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Triglyceride to HDL-cholesterol ratio as an independent risk factor for the poor development of coronary collateral circulation in elderly patients with ST-segment elevation myocardial infarction and acute total occlusion.
Liu, GY, Meng, XX, Zhang, Z
Medicine. 2018;(39):e12587
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Abstract
To determine the prognostic role of triglyceride (TG) to high-density lipoprotein cholesterol (HDL) ratio for poorly developed coronary collateral circulation (CCC) in elderly patients with ST-segment elevation myocardial infarction (STEMI) and acute total occlusion (ATO).As a retrospective case-control study, elderly patients (age ≥60 years) with both STEMI and ATO (n = 346) were classified as having either poorly- or well-developed CCC (Rentrop grades 0-1 and 2-3, respectively). The ratio of TG/HDL was calculated according to the detected levels of TG and HDL. The difference of TG/HDL ratio in those 2 groups was compared by Student t test, and multivariate logistic regression analysis indicating occurrence of poorly developed CCC was performed. Receiver operator characteristic curve (ROC) analysis of TG/HDL ratio which determine the optimal cut-off value of TG/HDL ratio was applied.The TG/HDL ratio was significantly higher in patients with poorly developed CCC than in those with well-developed CCC (2.88 ± 2.52 vs 1.81 ± 1.18, P < .001). In multivariate logistic regression analysis, higher TG/HDL ratio (OR 1.789, 95% CI 1 . 346-2.378, P < .001) and the presence of left circumflex branch of coronary artery (LCX) occlusion (OR6.235, 95% CI 2.220-17.510, P = .001) were emerged as independent positive predictors of poor development of CCC, whereas presence of right coronary artery (RCA) occlusion (OR 0.474, 95% CI 0.265-0.850, P = .002) and onset time (OR 0.693, 95% CI 0.620-0.775, P < .001) were found as negative indicators. The optimal cut-off value of TG/HDL ratio was found as 1.58 in ROC analysis, which yielded an area under the curve value of 0.716 (95% CI 0.654-0.778, P < .001) and demonstrated a sensitivity of 80.9% and a specificity of 59.3% for prediction of poorly developed CCC.TG/HDL ratio is an independent risk factor for predicting poor development of CCC in elderly patients with STEMI and ATO.
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A high legume low glycemic index diet improves serum lipid profiles in men.
Zhang, Z, Lanza, E, Kris-Etherton, PM, Colburn, NH, Bagshaw, D, Rovine, MJ, Ulbrecht, JS, Bobe, G, Chapkin, RS, Hartman, TJ
Lipids. 2010;(9):765-75
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Abstract
Clinical studies have shown that fiber consumption facilitates weight loss and improves lipid profiles; however, the beneficial effects of high fermentable fiber low glycemic index (GI) diets under conditions of weight maintenance are unclear. In the Legume Inflammation Feeding Experiment, a randomized controlled cross-over feeding study, 64 middle-aged men who had undergone colonoscopies within the previous 2 years received both a healthy American (HA) diet (no legume consumption, fiber consumption = 9 g/1,000 kcal, and GI = 69) and a legume enriched (1.5 servings/1,000 kcal), high fiber (21 g/1,000 kcal), low GI (GI = 38) diet (LG) in random order. Diets were isocaloric and controlled for macronutrients including saturated fat; they were consumed each for 4 weeks with a 2-4 week break separating dietary treatments. Compared to the HA diet, the LG diet led to greater declines in both fasting serum total cholesterol (TC) and low density lipoprotein cholesterol (LDL-C) (P < 0.001 and P < 0.01, respectively). Insulin-resistant (IR) subjects had greater reductions in high density lipoprotein cholesterol (HDL-C; P < 0.01), and triglycerides (TAG)/HDL-C (P = 0.02) after the LG diet, compared to the HA diet. Insulin-sensitive (IS) subjects had greater reductions in TC (P < 0.001), LDL-C (P < 0.01), TC/HDL-C (P < 0.01), and LDL-C/HDL-C (P = 0.02) after the LG diet, compared to the HA diet. In conclusion, a high legume, high fiber, low GI diet improves serum lipid profiles in men, compared to a healthy American diet. However, IR individuals do not achieve the full benefits of the same diet on cardiovascular disease (CVD) lipid risk factors.