Erectile dysfunction and cardiovascular risk factors in a Mediterranean diet cohort.

BACKGROUND: Erectile dysfunction affects more than 100 million men worldwide, with a wide variability in prevalence. An overall association of cardiovascular risk factors, lifestyle and diet in the context of ED in a Mediterranean population is lacking. AIM: To assess ED prevalence and associated factors in a Mediterranean cohort of non-diabetic patients with cardiovascular risk factors. METHODS: Observational, cross-sectional study of patients aged over 40 treated at cardiovascular risk units in Catalonia. Anthropometric data, risk factors, lifestyle and diet habits were recorded. ED was assessed using the International Index of Erectile Function. RESULTS: Four hundred and forty patients included, 186 (42.3%) with ED (24.8% mild, 6.8% moderate and 10.7% severe). ED presence and severity were associated with age, obesity, waist circumference, hypertension, antihypertensive treatment and ischaemic disease. Patients with ED were more frequently smokers, sedentary and consumed more alcohol. In multivariate analysis, consumption of nuts (> twice a week) (OR 0.41 (95% CI 0.25 to 0.67) and vegetables (≥ once a day) (OR 0.47 (95% CI 0.28-0,77)), were inversely related to ED. Obesity (as BMI ≥ 30 kg/m(2) ) (OR 2.49 (95% CI 1.48-4.17)), ischaemic disease (OR 2.30 (95% CI 1.22 to 4.33), alcohol consumption (alcohol-units a day) (OR 1.14 (95% CI 1.04 to 1.26), and age (year) (OR = 1.07 (95% CI 1.04-1.10) were directly related to ED. CONCLUSION: Erectile dysfunction is a common disorder in patients treated in lipid units in Catalonia for cardiovascular risk factors. This condition is associated with age, obesity, ischaemic disease and unhealthy lifestyle habits.

Hyperlipoproteinaemia(a) is a common cause of autosomal dominant hypercholesterolaemia.

UNLABELLED: Autosomal dominant hypercholesterolaemia (ADH) are a heterogeneous group of monogenic lipid disorders. The plasma level of lipoprotein(a) (Lp(a)) is a heritable trait associated with increased coronary heart disease (CHD) risk. OBJECTIVE: To evaluate the frequency of elevated Lp(a) as a cause of ADH and the characteristics of subjects with high Lp(a) (hyperLp(a)). MATERIAL AND METHODS: 200 healthy subjects and 933 unrelated Spanish subjects with a clinical diagnosis of ADH who were screened for low-density lipoprotein receptor (LDLR) and apolipoprotein B (APOB) gene mutations. Standard cardiovascular risk factors and blood lipid levels, including Lp(a), were evaluated. HyperLp(a) was defined as Lp(a) levels >or=95th centile of control values. RESULTS: Lp(a) was higher in 263 subjects without LDLR or APOB mutations (nonLDLR/nonAPOB group) than in 670 subjects with mutations (FH group): 40.0 mg/dl (interquartile range (IR) 15.0-89.0) versus 31.0 mg/dl (IR 11.0-73.7) respectively, p = 0.002. HyperLp(a) was present in 23% of ADH subjects (odds ratio (OR) 5.6 (95% CI, 2.9 to 10.7) versus controls) and 29% of nonLDLR/nonAPOB subjects (OR 7.7; 3.9 to 15.4). After adjusting for Lp(a), LDL cholesterol levels were <95th centile in 28 (10.6%) nonLDLR/nonAPOB subjects and in 9 (1.3%) FH subjects. Lp(a) levels were nonsignificantly higher in ADH subjects with early-onset CHD than in those without (43.5 mg/dl, (IR, 12.0-82.0) versus 31.7 mg/dl (11.8-76.5), respectively). CONCLUSIONS: HyperLp(a) is responsible for ADH in approximately 6% of nonLDLR/nonAPOB subjects. HyperLp(a) would not appear to be a risk factor for early-onset CHD in ADH, independently of whether genetic defects have or have not been demonstrated.

Effect of apolipoprotein E polymorphism on renal transplantation.

