Myocardial Infarction Subjects Research Articles

Decreased Levels Of Erythrocyte Glutathione In Patients With Myocardial Infarction

Background: Although experimental and clinical studies have demonstrated that evidence of oxidative stress in myocardial damage caused by reperfusion, defined as an imbalance between pro-oxidants and antioxidants. Glutathione (GSH) plays an important role in autoxidation of oxygen free radical (OFR) involved in diseases such as atherosclerosis, rheumatoid arthritis, and reoxygenation injury. Aim of the Study: The present study, to determined erythrocyte GSH levels in patients with myocardial infarction (MI). Material and Methods: Erythrocyte GSH levels were determined in 50 patients with MI and 45 age matched healthy controls. Erythrocyte GSH levels were measured by using Beutler method, also lipid profile was analyzed enzymatically. Malonaldehyde (MDA) levels were estimated by thiobarbituric acid reaction. Results are expressed as Mean±SD. Sigma stat version 3.0 was used for statistical analysis. P-value of less than 0.001 and 0.05 was considered to indicate statistical significance. Results: Glutathione levels were significantly decreased (p<0.001) in MI as compared to control. Malonaldehyde levels were significantly higher (p<0.001) in MI as compared to control. Also, total cholesterol and triglycerides were significantly higher (p<0.05) in MI subjects as compared to control. Significant correlation between MDA and GSH levels (r = -0.94, p<0.001) were also found. Conclusion: The Results suggest that decreased in GSH levels may be associated with enhanced protective mechanism to oxidative stress in MI.

Occupational magnetic field exposure and myocardial infarction incidence.

Studies on healthy volunteers have seen reduced heart rate variability after exposure to extremely low-frequency electric and magnetic fields (EMF). Because reduced heart rate variability has been linked to cardiovascular disease risk, it has been hypothesized that exposure to EMF might increase the risk of cardiovascular disease. One epidemiologic study has shown increased mortality from cardiovascular conditions in utility workers with elevated exposure to magnetic fields, but several other epidemiologic studies have failed to confirm this result. We tested the hypothesis that occupational EMF exposure increases the risk of myocardial infarction in a large population-based case-control study of myocardial infarction, with detailed information on potential confounders. We used data from the SHEEP study, which is a population-based case-control study of acute myocardial infarction in Stockholm. Occupational EMF exposure was based on job titles 1, 5, and 10 years before diagnosis. We used 2 approaches to classify exposure: first, specific individual job titles with presumed elevated EMF exposure, and second, classification of subjects according to a job-exposure matrix. We found no increased risk of myocardial infarction in subjects classified as having elevated EMF exposure. For the highest exposure category of > or = 0.3 microT according to the job-exposure matrix, the adjusted relative risk was = 0.57 (95% confidence interval = 0.36-0.89). The results of this study do not support the hypothesis that occupational EMF exposure increases the risk of myocardial infarction.

Should oral glucose tolerance test be a routine examination after a myocardial infarction?

Background: Diabetes mellitus (DM) and impaired glucose tolerance (IGT) are important cardiovascular risk factors. The objective of this study was to assess the prevalence of DM and IGT in patients discharged from the CCU without known DM after a myocardial infarction. Methods: One hundred and ten patients, men and women aged 31–80 years with a myocardial infarction 1–12 months before inclusion were examined with oral glucose tolerance test. Patients with known DM were excluded. A standard oral glucose test (OGTT) with 75 g of glucose was performed. Results: IGT was observed in 29 (26%) patients and DM in 13 (12%) patients in the OGTT. If only fasting plasma glucose (FPG) was used alone five (38.5%) patients with diabetes subjects and three (10.3%) with IGT were identified. Thus, a FPG test alone identified only 19.0% of the patients with pathological OGTT. The prevalence of DM and IGT in patients discharged from the CCU after a myocardial infarction without known DM diagnosis was high (38%). A fasting glucose alone failed to identify more than 80% of the patients with pathological glucose tolerance in this study. Conclusion: Since pathological glucose tolerance is an important cardiovascular risk factor, oral glucose tolerance test should be considered as a routine test after a myocardial infarction in subjects without known DM.

