Effects of a healthy diet enriched or not with pecan nuts or extra-virgin olive oil on the lipid profile of patients with stable coronary artery disease: a randomised clinical trial.

BACKGROUND: The present study aimed to assess the effect of a healthy diet, enriched or not with pecan nuts or extra-virgin olive oil, on the lipid profile of patients with stable coronary artery disease (CAD). METHODS: This was a randomised clinical trial conducted for 12 weeks with patients aged between 40 and 80 years with stable CAD for more than 60 days. Individuals were randomised into groups [control group (CG) with 67 patients, pecan nut group (PNG) with 68 patients and olive oil group (OOG) with 69 patients]. The CG was prescribed a healthy diet according to the nutritional guidelines; the PNG was prescribed the same healthy diet plus 30 g day-1 of pecan nuts; and the OOG was prescribed a healthy diet plus 30 mL day-1 of extra-virgin olive oil. RESULTS: In total, 204 subjects were submitted to an intention-to-treat analysis. After adjustment for baseline values and type of statin used, there was no difference regarding low-density lipoprotein (LDL)-cholesterol (primary outcome), high-density lipoprotein (HDL)-cholesterol, LDL-cholesterol/HDL-cholesterol ratio and HDL-cholesterol/triglycerides ratio according to groups. However, the PNG exhibited a significant reduction in non-HDL-cholesterol levels [PNG: 114.9 (31) mg dL-1 ; CG: 127 (33.6) mg dL-1 ; OOG: 126.6 (37.4) mg dL-1 ; P = 0.033] and in the total cholesterol/HDL-cholesterol ratio [PNG: 3.7 (0.7); CG: 4.0 (0.8); OOG: 4.0 (0.8); P = 0.044] compared to the CG and OOG. CONCLUSIONS: Supplementing a healthy diet with 30 g day-1 of pecan nuts for 12 weeks did not improve LDL-cholesterol levels but may improve other lipid profile markers in patients with stable CAD.

Postprandial metabolism and inflammatory markers in overweight adolescents.

Lifestyle changes have an impact on lipid metabolism. The overload of circulating lipids may lead to endothelial dysfunction, oxidative stress and exaggerated inflammatory response, which may be further aggravated in the presence of overweight. This study aims to describe the postprandial metabolism and inflammatory response in overweight and normal-weight adolescents. Sixty-two adolescents aged 11-18 years were divided into two groups: overweight (OW; n=38) and normal weight (NW; n=24). Total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), triglycerides (TG), glucose, insulin, high-sensitivity C-reactive protein (hs-CRP), fibrinogen and leukocytes were collected for fasting and 4 and 6 h after a oral fat tolerance test (OFTT) consisting of a high-fat meal with 1.000 Kcal, 27.4% carbohydrates, 14.7% protein and 57.8% lipids (30.4% saturated, 32.7% monounsaturated, 26.5% polyunsaturated fatty acids and 288 mg TC). Data were analyzed with repeated measures ANOVA, multiple linear regression, and Pearson, Spearman and partial correlations. OW adolescents showed significantly higher fasting values of TC (P=0.036), LDL-C (P=0.010), fibrinogen (P=0.036) and hs-CRP (P=0.004). All variables, except for glucose, increased in response to OFTT, but there were no interactions between group and time. body mass index z-score was positively correlated to LDL-C, TG, fibrinogen and hs-CRP, and inversely correlated to HDL-C. In conclusion, adolescents with OW showed higher TC, LDL-C and inflammatory markers levels than NW adolescents. These findings have clinical implications for prevention of chronic diseases, as we spend most of our days in a postprandial state.

The effect of simvastatin in penile erection: a randomized, double-blind, placebo-controlled clinical trial (Simvastatin treatment for erectile dysfunction-STED TRIAL).

The aim of the study is to evaluate the effect of simvastatin in erectile dysfunction (ED) secondary to endothelial dysfunction. This study is a double-blind, randomized, placebo-controlled, clinical trial in patients with ED and endothelial dysfunction. Patients were randomized to receive 20 mg simvastatin (n = 21) or placebo (n = 20) daily for 6 months and subsequently 10 mg of vardenafil on demand for 4 weeks. Serum cholesterol, hormone profile, ultrasensitive C-reactive protein, the International Index of Erectile Dysfunction (IIEF) and the ED Index of Treatment Satisfaction were evaluated. There was a significant reduction in serum cholesterol in the treatment group. The hormonal profile remained unaltered. There was no difference in the IIEF between the groups at follow-up, although, at the beginning, 26% of the patients of both groups presented with mild ED and 74% with moderate-to-severe ED; at the end of the 7th month, all patients from the simvastatin group progressed to mild ED, compared with only 83% in the placebo group. There was no statistically significant difference in penile erection after intake of simvastatin or placebo. This study does not support the use of simvastatin as erectogenic medication. Further studies are necessary to verify if simvastatin has any beneficial effect on ED.