INTRODUCTION: Dyslipidemia is an important cardiovascular risk factor and is implicated in the pathogenesis of chronic graft failure in renal transplant recipients. Apolipoprotein E (apoE), a hepatic glycoprotein involved in lipid metabolism, has been associated with hypercholesterolemia and premature coronary disease. AIM: This study assessed the impact of apoE polymorphism on the evolution of renal transplant recipients. METHODS: A total of 517 patients (age, 47 +/- 14 years; 62% men), who had undergone renal transplantation at least 12 months before enrollment, were assessed (mean follow-up, 5.4 +/- 2.2 years). ApoE polymorphisms (E2, E3, and E4 alleles) were analyzed using polymerase chain reaction (PCR) using genomic DNA. Donor-recipient clinical variables were assessed using univariate methods and Cox multivariate regression model. RESULTS: Genotype frequency was as follows: E2/E2 <1%, E2/E3 10%, E3/E3 71%, E2/E4 2%, E3/E4 16%, and E4/E4 1%, with no differences between sexes. In the univariate study, E2/E4, E3/E4, and E4/E4 genotypes were related with poorer patient survival (P = .0045). In the multivariate study, the E4 allele was associated with a higher independent risk of graft loss (odds ratio [OR], 3.23; 95% confidence interval [CI], 1.44-7.21; P < .0001) and death of the patient (OR, 16.03; 95% CI, 3.28-75.18; P < .0001), but only in patients older than 60 years of age. In patients with the E4 allele, 45% of deaths were due to cardiovascular causes. CONCLUSIONS: The genetic polymorphism of apoE (E4 allele) has an independent negative impact on patient and graft survival in the long term, particularly in older patients.

Impact of carotid atherosclerosis as assessed by B-mode ultrasonography on the evolution of kidney transplantation.

UNLABELLED: Carotid arteriosclerosis is a marker of cardiovascular risk in the general population. Cardiovascular disease is highly prevalent in kidney transplant recipients. This study analyzed the impact of arteriosclerotic carotid lesions on the evolution of renal transplant recipients. METHODS: This prospective study was performed in 70 patients with renal transplantations (mean age 52 +/- 12 years; 67% men (n = 47). High-resolution B-mode ultrasonography (7.5 MHz) of both carotid arteries was performed at baseline to assess carotid caliber, mean and maximum intima-media thickness (IMT), presence of arteriosclerotic plaques (number and maximum height), and percentage stenosis. We analyzed the impact of carotid arteriosclerosis and various donor-recipient clinical covariables on long-term patient and graft survival. RESULTS: Mean follow-up was 9.7 +/- 2.5 years (2-14). Atheroma plaques were detected in 74% of patients (n = 52). The mean number of plaques was 3.96 +/- 2.88 and maximum plaque height was 2.49 +/- 0.97 mm. IMT was 0.71 +/- 0.21 mm (0.4-1.5) with 27% of patients (n = 19) having an IMT value greater than 0.8 mm. Sonographic signs of occlusion were evident in 13% (n = 9) and the mean occlusion was 33 +/- 11% (range 20%-45%). The presence of plaques was significantly associated with age (P = .002), hypertension and diabetes (P = .016), and hypercholesterolemia (P = .01). There was an association between age and arterial wall thickness (P = .042). Acute rejection was an independent risk factor for graft loss (OR 8.14, P = .003). The multivariate study identified carotid wall thickness as an independent risk factor for patient death (OR 12.7, P = .017). CONCLUSION: Carotid arteriosclerosis is highly prevalent among renal transplant recipients. Carotid lesions were an independent risk factor for long-term patient death. High-resolution ultrasound imaging of the carotid arteries was a useful, noninvasive diagnostic technique for accurate assessment of cardiovascular risk in renal transplant recipients.

Comparative study of a microporous cholestyramine analogue (filicol) and gemfibrozil for treatment of severe primary hypercholesterolemia. Short- and long-term results.