Influence of selected lifestyle factors on risk of acute myocardial infarction in subjects with familial predisposition for the disease

Background. The joint effect of family history of acute myocardial infarction (AMI) and selected adult life risk factors on the risk of the disease is not clear. Methods. We used the combined data set from three Italian case-control studies including 1,737 cases of incident, nonfatal AMI and 2,317 hospital controls, aged less than 75 years. An adult lifestyle risk score (ALRS) was computed, including tobacco, body mass index, physical activity, and consumption of coffee, alcohol, fish, and vegetables. Results. Compared to the reference category (subjects with no family history of AMI and low ALRS), the risk of AMI was 4.97 (95% confidence intervals, CI: 4.00–6.18) in subjects without family history and high ALRS, 2.19 (95% CI: 1.65–2.90) in subjects with family history and low ALRS, and 11.90 (95% CI: 8.94–15.84) in subjects with family history and high ALRS. Conclusions. The risk of AMI in subjects with a familial predisposition to ischaemic heart disease might be substantially reduced by intervention on selected lifestyle risk factors for AMI. In absolute terms, any such intervention would be more effective than a comparable one on subjects without a familial predisposition.

Diabetes and obesity in Northern Sweden: occurrence and risk factors for stroke and myocardial infarction.

The authors describe the occurrence of diabetes and obesity in the population of Northern Sweden and the role of diabetes in cardiovascular disease. Four surveys of the population aged 25 to 64 years were undertaken during a 14-year time span. Stroke events in subjects 35-74 years during 1985-92 and myocardial infarction in subjects 25-64 years 1989-93 were registered. The prevalence of diagnosed diabetes was 3.1 and 2.0% in men and women, respectively, and 2.6 and 2.7% for previously undiagnosed diabetes. During the 13-year observation period, BMI increased 0.96 kg/m(2) in men and 0.87 in women. The proportion of subjects with obesity (BMI>or=30) increased from 10.3% to 14.6% in men and from 12.5% to 15.7% in women. Hip circumference increased substantially more than waist circumference, leading to a decreasing waits-to-hip ratio (WHR). The relative risk for stroke or myocardial infarction was four to six times higher in a person with diabetes than in those without diabetes. The 28-day case fatality for myocardial infarction, but not for stroke, was significantly higher in both men and women with diabetes. Population-attributable risk for diabetes and stroke was 18% in men and 22% in women and for myocardial infarction it was 11% in men and 17% in women. Obesity is becoming more common, although of a more distal than central distribution. The burden of diabetes in cardiovascular diseases in Northern Sweden is high.

Comparing actual food intake and serum lipid profile with perceived dietary behavior in Korean myocardial infarction patients

The purpose of this study was to compare serum lipid profile and food intake with the perceived dietary behavior of Korean myocardial infarction (MI) patients. Seventy-five MI subjects were recruited from a university outpatient clinic in Chunan, Korea. Individual interviews were conducted to assess dietary behavior and food intake, and a fasting blood sample was obtained for analyzing the lipid profile. The mean cholesterol levels of 176 mg/dl for men and 198 mg/dl for women were lower than the national statistics of MI patients in Korea, and were consistent with their actual food intakes. Significant gender differences were found in serum triacylglycerol and the ratio of total cholesterol to high-density-lipoprotein cholesterol. The dietary behaviors of the subjects were significantly related to total energy intake. Cardiac risk management should focus on promoting the perceived dietary behavior of individuals to produce a balanced nutrient intake, and ultimately on reducing cardiac risk factors for MI patients.

Coronary calcification detected by electron-beam computed tomography and myocardial infarction. The Rotterdam Coronary Calcification Study.

Available data are insufficient to determine the relation between coronary calcification and coronary events in the general population. We cross-sectionally examined the association between coronary calcification and myocardial infarction in the prospective Rotterdam Coronary Calcification Study. From 1997 onwards, subjects were invited for electron-beam computed tomography scanning to detect coronary calcification. The study was embedded in the population-based Rotterdam Study. Calcifications were quantified in a calcium score according to Agatston's method. Calcium scores were available for 2,013 participants with a mean age of 71 years (standard deviation, 5.7 years). A history of myocardial infarction prior to scanning was present in 229 subjects. Compared to subjects in the lowest calcium score category (0-100), the age-adjusted odds ratio for myocardial infarction in subjects in the highest calcium score category (above 2,000) was 7.7 (95% confidence interval, 4.1-14.5) for men, and 6.7 (95% confidence interval, 2.4-19.1) for women. Additional adjustment for cardiovascular risk factors only slightly altered the estimates. The association was observed across all age subgroups, i.e. also in subjects of 70 years and older. A strong and graded association was found between coronary calcification and myocardial infarction. The association remained at high ages.

