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Objective: Combined hyperlipidaemia is a common and highly atherogenic lipid phenotype with multiple lipoprotein abnormalities that are difficult to normalise with single-drug therapy. The ATOMIX multicentre, controlled clinical trial compared the efficacy and safety of atorvastatin and bezafibrate in patients with diet-resistant combined hyperlipidaemia., Patients and Study Design: Following a 6-week placebo run-in period, 138 patients received atorvastatin 10mg or bezafibrate 400mg once daily in a randomised, double-blind, placebo-controlled trial. To meet predefined low-density lipoprotein-cholesterol (LDL-C) target levels, atorvastatin dosages were increased to 20mg or 40mg once daily after 8 and 16 weeks, respectively., Results: After 52 weeks, atorvastatin achieved greater reductions in LDL-C than bezafibrate (percentage decrease 35 vs 5; p < 0.0001), while bezafibrate achieved greater reductions in triglyceride than atorvastatin (percentage decrease 33 vs 21; p < 0.05) and greater increases in high-density lipoprotein-cholesterol (HDL-C) [percentage increase 28 vs 17; p < 0.01 ]. Target LDL-C levels (according to global risk) were attained in 62% of atorvastatin recipients and 6% of bezafibrate recipients, and triglyceride levels <200 mg/dL were achieved in 52% and 60% of patients, respectively. In patients with normal baseline HDL-C, bezafibrate was superior to atorvastatin for raising HDL-C, while in those with baseline HDL-C <35 mg/dL, the two drugs raised HDL-C to a similar extent after adjustment for baseline values. Both drugs were well tolerated., Conclusion: The results show that atorvastatin has an overall better efficacy than bezafibrate in concomitantly reaching LDL-C and triglyceride target levels in combined hyperlipidaemia, thus supporting its use as monotherapy in patients with this lipid phenotype.

Background: Considerable variability exists in the plasma lipid and lipoprotein response to statin treatment due, in part, to genetic factors. The gene for apolipoprotein E (ApoE) is polymorphic and the different genotypes modulate baseline lipid levels. The objective of the present study was to evaluate the effect of the apoE genotype on the lipoprotein response to pravastatin treatment in an outpatient population followed-up in several different clinics across Spain. Subjects and methods. Subjects (n=401; 56% female; mean age 57 years), who were hypercholesterolaemic despite a diet poor in saturated fat and cholesterol, were treated according to NCEP-ATP II guidelines. Plasma lipids and lipoproteins were measured centrally before and after 16 weeks of treatment with 20 mg day-1 of pravastatin., Results: ApoE genotype distributions were 3.2% with varepsilon2/3, 73.1% with varepsilon3/3 and 22.4% with varepsilon3/4 or varepsilon4/4. ApoE genotype did not have any effect on baseline lipid levels except on triglycerides such that the carriers of the varepsilon2 allele had concentrations significantly greater than those subjects with varepsilon3/3 genotype and carriers of the varepsilon4 allele after adjustment for age, gender and body mass index (BMI) (P < 0.001). Once adjusted for age, gender, BMI and baseline lipid levels, the apoE polymorphism did not significantly influence the plasma lipid and lipoprotein response to pravastatin., Conclusion: ApoE genotype appears not to influence the hypolipidaemic effect of pravastatin in patients monitored in a general outpatient setting.

