Controlling the thickness of the atherosclerotic plaque by statin medication.

Controlling the thickness of the atherosclerotic plaque by statin medication.
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DOI:
10.1371/journal.pone.0239953
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发表时间:
2020
期刊:
影响因子:
3.7
通讯作者:
Krawczyk JB
Krawczyk JB
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Formanowicz D;Krawczyk JB

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动脉粥样硬化是动脉壁的一种慢性炎症性疾病,是一个复杂的过程,其动态受到多种因素的影响。疾病控制包括通过服用他汀类药物来抑制疾病。减缓或停止斑块生长取决于开始他汀类药物治疗的患者年龄以及当时内膜中层 (IMT) 的厚度。在本文中,我们提出了一个数学模型来估计动脉粥样硬化状态组,从中使用他汀类药物可以抑制疾病。我们的模型是控制理论的,用生存理论的说法,估计集是生存核。据我们所知,这种动脉粥样硬化进展建模方法是原创的。我们计算了两个活力核心,每个核心针对不同的他汀类药物治疗剂量。每个内核都由向量[age,IMT]组成,可以通过该向量来抑制疾病。推而广之,该病不能被核心补充所抑制,这主要是由于疾病和患者年龄的增长。内核可视化早期和晚期治疗之间的权衡,这有助于临床医生决定何时开始他汀类药物治疗以及哪种他汀类药物剂量可能足够。
Atherosclerosis, a chronic inflammatory disorder of the arterial wall, is a complex process whose dynamics are affected by multiple factors. The disease control consists of restraining it by administering statins. Slowing down or halting the plaque growth depends on the patient age at which the statin treatment begins and on the thickness of the intima-media (IMT) at that time. In this paper, we propose a mathematical model to estimate the sets of atherosclerosis states, from which the use of statins can restrain the disease. Our model is control-theoretic, and the estimated sets are the viability kernels, in the parlance of viability theory. To our best knowledge, this way of modelling the atherosclerosis progression is original. We compute two viability kernels, each for a different statin-treatment dose. Each kernel is composed of the vector [age, IMT] from which the disease can be restrained. By extension, the disease can’t be restrained from the kernel complements, this being mainly because of the disease and patient-age advancement. The kernels visualise tradeoffs between early and late treatments, which helps the clinician to decide when to start the statin treatment and which statin dose may be sufficient.
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