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Biomedical subjects

M Sentí

Publications and source records attributed to M Sentí.

At least 19 recordsLinked to original sources
PubMed2002

Short-term mortality of myocardial infarction patients with diabetes or hyperglycaemia during admission.

AIM: The hypothesis that patients with hyperglycaemia during admission, regardless of previous diagnosis of diabetes, have worse prognosis than those with normal glucose values is controversial. The objective was to assess the role of hyperglycaemia on short-term mortality after myocardial infarction (MI). METHODS AND RESULTS: A cohort study nested in a prospective registry of MI patients in the reference hospital of Gerona, Spain was performed. All consecutive MI patients under 75 were registered between 1993 and 1996. Patient and clinical characteristics, including previous diagnosis of diabetes, glycaemia on admission and in the next four days, were recorded. Patients with glycaemia on admission or four day mean glycaemia >6.67 mmol/l were considered hyperglycaemic. The main outcome measure was mortality at 28 days. Of 662 patients with MI included, 195 (29.7%) had previously known diabetes mellitus, but 457 (69.0%) had glycaemia >6.67 mmol/l on admission. Patients with hyperglycaemia on admission were older, more often female, more frequently had a previous diagnosis of diabetes, developed more complications, and had higher 28 day mortality. The effect of admission glycaemia >6.67 mmol/l on 28 day mortality was independent of major confounding factors, particularly previous diagnosis of diabetes (OR=4.20, 95% confidence intervals 1.18 to 14.96). CONCLUSIONS: Higher 28 day mortality was observed among MI patients with glycaemia on admission >6.67 mmol/l compared with patients with lower levels, independently of major confounding variables and, particularly, previous diagnosis of diabetes. This early, simple, and inexpensive marker of bad prognosis after MI should prompt the application of more aggressive treatment of MI and risk factors and, probably, of glycaemia during admission.

Adult↗
PubMed2001

Interaction between the Gln-Arg 192 variants of the paraoxonase gene and oleic acid intake as a determinant of high-density lipoprotein cholesterol and paraoxonase activity.

Olive oil, rich in oleic acid, could play a particular beneficial role in the anti-atherogenic effects attributed to the Mediterranean diet. Paraoxonase (PON1) has emerged as the component of high-density lipoproteins (HDL) most likely to explain its ability to attenuate the oxidation of low-density lipoproteins. We hypothesised that oleic acid intake might be associated with changes in PON1-HDL associated particles, and investigated the impact, if any, on this association of the PON1-192 polymorphism, a common polymorphism that strongly modulates PON1 activity. Six hundred and fifty-four men randomly selected from the census were studied. Oleic acid intake was calculated from a 72-h recall questionnaire with specific software. Oleic acid intake groups (low vs. high) were created by stratifying the population according the median value as a cut-point. After adjusting for confounding variables, high oleic acid intake was associated with increased HDL cholesterol levels and PON1 activity only in subjects with the QR and the RR genotypes, respectively. Analyses of the variance showed a statistically significant interaction between PON1-192 genotypes and oleic acid intake for log PON1 activity (P=0.005) and a marginally significant interaction for HDL cholesterol (P=0.066). These results suggest that the beneficial effect of increasing oleic acid intake on HDL and PON1 activity at population level is especially observed in subjects carrying the R allele of the PON1-192 polymorphism.

Adult↗
PubMed2001

Physical activity modulates the combined effect of a common variant of the lipoprotein lipase gene and smoking on serum triglyceride levels and high-density lipoprotein cholesterol in men.

Physical activity has been identified as a protective factor against the occurrence and progression of coronary heart disease. The lipoprotein lipase (LPL) HindIII polymorphism has been associated with changes in triglyceride and high density lipoprotein (HDL)-cholesterol levels. We have investigated whether the association between the LPL HindIII genetic polymorphism and lipid levels is modified by physical activity. We have also tested the hypothesis that physical activity may interact with smoking and the LPL HindIII polymorphism to determine an individual's plasma lipid concentrations. A total of 520 men were selected from a representative sample used in a population study conducted in Gerona, Spain. The median value (291 kcal/day) of energy expenditure in leisure-time physical activity of the studied sample was selected as a cut-off to define sedentary or active subjects. Serum HDL-cholesterol was positively and significantly associated with the amount of daily energy expenditure in physical activity, whereas inverse associations were seen between physical activity and triglyceride concentration and with the triglyceride to HDL-cholesterol ratio. These effects were consistent across LPL HindIII genotypes. There was a statistically significant interaction between LPL genotype and smoking on lipid concentrations. No statistically significant differences were observed in lipid levels of active or sedentary non-smokers between H- carriers and H+H+ homozygotes for the LPL HindIII polymorphism. In smokers, sedentary H+H+ homozygotes showed significantly higher triglyceride and lower HDL-cholesterol concentrations than sedentary H- carriers. These differences were smaller and not statistically significant when lipid values of active H+H+ homozygotes were compared with active H- carriers. Among all subgroups, sedentary smokers with the H+H+ genotype had the most adverse lipid profile, which was considerably less adverse in H+H+ smokers who were physically active. These findings suggest that the presence of the H+H+ genotype has a deleterious effect on lipid profile in an adverse environment such as smoking, and that the expenditure of more than 291 kcal/day in physical activity attenuates this effect.