Background: We have previously reported that the decrease in high-density lipoprotein (HDL)-cholesterol that is observed in patients with untreated sarcoidosis is limited to those with active disease., Aim: To determine the effect of corticosteroids, used in the treatment of active sarcoidosis, on the reported lipoprotein metabolism abnormalities., Methods: We studied 62 patients with biopsy-proven sarcoidosis, all of them with active disease. Sarcoidosis activity was evaluated by means of clinical, chest X-ray, gallium-67 scan, serum angiotensin-converting enzyme (peptidyl-dipeptidase A) values, and pulmonary function tests. A total of 40 patients were not treated with prednisone and 22 patients were treated with prednisone. The mean daily prednisone dosage in the treated patients with sarcoidosis was 20 mg and the mean duration of prednisone therapy was 6 months. Analysis of lipoprotein metabolism included: serum cholesterol, low-density lipoprotein (LDL)-cholesterol, HDL-cholesterol, HDL(2)-cholesterol, HDL(3)-cholesterol, apolipoprotein (apo) A-I, apo B, and triglyceride concentrations., Results: When patients with active sarcoidosis not treated with prednisone were compared to those treated with prednisone, the former had significantly lower HDL-cholesterol (1.17+/-0.36 vs. 1.42+/-0.42 mmol/l; P=0.01) and HDL(2)-cholesterol (0.37+/-0.18 vs. 0.53+/-0.25 mmol/l; P=0.009) levels. Multiple regression analysis demonstrated that the HDL-cholesterol (P=0.004), HDL(2)-cholesterol (P=0.002), HDL(3)-cholesterol (P=0.02), and apo A-I (P=0.02) levels were the variables independently and significantly associated with steroid therapy., Conclusions: Corticosteroid therapy, used in the treatment of active sarcoidosis, increased HDL-cholesterol levels to those seen in inactive disease. These changes are manifestations of reducing disease activity.

C-reactive protein (CRP) is a non-specific but sensitive marker of underlying systemic inflammation. High CRP plasma levels correlate with risk for future cardiovascular events. The present study evaluated the effects of atorvastatin (10-40 mg) and bezafibrate (400 mg) on CRP concentrations after 6 and 12 months of treatment in 103 patients with combined (mixed) hyperlipidemia. The number of cardiovascular risk factors present in a given patient was associated with baseline CRP levels. After 6 months and 1 year, atorvastatin treatment was associated with significant (P<0.001) decreases from baseline of CRP concentrations by 29 and 43%, respectively, while bezafibrate-treated patients showed non-significant reductions of 2.3 and 14.6%, respectively (P=0.056 and 0.005 for the respective differences between the two treatment arms at 6 months and 1 year). The magnitude of change in CRP after 1 year was directly related to baseline CRP levels. Covariance analysis showed that CRP decreases in the atorvastatin group were unrelated to total cholesterol and LDL cholesterol reductions; however, they were directly related to triglyceride changes (r=0.28, P=0.047) and inversely related to HDL cholesterol changes (r=-0.28, P=0.045). A model including baseline CRP values and treatment effect showed that atorvastatin use was a significant predictor of change in CRP levels over time (beta=0.82, P=0.023). These results suggest a potential anti-atherosclerotic additional benefit of atorvastatin in patients at a risk of cardiovascular disease.

Hypocholesterolemia has been observed in several inflammatory diseases such as rheumatoid arthritis, myeloproliferative disorders, systemic lupus erythematosus and sarcoidosis. Serum amyloid A is an acute-phase reactant that is related to the high-density lipoprotein cholesterol. This review discusses the relationship between the activation of the cells of the monocyte-macrophage system, determined by the serum amyloid A levels, and the lipid metabolism, measured as alterations in plasma lipoprotein concentrations. The mechanisms of this association during acute inflammation are also discussed in this review.

Isolated low high-density lipoprotein cholesterol (HDLc) is a well-known risk factor for cardiovascular disease and is associated with arterial endothelium dysfunction. Several studies have shown that cholesterol lowering in patients with hypercholesterolemia improves endothelial function, but the effect of treating low HDLc levels remains unknown. We studied the effect of increasing HDLc on endothelial function in patients with coronary artery disease (CAD) and isolated low HDLc (HDLc) <0.91 mM, low-density lipoprotein cholesterol (LDLc) <4.1 mM, and triglycerides <2.8 mM. Flow-mediated endothelium-dependent dilatation (FMD) in response to reactive hyperemia was measured by brachial ultrasound, before and after bezafibrate treatment (400 mg daily for 6 months) in 16 patients with CAD and impaired FMD (<10%). After bezafibrate therapy, HDLc increased from 0.79-1.0 mM (p = 0.0008) at the expense of both HDL2 and HDL3 subfractions, apolipoprotein A-I increased from 1.04-1.19 g/l (p = 0.0012), and fibrinogen decreased from 4.45-3.39 g/l (p = 0.0007). The impaired FMD increased after bezafibrate treatment from a median of 2.5-12.3% (p = 0.0004). Endothelial function was normalized in eight patients (50%), improved in four (25%), and did not change in four (25%). These observations indicate that in patients with isolated low HDLc and CAD, bezafibrate treatment improves endothelial function of brachial arteries, increases HDLc and apolipoprotein A-I, and lowers fibrinogen concentrations.

