more females, lower calcium score and less prevalent cardiac risk factors compared to ICAD (<jats:italic>p<\/jats:italic>\u00a0&lt;\u00a00.05 for all). At peak stress, MAPSE and TAPSE failed to increase in both groups. LV septal and lateral s\u2019 increased in the two groups but the increment increase was less in CSX than ICAD (<jats:italic>p<\/jats:italic>\u00a0&lt;\u00a00.05) while other diastolic indices did not differ between groups (<jats:italic>p<\/jats:italic>\u00a0&gt;\u00a00.05 for all). CAC correlated modestly with LV and RV systolic velocities: septal s' (<jats:italic>r<\/jats:italic>\u00a0=\u00a0\u22120.65, <jats:italic>p<\/jats:italic>\u00a0&lt;\u00a00.001) lateral s' (r\u00a0=\u00a0\u22120.35, <jats:italic>p<\/jats:italic>\u00a0=\u00a00.04) and right s' (<jats:italic>r<\/jats:italic>\u00a0=\u00a0\u22120.53, <jats:italic>p<\/jats:italic>\u00a0=\u00a00.005) in CSX, while in ICAD patients only with RV s' (<jats:italic>r<\/jats:italic>\u00a0=\u00a0\u22120.58, <jats:italic>p<\/jats:italic>\u00a0=\u00a00.02). On multivariate model, only septal s' OR 1.816 (1.1090\u20133.820, <jats:italic>p<\/jats:italic>\u00a0=\u00a00.04) proved the most powerful independent predictor of CAC.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>Compromised LV longitudinal systolic velocities were more pronounced and calcium score as a surrogate for atherosclerosis was lower in CSX than ICAD. These findings strengthen the evidence for different pathogenesis of CSX compared to ICAD, with microvascular disease in the former and calcification in the latter.<\/jats:p><\/jats:sec>","DOI":"10.1111\/cpf.12733","type":"journal-article","created":{"date-parts":[[2021,10,30]],"date-time":"2021-10-30T12:40:30Z","timestamp":1635597630000},"page":"35-42","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["Longitudinal myocardial function is more compromised in cardiac syndrome X compared to insignificant CAD: Role of stress echocardiography and calcium scoring"],"prefix":"10.1111","volume":"42","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-8996-4257","authenticated-orcid":false,"given":"Ibadete","family":"Byty\u00e7i","sequence":"first","affiliation":[{"name":"Institute of Public Health and Clinical Medicine Ume\u00e5 University Ume\u00e5 90187 Sweden"},{"name":"Clinic of Cardiology University Clinical Centre of Kosovo Prishtina 10000 Kosovo"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Tarek M.","family":"Bengrid","sequence":"additional","affiliation":[{"name":"Tripoli university Tripoli 13275 Libya"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Michael Y.","family":"Henein","sequence":"additional","affiliation":[{"name":"Institute of Public Health and Clinical Medicine Ume\u00e5 University Ume\u00e5 90187 Sweden"},{"name":"Molecular and Clinic Research Institute St George University London and Brunel University London UB8 3PH 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