scholarly journals Management of High-Risk Atherosclerotic Patients by Statins May Be Supported by Logistic Model of Intima-Media Thickening

2021 ◽  
Vol 10 (13) ◽  
pp. 2876
Author(s):  
Dorota Formanowicz ◽  
Jacek B. Krawczyk ◽  
Bartłomiej Perek ◽  
Dawid Lipski ◽  
Andrzej Tykarski
Keyword(s):  
Logistic Model ◽  
Intima Media Thickness ◽  
Statin Treatment ◽  
Logistic Growth ◽  
Theoretic Model ◽  
Subsequent Paper ◽  
Logistic Curve ◽  
Atherosclerosis Progression ◽  
Media Thickness ◽  
Decision Making Processes

While the use of statins in treating patients with atherosclerosis is an undisputed success, the questions regarding an optimal starting time for treatment and its strength remain open. We proposed in our earlier paper published in Int. J. Mol. Sci. (2019, 20) that the growth of intima-media thickness of the carotid artery follows an S-shape (i.e., logistic) curve. In our subsequent paper in PLoS ONE (2020, 15), we incorporated this feature into a logistic control-theoretic model of atherosclerosis progression and showed that some combinations of patient age and intima-media thickness are better suited than others to start treatment. In this study, we perform a new and comprehensive calibration of our logistic model using a recent clinical database. This allows us to propose a procedure for inferring an optimal age to start statin treatment for a particular group of patients. We argue that a decrease in the slope of the IMT logistic growth curve, induced by statin treatment, is most efficient where the curve is at its steepest, whereby the efficiency means lowering the future IMT levels. Using the procedure on an aggregate group of severely sick men, 38 years of age is observed to correlate with the steepest point of the logistic curve, and, thus, it is the preferred time to start statin treatment. We believe that detecting the logistic curve’s steepest fragment and commencing statin administration on that fragment are courses of action that agree with clinician intuition and may support decision-making processes.

scholarly journals High-Sensitivity C-Reactive Protein and Carotid Intima Media Thickness as Markers of Subclinical Inflammation and Atherosclerosis in Pediatric Patients with Hypercholesterolemia

Molecules ◽  
2020 ◽  
Vol 25 (21) ◽  
pp. 5118
Author(s):  
Lana Blinc ◽  
Matej Mlinaric ◽  
Tadej Battelino ◽  
Urh Groselj
Keyword(s):  
Subclinical Atherosclerosis ◽  
Elevated Serum ◽  
High Sensitivity ◽  
Intima Media Thickness ◽  
Carotid Intima Media Thickness ◽  
Low Grade ◽  
C Reactive Protein ◽  
Atherosclerosis Progression ◽  
Reactive Protein ◽  
Media Thickness

Hypercholesterolemia is a major cause of atherosclerosis development and premature cardiovascular disease (CVD). It leads to inflammation, which further accelerates atherosclerosis progression. Familial hypercholesterolemia (FH) is an autosomal dominant disorder characterized by elevated serum LDL-c from birth, due to a disease-causing variant in one of the causative genes (LDLR, APOB, PCSK9). In polygenic hypercholesterolemia (PH), the disease-causing genetic variant is absent; it is likely the cumulative result of multiple single nucleotide polymorphisms in LDL metabolism-related genes and other factors, such as lifestyle and environment. In high risk groups, such as patients with FH, an effective primary prevention of CVD must begin in childhood. High-sensitivity C-reactive protein (hsCRP) and carotid intima media thickness (cIMT) are two potential minimally invasive correlates of inflammation and subclinical atherosclerosis progression. hsCRP and cIMT have been shown to be significantly increased in patients with FH and PH relative to healthy controls, with some studies yielding conflicting results. In this review, we aim to summarize current knowledge and recent findings regarding the applicability of hsCRP and cIMT as markers of low-grade inflammation and subclinical atherosclerosis, focusing especially on children and adolescents with hypercholesterolemia.

Air Pollution and Atherosclerosis: Progression of (Research Using) Intima-Media Thickness (IMT)

Epidemiology ◽  
2006 ◽  
Vol 17 (Suppl) ◽  
pp. S241
Author(s):  
N Künzle ◽  
M Jerrett ◽  
K Watson Nelson ◽  
W J Mack ◽  
D Moore ◽  
...  
Keyword(s):  
Air Pollution ◽  
Intima Media Thickness ◽  
Atherosclerosis Progression ◽  
Media Thickness

Abstract 194: Rosuvastatin Reduces Progression of Carotid Atherosclerosis within 12 Months of Treatment: The METEOR Trial

