Chaitu Cheruvu1, Bruce Precious1, Christopher Naoum1, Philipp Blanke1, Amir Ahmadi2, Jeanette Soon1, Chesnaldey Arepalli1, Heidi Gransar3, Stephan Achenbach4, Daniel S Berman5, Matthew J Budoff6, Tracy Q Callister7, Mouaz H Al-Mallah8, Filippo Cademartiri9, Kavitha Chinnaiyan10, Ronen Rubinshtein11, Hugo Marquez12, Augustin DeLago13, Todd C Villines14, Martin Hadamitzky15, Joerg Hausleiter16, Leslee J Shaw17, Philipp A Kaufmann18, Ricardo C Cury19, Gudrun Feuchtner20, Yong-Jin Kim21, Erica Maffei9, Gilbert Raff10, Gianluca Pontone22, Daniele Andreini22, Hyuk-Jae Chang23, James K Min24, Jonathon Leipsic25. 1. Department of Radiology, University of British Columbia, Vancouver, BC, Canada. 2. Department of Medicine, University of British Columbia, Vancouver, BC, Canada. 3. Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, CA, USA. 4. Department of Medicine, University of Erlangen, Erlangen, Germany. 5. Department of Imaging, Cedars Sinai Medical Center, Los Angeles, CA, USA. 6. Department of Medicine, Harbor UCLA Medical Center, Los Angeles, CA, USA. 7. Tennessee Heart and Vascular Institute, Hendersonville, TN, USA. 8. Department of Medicine, Wayne State University, Henry Ford Hospital, Detroit, MI, USA. 9. Cardiovascular Imaging Unit, Giovanni XXIII Hospital, Monastier, Treviso, Italy. 10. William Beaumont Hospital, Royal Oaks, MI, USA. 11. Department of Surgery, Curry Cabral Hospital, Lisbon, Portugal. 12. Department of Cardiology at the Lady Davis Carmel Medical Center, The Ruth and Bruce Rappaport School of Medicine, Technion-Israel Institute of Technology, Haifa, Israel. 13. Capitol Cardiology Associates, Albany, NY, USA. 14. Department of Medicine, Walter Reed Medical Center, Washington, DC, USA. 15. Division of Cardiology, Deutsches Herzzentrum Munchen, Munich, Germany. 16. Medizinische Klinik I der Ludwig-Maximilians-Universität München, Munich, Germany. 17. Division of Cardiology, Emory University School of Medicine, Atlanta, GA, USA. 18. University Hospital, Zurich, Switzerland. 19. Baptist Cardiac and Vascular Institute, Miami, FL, USA. 20. Department of Radiology, Medical University of Innsbruck, Innsbruck, Austria. 21. Seoul National University Hospital, Seoul, South Korea. 22. Department of Clinical Sciences and Community Health, University of Milan, Centro Cardiologico Monzino, IRCCS, Milan, Italy. 23. Division of Cardiology, Severance Cardiovascular Hospital and Severance Biomedical Science Institute, Yonsei University College of Medicine, Yonsei University Health System, Seoul, South Korea. 24. Department of Radiology, New York-Presbyterian Hospital and the Weill Cornell Medical College, New York, NY, USA. 25. Department of Medicine and Radiology, University of British Columbia, Vancouver, BC, Canada. Electronic address: jleipsic@providencehealth.bc.ca.