Introduction and Aims: In patients with coronary risk factors the presence of endothelial dysfunction in epicardial arteries has been documented. The purpose of this study was to determine whether endothelial dysfunction, documented hypercholesterolemic patients and angiographically normal coronary arteries, improves by reduction and normalization of lipid levels., Patients and Method: In 10 patients with hypercholesterolemia and normal coronary angiography, the endothelium-dependent coronary vasomotion was studied by intracoronary infusion of acetylcholine into the left anterior descending coronary artery. Vasomotion changes in response to acetylcholine were analyzed by quantitative angiography. Five patients without coronary risk factors and normal coronary arteries formed the control group. Patients with hypercholesterolemia were treated with lipid-lowering therapy (diet and lovastatin) and endothelial function was reevaluated after 24 +/- 4 months., Results: In the initial study, hypercholesterolemic patients compared with the control group showed a vasoconstrictor response to serial doses of acetylcholine(10(-6) M, 10(-5) M, 10(-4)M) indicative of endothelial dysfunction (study group: -0.3 +/- 10%, -6 +/- 4%, -18 +/- 10% vs control group: -0.6 +/- 6%, -2 +/- 6%, 3+/-6%; p < 0.01 to 10(-4) M acetylcholine dose. During follow-up hypercholesterolemic patients who a significant reduction in total cholesterol levels and LDL. Compared to first study, at follow-up, there was an improvement in the response to acetylcholine (-0.4 +/- 4%, -3 +/- 6%, -3 +/- 10%; p<0.001 vs basal values at 10(-4) M acetylcholine concentration). Reduction in total cholesterol during follow-up was related to the improvement in the vasoconstrictor response to acetylcholine (r=0.53; p< 0.05)., Conclusion: In patients with hypercholesterolemia and angiographycally normal coronary arteries with documented endothelial dysfunction, the reduction and normalization of lipid levels during follow-up may improve endothelium-dependent coronary vasomotion.

Background: At high doses, the pharmacokinetics of fluvastatin immediate-release (IR) are nonlinear, possibly due to saturation of hepatic uptake. Fluvastatin delivery to the liver in a slower but sustained fashion would be expected to avoid hepatic saturation without elevating systemic drug levels., Objective: This pooled analysis compared the efficacy and tolerability of extended-release (XL) 80-mg and IR 40-mg formulations of fluvastatin in lowering low-density lipoprotein cholesterol (LDL-C) and triglyceride (TG) levels and raising high-density lipoprotein cholesterol (HDL-C) levels in patients with hypercholesterolemia., Methods: Data were pooled from 3 double-blind, randomized, active-controlled, multicenter, parallel-group studies that compared changes in lipid and apolipoprotein levels with fluvastatin XL 80 mg at bedtime (HS) with changes in fluvastatin IR 40 mg HS or BID in patients aged > or =18 years with primary hypercholesterolemia (consistently elevated LDL-C level [> or =160 mg/dL] and plasma TG levels < or =400 mg/dL). The primary efficacy variable was percent change in LDL-C from baseline., Results: The pooled analysis provided an intent-to-treat efficacy study population of 1674 patients. At 4 weeks, fluvastatin XL 80 mg HS reduced LDL-C levels by a mean of 36.3% (median 38%), significantly greater than a mean reduction of 25.9% (median 27%) seen with fluvastatin IR 40 mg HS, and an incremental additional mean reduction in LDL-C of 10.4% (P < 0.001). At 4 and 24 weeks, fluvastatin XL 80 mg HS provided an LDL-C reduction equivalent to fluvastatin IR 40 mg BID (P < 0.001 for noninferiority). Significant, dose-related changes in HDL-C, LDL-C:HDL-C ratio, total cholesterol, TG, and apolipoprotein A-I and apolipoprotein B levels also occurred. Mean HDL-C level increased by 8.7% and median TG level decreased by 19% with fluvastatin XL 80 mg HS (P < 0.001 and P < 0.05 vs fluvastatin IR 40 mg HS, respectively). Maximum mean increases in HDL-C level (21%) and median decreases in TG level (31%) with fluvastatin XL 80 mg HS occurred in patients with type IIb dyslipidemia and the highest baseline TG. Adverse events were mild, with similar frequency in all treatment groups., Conclusions: Once-daily administration of fluvastatin XL 80 mg provides enhanced efficacy with an additional 10.4% reduction in LDL-C levels compared with fluvastatin IR 40 mg HS, and superior increases in HDL-C levels, particularly in patients with elevated TG levels (P < 0.05 vs fluvastatin IR 40 mg HS). Fluvastatin XL 80 mg HS has a good tolerability profile and is effective as starting and maintenance lipid-lowering treatment in patients with type II hypercholesterolemia.

