Precision medicine in coronary artery disease: Time for impl
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Coronary artery disease (CAD) has been viewed largely using a reductionist approach; management is thus primarily evidence-based. However, recent advances in biological, genetic, and molecular technologies and big-data analysis suggested that the traditional approach is too simple to capture the complexity at an individual level and thus holds only limited potential for further improvement. Understanding individual differences in patients with similar clinical presentations are critical for effective risk stratification, diagnosis, and therapeutic decision.

Individualized Antiplatelet Strategy after Coronary Intervention: Dual antiplatelet therapy (DAPT) is a cornerstone in preventing stent thrombosis and recurrent ischemic events after PCI, but the strategy and duration of DAPT remain controversial.

In the era of 1st generation DES, intensive and prolonged DAPT was the norm due to the relatively high rate of late stent thrombosis. Conceivably, bleeding was a major concern. Due to thinner stent struts, more biocompatible polymers, and favorable drug-eluting characteristics, new-generation DES is associated with a significantly lower stent thrombosis rate. Accordingly, there has been a trend toward shorter and more balanced DAPT, with a switch to monotherapy at 3 months or even earlier. In addition to DES type, clinical characteristics, the complexity of coronary anatomy, and presence of diabetes or renal dysfunction must be considered when assessing the risk of thrombotic events. Clearly, a “one size fits all” approach is inadequate; individualized programs that pinpoint optimal balance between thrombotic and bleeding risks are needed.

Anti-inflammatory Therapy in Progression of Coronary Artery Disease: Cholesterol is important for atherosclerosis development but must be viewed under schematic frameworks that also consider the complex interaction between inflammation and cholesterol. Chronic inflammation plays an important role in the initiation and progression of coronary atherosclerosis. Furthermore, uncontrolled inflammation renders coronary plaques “unstable” and vulnerable to rupture or erosion, and ultimately acute coronary events. Several pro-inflammatory cytokines, including C-reactive protein, tumor necrosis factor-?, and interleukin-6, have been shown to promote coronary atherosclerosis and serve as the independent risk factors for CAD. In the Canakinumab anti-inflammatory Thrombosis Outcome Study (CANTOS), the anti-interleukin-1? antibody canakinumab reduced the rate of recurrent cardiovascular events by 15% in patients with a history of myocardial infarction and an elevated baseline level of C-reactive protein.