Lipids and cardiovascular calcification: contributions to plaque vulnerability.
Lipids and cardiovascular calcification: contributions to plaque vulnerability.
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DOI：
10.1097/mol.0000000000000777
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发表时间：
2021-10-01
影响因子：
4.4
通讯作者：
Demer LL
中科院分区：
文献类型：
--
作者：
Hsu JJ;Tintut Y;Demer LL
心血管钙化是动脉粥样硬化病变的常见特征，长期以来被认为与心血管风险相关。脂蛋白在动脉粥样硬化中的作用也已确定，调脂治疗已显示出斑块消退的能力。然而，调脂治疗与钙化的关系更为复杂，目前还没有发现逆转或减弱患者钙化的药物治疗。在这篇综述中，我们总结了脂质和心血管钙化之间相互作用的最新进展，以及评估钙化动脉粥样硬化斑块易损性的新成像方式。最近的临床研究强调了脂蛋白亚型（如低密度和高密度脂蛋白颗粒以及脂蛋白（a）[Lp（a）]）与冠状动脉钙化和钙化性主动脉瓣疾病的相关性。此外，在人类和动物模型中，融合的18F-氟化钠正电子发射断层扫描和计算机断层扫描（18F-NaF PET/CT）成像在表征动脉粥样硬化斑块的微结构和脆弱性方面的效用的证据继续出现。脂质和心血管钙化之间的关系是复杂的，新的成像技术，如18F-NaF PET/CT成像，可以更好地识别疾病修饰疗法和预测钙化斑块的进展和稳定性，以帮助指导临床管理。
Cardiovascular calcification, a common feature of atherosclerotic lesions, is long known to associate with cardiovascular risk. The roles of lipoproteins in atherosclerosis are also established, and lipid-modifying therapies have shown capacity for plaque regression. However, the association of lipid-modifying therapies with calcification are more complex, and currently no medical therapies have been found to reverse or attenuate calcification in patients. In this revie, we summarize recent developments in understanding of the interplay between lipids and cardiovascular calcification, as well as new imaging modalities for assessing calcified atherosclerotic plaque vulnerability. Recent clinical studies have highlighted the associations of lipoprotein subtypes, such as low-density and high-density lipoprotein particles, as well as lipoprotein (a) [Lp(a)], with coronary calcification and calcific aortic valve disease. Further, evidence continues to emerge for the utility of fused 18F-sodium fluoride positron-emission tomographic and computed tomographic (18F-NaF PET/CT) imaging in characterizing the microarchitecture and vulnerability of atherosclerotic plaque, in both humans and animal models. The relationship between lipids and cardiovascular calcification is complex, and new imaging techniques, such as 18F-NaF PET/CT imaging, may allow for better identification of disease-modifying therapies and prediction of calcified plaque progression and stability to help guide clinical management.