Cholesterol, HDL↗
PubMed2001

Relationship of age-related myocardial infarction risk and Gln/Arg 192 variants of the human paraoxonase1 gene: the REGICOR study.

Paraoxonase1 (PON1) seems to exert a major antioxidant effect by removing lipid-peroxidation products. A common polymorphism of the PON1 gene, the PON1-192 genetic polymorphism, modulates PON1 activity and has been related in some studies to coronary heart disease. Oxidized LDL is believed to play a crucial role in the pathogenesis of atherosclerosis and there are studies providing support for the oxidative stress theory of aging. We have conducted a case-control study to determine whether PON1 activity and PON1-192 genetic variants have a different impact on myocardial infarction (MI) risk among individuals stratified by tertiles of age distribution. PON1-192 genotypes and PON1 activity were determined in 280 consecutive MI patients and 396 control subjects. Serum PON1 activity levels were significantly higher in controls than in MI patients [226 U/l (159-351) vs. 216 U/l (146-298), median (interquartile range), P=0.005]. A decline of PON1 activity levels with advancing age in subjects carrying the low-activity QQ genotype was observed, particularly in MI patients. PON1 activity and age negatively correlated in MI patients but not in controls. In the entire population, middle-aged and older subjects showed MI risks of 1.89 (P=0.012) and 2.69 (P<0.001) respectively, compared with young subjects. These risks increased to 2.41 (P=0.016) and 4.39 (P<0.001), respectively, in QQ homozygotes in comparison with younger QQ homozygotes, decreased to 1.53 (P=0.314) and 2.08 (P=0.112), respectively, in QR heterozygotes, and also lowered to 1.95 (P=0.410) and 0.51 (P=0.508) in RR homozygotes who were middle-aged and older, respectively, compared with younger RR carriers. The effect of PON1-192 genotypes on the association of the older age-category and MI risk was gene-dosage related. PON1 activity decreases as a function of age in subjects homozygous for the Q allele. Age may also act on MI risk as a function of PON1-192 alleles. The risk of MI increases with advancing age, principally among subjects carrying the low-activity QQ genotype.

Adult↗
PubMed2001

Paraoxonase1-192 polymorphism modulates the nonfatal myocardial infarction risk associated with decreased HDLs.

Serum paraoxonase1 (PON1), a high density lipoprotein (HDL)-linked enzyme, appears to have a role in the protection of low density lipoproteins from oxidative stress. PON1 enzyme activity for paraoxon as a substrate is modulated, along with others at the PON1 locus, by the PON1-192 polymorphism, which contains low paraoxon-activity and high paraoxon-activity alleles (Q and R, respectively). The association of PON1 with HDL suggests that impaired serum concentrations of the lipoprotein could have consequences for the susceptibility to oxidative stress. Because PON1-192 polymorphism strongly influences PON1 activity toward paraoxon, we tested the hypothesis that this polymorphism may modulate the myocardial infarction (MI) risk associated with low HDL cholesterol concentrations. Two hundred eighty consecutive MI patients and 396 control subjects were studied. When considered as a whole, PON1-192 genetic polymorphism was not associated with higher MI risk. In the entire population, decreased HDL cholesterol concentration (<0.90 mmol/L in men and <1.11 mmol/L in women) conferred an MI risk of 2.56 (P=0.0001) compared with normal HDL levels. The risk increased to 4.51 (P<0.0001) in QQ homozygous HDL-deficient subjects relative to QQ homozygotes with normal HDL levels, decreased to 1.83 (P=0.1046) in QR heterozygote HDL-deficient subjects, and also decreased (to 1.41, P=0.6243) in RR homozygote HDL-deficient individuals compared with RR carriers with normal HDL cholesterol concentration. The effect of PON1-192 genotypes on the association of low HDL cholesterol levels and MI was related to gene dosage. A significantly decreased enzyme activity was found in HDL-deficient MI patients compared with HDL-deficient control subjects (median 208 U/L [interquartile range 136 to 298 U/L] versus median 235 U/L [interquartile range 163 to 350 U/L], respectively; P=0.025]. QQ homozygous MI patients showed the greatest difference of PON1 activity levels between normal and HDL-deficiency state groups (14.9%, P=0.002). Our observations raise the question of whether the decrease in PON1 activity and the MI risk associated with HDL deficiency are more evident in the low paraoxon-activity QQ genotype. It can be argued that the low paraoxon-activity QQ genotype, which may be adequate to prevent lipid peroxidation in normolipidemic subjects, may be insufficient when an HDL-deficiency state and low PON1 activity reflecting oxidative stress coexist. The risk of nonfatal MI is increased in HDL-deficiency states, principally among subjects carrying the low paraoxon-activity QQ genotype.

