Prediction of angiographic change in native human coronary arteries and aortocoronary bypass grafts. Lipid and nonlipid factors.

Blankenhorn, David H.; Alaupovic, Petar; Wickham, Emily; Chin, Hyunsook; Azen, Stanley P.

doi:10.1161/01.cir.81.2.470

Cited by 271 publications

(148 citation statements)

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“…29 However, influence of apoCIII and apoE distribution between lipoproteins on cardiovascular risk was suggested by other studies. ApoCIII associated with HDL (CIII LpnonB) was negatively correlated with lesion progression in CLAS study 30 whereas apoCIII associated with apoB containing lipoprotein (CIII LpB) was positively correlated with lesion progression in MARS study. 31 Studies on animal models, including transgenic 32 -35 or knock-out mice 36 -40 and familial studies 41,42 suggest that apoE can prevent coronary heart disease.…”

Section: Introductionmentioning

confidence: 90%

Negative and independent influence of apolipoprotein E on C-reactive protein (CRP) concentration in obese adults. Potential anti-inflammatory role of apoE in vivo

et al. 2001

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BACKGROUND: Obesity is frequently associated with an increase in the early inflammation marker C-reactive protein (CRP), insulin resistance and changes in lipoprotein metabolism. Increased CRP is known as an independent cardiovascular risk factor. Since the apolipoproteins (apo) E and CIII components of HDL are associated with reduced cardiovascular risk and since apoE has in vitro anti-inflammatory effect, we have investigated the relationships between apoE, apoCIII (in apoB and non apoB containing lipoproteins) and CRP in obese adults. METHODS:The following parameters from 34 healthy obese fasting women (age 22 -64 y, body mass index (BMI) 28 -68 kg=m 2 ) were measured: (1) ApoE and apoCIII, in total plasma, in apoB-(E LpB, CIII LpB) and non-apoB-containing lipoproteins (E LpnonB, CIII LpnonB); (2) CRP and cytokine secreted by adipose tissue (TNF-a and its soluble receptor TNFR2); (3) triglyceride, HDL-cholesterol, systolic blood pressure, diastolic blood pressure, waist and hip circumferences, insulin, glucose. HOMA, a marker of insulin sensitivity, and the ratio E=CIII in LpB and LpnonB were calculated. RESULTS: CRP was positively correlated with BMI (P < 0.05), waist circumference (WC, P < 0.05), triglyceride (P < 0.05) and negatively correlated with apoE (P < 0.01) and E LpnonB (P < 0.05). Two multiple regression models including parameters related to CRP with a P < 0.25 were run stepwise to assess their independent contribution to CRP concentration. In the first model (including BMI, WC, HOMA, insulin, triglyceride, apoE, E LpnonB), apoE was the best predictor of CRP (P ¼ 0.01) together with triglyceride (P ¼ 0.02) and BMI (P ¼ 0.08). The second model took into account E=CIII LpnonB ratio with the parameters included in the first model. In this second model, E=CIII LpnonB was the best predictor of CRP (P ¼ 0.007), explaining 39% of CRP variance. CONCLUSION: ApoE is strongly correlated with CRP and could have an anti-inflammatory effect in vivo in obese subjects. This correlation could be limited to LpnonB lipoproteins, depending on their apoE and CIII relative content.

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Section: Introductionmentioning

confidence: 90%

Negative and independent influence of apolipoprotein E on C-reactive protein (CRP) concentration in obese adults. Potential anti-inflammatory role of apoE in vivo

et al. 2001

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“…42 This was the first clear indication of the importance of triglyceride-rich lipoproteins in lesion progression, an effect manifested after LDL-C was removed as a risk factor.…”

Section: Early Trialsmentioning

confidence: 97%

“…The results of imaging studies can provide entirely new hypotheses. For example, as observed in CLAS 42 and MARS, 53 when LDL-C is aggressively reduced, triglyceride-rich lipoproteins assume control of atherogenesis. It is important to expand the scope of in vivo lesion staging to take full advantage of the new intervention targets that now seem possible.…”

Section: Hypothesis Testing and Trial Designmentioning

confidence: 99%

George Lyman Duff Memorial Lecture. Arterial imaging and atherosclerosis reversal.