Abstract
BACKGROUND: Coronary computed tomography angiography (coronary CTA) can prognosticate outcomes in patients without modifiable risk factors over medium term follow-up. This ability was driven by major adverse cardiovascular events (MACE). OBJECTIVE: Determine if coronary CTA could discriminate risk of mortality with longer term follow-up. In addition we sought to determine the long-term relationship to MACE. METHODS: From 12 centers, 1884 patients undergoing coronary CTA without prior coronary artery disease (CAD) or any modifiable CAD risk factors were identified. The presence of CAD was classified as none (0% stenosis), mild (1% to 49% stenosis) and obstructive (≥50% stenosis severity). The primary endpoint was all-cause mortality and the secondary endpoint was MACE. MACE was defined as the combination of death, nonfatal myocardial infarction, unstable angina, and late target vessel revascularization (>90 days). RESULTS: Mean age was 55.6 ± 14.5 years. At mean 5.6 ± 1.3 years follow-up, 145(7.7%) deaths occurred. All-cause mortality demonstrated a dose-response relationship to the severity and number of coronary vessels exhibiting CAD. Increased mortality was observed for >1 segment non-obstructive CAD (hazard ratio [HR]:1.73; 95% confidence interval [CI]: 1.07-2.79; p = 0.025), obstructive 1&2 vessel CAD (HR: 1.70; 95% CI: 1.08-2.71; p = 0.023) and 3-vessel or left main CAD (HR: 2.87; 95% CI: 1.57-5.23; p = 0.001). Both obstructive CAD (HR: 6.63; 95% CI: 3.91-11.26; p < 0.001) and non-obstructive CAD (HR: 2.20; 95% CI: 1.31-3.67; p = 0.003) predicted MACE with increased hazard associated with increasing CAD severity; 5.60% in no CAD, 13.24% in non-obstructive and 36.28% in obstructive CAD, p < 0.001 for trend. CONCLUSIONS: In individuals being assessed for CAD with no modifiable risk factors, all-cause mortality in the long term (>5 years) was predicted by the presence of more than 1 segment of non-obstructive plaque, obstructive 1- or 2-vessel CAD and 3 vessel/left main CAD. Any CAD, whether non-obstructive or obstructive, predicted MACE over the same time period.
BACKGROUND: Coronary computed tomography angiography (coronary CTA) can prognosticate outcomes in patients without modifiable risk factors over medium term follow-up. This ability was driven by major adverse cardiovascular events (MACE). OBJECTIVE: Determine if coronary CTA could discriminate risk of mortality with longer term follow-up. In addition we sought to determine the long-term relationship to MACE. METHODS: From 12 centers, 1884 patients undergoing coronary CTA without prior coronary artery disease (CAD) or any modifiable CAD risk factors were identified. The presence of CAD was classified as none (0% stenosis), mild (1% to 49% stenosis) and obstructive (≥50% stenosis severity). The primary endpoint was all-cause mortality and the secondary endpoint was MACE. MACE was defined as the combination of death, nonfatal myocardial infarction, unstable angina, and late target vessel revascularization (>90 days). RESULTS: Mean age was 55.6 ± 14.5 years. At mean 5.6 ± 1.3 years follow-up, 145(7.7%) deaths occurred. All-cause mortality demonstrated a dose-response relationship to the severity and number of coronary vessels exhibiting CAD. Increased mortality was observed for >1 segment non-obstructive CAD (hazard ratio [HR]:1.73; 95% confidence interval [CI]: 1.07-2.79; p = 0.025), obstructive 1&2 vessel CAD (HR: 1.70; 95% CI: 1.08-2.71; p = 0.023) and 3-vessel or left main CAD (HR: 2.87; 95% CI: 1.57-5.23; p = 0.001). Both obstructive CAD (HR: 6.63; 95% CI: 3.91-11.26; p < 0.001) and non-obstructive CAD (HR: 2.20; 95% CI: 1.31-3.67; p = 0.003) predicted MACE with increased hazard associated with increasing CAD severity; 5.60% in no CAD, 13.24% in non-obstructive and 36.28% in obstructive CAD, p < 0.001 for trend. CONCLUSIONS: In individuals being assessed for CAD with no modifiable risk factors, all-cause mortality in the long term (>5 years) was predicted by the presence of more than 1 segment of non-obstructive plaque, obstructive 1- or 2-vessel CAD and 3 vessel/left main CAD. Any CAD, whether non-obstructive or obstructive, predicted MACE over the same time period.
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