Atherosclerosis (AS) is the primary pathological result of obesity. Vulnerable AS plaques cause
fatal clinical end points such as myocardial infarction and stroke. To prevent this, improvements
in early diagnosis and treatment are essential. Because vulnerable AS plaques are frequently
nonstenotic, they are preclinically undetectable using conventional imaging. Levels
of blood lipids, C-reactive protein, and interleukin-6 are increased, but are insufficient to indicate
the process of critical perpetuation before the end points present.
More specific biomarkers
(e.g. troponin, copetin, natriuretic peptides, growth differentiation factor-15, or soluble
ST2) indicate the acute coronary syndrome or cardiac insufficiency, but not a critical destabilization
of AS lesions in coronary or carotid arteries. Thus, valuable time (months to years) that
could be used to treat the patient is wasted. An improved management of this dilemma may
involve better detection of variations in degrees of immune inflammation in plaques by using
new biomarkers in blood and/or within the lesion (molecular imaging). Macrophage and T-cell
polarization, and innate and adaptive immune responses (e.g. Toll-like receptors) are involved
in this critical process. New biomarkers in these mechanisms include pentraxin 3, calprotectins
S100A8/S100A9, myeloperoxidase, adiponectin, interleukins, and chemokines.
may also be candidates for molecular imaging using nuclear (magnetic resonance) imaging
tools. Nevertheless, the main challenge remains: which asymptomatic individual should
be screened? At which time interval? Intense interdisciplinary research in laboratory medicine
(biomarkers), nanomedicine (nanoparticle development), and radiology (molecular imaging)
will hopefully address these questions.