Heo Gyu S, Sultan Deborah, Liu Yongjian
Mallinckrodt Institute of Radiology, Washington University, St. Louis, MO, USA.
Mallinckrodt Institute of Radiology, Washington University, St. Louis, MO, USA -
Q J Nucl Med Mol Imaging. 2020 Mar;64(1):4-20. doi: 10.23736/S1824-4785.20.03230-6. Epub 2020 Feb 18.
Cardiovascular disease (CVD) remains the leading cause of death worldwide despite advances in diagnostic technologies and treatment strategies. The underlying cause of most CVD is atherosclerosis, a chronic disease driven by inflammatory reactions. Atherosclerotic plaque rupture could cause arterial occlusion leading to ischemic tissue injuries such as myocardial infarction (MI) and stroke. Clinically, most imaging modalities are based on anatomy and provide limited information about the on-going molecular activities affecting the vulnerability of atherosclerotic lesion for risk stratification of patients. Thus, the ability to differentiate stable plaques from those that are vulnerable is an unmet clinical need. Of various imaging techniques, the radionuclide-based molecular imaging modalities including positron emission tomography and single-photon emission computerized tomography provide superior ability to noninvasively visualize molecular activities in vivo and may serve as a useful tool in tackling this challenge. Moreover, the well-established translational pathway of radiopharmaceuticals may also facilitate the translation of discoveries from benchtop to clinical investigation in contrast to other imaging modalities to fulfill the goal of precision medicine. The relationship between inflammation occurring within the plaque and its proneness to rupture has been well documented. Therefore, an active effort has been significantly devoted to develop radiopharmaceuticals specifically to measure CVD inflammatory status, and potentially elucidate those plaques which are prone to rupture. In the following review, molecular imaging of inflammatory biomarkers will be briefly discussed.
尽管诊断技术和治疗策略取得了进展,但心血管疾病(CVD)仍然是全球主要的死亡原因。大多数心血管疾病的根本原因是动脉粥样硬化,这是一种由炎症反应驱动的慢性疾病。动脉粥样硬化斑块破裂可导致动脉阻塞,进而导致缺血性组织损伤,如心肌梗死(MI)和中风。临床上,大多数成像方式基于解剖结构,提供的关于影响动脉粥样硬化病变易损性的正在进行的分子活动的信息有限,无法用于患者的风险分层。因此,区分稳定斑块和易损斑块的能力是尚未满足的临床需求。在各种成像技术中,基于放射性核素的分子成像方式,包括正电子发射断层扫描和单光子发射计算机断层扫描,具有在体内无创可视化分子活动的卓越能力,可能成为应对这一挑战的有用工具。此外,与其他成像方式相比,放射性药物成熟的转化途径也可能促进从实验室发现到临床研究的转化,以实现精准医学的目标。斑块内发生的炎症与其破裂倾向之间的关系已有充分记录。因此,人们一直在积极致力于开发专门用于测量心血管疾病炎症状态的放射性药物,并有可能阐明那些易于破裂的斑块。在以下综述中,将简要讨论炎症生物标志物的分子成像。