Plasma concentration of C-reactive protein and risk of ischemic stroke and transient ischemic attack: the Framingham study.

The role of C-reactive protein (CRP) as a novel plasma marker of atherothrombotic disease is currently under investigation. Previous studies have mostly related CRP to coronary heart disease, were often restricted to a case-control design, and failed to include pertinent risk factors to evaluate the joint and net effect of CRP on the outcome. We related plasma CRP levels to incidence of first ischemic stroke or transient ischemic attack (TIA) in the Framingham Study original cohort. There were 591 men and 871 women free of stroke/TIA during their 1980 to 1982 clinic examinations, when their mean age was 69.7 years. CRP levels were measured by using an enzyme immunoassay on previously frozen serum samples. Analyses were based on sex-specific CRP quartiles. Risk ratios (RRs) were derived, and series of trend analyses were performed. During 12 to 14 years of follow-up, 196 ischemic strokes and TIAs occurred. Independent of age, men in the highest CRP quartile had 2 times the risk of ischemic stroke/TIA (RR=2.0, P=0.027), and women had almost 3 times the risk (RR=2.7, P=0.0003) compared with those in the lowest quartile. Assessment of the trend in risk across quartiles showed unadjusted risk increase for men (RR=1.347, P=0.0025) and women (RR=1.441, P=0.0001). After adjustment for smoking, total/HDL cholesterol, systolic blood pressure, and diabetes, the increase in risk across CRP quartiles remained statistically significant for both men (P=0.0365) and women (P=0.0084). Independent of other cardiovascular risk factors, elevated plasma CRP levels significantly predict the risk of future ischemic stroke and TIA in the elderly.

Methylenetetrahydrofolate reductase gene polymorphism and risk of premature myocardial infarction.

Elevated plasma homocysteine level is an independent risk factor for cardiovascular disease. A common mutation (nucleotid 677C-T) in the gene coding for methylenetetrahydrofolate reductase (MTHFR) has been reported to reduce the enzymatic activity of MTHFR and is associated with elevated plasma levels of homocysteine, especially in subjects with low folate intake. Methylenetetrahydrofolate reductase T/T genotype may be a risk factor for premature MI in Turkish population who are known to have low folate levels. The study group was comprised of 96 men (aged <45 years) with premature myocardial infarction (MI) and 100 age- and gender-matched controls who had no history or clinical evidence of coronary artery disease (CAD) and/or MI. DNA was extracted from peripheral blood and genotypes were determined by polymerase chain reaction, restriction mapping with HinfI, and gel electrophoresis. Conventional risk factors for CAD were prospectively documented. Allele and genotype frequencies among cases and control subjects were compatible with Hardy-Weinberg equilibrium. The frequencies of T/T, C/T, and C/C genotypes among patients with MI and control subjects were 15.6, 40.6, and 43.8%, and 5, 35, and 60%, respectively. Multivariate analyses identified smoking, MTHFR C/T polymorphism, diabetes mellitus, family history of CAD, and hypertension as the independent predictors of premature MI. Defining patients with non-T/T genotype (C/C and C/T combined) as reference, the relative risk of MI for subjects with T/T genotype was 5.94 (95% confidence interval: 1.96-18.02, p = 0.0016). Our findings suggest that C677T transition in the MTHFR gene may be a risk factor for premature MI in Turkish men.

Coronary Calcification Detected by Electron-Beam Computed Tomography and Coronary Heart Disease: The Rotterdam Study.

