Akihiro Nakajima1, Vijaykumar Subban2, Michele Russo1, Krzysztof L Bryniarski3, Osamu Kurihara1, Makoto Araki1, Yoshiyasu Minami4, Tsunenari Soeda5, Taishi Yonetsu6, Filippo Crea7, Masamichi Takano8, Takumi Higuma9, Tsunekazu Kakuta10, Tom Adriaenssens11, Niklas F Boeder12, Holger M Nef12, Owen C Raffel13, Iris McNulty1, Hang Lee14, Sunao Nakamura15, Jabir Abdullakutty16, Rony Mathew16, Mullasari Ajit Sankardas2, Ik-Kyung Jang17. 1. Cardiology Division, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA. 2. Institute of Cardiovascular disease, Madras Medical Mission, Chennai, India. 3. Cardiology Division, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA; Institute of Cardiology, Jagiellonian University Medical College, Kraków, Poland. 4. Department of Cardiovascular Medicine, Kitasato University School of Medicine, Sagamihara, Kanagawa, Japan. 5. Department of Cardiovascular Medicine, Nara Medical University, Kashihara, Nara, Japan. 6. Department of Interventional Cardiology, Tokyo Medical and Dental University, Tokyo, Japan. 7. Department of Cardiovascular and Thoracic Science, Catholic University of the Sacred Heart, Fondazione Policlinico Agostino Gemelli IRCCS, Roma, Italy. 8. Cardiovascular Center Nippon Medical School Chiba Hokusoh Hospital, Inzai, Chiba, Japan. 9. Division of Cardiology, Department of Internal Medicine, St. Marianna University School of Medicine, Kanagawa, Japan. 10. Department of Cardiology, Tsuchiura Kyodo General Hospital, Tsuchiura, Ibaraki, Japan. 11. Department of Cardiovascular Medicine, University Hospitals Leuven, Leuven, Belgium. 12. Department of Cardiology, University of Giessen, Giessen, Germany. 13. Department of Cardiology, The Prince Charles Hospital, Brisbane, QLD, Australia.; Queensland University of Technology, Queensland, Australia; University of Queensland, Queensland, Australia. 14. Biostatistics Center, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA. 15. Interventional Cardiology Unit, New Tokyo Hospital, Chiba, Japan. 16. Lisie Heart Institute, Lisie Hospital, Kochi, India. 17. Cardiology Division, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA; Division of Cardiology, Kyung Hee University Hospital, Seoul, Republic of Korea. Electronic address: ijang@mgh.harvard.edu.
Abstract
BACKGROUND: South Asians, and Indians in particular, are known to have a higher incidence of premature atherosclerosis and acute coronary syndromes (ACS) with worse clinical outcomes, compared to populations with different ethnic backgrounds. However, the underlying pathobiology accounting for these differences has not been fully elucidated. METHODS: ACS patients who had culprit lesion optical coherence tomography (OCT) imaging were enrolled. Culprit plaque characteristics were evaluated using OCT. RESULTS: Among 1315 patients, 100 were South Asian, 1009 were East Asian, and 206 were White. South Asian patients were younger (South Asians vs. East Asians vs. Whites: 51.6 ± 13.4 vs. 65.4 ± 11.9 vs. 62.7 ± 11.7; p < 0.001) and more frequently presented with ST-segment elevation myocardial infarction (STEMI) (77.0% vs. 56.4% vs. 35.4%; p < 0.001). On OCT analysis after propensity group matching, plaque erosion was more frequent (57.0% vs. 38.0% vs. 50.0%; p = 0.003), the lipid index was significantly greater (2281.6 [1570.8-3160.6] vs. 1624.3 [940.9-2352.4] vs. 1303.8 [1090.0-1757.7]; p < 0.001), and the prevalence of layered plaque was significantly higher in the South Asian group than in the other two groups (52.0% vs. 30.0% vs. 34.0%; p = 0.003). CONCLUSIONS: Compared to East Asians and Whites, South Asians with ACS were younger and more frequently presented with STEMI. Plaque erosion was the predominant pathology for ACS in South Asians and their culprit lesions had more features of plaque vulnerability. CLINICAL TRIAL REGISTRATION: http://www.clinicaltrials.gov, NCT03479723.
BACKGROUND: South Asians, and Indians in particular, are known to have a higher incidence of premature atherosclerosis and acute coronary syndromes (ACS) with worse clinical outcomes, compared to populations with different ethnic backgrounds. However, the underlying pathobiology accounting for these differences has not been fully elucidated. METHODS: ACS patients who had culprit lesion optical coherence tomography (OCT) imaging were enrolled. Culprit plaque characteristics were evaluated using OCT. RESULTS: Among 1315 patients, 100 were South Asian, 1009 were East Asian, and 206 were White. South Asian patients were younger (South Asians vs. East Asians vs. Whites: 51.6 ± 13.4 vs. 65.4 ± 11.9 vs. 62.7 ± 11.7; p < 0.001) and more frequently presented with ST-segment elevation myocardial infarction (STEMI) (77.0% vs. 56.4% vs. 35.4%; p < 0.001). On OCT analysis after propensity group matching, plaque erosion was more frequent (57.0% vs. 38.0% vs. 50.0%; p = 0.003), the lipid index was significantly greater (2281.6 [1570.8-3160.6] vs. 1624.3 [940.9-2352.4] vs. 1303.8 [1090.0-1757.7]; p < 0.001), and the prevalence of layered plaque was significantly higher in the South Asian group than in the other two groups (52.0% vs. 30.0% vs. 34.0%; p = 0.003). CONCLUSIONS: Compared to East Asians and Whites, South Asians with ACS were younger and more frequently presented with STEMI. Plaque erosion was the predominant pathology for ACS in South Asians and their culprit lesions had more features of plaque vulnerability. CLINICAL TRIAL REGISTRATION: http://www.clinicaltrials.gov, NCT03479723.