scholarly journals Predicting Locations of High-Risk Plaques in Coronary Arteries in Patients Receiving Statin Therapy

2018 ◽  
Vol 37 (1) ◽  
pp. 151-161 ◽  
Author(s):  
Ling Zhang ◽  
Andreas Wahle ◽  
Zhi Chen ◽  
John J. Lopez ◽  
Tomas Kovarnik ◽  
...  
Author(s):  
Kyeong-Hyeon Chun ◽  
Jung Mi Park ◽  
Chan Joo Lee ◽  
Jaewon Oh ◽  
Sungha Park ◽  
...  

2021 ◽  
Vol 10 (7) ◽  
pp. 1480
Author(s):  
Keishi Ichikawa ◽  
Toru Miyoshi ◽  
Kazuhiro Osawa ◽  
Takashi Miki ◽  
Hiroshi Ito

Objective: To evaluate the association of serum malondialdehyde low-density lipoprotein (MDA-LDL), an oxidatively modified LDL, with the prevalence of high-risk plaques (HRP) determined with coronary computed tomography angiography (CTA) in statin-treated patients. Methods: This study was a single-center retrospective cohort comprising 268 patients (mean age 67 years, 58% men) with statin therapy and who underwent coronary CTA for suspected stable coronary artery disease. Patients were classified into two groups according to median MDA-LDL level or median LDL-C level. Coronary CTA-verified HRP was defined when two or more characteristics, including positive remodeling, low-density plaques, and spotty calcification, were present. Results: Patients with HRP had higher MDA-LDL (p = 0.011), but not LDL-C (p = 0.867) than those without HRP. High MDA-LDL was independently associated with HRP (odds ratio 1.883, 95% confidential interval 1.082–3.279) after adjustment for traditional risk factors. Regarding incremental value of MDA-LDL for predicting CTA-verified HRP, addition of serum MDA-LDL levels to the baseline model significantly increased global chi-square score from 26.1 to 32.8 (p = 0.010). Conclusions: A high serum MDA-LDL level is an independent predictor of CTA-verified HRP, which can lead to cardiovascular events in statin-treated patients.


2009 ◽  
Vol 9 (5) ◽  
pp. 299-308 ◽  
Author(s):  
Richard H. Chapman ◽  
Allison A. Petrilla ◽  
Lance Berman ◽  
Joshua S. Benner ◽  
Simon S.K. Tang

JAMA ◽  
2004 ◽  
Vol 292 (3) ◽  
pp. 377 ◽  
Author(s):  
Antonio M. Gotto, Jr

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Yiannis S Chatzizisis ◽  
Konstantinos Toutouzas ◽  
Andreas A Giannopoulos ◽  
Maria Riga ◽  
Antonios P Antoniadis ◽  
...  

Background: High risk plaque accounts for the majority of acute coronary events. Low endothelial shear stress (ESS) is a key factor of the natural history of atherosclerosis. The role of ESS in high risk plaque formation is not well studied in man. Hypothesis: To explore the association of low ESS with high risk plaque and to identify the ESS milieu and vascular remodeling response in high risk vs. non high risk plaque. Methods: 35 coronary arteries from 30 patients were 3D reconstructed with fusion of coronary angiography and optical coherence tomography (Fig A-D) . ESS was calculated in the 3D reconstructed arteries using computational fluid dynamics (Fig E) and classified into low, moderate and high in 3 mm long segments. In each segment: i) fibroatheromas were classified into high risk and non high risk based on fibrous cap thickness and lipid pool size ii) vascular remodeling was classified into constrictive, compensatory and expansive. Results: Fibroatheromas in low ESS segments had significantly thinner fibrous cap compared to high ESS segments (89±84 vs.138±83 μm, p<0.05). Lipid pool size was comparable across all ESS categories. The majority of low ESS segments co-localized with high risk plaques (29 vs. 9%, p<0.05), whereas the majority of high ESS co-localized with non high risk plaques (24 vs. 9%, p<0.05, Fig F ). Compensatory and expansive remodeling was the predominant remodeling response in low ESS segments containing high risk plaques. In non-stenotic fibroatheromas (expansive or compensatory remodeling) low ESS was predominantly associated with high risk plaques (29 vs. 3%, p<0.05) whereas high ESS was associated with non high risk plaques (Fig F) . Conclusions: Novel combined anatomic and functional imaging with 3D OCT showed that low ESS and non-constrictive remodeling are associated with high risk plaque in man. Further studies are needed to assess the role of ESS and vascular remodeling in high risk plaque rupture and precipitation of clinical outcomes.