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Michiel L Bots ◽  
Joel S Raichlen ◽  
Gregory W Evans ◽  
Mike K Palmer ◽  
Daniel H O’Leary ◽  
...  
Keyword(s):  
Carotid Artery ◽  
Controlled Trial ◽  
Intima Media Thickness ◽  
Carotid Intima Media Thickness ◽  
Rate Of Change ◽  
Double Blind ◽  
Atherosclerosis Progression ◽  
Media Thickness ◽  
The Difference ◽  
The Individual

Background: In several statin trials, vascular event rates for treatment groups begin to separate 1 year after commencement of treatment. For atherosclerosis progression, the temporal sequence of the effect has not been defined. We sought to determine the earliest time point at which significant differences in atherosclerosis progression rates were detectable after initiation of statin therapy using data from the METEOR trial (Measuring Effects on intima media Thickness: an Evaluation Of Rosuvastatin). Methods: METEOR was a double-blind, randomized, placebo-controlled trial among 984 low risk subjects, which studied the effect of LDL lowering with 40 mg rosuvastatin on the rate of change in carotid intima media thickness (CIMT) over time. Ultrasound assessments were made at 12 carotid artery sites at baseline and every 6 months up to two years. In these analyses, the data were cut at 6 months, 1 year, and 18 months, and compared with analysis of all data at 2 years, using the same statistical method. Results: The difference in rate of maximum CIMT progression for all carotid artery sites (primary endpoint - near and far walls of the left and right common carotid artery [CCA], carotid bulb and internal carotid artery) between the rosuvastatin and placebo groups was apparent 6 months after baseline (0.0023 mm/yr and 0.0106 mm/yr, respectively p =0.36). After 12 months CIMT progression rates were significantly different between groups: 0.0032 mm/yr and 0.0133 mm/yr (p=0.049). This divergence grew with further follow-up: − 0.0009 mm/yr and 0.0131 mm/yr after 18 months (p<0.0001), and − 0.0014 mm/yr and 0.0131 mm/yr after 24 months of treatment (p<<178>0.0001). For the individual carotid artery segments, significant differences were seen at 12 months for the mean CIMT of the CCA, and at 18 months for the maximum CIMT of the bulb and the CCA. Conclusion: Aggressive LDL lowering with rosuvastatin exerts its beneficial effect on atherosclerosis during the first year of treatment, which parallels the timing of event rate reduction seen in clinical trials. These findings suggest that, in trials examining the effects of treatment on CIMT progression, a duration of 12 months may be adequate, given sufficient sample size, high precision of measurements, and treatment effect.

Abstract 17808: Fasting Levels of High-sensitive Growth Hormone in Males are Associated to Carotid Intima Media Thickness and are Reduced by Treatment With Fluvastatin

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Erik Hallengren ◽  
Peter Almgren ◽  
Maria Rosvall ◽  
Gerd Östling ◽  
Margaretha Persson ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Growth Hormone ◽  
Controlled Trial ◽  
Intima Media Thickness ◽  
Carotid Intima Media Thickness ◽  
Statin Treatment ◽  
Linear Regression Models ◽  
Double Blind ◽  
Cross Sectional ◽  
Media Thickness

Introduction: Growth hormone (GH) has been linked to cardiovascular disease and lipid metabolism but the exact mechanisms of this association are still unclear. Objectives: We here test if GH is cross-sectionally associated to carotid intima media thickness (IMT) and whether treatment with fluvastatin have any effects on the fasting level of GH in a randomized controlled trial of carotid IMT progression. Methods: We examined the association between GH and IMT in 4425 individuals (aged 46-68 years) included in the baseline examination (1991-1994) of the Malmö Diet and Cancer cardiovascular cohort (MDC-CC). From that cohort we then studied 472 individuals (aged 50-70 years) who also participated (1994-1999) in the β-Blocker Cholesterol-Lowering Asymptomatic Plaque Study (BCAPS), a randomized, double blind, placebo-controlled, single-center clinical trial. Using multivariate linear regression models we related the change in GH-levels at 12 months compared to baseline to treatment with fluvastatin. Results: In MDC-CC fasting values of GH exhibited a positive cross-sectional relation to the IMT at the carotid bifurcation after adjustment for traditional cardiovascular risk factors (p=0.002). In a gender-stratified analysis the association were positive and significant for males (p=0.005), but not for females (p=0.09). In males in BCAPS treated with fluvastatin there tended to be a greater reduction of GH after 12 months when compared to subjects not receiving fluvastatin (p=0.05) (Table). Fasting levels of GH did not interact with the different treatment regimes’ effect on the IMT. Conclusions: We here demonstrate that higher fasting levels of GH are associated to thicker IMT in the carotid bulb and that statin treatment may reduce fasting levels of GH in males. Our results are in line with previous results with GH being associated to cardiovascular disease. The effects of statin treatment on GH are small and need to be confirmed in a larger trial.

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