The hypolipidemic effect of gemfibrozil in severe hypercholesterolemia is not well established. Fifty patients with primary hypercholesterolemia (including 18 patients with familial hypercholesterolemia) and stable low-density lipoprotein cholesterol levels greater than 3.90 mmol/L (greater than 150 mg/dL) (6.10 +/- 1.30 [SD] mmol/L; 236 +/- 50 mg/dL) while on a hypolipidemic diet were assigned to treatment for 12 weeks with either 9 g/d of filicol, a microporous cholestyramine analogue, or 1.2 g/d of gemfibrozil in a randomized clinical trial. Tolerance was good with both drugs. Filicol and gemfibrozil caused similar decrements of total cholesterol (14% for both), low-density lipoprotein cholesterol (20% and 18%, respectively), and apolipoprotein B (16% and 21%, respectively). Close to 40% of the patients had decreases of greater than 25% in low-density lipoprotein cholesterol levels with both drugs. Gemfibrozil, but not filicol, significantly increased plasma high-density lipoprotein cholesterol (16%) and apolipoprotein A-I (17%) levels and reduced triglyceride levels (35%). No loss of efficacy was observed with either drug in subsets of patients who had a good 12-week response rate and had extended therapy for up to 12 months. This study demonstrates that gemfibrozil may have a beneficial effect on all aspects of the plasma lipid profile in patients with severe hypercholesterolemia, a clinical situation where it can be used with potential advantages over standard doses of anion-exchange resins.

Effect of apolipoprotein E polymorphism on the serum lipid response to a hypolipidemic diet rich in monounsaturated fatty acids in patients with hypercholesterolemia and combined hyperlipidemia.

We investigated the effect of variation at the apolipoprotein (apo) E gene locus on the serum lipid response to a hypolipidemic diet rich in monounsaturated fatty acids (MUFA). Lipoprotein changes were assessed in 122 outpatients with type IIa (n = 70) and type IIb (n = 52) hyperlipidemia [80 men and 42 women with apo E phenotypes 3/2 (n = 27), 3/3 (n = 48), and 4/3 (n = 47)] who were switched from their basal diet containing 40% fat (22% MUFA) to an isoenergetic diet containing 31% fat (MUFA content similar to that of the basal diet) for 12 wk. Significant (P < 0.005) reductions of total, LDL, and VLDL cholesterol; triglycerides; and apo B occurred in subjects regardless of WHO phenotype. Triglycerides and VLDL cholesterol decreased more in type IIb than in type IIa subjects: 25% vs 12% and 21% vs 15%, respectively (P = 0.01). HDL cholesterol tended to decrease only in women. The heterogeneity of lipoprotein responses to dietary intervention was unrelated to apo E phenotypes. In these hyperlipidemic subjects, however, diet-induced favorable changes in serum lipoproteins were selectively influenced by WHO phenotype.

Correlation between Apolipoprotein-E polymorphism and Alzheimer's disease pathology.

Alzheimer's disease (AD) and small vessel disease dementia (SVDD) are common causes of dementia. The ApoE genotype has been proposed as a risk factor for AD. The frequency of the three ApoE alleles was correlated with the neuropathological changes of AD (senile plaques, neurofibrillary tangles and amyloid angiopathy) and SVDD (status lacunaris, status cribosus, leucoencephalopathy, micronecrosis and vascular fibrohyalinosis) in order to validate previous ApoE genotyping results in AD and to identify pre-clinical AD. Representative cerebral regions (cortex, gyrus cinguli, putamen, hippocampus, white matter) from 28 AD cases, 7 SVDD and 38 non-neurological controls were studied using classical histological techniques and immunohistochemistry for tau protein and amyloid-beta. The frequency of the ApoE allele 4 was significantly increased not only in AD patients but also in aged controls. However, following a detailed histopathological examination was found 62% of this group to exhibit histological changes associated with AD in limited brain areas (entorhinal region, hippocampus and adjacent temporal cortex or entorhinal region and hippocampus, or only in the entorhinal region), but 87% of these cases were found to be ApoE4 positive. The significant differences found in the distribution of ApoE allele frequencies were more marked when these cases were excluded from the control group and included as AD cases. In contrast, the frequency of the ApoE allele 2 is significantly increased in SVDD patients. Using histological techniques we confirmed the clinical diagnoses of all cases and classified the AD patients according to the severity of cortical pathology related to AD, while re-grouping from the control group those cases which had no clinical history of the disease but exhibited typical AD and SVDD histological lessions which could be considered as "pre-clinical" forms of these diseases.

Lack of interaction of apolipoprotein E phenotype with the lipoprotein response to lovastatin or gemfibrozil in patients with primary hypercholesterolemia.

