Premature coronary artery disease: An inferred cardiovascular variant or a South Asian genetic disorder? Jeetesh V. Patel 1 , Shridhar Dwivedi 2 , Elizabeth A. Hughes 1 , Gregory Y. H. Lip 1 1 Haemostasis, Thrombosis and Vascular Biology Unit, University Department of Medicine, City Hospital, Birmingham, UK; 2 Preventative Cardiology, University College of Medical Sciences, University of Delhi, Delhi, India Editorial Focus Correspondence to: Dr. Jeetesh Patel Haemostasis, Thrombosis and Vascular Biology Unit University Department of Medicine City Hospital, Birmingham, UK Tel: +44 0121 507 5080, Fax: +44 121 554 4083 E-mail: Jeetesh.Patel@swbhl.nhs.uk Received May 6, 2008 Accepted May 6, 2008 Prepublished online May 7, 2008 doi:10.1160/TH08-05-0286 Thromb Haemost 2008; 99: 991–992 C oronary artery disease (CAD) is the leading cause of mor- bidity and mortality in both the developed and developing world, and in particular, people originating from the In- dian subcontinent appear to have a particular susceptibility (1–6). Contextually, age standardised rates of death from CAD in India were 127% higher than that in the US during 2002 (7), and deaths from this disease are projected to afflict some 2 million resident Indians by year 2010. Not only is the disease burden on the Indian subcontinent estimated to be the highest worldwide (8, 9) but there also is a markedly earlier progression of disease within the resident population (10). Indeed, the terms ‘pre- mature-’, ‘early onset-’ and ‘young-’ CAD were almost exclus- ively used by authors between the 1970s to the 1990s to distin- guish the impact of CAD on the Indian subcontinent (11–13). Despite a growing global familiarity of these terms and as- sociated definitions (Table 1), this condition is altogether less frequently looked at in the West (14), which may underline the ominous ancestral relationship between CAD with the Indian subcontinent. Given the wide interest into the underlying patho- physiology of atherogenesis, and more specifically, CAD itself (15–18) relatively little interest has been directed to ethnic pre- disposition to premature CAD. However, is there really any pathological or etiological basis to characterise ‘premature’ CAD per se? In the May issue issue 991 Table 1: The evolution of premature coronary ar- tery disease (CAD). Definition Upper age limit (years) Study population, CAD patients Reference Young CAD ≤45 men and women Singapore 26 ≤40 men and women Nine countries study of patients (Auckland, New Zealand; Melbourne, Australia; Los Angles/Atlanta, USA; Cape Town, South Africa; Tel Aviv, Israel; Heidelberg, Germany; Edinburgh, UK; Bombay, India, Singapore) 27 ≤45 women Canada 28 ≤40 men and women Shinshu, Japan 29 ≤40 men & women Poland 30 Premature CAD ≤50 men, ≤60 women Baltimore, US 31 ≤50 men Australia 32 ≤40 men and women Singapore 33 ≤45 men, ≤55 women London, UK 34 ≤45 men Turkey 35 ≤45 men and women Lucknow, India 36 ≤49 men Pozna¡, Poland 37 ≤45 men and women Tehran, Iran 38 Early onset CAD ≤45 men and women Israeli Jewish CAD patients in Tel-Aviv, Israel 39 California 14 ≤45 men and women © 2008 Schattauer GmbH, Stuttgart For personal or educational use only. No other uses without permission. All rights reserved. Downloaded from www.thrombosis-online.com on 2017-06-26 | IP: 54.191.40.80