P22 We examined the association between coronary calcification detected by electron-beam computed tomography (EBT) and the presence of myocardial infarction, stratified for gender and age. We performed a cross-sectional study among elderly subjects, participants from the population-based Rotterdam study. Baseline data were collected in 1990-1993. During the third examination phase (1998-2000), subjects were invited for EBT scanning to detect coronary calcification. Calcified lesions were quantified according to Agatston’s method. Calcium scores were available for 1874 of 2263 subjects who underwent EBT scanning. A history of myocardial infarction was defined as the occurrence of a myocardial infarction before baseline or during follow-up but before EBT scanning.Mean age (SD) of the 997 women and 877 men was 71 (5.7) years. The calcium score showed a graded association with the presence of myocardial infarction. Compared to the lowest calcium score category (0 - 100), the age-adjusted odds ratio for myocardial infarction in subjects with calcium score &gt; 2000 was 9.2 (95% CI 4.7 - 18.3) for men, and 10.0 (95% CI 3.4 - 29.8) for women. Additional adjustment for cardiovascular risk factors hardly changed the estimates. The association remained present in subjects above 70 years of age. In conclusion, in this population-based study, a strong association between coronary calcification and myocardial infarction was present in both men and women, which remained present at high age. Although results from prospective data in unselected populations have to be awaited, this study suggests that EBT is a promising tool for the detection of subjects at high-risk of coronary events in the general population.

A polymorphism in the gene for IGF-I: functional properties and risk for type 2 diabetes and myocardial infarction.

Evidence is accumulating that low levels of IGF-I play a role in the pathogenesis of type 2 diabetes and cardiovascular diseases. We examined the role of a genetic polymorphism in the promoter region of the IGF-I gene in relation to circulating IGF-I levels and growth measured as body height, and we studied the relationship of this polymorphism with type 2 diabetes and myocardial infarction. The relation between the IGF-I polymorphism and body height was assessed in a population-based sample of 900 subjects from the Rotterdam Study. Within each genotype stratum, 50 subjects were randomly selected for a study of the relation of this polymorphism with serum IGF-I levels. To assess the risk for type 2 diabetes, we studied 220 patients and 596 normoglycemic control subjects. For myocardial infarction, 477 patients with evidence of myocardial infarction on electrocardiogram and 808 control subjects were studied. A 192-bp allele was present in 88% of the population, suggesting that this is the wild-type allele from which all other alleles originated. Body height was, on average, 2.7 cm lower (95% CI for difference -4.6 to -0.8 cm, P = 0.004), and serum IGF-I concentrations were 18% lower (95% CI for difference -6.0 to -1.3 mmol/l, P = 0.003) in subjects who did not carry the 192-bp allele. In noncarriers of the 192-bp allele, an increased relative risk for type 2 diabetes (1.7 [95% CI 1.1-2.7]) and for myocardial infarction (1.7 [95% CI 1.1-2.5]) was found. In patients with type 2 diabetes, the relative risk for myocardial infarction in subjects without the 192-bp allele was 3.4 (95% CI 1.1-11.3). Our study suggests that a genetically determined exposure to relatively low IGF-I levels is associated with an increased risk for type 2 diabetes and myocardial infarction.

Quantitative ultrasonic tissue characterization can identify high-risk atherosclerotic alteration in human carotid arteries.

Recently, ultrasonic tissue characterization of the composition of plaques has been performed in a quantitative fashion on the basis of integrated backscatter (IBS) analysis, but most of those studies have used high-frequency ultrasound to obtain microscopic images. We performed B-mode measurement and IBS signal analysis with acoustic densitometry with a 7.5-MHz linear-array transducer in freshly excised human aortas (n=58) (normal, atheromatous, and fibrous tissue) obtained at autopsy. Atheromatous and fibrous tissue had a similar intima-media thickness (IMT), but the IBS value in atheromatous specimens was lower than that in fibrous specimens. We further applied this method to human carotid ultrasonography. The subjects were young (80 regions), middle aged with 1 or no coronary risk factors (low risk) (120 regions), middle aged with >/=2 coronary risk factors (high risk) (240 regions), or elderly (80 regions) or were patients with myocardial infarction (MI) with multivessel disease (90 regions). The IMT was similar in middle-aged, elderly, and MI subjects. In contrast, the IBS value was significantly higher in elderly subjects and lower in high-risk middle-aged and MI subjects compared with that in low-risk middle-aged subjects. The percent of regions diagnosed as atheromatous (IBS less than mean minus 2-SD value of IBS in young subjects) was 11% in low-risk middle-aged subjects, 29% in high-risk middle-aged subjects, and 63% in the MI group. In conjunction with conventional B-mode imaging, IBS analysis with carotid ultrasonography appeared to provide prognostic information to identify a high-risk group with systemic atherosclerosis, which could lead to coronary heart disease in individuals with early-stage disease.