Background: The aim of this work was to evaluate the role of homocysteine, and the MTHFR 677C-->T allele as risk factors for premature coronary artery disease and to analyse the inheritance of this metabolic disorder., Material and Methods: Case-control and family studies were performed in a sample of 76 male patients (age < 55), 95 age-matched controls and 89 patients' offspring. Plasma total homocysteine concentrations, its nutritional determinants and the frequency of the MTHFR 677C-->T allele were measured, in addition to conventional risk factors., Results: Mild hyperhomocysteinemia (above the 90th percentile of the control group) was seen in 22.4% of patients (P = 0.02) and was an independent predictor of premature coronary artery disease (odds ratio of 3.2). The frequencies of the 677T allele in patients and controls were 0.37 and 0.36 and those of the TT genotype were 0.15 and 0.14, respectively. Homozygosity for the 677T allele was associated with significantly higher homocysteine values (P < 0.00001). Among TT patients, 64% had mild hyperhomocysteinemia, as compared to 23% of TT controls. Mild hyperhomocysteinemia showed a strong hereditary component, as 36% of patients' offspring had homocysteine levels above the age-adjusted 90th percentile compared to only 13% of patients' spouses. Among children with the TT genotype, the proportion raised to 83% (P < 0.001)., Conclusion: In this Spanish population, mild hyperhomocysteinemia is associated with the risk of premature coronary artery disease and is highly prevalent in offspring of patients with this condition. The MTHFR TT genotype is associated with hyperhomocysteinemia, but not with coronary artery disease.

Background: Patients with coronary artery disease (CAD) associated with peripheral (PAD) or cerebrovascular disease (CVD), a condition called diffuse atherosclerosis, have a higher risk of death than patients with isolated CAD. The prevalence of diffuse atherosclerosis and the atherogenic risk factors associated with this condition in our geographic area have not been described previously., Methods: A cohort of 2597 patients (62 +/- 10.8 years, 665 women) consecutively admitted at Bellvitge Hospital because of acute coronary syndromes were studied. CAD patients were divided in two groups with diffuse and located atherosclerosis according to whether they had or they had not an associated PAD or CVD. Baseline history, physical data and lipid profile were recorded in each patient according to a standardized questionnaire., Results: A total of 370 patients (14.2%) had diffuse atherosclerosis. Among them, there were more men and women older than 55 years than among those with isolated CAD. Patients with diffuse atherosclerosis were more frequently hypertensive, diabetic and former smokers than those with isolated CAD (60.5% vs. 49.4%, P < 0.01; 37.4% vs. 24.5%, P < 0.01; and 47% vs. 35.7%, P < 0.01, respectively). There were no significant differences in the mean values of total cholesterol (TC), low-density cholesterol (LDL-C), high-density cholesterol (HDL-C) and triglycerides between both groups of patients, but patients with diffuse atherosclerosis had a lower HDL-C/TC ratio, with borderline statistical significance (0.18 +/- 0.06 vs. 0.19 +/- 0.06, P = 0.06). Using multiple logistic regression analysis, the variables associated with diffuse atherosclerosis in men were age greater than 55 years (OR 1.97, CI 1.33-2.93), hypertension (OR 1.50, CI 1.14-2.20), diabetes (OR 1.78, CI 1.20-2.70), smoking (former smokers) (OR 2.09, CI 1.36-3.24) and HDL-C/TC < 0.20 (OR 1.60, CI 1.18-2.17); and in women hypertension (OR 3.43, CI 1.48-7.94) and diabetes (OR 2.58, CI 1.55-4.80)., Conclusions: Clinically overt diffuse atherosclerosis is a relatively common disease. Older patients and those with hypertension, diabetes or low HDL-C/TC ratio are more likely to have diffuse atherosclerosis than those without these conditions.