The magnitude of serum lipid changes in response to hypolipidemic drugs varies considerably between individuals. These differences may be due to interactions between genetic and environmental factors that effect drug bioavailability or the capacity of the lipid-regulating enzyme and receptor targets to be affected. The apolipoprotein E (apoE) gene locus has been examined in this regard, but reports are conflicting on the effect of its variability on the response to hypolipidemic drugs. We investigated the effect of apoE polymorphism on the serum lipid response to the hepatic hydroxymethyl glutaryl coenzyme A (HMG CoA) reductase inhibitor lovastatin and the fibric acid derivative gemfibrozil. Lipoprotein changes were assessed after 12 weeks of therapy in 106 patients with primary hypercholesterolemia and combined hyperlipidemia treated with lovastastin and in 63 given gemfibrozil therapy. No significant effect of the apoE phenotypes E3/2, E3/3, or E4/3 on the heterogeneity of lipid responses to either drug was found.

High-monounsaturated fat, olive oil-rich diet has effects similar to a high-carbohydrate diet on fasting and postprandial state and metabolic profiles of patients with type 2 diabetes.

Whether metabolic control in type 2 diabetes mellitus (DM) is best achieved with the traditional high-carbohydrate (CHO), low-fat diet or a low-CHO, high-fat diet is still controversial. In a randomized crossover study, we compared the effects of a low-fat (30% of daily energy) diet and a high-fat (40% of daily energy), high-monounsaturated-fat diet for 6 weeks each on fasting and postprandial glucose, insulin, and lipoprotein concentrations in 12 patients with well-controlled type 2 DM (fasting blood glucose, 176 +/- 54 mg/dL; hemoglobin A1c, 6.4% +/- 0.7%) and no overt dyslipidemia (serum total cholesterol, 235 +/- 43 mg/dL; triglycerides, 180 +/- 63 mg/dL). Home-prepared foods were used and olive oil was the main edible fat, accounting for 8% and 25% of daily energy requirements in the low-fat and high-fat diets, respectively. For postprandial studies, the same mixed meal containing 36% fat was used in both dietary periods. Body weight and fasting and 6-hour postprandial blood glucose, insulin, and lipoprotein levels were similar after the two diets. The mean incremental area under the curve of serum triglycerides 0 to 6 hours after the challenge meal, adjusted for baseline levels, did not change significantly after the high-fat diet compared with the low-fat diet (1,484 +/- 546 v 1,714 +/- 709 mg x 6 h/dL, respectively, P = .099). Mean postprandial triglyceride levels at 6 hours were increased about 2 times over fasting levels and were still greater than 300 mg/dL after either diet. A diet high in total and monounsaturated fat at the expense of olive oil is a good alternative diet to the traditional low-fat diet for patients with type 2 DM. However, ongoing postprandial hypertriglyceridemia with either diet points to the need for other therapies to decrease triglyceride-rich lipoproteins (TRL) and the inherent atherogenic risk in type 2 diabetics.

Randomized crossover study of gemfibrozil versus lovastatin in familial combined hyperlipidemia: additive effects of combination treatment on lipid regulation.

The most appropriate therapy for combined hyperlipidemia remains to be determined. We compared the lipid-regulating effects of gemfibrozil and lovastatin in 30 patients with familial combined hyperlipidemia (FCHL) in a randomized, double-blind, placebo-controlled crossover study including 8-week courses of one drug followed by a washout period and a crossover phase to the alternate drug. After completion of the trial, open-label combination therapy was given for up to 12 months. Lovastatin was more efficacious than gemfibrozil in the reduction of total cholesterol (23% v. 9%, P<.001) and low-density lipoprotein (LDL) cholesterol (28% v. 2%, P<.001), whereas gemfibrozil surpassed lovastatin in the reduction of triglycerides (48% v. 0%, P<.001) and very-low-density lipoprotein (VLDL) cholesterol (50% v. 19%, P = .005) and the increase of high-density lipoprotein (HDL) cholesterol (18% v. 4%, P = .005). Lovastatin caused a greater decline in total apolipoprotein B (apo B) and LDL apo B than gemfibrozil, whereas VLDL apo B decreased only after gemfibrozil therapy. Drug-induced changes in lipoprotein composition indicated that gemfibrozil reduced both the number and size of VLDL particles and lovastatin decreased the number of LDL particles. Combined treatment was safe and had additive effects on lipids, causing significant (P<.001) reductions in total cholesterol (32%), triglycerides (51%), LDL cholesterol (34%), and apo B (26%) and an increase in HDL cholesterol (19%). Target LDL cholesterol levels were achieved only in 11% of patients given gemfibrozil alone and triglycerides decreased to target levels in 22% after lovastatin alone, whereas combined therapy normalized both lipid fractions in 96% of patients. Thus, in FCHL, gemfibrozil has no effect on LDL cholesterol levels but favorably influences the putative atherogenic alterations of lipoprotein composition that are related to hypertriglyceridemia. Conversely, lovastatin markedly decreases LDL cholesterol but has little effect on triglyceride-rich lipoproteins. Combination treatment safely corrects all of the lipid abnormalities in most patients.