Smokeless tobacco as a possible risk factor for myocardial infarction: a population-based study in middle-aged men

OBJECTIVESTo explore whether the use of snuff affects the risk of myocardial infarction (MI).BACKGROUNDSnuff and other forms of smokeless tobacco are widely used in some populations. Possible health hazards associated with the use of smokeless tobacco remain controversial.METHODSIn a population-based study within the framework of the Northern Sweden center of the World Health Organization Multinational Monitoring of Trend and Determinants in Cardiovascular Disease (WHO MONICA) Project, tobacco habits were compared in 25- to 64-year-old men with first-time fatal or nonfatal MI and referent subjects matched for age and place of living (687 cases, 687 referents).RESULTSThe unadjusted odds ratio (OR) for MI in regular cigarette smokers as compared with men who never used tobacco was 3.65 (95% confidence interval [CI] 2.67 to 4.99). When nonsmoking regular snuff dippers were compared with never-users of tobacco, the unadjusted OR was 0.96 (0.65 to 1.41). After adjustment for multiple cardiovascular risk factors, the OR was 3.53 (95% CI 2.48 to 5.03) for regular smoking and 0.58 (95% CI 0.35 to 0.94) for regular snuff dipping. Restricting the analyses to fatal cases of myocardial (including sudden death) showed a tendency towards increased risk among snuff dippers 1.50 (95% CI 0.45 to 5.03).CONCLUSIONSThe risk of MI is not increased in snuff dippers. Nicotine is probably not an important contributor to ischemic heart disease in smokers. A possible small or modest detrimental effect of snuff dipping on the risk for sudden death could not be excluded in this study due to a limited number of fatal cases.

The Relationship Between Polymorphisms in the Endothelial Cell Nitric Oxide Synthase Gene and the Platelet GPIIIa Gene With Myocardial Infarction and Venous Thromboembolism in African Americans

To determine whether the polymorphic dinucleotide repeats found in intron 4 of the endothelial cell nitric oxide synthase (ecNOS) gene and the platelet GPIIIa PLA(1)/A(2) polymorphism are associated with myocardial infarction (MI) and venous thromboembolism (VTE) in African Americans. Because these two genes may interact physiologically, the third objective was to determine if there was a relationship between the polymorphisms with respect to MI and VTE. A hospital-based case-control study. After informed consent was obtained, blood used for DNA extraction was drawn from the subjects. The study was conducted in the Anticoagulant Clinic and the Cardiology Clinic at Grady Memorial Hospital in Atlanta Georgia. Subjects were recruited from African-American patients with a reported history of MI (n = 110) or VTE (n = 91). Control subjects (n = 185) without a history of cardiovascular or venous disease were recruited from an outpatient clinic. The 393 ecNOS allele was more common among MI cases (36%; p = 0.01) and VTE cases (35%; p = 0.04) than among control subjects (26%). There was no association between the GPIIIa genotypes and either MI or VTE. However, among the MI subjects, there was a strong association between the ecNOS 393/393 genotype and the Pl(A2) allele. It was also found that the frequency of the 393 allele was higher in African-American persons (0.26) compared with what has been reported for Australian Caucasians (0. 14) and Japanese (0.10). The 393 allele but not the Pl(A2) allele was significantly associated with both MI and VTE in African Americans. Homozygosity for the 393 allele was significantly associated to the diagnosis of MI prior to the age of 45. The combination of the 393 allele and a Pl(A2) allele was also highly associated with MI. The frequency of the 393 allele was significantly higher in African Americans than what has been reported for other populations. This study furthers not only extends the association of the 393 allele to VTE but has demonstrated an interaction with the Pl(A2) allele with respect to MI.

Serum ferritin and risk of myocardial infarction in the elderly: the Rotterdam Study

