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Results of numerous epidemiologic studies indicate that elevated serum cholesterol, especially the LDL fraction, is a major cause of coronary heart disease (CHD). Epidemiologic and angiographic evidence from primary and secondary prevention studies involving several HMG-CoA reductase inhibitors (statins) indicate that decreasing elevated serum cholesterol concentration (specifically LDL-cholesterol) can reduce the incidence of CHD and/or progression of atherosclerosis and results in a decrease in associated morbidity and mortality. It has been estimated that each 1% reduction in LDL-cholesterol concentration may result in a 1% decrease in the incidence of CHD. Furthermore, an analysis of pooled data from primary and secondary prevention studies found that treatment with a statin for a median duration of 5.4 years was associated with a 31% and 21% reduction in the risk of major coronary events and total mortality, respectively. This paper deals with the pharmacology of statins, specially with the pleiotropic effects of these drugs.

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Results of numerous epidemiologic studies indicate that elevated serum cholesterol, especially the LDL fraction, is a major cause of coronary heart disease (CHD). Epidemiologic and angiographic evidence from primary and secondary prevention studies involving several HMG-CoA reducíase inhibitors (statins) indicate that decreasing elevated serum cholesterol concentration (specifically LDL-cholesterol) can reduce the incidence of CHD and/or progression of atherosclerosis and results in a decrease in associated morbidity and mortality. It has been estimated that each 1 percent reduction in LDL-cholesterol concentration may result in a 1 percent decrease in the incidence of CHD. Furthermore, an analysis of pooled data from primary and secondary prevention studies found that treatment with a statin for a median duration of 5.4 years was associated with a 31 percent and 21 percent reduction in the risk of major coronary events and total mortality, respectively. This paper deals with the pharmacology of statins, specially with the pleiotropic effects ofthese drugs.

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Background: High density lipoproteins are an heterogeneous population of particles. Two main subpopulations have been identified, one contains Apo A-I and Apo A-II and is denominated LpA-I:A-II and another one contains only Apo A-I and is denominated LpA-I. Aim: To measure the concentrations of these particles in patients with stable coronary artery disease. Patients and Methods: Serum lipids, A-I and B apolipoproteins, LpA-I, LpA-I:A-II and LpB particles were measured in 73 men aged 33 to 82 years with angiographically documented coronary artery disease (CAD) and 33 control subjects aged 39 to 76 years. LpA-I, LpA-I:A-II and LpB were measured by a noncompetitive enzyme linked immunoassay using previously characterized monoclonal antibodies against ApoA-I, ApoA-II and apoB. Results: Patients with CAD had significantly higher mean levels of LDL cholesterol than the control group (p= 0.038). The mean concentration of LpA-I particles in patients with CAD was significantly lower (p= 0.031) than in control subjects, while the concentration of LpA-I:A-II particles was significantly higher (p=0.016). The percentage of coronary stenosis correlated negatively with LpA-I and positively with LpA-I:A-II. The best relative risk (RR) indicator in these patients was LDL-cholesterol. The relative risk increases 2.5 fold when LpA-I falls below the cut-off level. Likewise, the relative risk increases 3-fold when LpA-I:A-II raises over the cut-off level. Conclusions: Our findings indicate that the quantification of LpA-I and LpA-I:A-II particles might allow a more accurate evaluation of the CAD risk than HDL cholesterol. LpA-I might represent the antiatherogenic fraction of HDL

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A significant factor associated with hiperglicaemia in diabetes is the resultant post-translation non-enzymatic glycation of plasma and cellular proteins. This process occurs in vivo by direct chemical reaction of glucose with protein alfa and epsilon amino groups. Because of the diverse evidences for direct involvement of non-enzymatic glycation of lipoproteins in the accelerated development of atherosclerosis in diabetic patients, most attention has been focused on the pathological properties of glycated lipoproteins. Glycation of LDL was found significantly increased in diabetic patients compared with normal subjects, even in the presence of good glycemic control. Metabolic abnormalities associated with glycation of LDL incluye diminished recognition of LDL by the classical LDL receptor, and enhancement uptake of LDL by a low-affinity, high capacity receptor pathway on macrophages, thus stimulating foam cell formation, an early feature of atherosclerosis. Moreover, glycated LDL are more susceptible to oxidative modification than non-glycated LDL and glycation of LDL may alter their structure sufficiently to render them immunogenic. Being immunogenic, glycated-LDL accumulates in plasma and may enhance cholesterol ester accumulation in macrophages. Non-enzymatic glucation of HDL impairs its recognition by cells and induce a diminished efflux of cholesterol from cells membranes to HDL particles. Furthermore, glycated apolipoprotein A-l isolated from plasma of diabetic subjetcs was deficient in activating lecithin: cholesterol acyl transferase, the driving force in reverse cholesterol transport, pathway responsable of the antiatherogenic properties of HDL