C-reactive protein in acute coronary syndrome: association with 3-year outcomes

Inflammatory markers have been associated with clinical outcome in patients with acute coronary syndrome (ACS). The present study evaluated the role of high-sensitivity C-reactive protein (CRP) measurements as a predictor of late cardiovascular outcomes after ACS. One hundred and ninety-nine ACS patients in a Coronary Care Unit from March to November 2002 were included and were reassessed clinically after ~3 years. Clinical variables and CRP levels were evaluated as predictors of major cardiovascular events (MACE, defined as the occurrence of cardiac death, ischemic stroke or myocardial infarction) and mortality. Statistical analyses included Cox multivariable analysis and survival curves (Kaplan-Meier). Of the 199 patients, 11 died within 1 month (5.5 percent). Of the 188 remaining patients, 22 died after a mean follow-up of 2.9 ± 0.5 years. Baseline CRP levels for patients with MACE (N = 57) were significantly higher than those of patients with no events (median = 0.67 mg/L; 25th-75th percentiles = 0.32 and 1.99 mg/L vs median = 0.45 mg/L; 25th-75th percentiles = 0.24 and 0.83 mg/L; P < 0.001). Patients with CRP levels >3 mg/L had a significantly lower survival than the other two groups (1-3 and <1 mg/L; P = 0.001, log-rank test). The odds ratio for MACE was 7.41 (2.03-27.09) for patients with CRP >3 mg/L compared with those with CRP <1 mg/L. For death by any cause, the hazard ratio was 4.58 (1.93-10.86). High CRP levels predicted worse long-term outcomes (MACE and death by any cause) in patients with ACS.

C-reactive protein in acute coronary syndrome: association with 3-year outcomes.

Inflammatory markers have been associated with clinical outcome in patients with acute coronary syndrome (ACS). The present study evaluated the role of high-sensitivity C-reactive protein (CRP) measurements as a predictor of late cardiovascular outcomes after ACS. One hundred and ninety-nine ACS patients in a Coronary Care Unit from March to November 2002 were included and were reassessed clinically after approximately 3 years. Clinical variables and CRP levels were evaluated as predictors of major cardiovascular events (MACE, defined as the occurrence of cardiac death, ischemic stroke or myocardial infarction) and mortality. Statistical analyses included Cox multivariable analysis and survival curves (Kaplan-Meier). Of the 199 patients, 11 died within 1 month (5.5%). Of the 188 remaining patients, 22 died after a mean follow-up of 2.9 +/- 0.5 years. Baseline CRP levels for patients with MACE (N = 57) were significantly higher than those of patients with no events (median = 0.67 mg/L; 25th-75th percentiles = 0.32 and 1.99 mg/L vs median = 0.45 mg/L; 25th-75th percentiles = 0.24 and 0.83 mg/L; P < 0.001). Patients with CRP levels >3 mg/L had a significantly lower survival than the other two groups (1-3 and <1 mg/L; P = 0.001, log-rank test). The odds ratio for MACE was 7.41 (2.03-27.09) for patients with CRP >3 mg/L compared with those with CRP <1 mg/L. For death by any cause, the hazard ratio was 4.58 (1.93-10.86). High CRP levels predicted worse long-term outcomes (MACE and death by any cause) in patients with ACS.

Emerging risk factors and early atherosclerosis indices in subjects with impaired glucose tolerance.

AIM: To evaluate the response to an oral lipid overload, inflammatory markers and carotid intima-media thickness in subjects with impaired glucose tolerance. METHODS: 54 subjects, both sexes, 58 y-old average were submitted to 1) Clinical evaluation 2) Glucose tolerance test with 75 g glucose; classified as normal (2 h plasma glucose<140 mg/dl, n=37) or IGT (2 h G 140-200 mg/dl, n=17), 3) 12 h fasting sample (plasma glucose, lipids, C-reactive protein, fibrinogen and HOMA-IR calculation); 4 and 6 h after the oral lipid overload (1000 kcal, lipids 65 g) glycemia, fibrinogen and triglycerides were reevaluated. Intima-media thickness was calculated by the average of 6 measurements (3 highest of each carotid) evaluated by ultrasonography (7 MHZ transducer). RESULTS: The IGT group had higher (P<0.001) fasting plasma glucose (89.4 +/- 13 vs 104.4 +/- 8 mg/dl), HOMA-IR (1.69 +/- 1.2 vs 2.93 +/- 2.2) and waist (91 +/- 14 vs 101 +/- 9 cm), similar fasting lipids, intima-media thickness (P=0.58) and post-oral lipid overload triglycerides (P=0.74), but higher fibrinogen (284.3 +/- 6 and 305 +/- 10 mg/dl, P=0.05) and C-reactive protein (2.11 +/- 0.33 and 4.19 +/- 0.65 mg/l, P=0.003). C-reactive protein was positively correlated with HOMA-IR (r=0.45, P=0.001), fasting plasma glucose (r=0.43, P=0.002) and waist (r=0.45, P=0.0006), but not with postprandial lipids. CONCLUSION: A higher C-reactive protein in IGT, and its positive correlation with insulin resistance indices, but not with postprandial lipaemia, suggests that the clustering of these factors, characteristic of the metabolic syndrome, occurs earlier than postprandial lipid abnormalities.