The genetic and biochemical basis of fish-eye disease (FED) was investigated in a 63-year-old female proband with low plasma HDL cholesterol. Analyses of corneal and plasma lipids of the proband were consistent with impaired lecithin:cholesterol acyltransferase (LCAT) activity. Free cholesterol and phospholipid levels were elevated relative to control values, whereas cholesteryl ester levels were greatly reduced. Fatty acid compositions of corneal lipids from the proband and control subjects differ from the respective fatty acid compositions of their plasma lipids. This suggests that the metabolic pathways and acyl chain specificities for phospholipid, cholesteryl ester, and triglyceride metabolism within the cornea are distinct from those of plasma. Sequencing of the LCAT gene from the proband revealed a novel mutation at nucleotide 399, corresponding to an Arg99-->Cys substitution. Secretion of LCAT (Arg99-->Cys) by transfected COS-6 cells was approximately 50% of that of the wild type, but its specific activity against reassembled HDL was 93% lower than that of wild-type LCAT. The specific activities of wild-type and LCAT (Arg99-->Cys) against LDL were reduced similarly, suggesting that the appearance of the FED phenotype does not require enhanced activity against LDL. Our data support the hypothesis that FED is a partial LCAT deficiency in which poor esterification in specific types of HDL particles may contribute to the appearance of the corneal opacities.

Background: The role of lipoproteins as markers of peripheral arterial disease (PAD) is not well defined., Methods: We measured both lipid and non-lipid risk factors in 51 male patients with angiographically proven PAD and in 56 control subjects. The independent association of risk factors with PAD was evaluated by means of a multiple logistic regression analysis., Results: The levels of cholesterol bound to high density lipoprotein (HDLc) and to its subfraction HDL2 were lower and triglycerides were higher in patients than in control subjects (1.0 +/- 0.3 vs 1.2 +/- 0.3, p < 0.003; 0.4 +/- 0.2 vs 0.5 +/- 0.3, p < 0.03; and 1.8 +/- 1.2 vs 1.3 +/- 0.7, p < 0.02, respectively). Total cholesterol and LDLc levels were similar in both groups. In the multiple logistic regression analysis that was done with lipid parameters, a statistically significant association of triglycerides (OR = 1.73; CI95% = 1.06-2.80) and HDLc (OR = 0.15; CI95% = 0.05-0.50) with PAD was observed, while HDL subfractions and apolipoproteins were not significantly associated. In the multiple logistic regression analysis that was done with non-lipid parameters, hypertension (OR = 5.35; CI95% = 1.86-15.4) and smoking (packs-year) (OR = 1.04; CI95% = 1.10-1.06) were the only significantly associated with PAD. When lipid and non-lipid parameters were included in the regression analysis, a statistically significant association between hypertension, smoking and HDLc with PAD was observed., Conclusions: Among lipid risk factors, a low HDLc and high triglycerides, and among non-lipid risk factors hypertension and smoking, are significantly and independently associated with lower limb arteriopathy.