Aged↗
PubMed2000

Effect of physical activity on lipid levels in a population-based sample of men with and without the Arg192 variant of the human paraoxonase gene.

The prevalence of cardiovascular risk factors in Gerona, Spain, is high for the low myocardial infarction incidence and mortality rates in the province. Physical activity is a protective factor against coronary heart disease. We investigated whether the genetic variants Q and R of the paraoxonase Gln-Arg 192 polymorphism were involved in different responses of lipids to physical activity. Serum triglycerides, HDL-cholesterol concentrations, and the paraoxonase Gln-Arg 192 polymorphism were determined in 262 men randomly selected from a representative population sample in a cross-sectional study conducted in Gerona, Spain. The Minnesota Leisure Time Physical Activity Questionnaire was used to assess energy expenditure in leisure time physical activity. No differences were found in lipid levels among tertiles of physical activity distribution in subjects with the QQ genotype. However, R carriers showed a significant decreasing trend in triglyceride levels and in log-triglyceride-to-HDL-cholesterol ratio and a significant increasing trend in HDL-cholesterol concentration with the amount of physical activity. R carriers included in the low tertile of physical activity distribution had HDL-cholesterol levels significantly lower than those of QQ homozygous men in the same physical activity category (1.04 mmol/L vs. 1.22 mmol/L, P = 0.024). R carriers of the higher tertile of physical activity distribution showed the most favorable lipid profile in this genetic group. A statistically-significant interaction between paraoxonase genotypes and physical activity was observed for log triglycerides (P = 0.018), HDL-cholesterol concentration (P = 0.017), and log triglyceride-to-HDL-cholesterol ratio (P = 0.008). The beneficial association of the amount of physical activity and lipid traits found in men with the R allele suggests that this population subgroup needs to be physically active to achieve a favorable lipoprotein phenotype similar to that observed in QQ homozygous men.

Adult↗
PubMed2000

Relationship of abdominal adiposity and dyslipemic status in women with a common mutation in the lipoprotein lipase gene. The REGICOR investigators.

Abdominal obesity constitutes an important risk factor for cardiovascular disease. Hypertriglyceridemia and low high-density lipoprotein (HDL) cholesterol concentration constitute the major lipid alterations observed in obesity. A common variant of the lipoprotein lipase (LPL) gene, the HindIII polymorphism, has been found to be associated with changes in triglyceride and HDL-cholesterol levels. We have investigated the impact of the LPL HindIII polymorphism on the relationship between abdominal adiposity and lipoprotein concentrations in 156 randomly selected women in a cross-sectional study conducted in the province of Gerona, in the northeast of Spain. The waist-to-hip ratio was used as an estimate of regional fat distribution. Serum lipid and lipoprotein measurements as well as lipoprotein lipase-HindIII genotypes were determined. Percentile 50 of waist-to-hip ratio (WHR) (0.81) was used as a cutoff to define low or high WHR groups, which significantly differed in blood pressure and lipid trait concentrations. Serum triglyceride concentrations and mean log triglyceride-to-HDL-cholesterol ratio were significantly higher in H+ homozygous women compared with H- carriers. Whereas no statistically-significant differences were observed in HDL-cholesterol concentration and log triglyceride-to-HDL-cholesterol ratio of H- carriers between WHR groups, H+ homozygous women showed significant differences in these lipid traits. It is noteworthy that high-WHR H- carrier women showed a mean HDL-cholesterol value similar to those of both genotypes in the low WHR group. A statistically significant interaction between WHR and genotype was observed for HDL-cholesterol concentration (P=0. 027) and log triglyceride-to-HDL-cholesterol ratio (P=0.040). These results stress the compensating effects that weight loss may have on women with adverse genetic factors. From a complementary viewpoint, the presence of the H- allele seems to confer a protective lipid profile, even when an adverse anthropometric factor such as abdominal adiposity is present.

