Page 12 - Rob Holtackers
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            Coronary artery disease (CAD) is the most common of the cardiovascular diseases and
            involves the gradual build-up of fatty streaks or ‘plaques’ in the coronary arteries, also
            known as atherosclerosis. In a period that may extend over tens of years, the coronary
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            arteries slowly narrow and stiffen over time (Figure 1.1).  The narrowing of the arteries
            prevents oxygenated blood from reaching the cardiomyocytes, which may cause chest
            pain and discomfort known as ‘angina’. While angina is generally experienced with
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            physical  activity  first,  emotional  stress  may  also  trigger  pain  during  rest.   As
            atherosclerotic plaques increase in size over time, a lipid-rich necrotic core can form
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            that is separated from the vessel lumen by a fibrous cap.  This cap averts contact of the
            thrombogenic core substituents with the blood flow. Specific plaque features, such as
            intra-plaque hemorrhage, may develop that are known to destabilize plaques that make
            them  more  vulnerable  to  rupture.   With  sudden  rupture  of  the  fibrous  cap,  the
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            thrombogenic plaque material is released into the blood stream triggering a cascade of
            events. Immediate blood clotting results, which may occlude the coronary artery and
            thereby cutting off the blood supply to the tributary tissue. The resulting ischemia leads
            to  rapid  degeneration  and  subsequent  necrosis  of  the  cardiomyocytes,  called
            myocardial infarction (MI).

            Among cardiovascular diseases, CAD ranks as the most prevalent with approximately
            8.9 million (16%) annual deaths worldwide, leaving it the leading cause of death in























            Figure 1.1: Schematic overview of the progression of atherosclerosis. Through a complex series
            of cellular events within the arterial wall, a fatty streak or ‘plaque’ is formed between the inner
            lining (endothelium) and middle layer (tunica media) of the blood vessel. Over time, this plaque
            undergoes extensive remodeling and increases in size, thereby potentially narrowing the vessel
            lumen. Specific processes, such as intra-plaque hemorrhage and thinning of the fibrous cap, may
            destabilize the plaque making it vulnerable to rupture. Ultimately, in case the plaque ruptures,
            the thrombogenic plaque contents are exposed to the blood stream, leading to immediate blood
            clotting and obstructing or completely blocking blood flow downstream. Image adapted from the
            ‘Arteries atherothrombosis’ dataset by Servier Medical Art.
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