Statins and the coronary plaque calcium “paradox”: Insights from non-invasive and invasive imaging

Ferencik, Maros; Chatzizisis, Yiannis S.

doi:10.1016/j.atherosclerosis.2015.05.021

Cited by 16 publications

(10 citation statements)

References 18 publications

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“…We can see that the exponential function shown in Figure 6 represents quite faithfully what we know about the statin effect: administering statins diminishes hsCRP first quickly and then slowly. Beneficial role of statins in coronary artery disease has been widely discussed in [64]. Based on clinical experience it seems to us that an initial reduction of IMT, in a course of statin treatment, is large because of shrinkage and fibrosis of the plaque.…”

Section: Plaque Sensitivity To Statins—3-hydroxy-3-methylglutaryl mentioning

confidence: 99%

A Control-Theoretic Model of Atherosclerosis

Formanowicz

Krawczyk

Perek

et al. 2019

IJMS

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We propose a control-theoretic aggregate model of the progression of atherosclerosis plaque, a chronic inflammatory disease of the arterial wall, to study the basic features of this disease. In the model, we exploit the role of inflammation in the disease progression, and use statins—drugs commonly recommended in atherosclerosis—to control this progression. We use a logistic function to allow for constrained growth of plaque. In the model, both the patient’s age and overall health impact the plaque growth and its sensitivity to statins. The model parameters are estimated using original data, or calibrated using published research as well as our own clinical and laboratory studies. We contend that our model helps to gauge the statins’ impact on a patient’s plaque thickness, hence the disease’s progression and cardiovascular risk, without requiring artery scans.

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Section: Plaque Sensitivity To Statins—3-hydroxy-3-methylglutaryl mentioning

confidence: 99%

A Control-Theoretic Model of Atherosclerosis

Formanowicz

Krawczyk

Perek

et al. 2019

IJMS

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“…Rather, calcification serves as an endpoint to inflammation-driven remodeling. Due to their anti-inflammatory action, statins may prevent calcification if given prior to the onset of mineralization, but once the remodeling has begun, statins accelerate the onset of calcification 13 and may also directly stimulate osteogenic responses.…”

Section: Diversity In Calcification Initiatorsmentioning

confidence: 99%

Giving Calcification Its Due: Recognition of a Diverse Disease

Hutcheson

Blaser

Aikawa

2017

Circulation Research

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“…Moreover, several randomized studies involving patients without kidney disease have demonstrated that statins promote coronary atheroma calcification independent of their plaque-regressive effects, and which also did not correlate with a greater risk of CV events [ 36 , 37 ]. Statins change the composition of the coronary atheroma, thicken the fibrous cap, replace the central lipid pool with calcification and fibrosis, decrease plaque volume, and reduce inflammation [ 38 , 39 ]. These shifts in plaque components with increased calcium content stabilize vulnerable plaques, reducing the risk of rupture.…”

Section: Discussionmentioning

confidence: 99%

Does Statin Therapy Reduce the Risks of Mortality and Major Adverse Cardiac and Cerebrovascular Events in Young Adults with End-Stage Renal Disease? Population-Based Cohort Study

Cheng

Yang

et al. 2021

JCM

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Among hemodialysis patients aged more than 40 years old, previous large-scale studies showed statin treatment had no effect on reducing cardiovascular adverse events. However, young-adult-onset end-stage renal disease (ESRD) patients have different physicosocial factors compared to older ESRD patients. The benefit of statins in such a specific group has not been well evaluated. Through the use of Taiwan’s National Health Insurance Research Database (NHIRD), young adult patients aged 20–40 with incident ESRD requiring permanent dialysis between 1 January 2003 and 31 December 2015 were identified. The enrollees were further divided into two groups depending on whether they received statin therapy for more than 90 days (statin group) or never received any statin (nonstatin group) in the first year after initiation of dialysis. Propensity score weighting (PSW) was used to balance the baseline characteristics between the two groups. After PSW, the statin group (n = 771) exhibited a higher rate of major adverse cardiac and cerebrovascular events (MACCEs) (2.65% vs. 1.44%, hazard ratio (HR): 1.87, 95% confidence interval (CI): 1.43–2.45), and acute myocardial infarction (1.51% vs. 0.30%, HR: 5.34, 95% CI: 3.40–8.39) compared to the nonstatin group (n = 1709). The risk of all-cause mortality, cardiovascular (CV) death. and stroke did not significantly differ between the two groups. Similar to older patients, this study demonstrated that statin therapy cannot offer any protective effects in reducing CV outcomes among young adult ESRD patients undergoing dialysis.

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Statins and the coronary plaque calcium “paradox”: Insights from non-invasive and invasive imaging

Cited by 16 publications

References 18 publications

A Control-Theoretic Model of Atherosclerosis

A Control-Theoretic Model of Atherosclerosis

Giving Calcification Its Due: Recognition of a Diverse Disease

Does Statin Therapy Reduce the Risks of Mortality and Major Adverse Cardiac and Cerebrovascular Events in Young Adults with End-Stage Renal Disease? Population-Based Cohort Study

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