Abdomen↗
PubMed2000

Differential effects of smoking on myocardial infarction risk according to the Gln/Arg 192 variants of the human paraoxonase gene.

Paraoxonase (PON1) seems to exert a major antioxidant effect by removing lipid peroxidation products. A common polymorphism of the PON1 gene modulates paraoxonase activity and has been related in some studies to coronary heart disease. PON1 genetic polymorphism includes PON1 Q, an isoform with a low activity toward paraoxon hydrolysis that has a glutamine at position 192, and PON1 R, the high-activity isoform with an arginine at position 192. In the present study, we investigated whether smoking, which is related to increased susceptibility to lipoprotein oxidation, has a differential effect by PON1-192 genotype on the risk of myocardial infarction (MI). One hundred fifty-six consecutive MI patients and 310 control subjects were studied. PON1 genotypes in the controls were distributed as follows: 154 (49.7%) QQ, 123 (39.7%) QR, and 33 (10.6%) RR. This distribution did not significantly differ from that of the MI patients: 84 (53.8%) QQ, 60 (38.5%) QR, and 12 (7.7%) RR. Subjects were classified into two groups, those who never smoked (n = 209) and those who were current smokers (n = 135) or ex-smokers (n = 122). In the latter, the variable "cigarette packs smoked per year" was defined as the number of packs smoked daily multiplied by the number of smoking years. As expected, smoking was significantly associated with an increased MI risk in the overall group. Subjects were then stratified by PON1 genotype. The packs smoked per year were significantly associated with an increased MI risk only in QQ homozygotes. This risk was higher among those in the higher tertile for cigarette packs smoked per year (odds ratio [OR] = 5.24, 95% confidence interval = 1.67 to 16.44, Pfor trend <.001). In contrast, the packs smoked per year were not significantly associated with MI risk in R-carrier subjects. We conclude that the risk of MI associated with smoking appears to be increased in subjects who are homozygous for the low-activity PON1 QQ genotype compared with R carriers, and this risk seems to be time- and dose-dependent.

Aged↗
PubMed2000

Risk of myocardial infarction associated with Gln/Arg 192 polymorphism in the human paraoxonase gene and diabetes mellitus. The REGICOR Investigators.

AIMS: There is increasing evidence that paraoxonase, an HDL-linked enzyme, exerts its effect by removing lipid-peroxidation products. We have conducted a case-control study in Gerona, Spain, to find out whether paraoxonase1 polymorphism at codon 192 (Q and R alleles) is associated with increased risk of coronary heart disease, and how diabetes mellitus, associated with high oxidative risk, influences such an association. METHODS AND RESULTS: One hundred and fifty six consecutive myocardial infarction patients and 310 age- and sex-matched control subjects were studied. There were no differences in the distribution of genotype and allele frequencies between patients and controls. The odds ratios for diabetes and dyslipaemia in control and patients stratified by genotype group were compared. Whereas dyslipaemic status was significantly related to myocardial infarction in QQ homozygotes and R carriers, diabetes mellitus was significantly associated with myocardial infarction only in R-carrier subjects. In logistic regression analysis, diabetic R carriers demonstrated a more than two and a half-fold increase in myocardial infarction risk compared with non-diabetic R carriers (OR: 2.65, P<0.05). CONCLUSION: These data indicate that the R allele of the paraoxonase1-192 polymorphism is not an independent risk factor for myocardial infarction in our population. However, the interaction between this polymorphism and diabetes mellitus leads to increased myocardial infarction risk in diabetic patients with the R allele.

Aged↗
PubMed2000

Effect of simvastatin therapy on paraoxonase activity and related lipoproteins in familial hypercholesterolemic patients.