Elevated body iron stores have been suggested to be a risk factor for ischemic heart disease. We examined whether elevated serum ferritin concentrations, other indicators of iron status, and dietary iron affected the incidence of myocardial infarction (MI) in an elderly population. A nested, case-control study of 60 patients who had their first MI and 112 age- and sex-matched control subjects embedded in the population-based cohort of the Rotterdam Study. The age- and sex-adjusted risk of MI for subjects with serum ferritin concentrations > or = 200 microg/L was 1.82 (95% CI: 0.90, 3.69; P = 0.096). The odds ratio (OR) was 1.26 (95% CI: 0.98, 1.64; P = 0.078) for the highest tertile of serum ferritin and was only slightly altered in a multivariate model. Risk of MI associated with the highest tertile of ferritin was most evident in current or former smokers (OR: 1.68; 95% CI: 1.17, 2.47; P for trend = 0.008) and in subjects with hypercholesterolemia (OR: 1.43; 95% CI: 0.99, 2.11; P for trend = 0.056) or diabetes (OR: 2.41; 95% CI: 1.12, 7.67; P for trend = 0.027). No association with risk of MI was observed for tertiles of serum iron, serum transferrin, or total dietary iron. For dietary heme iron, risk of MI was significantly increased in a multivariate model in which dietary energy, fat, saturated fat, and cholesterol were adjusted for (OR: 4.01; 95% CI: 1.17, 15.87; P for trend = 0.031). In the presence of other risk factors, serum ferritin may adversely affect ischemic heart disease risk in the elderly.

三次元心磁図計測に基づく心筋梗塞・心室性期外収縮患者の周波数分析

We carried out 3D vector measurement of magneto-cardiograms (MCGs) of normal subjects and subjects with myocardial infarction (MI) or premature ventricular contraction (PVC), using a 3D second-order gradiometer connected to 39-channel SQUIDs, which can detect the magnetic field components perpendicular to the chest wall (Bz) and tangential to the chest wall (Bx, By) simultaneously. We used principal component analysis in order to compare the frequency characteristics in the MCG waveforms of MI, PVC, and normal subjects. The results showed that the frequencies in the MCG waveforms of MI and PVC subjects were dominated by lower frequencies (less than 10 Hz) than in normal MCGs, and that the score proportion characteristic of Bx was different from those characteristic of Bz and By.

Associations among serum lipoprotein(a) levels, apolipoprotein(a) phenotypes, and myocardial infarction in patients with extremely low and high levels of serum lipoprotein(a).

A high serum lipoprotein(a) [Lp(a)] level, which is genetically determined by apolipoprotein(a) [apo(a)] size polymorphism, is an independent risk factor for coronary atherosclerosis. However, the associations among Lp(a) levels, apo(a) phenotypes, and myocardial infarction (MI) have not been studied. Patients with MI (cases, n = 101, M/F: 86/15, age: 62+/-10y) and control subjects (n = 92, M/F: 53/39, age: 58+/-14y) were classified into quintile groups (Groups I to V) according to Lp(a) levels. Apo(a) isoform phenotyping was performed by a sensitive, high-resolution technique using sodium dodecyl sulfate-agarose/gradient polyacrylamide gel electrophoresis (3-6%), which identified 26 different apo(a) phenotypes, including a null type. Groups with higher Lp(a) levels (Groups II, III, and V) had higher percentages of MI patients than that with the lowest Lp(a) levels (Group I) (54%, 56%, or 75% vs. 32%, p<0.05). Groups with different Lp(a) levels had different frequency distributions of apo(a) isoprotein phenotypes: Groups II, III, IV, and V, which had increasing Lp(a) levels, had increasingly higher percentages of smaller isoforms (A1-A4, A5-A9) and decreasingly lower percentages of large isoforms (A10-A20, A21-A25) compared to Group I. An apparent inverse relationship existed between Lp(a) and the apo(a) phenotype. Subjects with the highest Lp(a) levels (Group V) had significantly (p<0.05) higher serum levels of total cholesterol, apo B, and Lp(a). Patients with MI and the controls had different distributions of apo(a) phenotypes: i.e., more small isoforms and more large size isoforms, respectively (A1-A4/A5-A9/A10-A20/A21-A25: 35.7%/27.7%/20.8%/15.8% and 22.8%/23.9%/29.4%/23.9%, respectively). Lp(a) (parameter estimate +/- standard error: 0.70+/-0.20, Wald chi2 = 12.4, p = 0.0004), apo(a) phenotype (-0.43+/-0.15, Wald chi2 = 8.17, p = 0.004), High-density lipoprotein-cholesterol, apo A-I, and apo B were significantly associated with MI after adjusting for age, gender, and conventional risk factors, as assessed by a univariate logistic regression analysis. The association between Lp(a) and MI was independent of the apo(a) phenotype, but the association between the apo(a) phenotype and MI was not independent of Lp(a), as assessed by a multivariate logistic regression analysis. This association was not influenced by other MI- or Lp(a)-related lipid variables. These results suggest that apo(a) phenotype contributes to, but does not completely explain, the increased Lp(a) levels in MI. A stepwise logistic regression analysis with and without Lp(a) in the model identified Lp(a) and the apo(a) phenotype as significant predictors for MI, respectively.

