{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,5]],"date-time":"2026-08-05T01:22:46Z","timestamp":1785892966603,"version":"3.56.0"},"reference-count":20,"publisher":"Oxford University Press (OUP)","issue":"12","license":[{"start":{"date-parts":[[2012,12,1]],"date-time":"2012-12-01T00:00:00Z","timestamp":1354320000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2012,12,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Aims<\/jats:title>\n                    <jats:p>Coronary telangiectasia (CT) is a rare congenital anomaly causing ventricular shunt and myocardial ischaemia. Its prevalence, genetic background, and impact in human hypertrophic cardiomyopathy (HCM) are unknown and were therefore investigated in this study.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods and results<\/jats:title>\n                    <jats:p>Among 445 patients with HCM, 195 had a coronary angiography and 124 a left ventricular endomyocardial biopsy. CT draining into the ventricular cavities was observed in 5 of 195 HCM patients (2.5%), whereas it was detected in 0.1% of 1000 consecutive subjects without congenital anomalies undergoing coronary angiography. Patients with CT-HCM underwent a total body computed tomography scan to investigate the presence of systemic vascular malformations. HCM-related MYH7, MYBPC3, TNNT2, and TPM1 genes and hereditary haemorragic telangiectasia-related endoglin and activin receptor-like kinase 1 genes were analysed. Histology, clinical profile, and outcome of CT-HCM patients were correlated with those of 22 control HCM patients. No mucocutaneous or systemic vascular malformations were detected. Gene analysis showed a MYH7 mutation in two patients, with an associated endoglin point mutation. Histology showed in the CT-HCM cohort a more pronounced myocardial fibrosis (29.8 \u00b1 3.8%) compared with HCM controls (13 \u00b1 2.6%), and disorganized cardiomyocytes separated by thin-walled large vessels adherent to the endocardium. Clinically, the CT-HCM cohort had a higher arrhythmic profile at diagnosis and increased incidence of implantable cardioverter defibrillator (ICD) implantations and arrhythmic deaths during a long-term follow-up.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>CT is detectable in 2.5% of HCM patients vs. 0.1% of the general population; it may derive from a co-existing endoglin gene mutation and cause a prominent, potentially arrhythmogenic myocardial fibrosis.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1093\/eurjhf\/hfs125","type":"journal-article","created":{"date-parts":[[2012,8,6]],"date-time":"2012-08-06T20:13:39Z","timestamp":1344284019000},"page":"1332-1337","source":"Crossref","is-referenced-by-count":3,"title":["Coronary Telangiectasia Associated with Hypertrophic 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