Human paraoxonase (PON1) is a calcium-dependent esterase closely associated with high density lipoprotein (HDL)-containing apolipoprotein AI (apoAI), which has been shown to confer antioxidant properties to HDL. PON1 has been recently implicated in the pathogenesis of atherosclerosis. Low PON1 activities have been found in familial hypercholesterolemia (FH) and diabetes mellitus. We have undertaken a study of the effect of the lipid-lowering drug simvastatin on serum PON1 activity (in relation to paraoxon and arylesterase activity), on apoAI-containing and apolipoprotein B (apoB)-containing lipoproteins, and on lipid peroxide concentrations in 64 (39 women and 25 men) unrelated FH patients. We have also analyzed the influence of the PON1-192 and PON1-55 genetic polymorphisms on the response of PON1 activity to simvastatin therapy. A venous blood sample for a baseline analysis and another after 4 months of simvastatin therapy at a dosage of 20 mg per day were taken. The major effect of simvastatin on lipid traits was to decrease serum cholesterol, low density lipoprotein (LDL) cholesterol, and lipid peroxide concentrations by 19.9%, 26.3%, and 37.3%, respectively. There was also a significant decrease in serum apoB, LDL apoB, and triglyceride concentrations (20.5%, 21.1%, and 15.6%, respectively). Conversely, simvastatin had no significant influence on very low density lipoprotein-lipid content, HDL cholesterol, apoAI concentrations, and lipoprotein AI and AI:AII particles. Remarkably, serum PON1 activity toward paraoxon significantly increased during treatment with simvastatin (168. 7+/-100.3 U/L before therapy versus 189.5+/-116.5 U/L after therapy, P:=0.005). Arylesterase activity displayed only a nonsignificant trend to increase after therapy. Whereas PON1 activity levels were significantly lower in FH patients before simvastatin therapy compared with those of 124 normolipidemic subjects (168.7+/-100.3 versus 207.6+/-125.2 U/L, respectively; P:<0.05), this difference disappeared after simvastatin therapy. After simvastatin therapy, a significantly negative correlation between PON1 activity and lipid peroxide concentration was observed (r=-0.35, P:=0.028). The latter also strongly correlated with LDL cholesterol concentration (r=0.64, P:<0.001). Serum PON1 activity levels were significantly lower in the low-activity PON1-192 QQ and PON1-55 M carriers than in R carriers and in LL carriers, respectively. No significant differences were found in the therapeutic response of PON1 activity between genotype groups (8.5% and 11.1% increase for QQ homozygous and R-carrier FH patients, respectively, and 12.7% and 9.5% increase for LL homozygotes and M carriers, respectively). We conclude that simvastatin may have important antioxidant properties through increasing serum PON1 activity, perhaps as a consequence of reducing oxidative stress, by a mechanism independent of apoAI-containing lipoprotein concentration and without the influence of PON1-192 and PON1-55 genetic polymorphisms. Further studies are clearly warranted to clarify the precise mechanism by which simvastatin therapy is associated with increased PON1 activity.

Anticholesteremic Agents↗
PubMed1998

Platelet glycoprotein IIb/IIIa genetic polymorphism is associated with plasma fibrinogen levels in myocardial infarction patients. The REGICOR Investigators.

Fibrinogen is the major ligand of platelet glycoprotein IIb/IIIa platelet receptor. Genes coding for platelet fibrinogen receptor glycoprotein IIb/IIIa are polymorphic. The PLA alloantigen has two antigenic determinants, PLA1 and PLA2, located in a 17-23 kD fragment of glycoprotein IIIa. We analyzed whether PLA genotype has any effect on plasma fibrinogen concentration and investigated if the effect has different magnitude in myocardial infarction patients compared with subjects free of angina or myocardial infarction. One hundred sixteen consecutive patients who suffered a myocardial infarction and 136 subjects recruited by random sampling from the local census were included in the study. PLA genotype distribution and allele frequencies in patients did not significantly differ from those in the control group. Mean fibrinogen concentration tended to be higher in controls with genotype PLA1PLA1 than in those with genotype PLA1PLA2 or PLA2PLA2, and in patients this difference reached statistical significance (p < 0.001). We conclude that the PLA polymorphism may be in linkage disequilibrium with another functional mutation in or near the promoter area of the fibrinogen gene or even in another gene, which controls the production or the clearance of fibrinogen.

Chi-Square Distribution↗
PubMed1998

The relationship between smoking and triglyceride-rich lipoproteins is modulated by genetic variation in the glycoprotein IIIa gene.