Cardiac troponin elevations in chronic renal failure: prevalence and clinical significance.

OBJECTIVES: The aim of the study was investigate the prevalence of abnormal values of cardiac troponin T (cTnT) and cardiac troponin I (cTnI) in patients with chronic renal failure (CRF) and their clinical significance. DESIGN AND METHODS: We investigated the concentrations of cTnT and cTnI in 49 CRF patients without heart disease or diabetes. Cardiac TnT values were measured with a second generation immunoassay and cTnI with two immunoassays with different analytical sensitivity. All CRF patients underwent regular clinical follow-up over a 18-month period. RESULTS: No patients with CRF had elevated values of cTnI when measured with one assay and only 2 patients displayed minimally elevated values with the second assay. In contrast, 23 CRF patients (47%) displayed cTnT concentrations elevated above the upper reference limit. The elevated cTnT values observed were below the values detected in acute myocardial infarction and were not associated with adverse cardiac events during follow-up. CONCLUSIONS: Mildly elevated cTnT concentrations are common in patients with CRF and do not appear to be associated with adverse coronary events.

In-vitro effect of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors on non-hepatic LDL receptor activity: evidence of lack of stimulatory effect of pravastatin.

BACKGROUND: It is speculated that, as a result of its tissue selectivity, pravastatin may be a safer drug than the lipophilic 3-hydroxy-3-methylglutaryl Coenzyme A (HMG-CoA) reductase inhibitors in combination therapy involving drugs with potential muscle toxicity. Several studies have shown specific inhibitory activity on hepatic cholesterogenesis and a potent induction of hepatic low-density lipoprotein (LDL) receptors. However, data about its effect on stimulation of LDL receptor activity on non-hepatic cells are not available. METHODS: Several experiments were carried out in order to assess the in-vitro effect of HMG-CoA reductase inhibitors on the activity of LDL receptors of human non-hepatic cells. Lymphocytes from both normolipidemic controls and patients with heterozygous familial hypercholesterolemia along with human fibroblasts were cultured in both the presence and absence of pravastatin and lovastatin. RESULTS: Pravastatin, at concentrations of 0.25-50 mumol/l, did not enhance the LDL receptor activity of lymphocytes derived from both patients with familial hypercholesterolemia and normolipidemic controls. In contrast, lovastatin, at concentrations of 0.25 mumol/l, increased the LDL receptor activity in both control lymphocytes and lymphocytes from patients with familial hypercholesterolemia by 121% and 148%, respectively. Fibroblast LDL receptor activity was not altered by pravastatin at a concentration of 50 mumol/l, whereas lovastatin at the same concentration increased the LDL uptake by 153%. CONCLUSION: From in-vitro experiments of LDL receptor activity stimulation, we conclude that pravastatin has little effect on non-hepatic cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of apolipoprotein polymorphisms in renal transplant recipients.

Cardiovascular disease (CVD) is the main cause of mortality among long-term renal transplant recipients (RTR). On the other hand, allograft chronic nephropathy is the primary cause of graft loss among long-term RTR. Hyperlipidemia is a predisposing factor for both conditions. Polymorphisms of the apolipoproteins modulate lipid metabolism. The aim of the study was to evaluate the effect of apo A-I, apo A-IV and apo C-III genotypes on the long-term results of renal transplantation. Clinical assessment (renal allograft and patient survival) and genotyping for apo A-I (+83C/T), apo C-III (Sst I), and apo A-IV (Thr347Ser and Gln360His) polymorphisms were evaluated in 516 kidney transplant patients and correlated with the clinical evolution over 12 months. The distribution of the apo A-I (+83C/T) polymorphisms was: CC 91.9%, CT 7.9%, and TT 0.2%. The apo C-III genotype showed: S1S1 84.4%, S1S2 15.2%, and S2S2 0.4%. The apo A-IV (Pvu II) polymorphism was: GG 82%, GT 18%, and 0% TT. Finally, the frequency of apo A-IV (Hinf I) polymorphism was: AA 69%, AT 27%, and TT 4%. The frequency of polymorphisms was similar between men and women. In conclusion, there was no significant influence of apolipoprotein polymorphisms on renal and patient survival.

