Percutaneous coronary intervention (PCI) continues to advance at pace with an ever-broadening indication. In this article we will review the recent technological advances in PCI that have enabled more complex coronary disease to be treated. The choice of revascularisation strategy must take into account the evidence—just because we can treat by PCI does not necessarily mean we should. When PCI is indicated, a safe, precision PCI approach guided by physiology, imaging and optimal lesion preparation should be the goal to obtain complete revascularisation and a durable long-term result. When these standards are adhered to, the outcomes can be excellent, in even complex coronary disease. We provide contemporary trial evidence to justify PCI and treatment algorithms that ensure optimal revascularisation decision making to achieve the best patient outcomes.

Aims To examine pericoronary (PCAT) and periaortic (PAAT) adipose tissue density on coronary computed tomography angiography (CCTA) for assessing arterial inflammation in Takayasu arteritis (TAK) and atherosclerosis. Methods and results PCAT and PAAT density was measured in coronary (n = 1016) and aortic (n = 108) segments from 108 subjects (TAK+coronary artery disease (CAD), n = 36; TAK, n = 18; atherosclerotic CAD, n = 32; matched controls, n = 22). Median PCAT and PAAT densities varied between groups (mPCAT: p < 0.0001; PAAT: p = 0.0002). PCAT density was 7.01 ± SEM 1.78 Hounsfield Unit (HU) higher in coronary segments from TAK+CAD patients than stable CAD patients (p = 0.0002), and 8.20 ± SEM 2.04 HU higher in TAK patients without CAD than controls (p = 0.0001). mPCAT density was correlated with Indian Takayasu Clinical Activity Score (r = 0.43, p = 0.001) and C-reactive protein (r = 0.41, p < 0.0001), and was higher in active versus inactive TAK (p = 0.002). mPCAT density above -74 HU had 100% sensitivity and 95% specificity for differentiating active TAK from controls (AUC=0.99 [95% CI 0.97-1]). The association of PCAT density and coronary arterial inflammation measured by 68Ga-DOTATATE positron emission tomography equated to an increase of 2.44 ± SEM 0.77 HU in PCAT density for each unit increase in 68Ga-DOTATATE maximum tissue-to-blood ratio (p = 0.002). These findings remained in multivariable sensitivity analyses adjusted for potential confounders. Conclusions PCAT and PAAT density are higher in TAK than atherosclerotic CAD or controls, and are associated with clinical, biochemical and PET markers of inflammation. Owing to excellent diagnostic accuracy, PCAT density could be useful as a clinical adjunct for assessing disease activity in TAK.

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