P. Rubba

Effects of short-term reduction in serum cholesterol with simvastatin in patients with stable angina pectoris and mild to moderate hypercholesterolemia

To evaluate the effects of short-term cholesterol-lowering treatment on myocardial effort ischemia, 22 patients with stable effort ischemia and mild to moderate hypercholesterolemia (low density lipoprotein [LDL] cholesterol 160 to 220 mg/dl) were randomly allocated at baseline (TO) in 2 groups. Group A included 12 patients treated with simvastatin 10 mg bid; group B included 10 patients treated with placebo. All patients underwent a treadmill electrocardiography (ECG) test; total cholesterol, HDL and LDL cholesterol, triglycerides, plasma, and blood viscosity were measured. All tests were repeated after 4 and 12 weeks. For 18 of the same patients (11 taking simvastatin, 7 receiving placebo), forearm strain-gouge plethysmography was performed at baseline and after 4 weeks, both at rest and during reactive hyperemia. At 4 and 12 weeks, group A showed a significant reduction in total cholesterol (p <0.05) and LDL (p <0.05), with unchanged HDL, triglycerides, blood, and plasma viscosity. Effort was unmodified, ST-segment depression at peak effort and ischemic threshold were significantly improved after 4 and 12 weeks (all p <0.05) with unchanged heart rate x systolic blood pressure product. A significant increase in the excess flow response to reactive hyperemia was detected in group A (p <0.03); group B showed no changes in hematochemical and ergometric parameters. These data suggest that cholesterol-lowering treatment is associated with an improvement in myocardial effort ischemia; this might be explained by a more pronounced increase of coronary blood flow and capacity of vasodilation in response to effort.

Carotid artery wall hypertrophy in children with metabolic syndrome

Preclinical vascular changes (increased stiffness and/or wall thickness) have been observed in children with known metabolic risk factors. Aim of the present study was to evaluate different carotid parameters, representative of vascular health, in children with and without metabolic syndrome (MS). We studied 38 children with MS (mean age 9.6±2.6 years; range 6–14 years) and 45 healthy age-matched subjects. Children who met three or more of the following criteria qualified as having the MS: fasting glucose >110 mg dl−1, fasting triglyceride concentration >100 mg dl−1, fasting high-density lipoprotein cholesterol concentration <50 mg dl−1 for females or <45 mg dl−1 for the males, waist circumference >75th percentile for age and gender and systolic or diastolic blood pressure >90th percentile for age, gender and height. Carotid B-mode ultrasound examinations were performed and intima–media thickness and diameters were measured in all subjects. Arterial geometry was further characterized by calculation of carotid cross-sectional area. Carotid intima–media thickness and lumen diameters were increased in children with MS as compared to children without MS. Moreover, carotid cross-sectional area was significantly higher in the group of children with MS 9.83±1.86 mm2 [mean±s.d.] compared with the control group: 7.77±1.72 mm2, P<0.001, even after adjustment for age, gender and height. Carotid hypertrophy is already detectable in children with MS. High-resolution B-mode ultrasound could provide a valuable tool for the cardiovascular risk stratification of children.

A case of association between type I hyperlipoproteinemia and systemic lupus erythematosus (SLE). Effects of steroid treatment

The case of a girl aged 19 yr with hypertriglyceridemia and systemic lupus erythematosus (SLE) is described. The girl had been admitted to a Lipid Outpatient Clinic in 1981 and diagnosed as having a Type I hyperlipidemia pattern. In November 1984 the patient acutely developed a SLE syndrome. Steroid treatment led to a dramatic fall of serum triglycerides from a starting value of 2100 mg/dl to 95 mg/dl. The role of steroids in completely correcting genetically deficient Lipoprotein Lipase Activity (LLA) is discussed.

Impaired endothelium-dependent vascular reactivity in patients with familial combined hyperlipidaemia

Background: Familial combined hyperlipidaemia (FCHL) is associated with a markedly increased risk of premature coronary artery disease. This study was designed to evaluate whether preclinical atherosclerotic functional abnormalities are detectable in the arteries of patients with FCHL. Methods: 60 subjects were recruited for the study: 30 probands of families with FCHL (mean (standard deviation (SD)) age 48 (10) years, 77% men), defined by fasting total plasma cholesterol or triglyceride concentration >250 mg/dl (>6.5 mmol/l cholesterol, >2.8 mmol/l triglyceride) and by the occurrence of multiple lipoprotein phenotypes within a family, and 30 age-matched and sex-matched healthy controls. All subjects underwent high-resolution B-mode ultrasound examination and the brachial arterial reactivity, a marker of endothelial function, was measured by a semiautomated computerised program. Lipid profile, resting blood pressure, body mass index (BMI), smoking status, insulin and homocysteine levels were also determined. Results: Compared with controls, patients with FCHL had significantly higher BMI, diastolic blood pressure and insulin levels. No difference was observed in baseline brachial diameter between the two groups (mean (SD) 3.45 (0.51) mm for FCHL v 3.60 (0.63) mm for controls; p = 0.17). In response to flow increase, the arteries of the controls dilated (mean (SD) 8.9% (4.9%), range 2.3–20.8%), whereas in the patients with FCHL, brachial arterial reactivity was significantly impaired (5.5% (2.5%), range 0–10.1%; p = 0.002). In multivariate linear regression analysis, apolipoprotein B and BMI were independent determinants of brachial artery response to reactive hyperaemia. Conclusions: The findings of our study suggest that vascular reactivity is impaired in the arteries of patients with FCHL.

Extracoronary atherosclerosis and genetic variants of apolipoprotein AI-CIII cluster in myocardial infarction survivors from southern Italy

The relationships between some genetic markers, as evaluated by DNA analysis, and ultrasound evidence of extracoronary athero-sclerosis, as detected by ultrasound methods, were evaluated in 39 myocardial infarction survivors of middle age and in 40 healthy controls of comparable age. Coronary heart disease (CHD) patients showed higher levels of triglycerides (P = 0.01) and greater number of exsmokers (P = 0.004). Carotid stenoses (> 15%) were detected in ten CHD patients and in two controls; iliac stenoses (> 15%) or abnormal ankle/arm ratio (< 0.97) were found in ten CHD patients and in one control; the scores of vascular disease severity in the myocardial infarction survivors were higher (Mann-Whitney test) than in controls (P < 0.01). Molecular genetic analysis of Sstl restriction fragment length polymorphism (RFLP) of the apolipoprotein (apo) AI-CIII cluster and of the apo B gene demonstrated a higher frequency of the S2 allele (SstI RFLP) in coronary patients than in controls (P = 0.04) and no significant differences in the frequencies of XbaI RFLP of the apo B gene between patients and controls. The relative risk of myocardial infarction associated with an abnormal vascular score (> 8) or with the presence of the rare allele S2 (SstI apo AI-CIII polymorphism) was estimated by odds ratios. The lower 95% limits of odds ratios were above 1 (indicating significant increase in the relative risk of myocardial infarction) both in the case of vascular score and that of SstI RFLP. These associations were independent of one another and of triglyceride levels. SstI RFLP association with CHD disappeared after adjustment for smoking habits. Ultrasound evidence of extracoronary atherosclerosis and SstI RFLP are markers of cardiovascular risk, which might be of help in identifying coronary-prone individuals, independently of the influence of life-style changes or ongoing treatments.

Nutrition and Antioxidants

In recent years, there has been a large amount of scientific and public interest in the possibility that antioxidant vitamins, in particular alpha-tocopherol (vitamin E) and beta-carotene (provitamin A), might represent safe means to prevent lipoprotein oxidation and antagonize the atherosclerotic process [1,2].