The 4G/5G polymorphism of the plasminogen activator inhibitor gene is associated with the time course of progression to acute coronary syndromes

The 4G allele of the plasminogen activator inhibitor (PAI-I) gene is associated with increased PAI-I levels. Increased PAI-I levels have been reported to be associated with atherothrombotic events. However, the significance of the 4G/5G polymorphism of the PAI-I gene in the pathogenesis of ischemic heart diseases has not been determined. We assessed the 4G/5G polymorphism of the PAI-I gene in 500 subjects including 148 normal controls, 23 subjects with normal coronary arteries, 28 subjects with a paradoxical acetylcholine response, 97 subjects with angina pectoris (AP) and 204 subjects with myocardial infarction (MI). We assessed the length of time between the first anginal pain and the onset of acute coronary syndromes (ACS) in the AP and MI subjects. Subjects who developed ACS within 2 months from the first anginal pain were categorized to have a rapid progression to ACS, and subjects who had had stable anginal pain more than 2 months were placed in the non-ACS group. Subjects in the ACS group were younger than those in non-ACS group ( P=0.012) The frequency of the 5G/5G genotype of the PAI-I gene was lower in the ACS (0.228) than in the non-ACS group (0.093) ( P=0.003). Multiple logistic analyses revealed that a younger age ( P=0.028, odds ratio=1.03) and the (4G/5G+4G/4G) genotype of the PAI-I gene ( P=0.008, odds ratio=2.68) were associated with the ACS group. We also assessed plasma PAI-I antigen levels in 78 subjects. Plasma PAI-I antigen levels in the non-ACS group were significantly lower than those in the ACS group ( P=0.050). Multiple regression analyses revealed that plasma PAI-I levels were determined by plasma insulin ( P<0.001) and the genotype of the PAI-I gene ( P=0.019). Higher plasma insulin levels and the (4G/5G+4G/4G) genotype of the PAI-I gene were associated with higher plasma PAI-I levels. The 4G/5G polymorphism of the PAI-I gene influenced not only plasma PAI-I antigen levels but also the time course of the progression to ACS in patients with coronary atherosclerosis.

4G/5G Polymorphism in the Promoter Region of the PAI-1 Gene Is not a Risk Factor for Familial Myocardial Infarction in Subjects over 45 Years

4G/5G Polymorphism in the Promoter Region of the PAI-1 Gene Is not a Risk Factor for Familial Myocardial Infarction in Subjects over 45 Years

Genetic polymorphisms of the renin-angiotensin system and angiographic extent and severity of coronary artery disease: the CORGENE study.

Genetic polymorphisms of the renin-angiotensin system (RAS) have been associated with coronary artery disease (CAD) but no relation between these polymorphisms and coronary atherosclerosis has yet been systematically evaluated. The CORGENE study is a cross-sectional study involving 463 Caucasians who underwent standardized coronary angiography for established or suspected CAD [156 patients with a previous myocardial infarction (MI), 307 without MI]. Four angiographic scores assessing the extent and severity of the coronary lesions were obtained from a double visual analysis of each angiogram, arbitration being achieved by a quantitative measurement. Three different genotypes were analyzed: the angiotensin I-converting enzyme insertion/deletion (ACE I/D) polymorphism, the Met to Thr change at position 235 of the angiotensinogen gene (AGT M235T) and the A to C transition at position 1166 of the angiotensin II type-1 receptor gene (AT1R A1166C). No significant association was observed between these polymorphisms and the clinical characteristics of MI and non-MI subjects. While most classical risk factors were positively correlated with the angiographic scores, no significant relationship could be established with the three genotypes (r ranging from -0.08 to 0.05). Only one significant correlation was observed: between the presence of the AGT 235T allele and the extent of the coronary lesions (r = -0.19, P = 0.04) in patients with low-risk status. These overall results are not in favor of a role of these RAS genetic polymorphisms in the development of coronary atherosclerosis.