Controlling the thickness of the atherosclerotic plaque by statin medication

被引:10
作者
Formanowicz, Dorota [1 ]
Krawczyk, Jacek B. [2 ]
机构
[1] Poznan Univ Med Sci, Dept Clin Biochem & Lab Med, Poznan, Poland
[2] Univ Sydney, Sch Math & Stat, Sydney, NSW, Australia
来源
PLOS ONE | 2020年 / 15卷 / 10期
关键词
INTIMA-MEDIA THICKNESS; CORONARY-HEART-DISEASE; C-REACTIVE PROTEIN; DENSITY-LIPOPROTEIN CHOLESTEROL; CARDIOVASCULAR RISK-FACTORS; CHRONIC KIDNEY-DISEASE; ALL-CAUSE MORTALITY; MATHEMATICAL-MODEL; CAROTID-ARTERY; MYOCARDIAL-INFARCTION;
D O I
10.1371/journal.pone.0239953
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
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 theviability 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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页数:20
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