Intravascular molecular imaging: translating pathophysiology of atherosclerosis into human disease conditions

Abstract

Progression of atherosclerotic plaque in coronary arteries is characterized by complex cellular and non-cellular molecular interactions. Within recent years, atherosclerosis has been recognized as inflammation-driven disease condition, where progressive stages are characterized by morphological changes in plaque composition but also relevant molecular processes resulting in increased plaque vulnerability. While existing intravascular imaging modalities are able to resolve key morphological features during plaque progression, they lack capability to characterize the molecular profile of advanced atherosclerotic plaque. Because hybrid imaging modalities may provide incremental information related to plaque biology, they are expected to provide synergistic effects in detecting high risk patients and lesions. The aim of this article is to review existing literature on intravascular molecular imaging approaches, and to provide clinically oriented proposals of their application. In addition, we assembled an overview of future developments in this field geared towards detection of patients at risk for cardiovascular events.

Multimodal photoacoustic imaging in analytic vulnerability of atherosclerosis

“…USI possesses a high tissue penetration depth, which enables the characterization of plaque burden over the entire vessel. However, an important limitation of this method is poor resolution, which prevents clear‐cut identification of high‐risk lesions, making it difficult to distinguish the fine composition within plaques [20].…”

“…This trait is also known as lipid-rich plaque. Lipid-rich plaques are formed by two important pathophysiological changes: first, lipid accumulation and fibrous cap thinning (less than 65 μm) [25] F I G U R E 1 Coarse visualization of pathologies associated with atherosclerotic lesions [20]. (a) Schematic characterization of a represent pathological intimal thickening with macrophages.…”

“…This trait is also known as lipid‐rich plaque. Lipid‐rich plaques are formed by two important pathophysiological changes: first, lipid accumulation and fibrous cap thinning (less than 65 μm) [25] and second, clustering of lipid‐loaded macrophages with blood inclusions [20]. The clinical manifestation of atherosclerosis is asymptomatic and relatively stable in its initial stage, but early diagnosis is critical for prevention and intervention to reverse its development.…”

“…(c) Thin cap fibroatheroma. Figure 1 is reproduced with permission from reference [20]. iRADIOLOGY and second, clustering of lipid-loaded macrophages with blood inclusions [20].…”

“…Figure 1 is reproduced with permission from reference [20]. iRADIOLOGY and second, clustering of lipid-loaded macrophages with blood inclusions [20]. The clinical manifestation of atherosclerosis is asymptomatic and relatively stable in its initial stage, but early diagnosis is critical for prevention and intervention to reverse its development.…”