Lipoprotein (a) and lipid and non-lipid risk factors in coronaries risk assessment.

PURPOSE: Several studies showed that elevated plasma levels of lipoprotein(a) [Lp(a)] represent a predictor for cardiovascular risk. Based on already existing literature data, we aim to study the relationship between Lp(a), lipids and other cardiovascular risk factors in individuals with or without coronary heart disease. METHODS: We performed a cross-sectional transversal study on 208 patients (100 men and 108 women) aged between 37-75, with or without old myocardial infarction. In all the patients were evaluated the cardiovascular risk factors, the plasma level of the lipid fractions and Lp(a). The relationship between Lp(a) and the lipid and non-lipid risk factors were evaluated by the logistic regression method. RESULTS: The myocardial infarction group had higher values of plasma levels of Lp(a) (0.37 +/- 0.28 vs. 0.29 +/- 0.23 g/L, p < 0.05), and LDL-C (125.66 +/- 41.21 vs. 113.44 +/- 46.64 mg/dL, p < 0.05), than the group without coronary heart disease, as well as higher values of plasmatic TC/HDL-C ratio (4.31 +/- 1.55 vs. 4.08 +/- 1.29, p < 0.05), with significantly decreased plasmatic levels of HDL-C (45.88 +/- 12.04 vs. 53.22 +/- 23.12 mg/dL, p < 0.05). The association between the high Lp(a) plasma levels and the severity of coronary vessels number involved was significant. Multivariate analysis performed with adjustments for cardiovascular risk factors showed that the Lp(a), LDL-C and CT/HDL-C ratio levels are significant and independent predictive markers of coronary heart disease. CONCLUSION: The results show that the high Lp(a) plasma levels represent an independent cardiovascular risk factor, with superior risk prediction than the conventional lipid fractions. Our results confirm the Lp(a) as a marker for cardiovascular risk assessment in clinical practice.

The correlation between alcohol consumption, lipids, apolipoproteins and coronary heart disease.

UNLABELLED: Moderate alcohol consumption is associated with a lower risk of coronary heart disease. Whether alcohol is truly protective or whether the amount, type, or pattern of intake is the most important is still under debate. The aim of this study was to evaluate the relationship between effect of presence, rhythm, frequency of alcohol consumption on lipid and apo-lipoproteic profile, and indirectly of cardiovascular risk. METHODS: We performed a cross-sectional transversal study on 105 patients free of coronary heart disease (men and women) aged 58.08 (10.43) years. Alcohol and dietary intakes were assessed by using validated questionnaires. The dosages of lipids were measured by the enzymatic method and the dosages of apolipoproteins were measured by immuno-turbidometric methods. RESULTS: Presence of chronic alcohol consumption independently correlated with HDL-Cholesterol (p < 0.5) and apoA-I levels (p < 0.05). Ethylic dose positively associated with HDL-C (r = 0.71, p = 0.003) and apoA-I levels (r = 0.65, p = 0.002). Mean HDL-C levels significantly increase from the <1 drink/day group (46.58 +/- 35.12) to >7 drinks/day group (55.54 +/- 49.12) (p < 0.05). apoA-I also had a higher mean level for the >7 drinks/day group (1.78 +/- 1.21) than the 1-6 drinks/day group (1.58 +/- 0.05) and than the <1 drink/day group (1.53 +/- 0.09). Differences were found to be significant (p < 0.05). CONCLUSION: Alcohol consumption interferes with lipids and lipoproteins balance and is one of the parameters that indirectly decrease the cardiovascular risk. A higher ethylic quantity and rhythm of consumption correlates with a higher protection offered by HDL-Cholesterol and apo A-I.

The impact of the metabolic syndrome on the patients with acute coronary syndrome.

BACKGROUND: The subjects with metabolic syndrome are an increased risk for the development of diabetes mellitus and cardiovascular disease as well as an increased mortality for cardiovascular disease in all causes. The prevalence of the metabolic syndrome after acute coronary syndrome has not been studied yet. We aimed to evaluate the prevalence of the metabolic syndrome and to evaluate its cardiovascular risk potential using the National Cholesterol Education Program's Adult Treatment Panel III (NCEP-ATP III) criteria. METHODS: We performed a cross sectional study in 256 patients with acute coronary syndrome. The definition of the metabolic syndrome was based on NCEP-ATP III criteria. The cardiovascular risk factors that define the metabolic syndrome and their correlation with the cardiovascular risk were evaluated by descriptive and interferential statistical methods. RESULTS: The prevalence of metabolic syndrome was 47.26%, as assessed by criteria of the NCEP-ATP III. The presence of the metabolic syndrome has been positively correlated with the cardiovascular risk (OR 1.29; 95% CI, 1.05-1.54, p=0.047). The cardiovascular risk has significantly correlated with the increasing of the components number that defines the metabolic syndrome. Among the components of the metabolic syndrome, HDL-Cholesterol was the most significantly correlated with the cardiovascular risk in the patients with acute coronary syndrome (OR 3.60; 95% CI 2.14-5.06; p=0.002). CONCLUSION: The prevalence of the metabolic syndrome according to the NCEP-ATP III criteria was high, and positively correlated with the cardiovascular risk in the patients with acute coronary syndrome. The cardiovascular risk rises proportionally with the number of metabolic components.

Recurrent thrombembolic risk in patients with multiple thrombophilic disorders.

Genetic mutations of the coagulation factors II and V (G20210A and G1691A - factor V Leiden)--as well as the one for methylene tetrahydrofolat reductase's (MTHFT) gene C677T are diseases with dominant autosomal transmission characterized by thromboembolic events leading to deep vein thrombosis and/or pulmonary embolism. The authors show the clinical observation of 2 cases of recurrent deep venous thrombosis evolving with pulmonary embolism in patients with genetic defects of the coagulating factors. The positive diagnostic was put on the paraclinical findings and the etiology was established from the homocysteine genetic modification of the G20210A prothrombin and factor V Leiden and MTHFT mutation. Publishing these cases will allow us to emphasize the importance of the genetic factors for thromboembolic episodes and especially for the consequences of the long-term anticoagulant therapy.