Diagnóstico de síndrome metabólico. Adecuación de los criterios diagnósticos en nuestro medio. Recomendaciones del foro HDL. Resumen ejecutivo / Diagnosis of Metabolic Syndrome. Adaptation of Diagnostic Criteria in Our Setting. Recommendations of the Hdl Forum

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El índice tobillo-brazo: un método incruento de evaluación del riesgo cardiovascular / The ankle/arm index: a noninvasive method for evaluating cardiovascular risk

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Metabolismo lipoproteico y deporte / Lipoprotein metabolism and sports

El ejercicio físico regular tiene efectos beneficiosos protegiendo contra el riesgo de presentar episodios de enfermedad cardiovascular. Los mecanismos a través de los que ejerce esta acción beneficiosa incluyen un efecto hipotensor, un aumento de la sensibilidad a la insulina y una mejoría en el perfil de los lípidos y lipoproteínas plasmáticas. El ejercicio físico regular ha demostrado en estudios caso-control y en estudios prospectivos que induce una disminución en la concentración plasmática de triglicéridos, de colesterol total y de colesterol transportado por las lipoproteínas de baja densidad (LDL) con aumento del colesterol vehiculizado por las lipoproteínas de alta densidad (HDL). Se ha observado una buena correlación entre los cambios favorables en las lipoproteínas plasmáticas y la dosis de ejercicio, principalmente en los individuos entrenados que hacen ejercicio moderado e intenso. De acuerdo con estos hechos, la actividad física regular junto a los adecuados cambios dietéticos y otros hábitos de vida saludable forman parte del tratamiento de los pacientes con hiperlipidemia y disminuyen el riesgo de sufrir enfermedad cardiovascular (AU)

Low-density lipoprotein particle size, triglyceride-rich lipoproteins, and glucose tolerance in non-diabetic men with essential hypertension.

The aim of the study is to investigate serum lipoproteins abnormalities including low-density lipoprotein (LDL) particle size, and their relationship with other cardiovascular risk factors in men with essential hypertension. Plasma glucose and serum insulin levels during oral glucose tolerance test (OGTT), serum lipoprotein(a), apolipoprotein (apo) A-I. apo B. cholesterol and triglycerides in serum and in lipoproteins, and LDL particle diameter were measured in thirty-eight consecutive newly-diagnosed non-diabetic untreated hypertensive men and 38 healthy male controls. Plasma glucose at baseline, 60 and 120 min during OGTT was significantly higher in patients than controls whereas serum insulin levels did not differ between patients and controls. Serum apo B and triglycerides were significantly raised in patients compared with controls (1.08 +/- 0.17 g/L [mean +/- SD] vs 0.97 +/- 0.22 g/L. p < 0.05, and 1.56 +/- 0.90 mmol/L vs 1.15 +/- 0.57 mmol/L, p < 0.05, respectively). Very-low-density lipoprotein (VLDL) triglycerides and LDL-cholesterol were increased in patients compared with controls (0.89 +/- 0.79 mmol/L and 0.54 +/- 0.35 mmol/L, p < 0.05, and 4.08 +/- 0.85 mmol/L and 3.60 +/- 0.92 mmol/L, p < 0.05, respectively) whereas high-density lipoprotein (HDL) cholesterol was lower in patients compared with controls 0.95 +/- 0.22 mmol/L and 1.07 +/- 0.20 mmol/L, p < 0.05). Adjustment for body mass index, abdominal/hip perimeter ratio and area under the glucose curve did not attenuate the relationship between hypertension and VLDL-triglycerides. Six patients and two controls had a mean LDL diameter < or = 25.5 nm and in the former serum triglycerides ranged from 1.86 mmol/L to 2.37 mmol/L. Mean LDL particle diameter in both patients and controls showed an inverse relationship with log-transformed serum triglycerides (r = - 0.51, p < 0.001 and r = - 0.47, p < 0.005, respectively). Among patients, those with serum triglycerides > or = [corrected] 1.58 mmol/L had a lesser mean LDL diameter than those with triglycerides above this threshold (25.78 +/- 0.47 nm vs 26.30 +/- 0.35 nm, p < 0.001). Higher plasma glucose, serum apo B and LDL-cholesterol as well as the decrease in serum HDL-cholesterol in patients with hypertension are consistent with high coronary heart disease risk. Not only mild hypertriglyceridemia but also high-normal serum triglycerides in themselves or as a surrogate of a predominance of small dense LDL particles in plasma convey an additional risk for cardiovascular disease in hypertensive patients even though routine plasma lipids are within or near normal range.

