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19th World Congress on Heart Disease



Mohammad Madjid, M.D., Texas Heart Institute, Houston, TX, USA


Atherosclerotic cardiovascular events result from two separate phases of mechanistic processes. Whereas lipid accumulation and chronic latent inflammation lead to development of atherosclerotic plaques over a period of years, certain internal or external factors can “trigger” the transformation of stable plaques into unstable plaques within hours to weeks, causing an acute coronary syndrome (ACS).

Many triggers act by stimulating the sympathetic nervous system or imposing extra physiologic, hemodynamic, or psychological stress, thereby inducing thrombosis, vascular inflammation, or rupture of high-risk, vulnerable plaques.

Such triggers can arise from a variety of situations and can be categorized as external (ie, natural disasters, cocaine, infectious organisms, emotional stress) or internal (ie, circadian variations). High-risk atherosclerotic plaques are commonly present but are not a prerequisite for trigger-induced ACS events. Cocaine abuse is a well-known trigger for acute coronary events and can exert its effects even in the absence of atherosclerotic lesions.

Infections are well-known triggers of ACS and have been studied rather extensively in this setting. Influenza, pneumonia, bacteremia, urinary tract infection, and other types of infection are associated with an increased risk of ACS. This fact is not surprising, given the critical role inflammation plays in the pathogenesis of ACS. Influenza vaccination has been proven to prevent ACS, and antiviral therapy after influenza infection has been suggested to prevent ACS and stroke.

Despite the important role of triggers in the pathogenesis of ACS, there is little consensus about how to develop and implement a comprehensive plan to control these factors. Rigorous basic, preclinical, and clinical studies are needed to identify and develop preventive and therapeutic measures against different triggers as a new approach to preventing cardiovascular events.



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