¹⁸F-sodium fluoride: An old tracer with a new promising clinical application

Excerpt

Atherosclerosis is among the leading causes of morbidity and mortality in developed countries.1 It is directly responsible for the majority of ischemic cardiovascular and cerebrovascular events, involved 7.0 and 2.8 million people every year, respectively.2 Vascular calcification is a complex biological process that is a hallmark of atherosclerosis.3 However, the complex atheroma pathogenesis process causes a late clinical diagnosis of atherosclerotic cardiovascular disease. Specifically, coronary atherosclerotic plaque rupture is the principal precipitant of acute myocardial infarction and an important cause of sudden cardiac death. Rupture is challenging to predict because most plaques are non-obstructive and are not identified by stress testing or coronary angiography.4,5 Furthermore, the rapid progression of existing vascular calcium is driven by ongoing microcalcification, carries a poor prognosis, and is not responsive to current medical therapies.6 Therefore, the early and effective detection, particularly of plaques vulnerable to rupture, of atherosclerotic disease is vital to the effective prevention and management of life-threatening cardiovascular events such as myocardial infarctions and cerebrovascular accidents.7 Assessment of Framingham risk factors such as dyslipidemia, hypertension, and diabetes can identify patients at risk of developing atherosclerotic disease but cannot clarify the extent or vulnerability of existing plaques. Clinical evaluations performed in symptomatic patients, such as the ankle-brachial index and cardiac stress tests, are useful to investigate the presence of intraluminal stenosis, but the degree of stenosis alone has not been shown to be predictive of plaque rupture.8,9 …