Decreased endogenous antioxidant enzymatic status in essential hypertension.

Several lines of evidence suggest that patients with essential hypertension have impaired endothelial nitric oxide activity and increased superoxide anion production. However, the mechanisms underlying these abnormalities remain unknown. We measured enzymatic superoxide dismutase (SOD) and glutathione peroxidase (GPX) activities in erythrocytes and whole blood, respectively, in 30 newly-diagnosed, normolipidaemic untreated mild hypertensive patients and in 164 age-matched healthy controls. SOD and GPX activities in hypertensive patients (806 +/- 225 U/Hb.g and 5491 +/- 2073 U/L, respectively) were significantly lower than in the control group (931 +/- 202 U/Hb.g and 6669 +/- 1560 U/L, respectively) (P < 0.005). No significant association was found between these antioxidant enzyme activities and blood pressure in normotensive controls. In the hypertensives, only log-transformed SOD activity showed a significant negative correlation with systolic and diastolic blood pressure (r = 0.37, P < 0.05; r = 0.64, P < 0.0001, respectively). The low endogenous antioxidant enzyme activities observed may in turn result in decreased superoxide anion removal leading to nitric oxide inactivation. Journal of Human Hypertension (2000) 14, 343-345

Differential expression of double-band apolipoprotein(a) phenotypes in healthy Spanish subjects detected by SDS-agarose immunoblotting.

A sodium dodecyl sulphate-agarose apolipoprotein(a) [apo(a)] phenotyping method was set up to attain accurate scanning densitometry of proteins. Serum samples from 99 healthy Spanish men were analysed and twenty-five different apo(a) isoforms (12 to 37 kringle 4 repeats) were detected. Double-band phenotypes accounted for 39.4% (n = 39) and three different patterns of protein expression were identified: pattern A (20.5% of double-band phenotyped samples) predominantly expressed the highest molecular weight isoform; pattern B (53.9%) mainly the lowest molecular weight isoform, and pattern AB (25.6%), expressed both isoforms equally. A significant linear association between expression pattern and lipoprotein(a) [Lp(a)] concentration > or = 0.30 g/l was observed. Single-band phenotyped samples (n = 60) were stratified according to apo(a) kringle 4 repeat categories and showed that 90% of isoforms < 20 K4 repeats had high Lp(a) concentrations (> or = 0.30 g/l), whereas isoforms with 20 to 24 or more than 24 kringle 4 repeats had Lp(a) concentrations > or = 0.30 g/l in 47% and 14%, respectively. A logistic regression model was fitted to test the association between apo(a) size, expression pattern and Lp(a) concentration. In this model, apo(a) isoform < 25 kringle 4 repeats was significantly associated with serum Lp(a) concentration > or = 0.30 g/l in both single and double-band phenotyped samples (odds ratio = 8.9, p < 0.001). In the latter, a differential expression pattern with respect to smaller size isoforms (pattern AB vs A) was significantly associated with Lp(a) concentration > or = 0.30 g/l (odds ratio = 17.97, P = 0.045). Heterogeneity in protein apo(a) size expressed according to kringle 4 repeat number could be categorized in heterozygous phenotypes as three patterns. When small-sized isoform was expressed (pattern B) or both isoforms were equally expressed (pattern AB), the probability of having Lp(a) > or = 0.30 g/l is higher.

Lacrimal immunoglobulins in rheumatoid arthritis patients with or without Sjögren's syndrome.

