Search

The association of stroke to acute myocardial infarction (AMI) may be considered either a consequence of the myocardial ischemia, or separate entity. Purpose: To appreciate the short term(30- days)evolution of subjects that associate an ischemic cerebral stroke to an AMI within minimum one and maximum 6 days from the onset of the myocardial infarction. Material and Methods: There were included 97 subjects during 2005-2008, divided in two groups: group A-association of stroke to AMI; groupB-case control, subjects with stroke and no AMI. Results: The cardiovascular burden did not differ significantly in the two groups.In the intra-group analysis the presence of peripheral arterial disease, high total cholesterol/HDL-cholesterol ratio and post-AMI atrial fibrillation correlated to a more severe neurological status (p<0.05,CI95%). The association of stroke to the AMI paradoxically leads to an appreciation of the neurological status at 30days (p<0.05,CI95%). The mortality did not differ significantly. Conclusions: The association of a an ischemic stroke to a myocardial infarction is not a negative shot term neurological prognostic factor, without significantly influencing the mortality. [ABSTRACT FROM AUTHOR]

The association of stroke and acute myocardial infarction may be considered either a consequence of stroke, or a separate entity. Purpose: To appreciate the short term (30-days) evolution of subjects that associate acute myocardial infarction to cerebral stroke within minimum one and maximum 7 days from the onset of the cerebral stroke using several parameters. Material and Methods: There were included 55 subjects divided in two groups: group A - association of myocardial infarction to stroke within 1 - 7 days from stroke's onset; group B - case control group having subjects with stroke and no myocardial infarction. Results: The burden of cardiovascular diseases did not differ significantly in the two groups, with the exception of hypertension and stroke history that were associated to group A, together with CRP presence, lower HDL cholesterol and higher CT/HDL cholesterol ratio when screened. In the intra-group analysis, persistent hypertension at 72 hours and hyperglycemia at 48 hours correlated to a severe neurological status (p<0.05, CI95%). The occurrence of myocardial infarction leads to a depreciation of the neurological status in group A subjects at 15 and 30 days when compared to group B subjects (p<0.05,CI95%). The mortality in the groups did not differ significantly. Conclusions: The association of a myocardial infarction to an ischemic stroke is an independent negative prognostic factor without influencing the mortality. When other risk factors are present they may be omitted in favor for myocardial infarction on the respect to 30-days prognosis. [ABSTRACT FROM AUTHOR]

Introduction: The prevalence of obesity is continuously increasing among children with high risk for dyslipidemic troubles. Objective: The aim of the present study was to determine the prevalence of lipid abnormalities among children and adolescents in our geographic area and to evaluate IDF dyslipidemic criteria at increased risk of developing metabolic syndrome. Material and methods: 50 obese children aged 3-19 yrs (first group - 15 children, under 10 yrs and the second group - 35 children, above 10 yrs) and 50 normostenic children (age- and gender- matched controls) were evaluated. Blood samples for serum lipids were collected in all children. Total cholesterol, HDLcholesterol, triglycerides were measured and LDL cholesterol was calculated. This values were compared with the values above the 90 th percentile for gender and age (for total cholesterol, LDL-cholesterol, triglycerides), and also with the values under the 5 th percentile (for HDL cholesterol). In addition, the results obtained from the evaluation of second lot had been compared with the IDF criteria, using a single cut point for all pediatric age groups. The statistical program SPSS was used. Results: Total cholesterol, LDL-cholesterol, triglycerides and triglyceride/ HDL, LDL/HDL cholesterol ratio were significantly higher among the obese children, compared to control group. HDL cholesterol was significantly lower among the obese children. From the evaluation of obese children separately (first, second lot and globally) the following results are: hypertriglyceridemia - 33,3%, 22,85%, 26%: high LDL cholesterol - 13,3%, 22,85%, 20%; low HDL cholesterol - 6,6%, 2,85%, 4%. Working with the IDF criteria on the second lot, the following prevalences were revealed: for hypertriglyceridemia - 2,85%, for low HDL cholesterol - 31,42%. Conclusions: The disorder of the lipid profile is present in 44% of our obese children, reporting to the normal values for age and gender. Evaluation of the individual results leads to underdiagnostication of the dyslipidemia reporting to the IDF criteria. [ABSTRACT FROM AUTHOR]

