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18F-Fluoride Imaging and Other Plaque-Seeking Diagnostic Strategies: Understanding the Reality and Setting the Ground Rules….

Identification and passivation of high-risk plaques prior to a clinical event should help prevent myocardial damage in patients with coronary atherosclerosis.1 However, it is becoming clear that chasing individual plaques may not be the best strategy. Atherosclerosis is a systemic disease and numerous plaques, in many vascular beds, may enlarge and result in plaque rupture.2 Therefore, the status and rate of evolution toward stability or instability of lesions is probably more important. During the process of maturation, high-risk plaques may undergo subclinical plaque ruptures and accelerate plaque expansion.3,4 High-risk plaques characteristically demonstrate optical coherence tomography (OCT)–detectable thin fibrous caps,5 computed tomographic (CT) angiography (CTA)–based large necrotic cores,6,7 and fluorodeoxyglucose (FDG)–positron emission tomography (PET)–related evidence of plaque inflammation.8 Core neovascularity and intraplaque hemorrhage contribute to instability. It is difficult to identify precise threshold points for these high-risk plaque characteristics that might trigger an event. However, the study of the pathophysiology of plaque vulnerability has advanced our understanding of acute coronary syndromes, and serial noninvasive imaging might derisk development of medical interventions for calming such lesions,9 even though a favorable pharmacological manipulation may not necessarily result in superior outcomes.10

See Article by Lee et al 

In addition to the large necrotic cores and inflamed thin fibrous caps, lesions with spotty calcification are associated with acute clinical events.11 Microcalcifications measuring >5 μm are common in the fibrous cap of atheroma12 but are too small to be identified by clinical CT. However, when vascular specimens are studied ex …