[Excessive intake of fats and cholesterol in hypercholesterolemic individuals. Effects of dietary intervention on plasma lipids and lipoprotein cholesterol]. / Ingesta excesiva de grasas y colesterol en individuos hipercolesterolémicos. Efectos de la intervención dietética sobre los lípidos plasmáticos y colesterol lipoproteico.

Preliminary evidences suggest that both the frequency of ischemic heart disease and the plasma cholesterol levels are increasing in the Spanish population, whose dietary habits are becoming progressively "westernized". In the present work we used the food frequency method to evaluate the dietary habits of 30 hypercholesterolemic subjects. These and another 65 free-living individuals of both sexes, ages 18-77 yrs, with plasma cholesterol 301 +/- 41 mg/dl or 7.80 +/- 1.06 mmol/l (means +/- SD) were submitted to a hypolipidemic diet similar to the mediterranean diet in order to assess effects on plasma lipids and lipoprotein cholesterol. The usual diet contained (% kcal/day): total fat 37, saturated fat (S) 12, monoinsaturated fat 16 and poliinsaturated fat (P) 6, with P/S = 0.5 and a daily cholesterol intake of 506 mg. During dietary intervention, respective changes were: -7%, -5%, -1%, +2%, +0.6, and -304 mg. After a 3 - month dietary period, significant (p less than 0.001) decreases occurred in total plasma cholesterol (-40 mg/dl or -1.04 mmol/l, -14%), LDL-cholesterol (-35 mg/dl or -0.91 mmol/l, -16%) and triglycerides (-5 mg/dl or -0.28 mmol/l, -14%), while HDL-cholesterol and body weight did not change. Similar effects were obtained when diet was continued for 1 yr in a subgroup of 40 individuals. The responses of plasma cholesterol to dietary change had a normal distribution, with 17% hyporresponses and 15% hyperresponses. A marked decrease (-36%) of plasma triglycerides was observed in 12 subjects with IIb hyperlipidemia. The total cholesterol/HDL-cholesterol and LDL-cholesterol/HDL-cholesterol ratios improved in both men and women.(ABSTRACT TRUNCATED AT 250 WORDS)

[Carotid atherosclerosis evaluated by two-dimensional ultrasonography in patients with primary hypercholesterolemia]. / Aterosclerosis carotídea evaluada por ecografía bidimensional en pacientes con hipercolesterolemia primaria.

BACKGROUND: Two-dimension ultrasonography permits to noninvasively quantify extracoronary atherosclerosis. The objective of this study was to assess preclinical atherosclerosis of the extracranial carotid arteries in patients with primary hypercholesterolemia. METHODS: Lipid and nonlipid cardiovascular risk factors were evaluated in 206 patients with dyslipidemia (127 men and 79 women, mean age 49 years, range 18-75), and a multifactorial cardiovascular risk profile was constructed for each patient. Ultrasound measurements of the intima-media thickness in the common carotid artery of each side were taken, and the number and height of any atheroma plaques present were quantified. RESULTS: Asymptomatic plaques were found in 120 patients (58%), and were more frequent in men than in women (65 vs 47%, p = 0.009), and in patients with than in those without prior coronary heart disease (80 vs 50%, p < 0.001). Both intimal thickening, indicative of early atherosclerosis, and the extent of arterial wall involvement with plaques, which represents an advanced stage of the disease, increased significantly with age and with increasing multifactorial cardiovascular risk, reflecting a positive relation between signs of atherosclerosis and the burden of risk factors. Intima-media thickness also increased with increasing plaque score, indicating the generalization of atherosclerosis. CONCLUSIONS: The high prevalence of preclinical carotid atherosclerosis confirms the atherogenic risk of primary dyslipidemias. The relation between carotid lesions and both coronary heart disease and multifactorial risk supports the validity of arterial ultrasound studies for cardiovascular risk prediction.