Serum paraoxonase (PON1) is the main enzyme that confers antioxidant properties of HDL-lipoprotein, beeing responsible for the mechanism by which they inhibit the oxidation of LDL and HDL itself. It is a calcium-dependent enzyme associated HDL, able to hydrolyze oxidized fatty acids in phospholipids and reduce fat accumulation from oxidized LDL, thus inhibiting pro-inflammatory response promoted by these [1]. A low serum PON activity is correlated with an increased risk of coronary disease, carotid atherosclerosis and myocardial infarction [2]. Variation of PON activity is influenced both by genetic factors - PON polymorphism and acquired factors [3]. [ABSTRACT FROM AUTHOR]

Introduction. Apolipoprotein E plays a crucial role in Gaucher disease's pathogenesis. Materials and Methods. The aim of our study was to identify the allelic variants of apolipoprotein E (ApoE) gene in Romanian type 1 Gaucher disease patients. Fourtyone patients, 31 receiving enzyme replacement therapy (group A) and 10 untreated (grup B) were analized. Plasma levels of total cholesterol, HDL, LDL-cholesterol, triglycerides and apolipoprotein E were determined by enzymatic methods. 41 patients have been also genotyped for ApoE polymorphism by PCR-RFLP. Results. Globally, three genotypes were identified: ϵ3/ϵ3, ϵ3/ϵ4 and ϵ2/ϵ3 in 75.6%, 14.6% and respectively 9.8% of the patients. The plasma level of Apo E was increased up to 6.20+3.86 x ULN (upper limit normal) globally (A+B), but values were different depending on the genotype: lower for genotype ϵ3/ϵ4 (3.06+1.81xULN), compared with ϵ3/ϵ3 (6.80+4.11xULN) and ϵ2/ϵ3 (6.26+1.15xULN) (p<0.05 for each). Triglycerdemia in patients carrying genotype ϵ2/ϵ3: 1.15+0.39 x ULN was superior than the values determined for genotype ϵ3/ϵ4: 0.81+0.26 (p>0.05) and for genotype ϵ3/ϵ3: 0.70+0.30 x LSN (p<0.05). The same trend of variation for ApoE and triglycerides depending onto genotype maintained similarly within group A. Plasma level of ApoE significantly correlated with triglyceridemia for all three genotypes r=0.57; 0.72; 0.85, respectively for ϵ3/ϵ3, ϵ3/ϵ4 and ϵ2/ϵ3. ERT, for 3 years, has the following consequences: decreasing level of ApoE from 8.61+6.0x to 5.42 +2.56 xULN (p >0.05), globally, in A+B; decreasing triglyceridemia - reaching the significance point for carriers of ϵ3/ϵ3 allelas - from 0.93+0.30 xULN to 0.61+0.25xULN and increasing HDL-cholesterol from 0.86+0.5x to 1.31+0.32 x LLN (lower limit normal) (p<0.05), globally, in A+B. Conclusion. This study reports the allela distibution of ApoE gene in patients with Gaucher disease, compared with general population. Plasma levels of ApoE are significantly raised and still remain high after 3 years of ERT, correlated with triglyceridemia, for all genotypes. The presence of ϵ4 allela does not results in dyslipidemic changes in treated patients, but presence of ϵ2 allela induces hypertriglyceridemia. [ABSTRACT FROM AUTHOR]

We know from literature that moderate alcohol consumption combined with physical strain leads to HDL-cholesterol increase, platelet adhesion impact through the antioxidant effect of the resveratrol and quercetine contained in red wine, and positively influences fibrinogen decrease and NO increase, and all these effects play an eventual inhibition role of the blood vessels muscles' proliferation, a stabilization of the aterosclerotic plate and endothelial disfunction correction. [ABSTRACT FROM AUTHOR]