ABSTRACT

Introduction Coronary artery disease (CAD) is the commonest cause of death in the developed world, and is ever increasing in developing countries.1

The burden of disease in terms of mortality, morbidity, and socio-economic hardship is considerable. Traditional risk factors of atherosclerosis such as hypertension, tobacco smoking, diabetes mellitus and hyperlipidaemia have been estimated to account for only about 50% of clinical cases of CAD.2 A number of potential ‘novel’ cardiovascular risk factors are emerging: one of which is chronic infection.3-5

Historically, the concept that infection could be an aetiological factor in atherosclerosis was proposed as early as 1859 by Virchow,6 followed by Osler7 in 1908, Frothingham8 in 1911 and Ophuls9 in 1921. Infections (micro-organisms and their products), alone and in conjunction with conventional cardiovascular risk factors (LDL cholesterol, smoking), could act as forceful inflammatory stimuli systemically.10 These stimuli may drive the production (and lead to a dynamic interplay) of various inflammatory cells, cytokines and acute phase reactants in the circulation and on the vascular wall.10 Indeed, atherosclerosis is now acknowledged as an inflamma11

Research over the last century has implicated a number of micro-organisms that may serve as the potential link between inflammation and atherosclerosis (Table 7.1).12