Background: In May 1989 and June 1990, consensus conferences of treatment of hypertension and hypercholesterolemia respectively were held in Spain, at the General Division of Health Planning from the Ministry of Health. The objective of this article is to assess the effect of such conferences of physicians' knowledge, attitudes and practices., Subjects and Methods: Cross-sectional telephone survey was carried out in physicians of general medicine, family practice, internal medicine and cardiology specialties. 807 physicians were selected, 347 family physicians, 177 general practitioners, 156 cardiologists and 128 internists. A questionnaire of 30 items was designed to obtain information about demographic and professional characteristics, knowledge of the consensus conferences and attitudes related to a case of an otherwise healthy asymptomatic 48-years-old man., Results: The response rate was 57% (463 physicians), and 60% of physicians had knowledge about the conferences, being general practitioners the ones who had less knowledge of the conferences. The items about recommendations of diet and pharmacological treatment were property answered (about 50% of the physicians answered correctly). The mean of serum cholesterol when diet and drugs are recommended was 232 mg/dl (SD 23) (6.01 mmol/l) and 260 mg/dl (SD 25) (6.7 mmol/l) respectively. The first-choice cholesterol lowering drugs were statines. A patient was considered as hypertensive it the mean of systolic blood pressure was 149 mmHg (9.4) and the mean for diastolic blood pressure was 92 mmHg (3.8). The mean of diastolic blood pressure considered for drug treatment was 96.7 mmHg (SD 4.6). The first-choice antihypertensive drugs were angiotensin conversive enzyme inhibitors., Conclusions: Diffusion of the conferences has been unequal, being general practitioners less knowledgeable about the content of the conferences. Although physicians know reasonably well the recommendations about diet and drug treatments, the attitude in practice is more aggressive than recommended. Globally, the knowledge of the contents of the conferences was acceptable, although there were differences between specialties; however the effect on clinical practice is still low.

Purpose: To know the prevalence and types of dyslipidemia associated with xanthelasma., Patients and Methods: One hundred fifteen patients with xanthelasma and 105 age-matched control subjects without xanthelasma were evaluated in a cross-sectional study. Univariate and multivariate comparisons of lipid variables (including total cholesterol; triglycerides; very-low-, low-, and high-density lipoprotein cholesterol [VLDL-C, LDL-C, and HDL-C, respectively]; cholesterol of high density lipoprotein [HDL] subfractions 2 and 3 [HDL2-C and HDL3-C]; apolipoprotein (apo) A-I and B; and apo E phenotypes) and nonlipid coronary risk factors were made between patients with and without xanthelasma., Results: Patients with xanthelasma had higher levels of cholesterol, LDL-C, and apo B, and lower levels of HDL2-C than control subjects. The prevalence of the apo E4/E3 phenotype was higher in cases than in controls (P < 0.05). Patients with xanthelasma had a higher prevalence of personal and familiar history of cardiovascular disease and were more overweight than control subjects. A stepwise discriminant analysis disclosed an independent association of xanthelasma with lower HDL-C, HDL2-C, and HDL3-C levels in men, and with higher total cholesterol and lower HDL2-C levels in women., Conclusions: Xanthelasma appears to be associated with qualitative and quantitative abnormalities of lipid metabolism that may favor lipid deposition in the skin and arterial wall. The findings support the notion that xanthelasma is a marker of dyslipidemia, and underline the need to determine a full lipid profile in these patients to detect those potentially at increased risk of cardiovascular disease.

Background: The distribution of serum fibrinogen levels and factor VII in a population of dyslipemic women and their association with other cardiovascular risk factors are herein described., Methods: Dyslipemic women between 40-70-years of age without cardiovascular disease and with no hypolipemic treatment who attended 21 primary health care consultations were studied. The following data were collected in a questionnaire: smoking habit, high blood pressure, alcohol consumption and menopause. The analytical parameters determined were: total cholesterol, LDL-cholesterol, HDL-cholesterol, triglycerides, fibrinogen and factor VII. The Pearson correlation coefficient was determined to evaluate the association of fibrinogen and factor VII with other cardiovascular risk factors., Results: Serum fibrinogen levels correlated positively with LDL-cholesterol and with the body mass index and negatively with HDL-cholesterol. Factor VII correlated positively with the triglycerides and total cholesterol. No significant differences were observed in the hematic factors among the hypertensive women and those who were not hypertensive. The same was observed in diabetic and in the pre- and postmenopausal women., Conclusions: In this transversal study a relationship was found between serum fibrinogen level and factor VII activity and other known cardiovascular risk factors.

A sensitive and specific enzyme-linked immunosorbent assay (ELISA) for human apolipoprotein E (apo E) quantification using commercially available reagents is described. The assay is a noncompetitive, sandwich ELISA in which the wells were coated with a monoclonal EO1 antibody anti-human apo E and detected with a polyclonal antibody-peroxidase conjugate anti-apo E. The mean apo E concentration in 168 middle-aged subjects randomly selected from general population was 51.7 +/- 12.4 mg/liter. Apo E levels were highly correlated with apo E phenotypes. Apo E polymorphism, which shows a modulating effect in the catabolism of apo E containing lipoproteins, may explain a large fraction, 18.5%, of the variability of serum apo E levels in middle-aged population. Isoforms apo E2 and apo E4 have an opposite effect on the regulation of serum apo E concentrations. Individuals that express apo E2 isoform present higher apo E levels (65.5 mg/liter for apo E2/E3), whereas the average of individuals with apo E4 is lower (42.8 mg/liter for apo E4/E3) than general population.