The aim of the present study was to analyse immunoglobulin G, A, and M levels in tears of patients with rheumatoid arthritis with or without keratoconjunctivitis sicca (KS) which define Sjögren's syndrome (SS). Tears were collected from the lower cul-de-sac by capillarity (100-300 microl). Tear IgG, IgA and IgM levels were determined by radial immunodiffusion. Samples diluted 1:10 were used for IgA and IgG and non-diluted ones for IgM. Fifty-three patients with rheumatoid arthritis and 30 healthy control subjects were studied. In all individuals IgA predominated in tears, IgG levels were low but with a very wide range and IgM was present in very low concentrations. The IgG concentration in tears showed statistically significant differences between the control group and that of rheumatoid arthritis and KS. IgG in tears correlated positively with the rose bengal test (r=0.2848, p<0.05) and negatively with the Schirmer test (r=0.3042, p<0.05). Tear IgG measurement might provide a marker for eye involvement in patients with rheumatoid arthritis and KS which define SS.

Thrombomodulin and induced tissue factor expression on monocytes as markers of diabetic microangiopathy: a prospective study on hemostasis and lipoproteins in insulin-dependent diabetes mellitus.

Vascular complications are the main cause of morbidity in diabetes mellitus. To evaluate lipoprotein and hemostatic parameters and their relationship with clinically detectable microangiopathy, we studied 58 insulin-dependent diabetes mellitus patients and 60 controls matched for age, sex, and body mass index. Thirteen patients presented clinically detectable microangiopathy (8 retinopathy and 5 both retinopathy and microalbuminuria). A cross-sectional study of lipid profile, coagulation parameters, and a flow-cytometric evaluation of tissue factor expression in normal monocytes induced by patient plasma were performed. Patients were re-evaluated for microangiopathy in a 3-year median follow-up. Patients showed triglyceride enrichment in low (P = 0.00002) and high density lipoproteins (P = 0.004) and increased levels of D-dimer (P < 0.00001), prothrombin fragment 1 + 2 (P < 0.00001), and thrombin-antithrombin III complex (P = 0.0001). Patients with clinically detectable microangiopathy had increased type 1 plasminogen activator inhibitor (P = 0.00001), thrombomodulin (P = 0.02), and induced monocyte tissue factor expression (P < 0.00001). Nine patients developed clinically detectable microangiopathy in the follow-up and the only predictive variable was increased induced tissue factor expression. In conclusion, in these patients elevated thrombin and fibrin generation reflects a hypercoagulable state but clinically detectable microangiopathy seems related to endothelial cell injury markers and to increased induced tissue factor expression on monocytes.

Interaction of family history of atherosclerosis with atherogenic lipid traits in men with non-coronary atherosclerosis.

Family history of atherosclerosis has been recognised as an nonmodifiable cardiovascular risk factor. Lipid levels, together with hypertension and diabetes, appear to have an inheritable component. The aim of the study was to ascertain whether lipoprotein abnormalities of 169 adult patients with non-coronary atherosclerosis were associated with a family history of atherosclerosis. Besides intermediate density lipopoprotein composition and Lp(a) levels, we focused on apo(a) and apo E phenotypes, LDL cholesterol/apo B ratio, VLDL triglyceride/HDL cholesterol ratio, and environmental factors. We found that patients with a family history of atherosclerosis had a higher prevalence of VLDL triglyceride/HDL cholesterol ratio above 1.8 (51.3% vs 34.7%) than patients without. Similarly, there was a significant inverse correlation between both considered ratios (r = -0.24, p < 0.05). The odds ratio of the presence of both abnormal ratios (4.60, 95% CI, 1.41-15.00) and low molecular weight apo(a) isoforms (3.30, 95% CI, 1.05-10.30 and family history of atherosclerosis was independent of smoking and hypertension. Apo(a) isoform size seems to be more important than Lp(a) concentrations in the family history of atherosclerosis risk determination. Subsequent analysis showed that patients with a family history of atherosclerosis had a greater-than-fourfold increased risk of having one or both abnormal ratios reflecting metabolic disturbances which probably constitute a combined trait. Family history of atherosclerosis may constitute a specific lipoprotein-related marker of atherosclerosis. Such a marker often precedes the onset of overt disease and may contribute to identifying patients with an atherogenic lipoprotein profile even in the absence of classical lipid risk factors.

Autonomic dysfunction in patients with non-alcoholic chronic liver disease.