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Desde que Miller en 1982, describiera la clasificación de los quistes mamarios de acuerdo a su concentración de electrólitos (relación K+/Na+) y posteriormente se demostrara una relación entre el tipo de quistes y el riesgo de cáncer de mama, se han realizado numerosos estudios tendientes a demostrar que los quistes se diferencian en otros aspectos, y a tratar de encontrar evidencias de una justificación para el mayor riesgo de cáncer de mama asociadas a los niveles de colesterol y lipoproteínas plasmáticas y de la evidencia de una relación entre diversos ácidos grasos y fenómenos de carcinogénesis en colon y mama, no hay estudios suficientes que evalúen específicamente la presencia de colesterol, triglicéridos y lipoproteínas en el líquido de quistes mamariosy relacionarla con la concentración de cationes, se estudió el líquido de 30 quistes mamarios, aspirado por punción de aguja fina. Se determinó, mediante potenciometría directa de ion selectivo, la concentración de sodio y potasio. La concentración de colesterol, triglicéridos y HDL se midió con método colorimétrico enzimático en fotémetro de flujo continuo. El colesterol LDL se calculó según la fórmula de Friedwald. Se encontraron 12 quistes de tipo I, 15 de tipo II (K+/Na+< 0,66) y 3 de tipo III (intermedio). La concentración promedio de triglicéridos fue 170,5 mg por ciento (DE 226,7); colesterol total 614,1 mg por ciento (DE 308,1); colesterol-HDL: 321,4 mg por ciento (DE 157,5) y colesterol-LDL 258,6 mg por ciento (DE 244,2). No hubo diferencias significativas en las concentraciones de ninguno de ellos entre los quistes de tipo I y los de tipo II. No se encontró relación entre la concentración de potasio y la concentración de colesterol triglicéridos, HDL y LDL

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Se realiza un estudio de medición de presión pulmonar en un grupo de 24 niños con hiperplasia adenoamigalina severa que presentan crisis de apnea obstructiva durante el sueño y se compara con un grupo de 10 niños sanos. Las edades de los niños fluctuan entre los 2 y 8 años. A todos se les efectuó un electrocardiograma (ECG) y un ecocardiograma Doppler (ECO-D) midiendo la presión media pulmonar (PMP), presión sistólica (PS) y la presión diastólica (PD). En todos los niños las mediciones de presión pulmonar y el ECG, estuvieron dentro de rangos normales no demostrando hipertensión pulmonar (HTP)

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Se midieron las concentraciones séricas y la distribución de frecuencia de lipoproteína (a) en 71 niños caucásicos y 41 pehuenches (de 6 a 15 años de edad) que habitan en la zona del Alto Bío-Bío, VIII Región geopolítica de Chile. Adicionalmente se registraron las isoformas de apolipoproteína (a) en 50 de los participantes. Las concentraciones de lipoproteína (a) fueron 10,5 ñ 6,2 y 21,3 ñ 34,5 mg/dl, respectivamente, en los niños pehuenches y caucásicos (p< 0,001). La distribución de las frecuencias de ambos grupos mostró inclinación hacia las concentraciones más bajas de una curva normal. La prevalencia de concentraciones séricas de lipoproteína (a) consideradas riesgosas en términos de enfermedades cardiovasculares (> 30 mg/dl) fue de 21,1 por ciento y 7,3 por ciento, respectivamente, para niños caucásicos y pehuenches. En los caucásicos se observó una correlación inversa entre el tamaño de la isoforma de apolipoproteína (a) y la concentración plasmática de lipoproteína (a) (r=0,77), lo que fue menos claro en la población pehuenche (r=0,33)

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Lipoprotein(a) is considered an independent cardiovascular risk factor. Forty four children aged between 3 and 18 years old with family history of coronary artery disease and 44 age and sex matched controls were studied. A fasting blood sample was obtained to measure total, HDL and LDL, cholesterol, triglycerides. A1 and B apoproteins and lipoprotein (a). Comparaed to controls, children with family history of coronary disease had higher total cholesterol (177ñ35 and 159ñ23 mg/dl respectively). LDL cholesterol (112ñ34 and 94ñ21 mg/dl respectively), triglycerides (89ñ38 and 71ñ25 mg/dl respectively), apoprotein B (85ñ17 and 65ñ13 mg/dl respectively), and lipoprotein (a) (40ñ50 and 23ñ31 mg/dl respectively). Thirty two percent of children with positive family history had lipoprotein (a) levels over 30 mg/dl, compared to 23 percent of controls. Children with family history of coronary artery disease have higher levels of cholesterol, triglycerides and lipoprotein (a) than matched controls

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