Blankenhorn

Hodis

1994

Arterioscler Thromb

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202

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This review explores evidence for the reversibility of atherosclerosis and augmentation of angiography with noninvasive arterial wall imaging. Meta-analysis from coronary angiographic trials demonstrates that regression and stabilization are 1.5 to 2 times more common in treated than placebo subjects, and progression is reduced by half in treated subjects. Odds ratios for clinical coronary events are significantly reduced with treatment. Lesion improvement occurs more readily in women than men and more so in women receiving concomitant estrogen replacement therapy. Lesions with >50% diameter stenosis (%S) at baseline respond more readily to lipid lowering than those <50%S, whereas reduction in coronary events is related to stabilization of lesions <50%S. Lipoproteins have a differential effect on lesion progression according to lesion size, and triglyceride-rich lipoproteins play an important role in the progression of coronary artery lesions <50%S. Improved therapeutic regimens to alter progression of atherosclerosis may require adjunctive therapy, such as with antioxidants or hormone replacement therapy, in concert with low-density lipoprotein cholesterol reduction to prevent new lesion formation or early lesion progression. Sequential coronary angiographic determination of progression evaluated by both quantitative coronary angiography and global change score, a visual assessment of overall lesion change, predicts clinical coronary events. Only inferences about the state of the arterial wall can be made from angiography, because it delineates only the lumen. Therapy testing and study of atherosclerosis progression can be improved with noninvasive B-mode ultrasonographic imaging of the distal common carotid artery far-wall intima-media thickness (IMT), a reliable measure of early preintrusive atherosclerosis. Measurement of common carotid IMT is useful for the study of coronary artery risk factors and can augment studies of coronary artery intrusive lesions, because it is associated with coronary artery disease. B-mode measurement of common carotid IMT has the potential of serving as a noninvasive surrogate end point for clinical coronary events. Screening for peripheral vessel changes indicative of high risk for coronary artery disease is possible and cost-effective with the noninvasive procedures now available. (Arterioscler Thromb. 1994;14:177-192.) Key Words • atherosclerosis • angiography • ultrasound • regression • clinical trials • intima-media thickness • quantitative computerized angiography • common carotid artery • coronary arteries • meta-analysis E vidence that progression of atherosclerosis can be retarded and atherosclerotic lesions can regress derives from several sources. These sources include studies of arterial lesions obtained at autopsy from starved human populations, animal experimentation, and clinical trials using serial angiography. In the first half of this article, we review serial angiographic evidence for atherosclerotic lesion improvement induced by diverse modes of int...

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“…In the Cholesterol and Recurrent Events (CARE) study, LpB:C-III was strongly and independently associated with the risk of CVD (26). However, the concentration of apoC-III in HDL (HDL apoC-III) was the major predictor of global coronary atherosclerosis progression in subjects treated with niacin-colestipol (Cholesterol Lowering Atherosclerosis Study [CLAS]) (27). The important role of apoC-III in lipoprotein metabolism and as a risk factor for CVD means that treatments aimed at affecting apoC-III levels are of great interest.…”

mentioning

confidence: 99%

Atorvastatin Decreases Apolipoprotein C-III in Apolipoprotein B-Containing Lipoprotein and HDL in Type 2 Diabetes

Dallinga‐Thie

Berk-Planken²,

Bootsma³

et al. 2004

Diabetes Care

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OBJECTIVE -Apolipoprotein (apo)C-III is a constituent of HDL (HDL apoC-III) and of apoB-containing lipoproteins (LpB:C-III). It slows the clearance of triglyceride-rich lipoproteins (TRLs) by inhibition of the activity of the enzyme lipoprotein lipase (LPL) and by interference with lipoprotein binding to cell-surface receptors. Elevated plasma LpB:C-III is an independent risk factor for cardiovascular disease. We studied the effect of atorvastatin on plasma LpB:C-III and HDL apoC-III. RESEARCH DESIGN AND METHODS-We studied the effect of 30 weeks' treatment with 10 and 80 mg atorvastatin on plasma apoC-III levels in a randomized, double-blind, placebo-controlled trial involving 217 patients with type 2 diabetes and fasting plasma triglycerides between 1.5 and 6.0 mmol/l.RESULTS -Baseline levels of total plasma apoC-III, HDL apoC-III, and LpB:C-III were 41.5 Ϯ 10.0, 17.7 Ϯ 5.5, and 23.8 Ϯ 7.7 mg/l, respectively. Plasma apoC-III was strongly correlated with plasma triglycerides (r ϭ 0.74, P Ͻ 0.001). Atorvastatin 10-and 80-mg treatment significantly decreased plasma apoC-III (atorvastatin 10 mg, 21%, and 80 mg, 27%), HDL apoC-III (atorvastatin 10 mg, 22%, and 80 mg, 28%) and LpB:C-III (atorvastatin 10 mg, 23%, and 80 mg, 28%; all P Ͻ 0.001). The decrease in plasma apoC-III, mainly in LpB:C-III, strongly correlated with a decrease in triglycerides (atorvastatin 10 mg, r ϭ 0.70, and 80 mg, r ϭ 0.78; P Ͻ 0.001). Atorvastatin treatment also leads to a reduction in the HDL apoC-III-to-HDL cholesterol and HDL apoC-III-to-apoA-I ratios, indicating a change in the number of apoC-III per HDL particle (atorvastatin 10 mg, Ϫ21%, and 80 mg, Ϫ31%; P Ͻ 0.001).CONCLUSIONS -Atorvastatin treatment resulted in a significant dose-dependent reduction in plasma apoC-III, HDL apoC-III, and LpB:C-III levels in patients with type 2 diabetes. These data indicate a potentially important antiatherogenic effect of statin treatment and may explain (part of) the triglyceride-lowering effect of atorvastatin.

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Prediction of angiographic change in native human coronary arteries and aortocoronary bypass grafts. Lipid and nonlipid factors.

Cited by 271 publications

References 33 publications

Negative and independent influence of apolipoprotein E on C-reactive protein (CRP) concentration in obese adults. Potential anti-inflammatory role of apoE in vivo

Negative and independent influence of apolipoprotein E on C-reactive protein (CRP) concentration in obese adults. Potential anti-inflammatory role of apoE in vivo

George Lyman Duff Memorial Lecture. Arterial imaging and atherosclerosis reversal.

Atorvastatin Decreases Apolipoprotein C-III in Apolipoprotein B-Containing Lipoprotein and HDL in Type 2 Diabetes

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