AIMS: To assess the presence of autonomic neuropathy in patients with non-alcoholic chronic liver disease and its relationships with the severity of liver damage. METHODS: Thirty non-alcoholic patients with chronic liver disease and 26 healthy control subjects were studied. The silicone imprint technique was used to quantify the number of functioning sweat glands in order to assess peripheral sympathetic dysfunction. Heart rate variations in response to deep breathing at 6 per minute (deltaR6), to a Valsalva maneuver, and with orthostatism (RRmax/RRmin) were determined to assess parasympathetic vagal function. RESULTS: Mean values for autonomic tests were significantly lower in the group of patients with non-alcoholic chronic liver disease than in the control subjects. The number of activated sweat glands in the foot was abnormal in 19 (63%) patients. Among vagal tests, Valsalva ratio was abnormal in 14 (46%) and deltaR6 in 11 (36%) patients with liver disease. Vagal neuropathy (two or more abnormal heart rate tests) was definite in nine patients (30%). CONCLUSIONS: A high prevalence of abnormalities in both sympathetic and parasympathetic function tests, with a poor relationship with liver function parameters, has been found in patients with non-alcoholic chronic liver disease.

Interrelationship of triglyceride-rich lipoproteins, serum lipoprotein (a) concentration and apolipoprotein(a) size.

At present, the biochemical mechanisms underlying lipoprotein(a) (Lp(a)) metabolism are not fully understood. We analysed sera from 202 patients with atherosclerotic disease and 109 healthy subjects as a control group to investigate the possible relationship between triglyceride-rich lipoproteins (TRL) and serum lipoprotein(a) levels. To assess the influence of apolipoprotein (apo) (a) isoforms on the Lp(a)-TRL association, the apo(a) phenotypes of 177 patients and 95 controls were included in the analysis. Patients with atherosclerotic disease showed triglyceride levels almost within the normal range. There was no significant correlation between serum Lp(a) levels and triglyceride concentrations, or between Lp(a) and TRL levels in either group. When a subset of subjects from each group with serum triglycerides above 1.7 mmol l-1 was considered, a significant negative correlation between lipid concentration of very low density lipoproteins (VLDL) and serum Lp(a) levels was found only in patients. Control subjects with triglyceride levels under or over 1.7 mmol l-1 showed similar median Lp(a) levels (0.06 gl-1), in contrast to atherosclerotic patients, in whom median Lp(a) concentration was higher in the subset with serum triglycerides under 1.7 mmol l-1 than in those with triglyceride concentration above this value (0.16 vs. 0.13 gl-1). When patients with triglyceride concentrations above 1.7 mmol l-1 were classified into quartiles according to VLDL lipid concentration, subjects with the highest quartiles showed the lowest Lp(a) median levels. Despite the dependence of the Lp(a) concentration on apo(a) size isoforms, we found no effect of apo(a) genetic polymorphism on triglyceride levels or on TRL concentrations. We conclude that the variation in TRL metabolism may constitute a source of variation in serum Lp(a) concentrations that is independent of the genetically determined apo(a) molecule size.

Increased radionuclide uptake on bone scintiscans: a common but not clinically significant finding for human immunodeficiency virus type 1-infected patients free of osteoarticular symptoms.

The aim of this study was to describe findings of bone scintiscans and their clinical significance for patients infected with human immunodeficiency virus type 1 (HIV-1); 33 HIV-1-infected patients (22 men and 11 women) free of osteoarticular symptoms were included in the study. Plain bone roentgenograms, bone mineral contents (measured by dual-photon absorptiometry), and scintiscans (determined with 99mTc diphosphonate) were obtained for all subjects. Plain bone roentgenograms showed no abnormalities, and bone mineral contents were within the normal range for all patients. Radionuclide bone scans were unremarkable for eight patients (24%) and showed symmetrical abnormally increased uptake in the epiphyseal region of the appendicular skeleton in 25 (76%). Follow-up of the patients for > or = 1 year ruled out subsequent development of osteoarticular disorders. Generalized, symmetrical increased radionuclide uptake on bone scans is a common finding for HIV-1 infected patients free of osteoarticular symptoms. This finding is probably related to bone marrow hypercellularity and is of no clinical significance; therefore, other diagnostic procedures are not required in the workup of these patients.