Objective Data describing clinical relevance of chronic total occlusion (CTO) identified by coronary CT angiography (CCTA) have not been reported to date. We investigated the prognosis of CTO on CCTA.
Methods We identified 22 828 patients without prior known coronary artery disease (CAD), who were followed for a median of 26 months. Based on CCTA, coronary lesions were graded as normal (no atherosclerosis), non-obstructive (1%–49%), moderate-to-severe (50%–99%) or totally occluded (100%). All-cause mortality, and major adverse cardiac events defined as mortality, non-fatal myocardial infarction and late coronary revascularisation (≥90 days after CCTA) were assessed.
Results The distribution of patients with normal coronaries, non-obstructive CAD, moderate-to-severe CAD and CTO was 10 034 (44%), 7965 (34.9%), 4598 (20.1%) and 231 (1%), respectively. The mortality rate per 1000 person-years of CTO patients was non-significantly different from patients with moderate-to-severe CAD (22.95; 95% CI 12.71 to 41.45 vs 14.46; 95% CI 12.34 to 16.94; p=0.163), and significantly higher than of those with normal coronaries and non-obstructive CAD (p<0.001 for both). Among 14 382 individuals with follow-up for the composite end point, patients with CTO had a higher rate of events than those with moderate-to-severe CAD (106.56; 95% CI 76.51 to 148.42 vs 65.45; 95% CI 58.01 to 73.84, p=0.009). This difference was primarily driven by an increase in late revascularisations in CTO patients (27 of 35 events). After multivariable adjustment, compared with individuals with normal coronaries, the presence of CTO conferred the highest risk for adverse cardiac events (14.54; 95% CI 9.11 to 23.20, p<0.001).
Conclusions The detection of CTO on non-invasive CCTA is associated with increased rate of late revascularisation but similar 2-year mortality as compared with moderate-to-severe CAD.
Trial registration number NCT01443637.
- cardiac computer tomographic (ct) imaging
- heart disease
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Contributors Drs MPO and FYL contributed to data analysis and interpretation as well as drafting, critical revision and final approval of the manuscript. Drs YL, SA, MHAl-M, DA, JJB, DSB, MJB, FC, TQC, H-JC, KC, BJWC, RCC, ADL, GMF, MH, JH, PAK, Y-JK, JAL, EM, HM, GP, GR, RR, LJS, TCV, MG, ECJ and JMP contributed to data acquisition and interpretation as well as critical revision and final approval of the manuscript. Dr HG contributed to data analysis as well as critical revision and final approval of the manuscript. Dr JKM contributed to planning, design, conduction and reporting of the work described in the article as well as critical revision and final approval of the manuscript. Dr JKM is responsible for the overall content as guarantor.
Funding The research reported in this publication was funded, in part, by the Heart, Lung and Blood Institute of the National Institutes of Health (Bethesda, Maryland, USA) under award number R01 HL115150, and also supported, in part, by the Dalio Institute of Cardiovascular Imaging (New York, New York, USA) and the Michael Wolk Heart Foundation (New York, New York, USA).
Competing interests Dr JKM receives funding from the Dalio Foundation, National Institutes of Health and GE Healthcare. Dr JKM serves on the scientific advisory board of Arineta and GE Healthcare, and has an equity interest in Cleerly. All other coauthors have no relevant disclosures.
Patient consent Obtained.
Ethics approval Weill Cornell Institutional Review Board.
Provenance and peer review Not commissioned; externally peer reviewed.
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