Medial Arterial Calcification: A Significant and Independent Contributor of Peripheral Artery Disease.

Medial Arterial Calcification: A Significant and Independent Contributor of Peripheral Artery Disease.
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DOI:
10.1161/atvbaha.121.316252
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发表时间:
2022-03
期刊:
Arteriosclerosis, thrombosis, and vascular biology
影响因子:
--
通讯作者:
St Hilaire C
St Hilaire C
中科院分区:
其他
文献类型:
--
作者:
St Hilaire C

文献摘要

相似文献

据估计,全世界有超过2亿人患有外周动脉疾病(PAD)。虽然术语“外周”可以指血管系统的任何外部分支,但本综述的重点是下肢动脉。PAD的最初后遗症通常包括运动引起的臀部和腿部抽筋疼痛或脱发和下肢皮肤变薄。PAD进展迅速,有时会导致无法愈合的溃疡和严重的肢体缺血,对活动能力和肌肉张力产生不利影响;急性肢体缺血是一种医疗紧急情况。PAD会导致巨大的疼痛和截肢的高风险,并最终使患者面临重大不良心血管事件的重大风险。这对患者的生活质量以及产生的医疗成本的负面影响是巨大的。动脉粥样硬化斑块是PAD的原因之一,然而,新出现的临床数据显示,非动脉粥样硬化性中层动脉钙化(MAC)是同样明显的因素。这篇ATVB in Focus文章将介绍有关MAC在PAD中的患病率和影响的最新临床研究结果,讨论导致下肢MAC的已知途径,并强调限制我们理解MAC发病机制的知识和工具方面的差距。
Over 200 million individuals world-wide are estimated to have Peripheral Artery Disease (PAD). While the term “peripheral” can refer to any outer branch of the vasculature, the focus of this review is on lower extremity arteries. The initial sequelae of PAD often include movement-induced cramping pain in the hips and legs or loss of hair and thinning of the skin on the lower limbs. PAD progresses, sometimes rapidly, to cause non-healing ulcers and critical limb ischemia which adversely affects mobility and muscle tone; acute limb ischemia is a medical emergency. PAD causes great pain and a high risk of amputation and ultimately puts patients at significant risk for major adverse cardiovascular events. The negative impact on patients’ quality of life, as well as the medical costs incurred, are huge. Atherosclerotic plaques are one cause of PAD, however emerging clinical data now shows that non-atherosclerotic medial arterial calcification (MAC) is an equal and distinct contributor. This ATVB In Focus article will present the recent clinical findings on the prevalence and impact of MAC in PAD, discuss the known pathways that contribute specifically to MAC in the lower extremity, and highlight gaps in knowledge and tools that limit our understanding of MAC pathogenesis.