Background: The aims of this study were to estimate the number of people who should receive some intervention (pharmacologic and/or dietetic) to reduce cholesterol concentrations and to evaluate selective case finding in comparison to opportunistic detection., Methods: Six hundred twenty-five individuals participating in a study of cardiovascular risk factors were included in the study. Those with total cholesterol concentrations (TC) greater than 6.2 mmol/l and those with CT concentrations greater than 5.2 mmol/l observed upon lipid profile analysis and history of cardiovascular disease and/or risk factors were considered as candidates. Out of these individuals, those with cholesterol concentrations linked to low density lipoproteins greater than 4.14 mmol/l or greater than 3.37 mmol/l and previous history of cardiovascular disease or two risk factors were considered candidates to undergo intervention to reduce cholesterol concentrations. Moreover, the number of individuals with CT concentrations greater than 6.2 mmol/l which would not be detected if CT was only determined in those who already had another cardiovascular risk factor was estimated., Results: 37.5% (CI 95%; 33.8%-41.5%) of the individuals required lipid profile and out of these 88.8% (CI 95%; 3.8%-92.4%) were candidates to receive intervention. Upon evaluating the efficacy of the strategy of selective case finding it was observed that the sensitivities of the risk factors were low, ranging from 22.6% in those with family history of cardiovascular disease to 34.8% in cases with personal history of high blood pressure., Conclusions: If selective case finding of high risk subjects was the only strategy applied, many individuals with hypercholesterolemia would remain undetected, therefore the strategy of opportunistic detection is preferable whenever possible.

Background: The aim of this study was to analyze the percentage of individuals with hypoalphalipoproteinemia and isolated hypertriglyceridemia which would not be detected if only total cholesterol were included in the initial detection of dyslipemia., Methods: Five hundred forty-one individuals participating in a study concerning factors of cardiovascular risk were included in the present study which consisted in a survey on risk factors and a medical examination. The population studied was divided according to the concentration of total cholesterol (TC) in desirable concentrations (5.2 mmol/l), intermediate (5.2-6.2 mmol/l) and elevated (6.2 mmol/l). The concentrations of cholesterol bound to high density lipoproteins (cHDL) less than 0.9 mmol/l and of triglycerides (TG) greater than 2.3 mmol/l were considered as high risk., Results: Hypoalphalipoproteinemia would not be detected in 2.9% of the population studied (IC 95%: 1.5%-4.3%) and isolated triglyceridemia in 2.4% (IC 95%: 1.1%-3.7%) if the cHDL and the TG were only determined in the individuals who had high or elevated CT concentrations and two or more cardiovascular risk factors., Conclusions: These data support the efficacy of CT as the only test for initial detection of dyslipemia and question the convenience of initial quantification of cHDL and triglycerides in all cases as some authors request.

We studied the lipidic metabolism and the atherogenic risk factors non related to lipidic metabolism in two groups of patients: group 1 with only coronary disease and group 2 with coronary disease and atherosclerosis in the cerebral and/or peripheric artery territories. Patients of group 2 showed a cholesterol, cLDL, and B-apoprotein titers significantly higher than group 1. Systolic and diastolic blood pressure were higher in group two. Also the incidence of diabetes mellitus in group 2 was higher than in group 1. In a stepwise discriminating analysis the diastolic arterial pressure and cholesterol titers were the parameters with a greatest predictive potential for the presence of localized or generalized ischemic disease. B-apoprotein was the lipidic parameter with the greatest predictive potential. All together these data suggest that in coronary patients, a discrete increase in plasma cholesterol can imply a risk of suffering ischemia in some other arterial territories. Diastolic blood pressure, cholesterol and diabetes mellitus are the factors with the highest predictive potential for the generalization of arteriosclerosis.