In the last year, several studies have reported conflicting results concerning an association between the PI(A2) allele of the PI(A1/A2) polymorphism of platelet glycoprotein IIIa and the risk of myocardial infarction. In the present study, we analyzed the hypothesis of whether glycoprotein IIIa genotypes have any association with lipids and lipoproteins as classical cardiovascular risk factors. Smoking, associated with changes in triglyceride-rich lipoprotein (TRL) concentrations and with both hypercoagulability and reduced fibrinolysis, was also analyzed as an environmental factor. Blood samples were obtained from 170 subjects (83 men and 87 women; mean age, 57 years; SD 15) recruited by random sampling from the census of Girona, Spain. Subjects were classified as current smokers (n=41) and nonsmokers or exsmokers (n=129). Whereas no differences were found in lipid and lipoprotein concentrations between smokers and nonsmokers in subjects with the PI(A1/A1) genotype, smokers with the PI(A1/A2) or PI(A2/A2) genotypes showed significantly higher triglyceride and very-low-density lipoprotein (VLDL) triglyceride concentrations than nonsmokers or exsmokers with the same genotypes. Similarly, the VLDL triglyceride/HDL cholesterol ratio was significantly different in subjects with the PI(A1/A2) or PI(A2/A2) genotypes stratified according to smoking status. Further analysis revealed a significant interaction between smoking and genotype when those homozygous for the allele PI(A1) were compared with one or two PI(A2) alleles for the three lipidic parameters. The observed effects appear to show links between smoking, triglyceride metabolism, and a glycoprotein involved in platelet aggregation. It is likely that the pI(A) polymorphism is in linkage disequilibrium with other functional mutations that might influence triglyceride metabolism under some environmental factors such as smoking. This finding may provide a new perspective in the complex relationship between glycoprotein IIIa gene, environment, and their interactions.

Adult↗
PubMed1998

[Anthropometric and dietary determinants of blood levels of HDL cholesterol in a population-based study. The REGICOR study. Researchers of the REGICOR study].

OBJECTIVES: The aim of the present study was to identify dietary and anthropometric factors influencing HDL cholesterol levels in the region of Girona. POBLATION AND METHODS: A cross-sectional study was designed with random recruitment and 798 men and 862 women were included. Anthropometric variables were collected, the energy expenditure in physical activity was calculated and a dietary questionnaire was supplied in order to obtain nutritional data. Furthermore, lipid levels and lipoprotein concentrations were determined. RESULTS: Significant differences were found in serum triglycerides, body mass index, glucose levels and alcohol intake between the upper and the lower tertils of HDL cholesterol in both men and women. In men, energy expenditure in physical activity was significantly associated with HDL cholesterol levels, as well as total fat and monounsaturated fat. In women, together with the waist-to-hip ratio and fasted glycemia, vitamin C was the dietary factor positively associated with HDL cholesterol levels. CONCLUSIONS: Moderate alcohol intake, physical activity, vitamin C consumption and optimizing body weight strongly contribute to increased HDL cholesterol levels in our region.

Adult↗
PubMed1997

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.

Adult↗
PubMed1996

Secondary prevention of coronary heart disease in patients with extracoronary atherosclerosis: a need for accuracy of low density lipoprotein determination.

According to the new guidelines of the National Cholesterol Education Program (NCEP) for secondary prevention in adults with evidence of coronary heart disease or other clinical atherosclerotic disease, lipoprotein analysis is required and classification is based on low density lipoprotein (LDL) cholesterol. The aim of the present study was to analyze the reliability of calculated LDL cholesterol by the Friedewald formula compared with measured LDL cholesterol after separation by ultracentrifugation in 202 male patients with extracoronary atherosclerosis (100 patients with ischemic cerebrovascular disease and 102 patients with peripheral vascular disease) and in 117 health control subjects. Calculated LDL cholesterol coincided with measured LDL cholesterol, with less than 10% error, in 118 patients (58.4%) with extracoronary atherosclerosis and in 87 controls (74.4%). Calculated LDL cholesterol was overestimated, with an error of 10% or more compared with measured LDL cholesterol, in 34.6% of patients and 22.2% of controls, and underestimated in 6.9% and 3.4% respectively. Despite a good correlation between calculated and measured LDL cholesterol, the intraclass correlation coefficients demonstrate a poor concordance between calculated and measured LDL cholesterol, both in patients and controls. The authors underline the need for caution in assessing the reliability of calculated LDL cholesterol.

Adult↗