Medicina ◽  
2008 ◽  
Vol 44 (5) ◽  
pp. 407 ◽  
Author(s):  
Sigita Kėvelaitienė ◽  
Rimvydas Šlapikas

During the last decade, the evidence of beneficial effects of cholesterol lowering in patients with coronary heart disease has been proven in many clinical trials. The National Cholesterol Education Program (NCEP) released 2004 update to the Adult Treatment Panel III (ATP III) guidelines. The new guidelines of European Society of Cardiology announced in 2007 support more intensive LDL-C lowering in patients at high risk of cardiovascular diseases. For patients at the highest risk of cardiovascular diseases (diabetic patients with coronary heart disease), the recommended LDL-C goal is <1.8 mmol/L. In very high-, high-, and moderately high-risk patients, statin therapy should be considered with a treatment targeting an LDL-C reduction of 30– 40%. Clinical studies have shown that statin therapy alone is not always effective, especially in patients with primary hypercholesterolemia. Furthermore, high doses of statins can increase the possibility of adverse events. The combination of statins with intestinal cholesterol absorption inhibitors is more effective than statin monotherapy in LDL-C lowering and is well tolerated.


2016 ◽  
Vol 157 (19) ◽  
pp. 746-752 ◽  
Author(s):  
László Márk ◽  
Győző Dani

The incidence and the public health importance of diabetes mellitus are growing continuously. Despite the improvement observed in the latest years, the leading cause of morbidity and mortality of diabetics are cardiovascular diseases. The diagnosis of diabetes mellitus constitutes such a high risk as the known presence of vascular disease. Diabetic dyslipidaemia is characterised by high fasting and postprandial triglyceride levels, low HDL level, and slightly elevated LDL-cholesterol with domination of atherogenic small dense LDL. These are not independent components of the atherogenic dyslipidaemia, but are closely linked to each other. Beside the known harmful effects of low HDL and small dense LDL, recent findings confirmed the atherogenicity of the triglyceride-rich lipoproteins and their remnants. It has been shown that the key of this process is the overproduction and delayed clearance of triglyceride-rich lipoproteins in the liver. In this metabolism the lipoprotein lipase has a determining role; its function is accelerated by ApoA5 and attenuated by ApoC3. The null mutations of the ApoC3 results in a reduced risk of myocardial infarction, the loss-of-function mutation of ApoA5 was associated with a 60% elevation of triglyceride level and 2.2-times increased risk of myocardial infarction. In case of diabetes mellitus, insulin resistance, obesity, metabolic syndrome and chronic kidney disease the non-HDL-cholesterol is a better marker of the risk than the LDL-cholesterol. Its value can be calculated by subtraction of HDL-cholesterol from total cholesterol. Target values of non-HDL-cholesterol can be obtained by adding 0.8 mmol/L to the LDL-cholesterol targets (this means 3.3 mmol/L in high, and 2.6 mmol/L in very high risk patients). The drugs of first choice in the treatment of diabetic dyslipidaemia are statins. Nevertheless, it is known that even if statin therapy is optimal (treated to target), a considerable residual (lipid) risk remains. For its reduction treatment of low HDL-cholesterol and high triglyceride levels is obvious by the administration of fibrates. In addition to statin therapy, fenofibrate can be recommended. Orv. Hetil., 2016, 157(19), 746–752.


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