Myocardial Infarction Odds Ratio Research Articles

A non-conservative polymorphism in the IL-6 signal transducer (IL6ST)/gp130 is associated with myocardial infarction in a hypertensive population

Inflammation is a key component in the development of atherosclerosis, and myocardial infarction (MI); therefore we investigated the association between an interleukin-6 signal transducer (IL6ST)/gp130 polymorphism, gp130 function and risk of MI. Structural modeling suggested that a non-conservative single nucleotide polymorphism in the gp130, Gly148Arg, can change the stability and functional properties of the molecule. In vitro studies were done with BAF/3 cells lacking endogenous gp130. Cells stably transfected with the gp130 148Arg variant proliferated less and showed slightly lower STAT-3 phosphorylation in response to gp130 stimulation as compared to cells transfected with gp130 148Gly. In a prospectively followed hypertensive cohort we identified 167 patients who suffered a MI during the study and compared them to matched controls (mean age 57 years, 73% males, n = 482). Carriers of the 148Arg variant ( f Arg = 0.12) of the gp130 receptor had decreased odds ratio for MI in univariate analysis (0.56, 95% CI 0.34–0.91, p = 0.02). In conclusion, a genetically determined structural variant of the IL-6 receptor subunit gp130 is, independently of other known risk factors, associated with decreased risk of MI. The variant is also associated with decreased IL-6 responsiveness and could lead to a configuration change in the gp130 receptor.

Neutrophil elastase gene variation and coronary heart disease

Identification and functional characterization of variants in the neutrophil elastase (ELA2) gene in cardiovascular disease. From participants of the ECTIM (Etude Cas-Témoins sur l'infarctus du Myocarde) Study with myocardial infarction (MI) 2082 chromosomes were genetically scanned; 990 patients with MI and 904 controls were genotyped for the common polymorphisms G-761A and S173S (C4890A). Expression vectors for Ela2 variants were transiently transfected, followed by Northern and Western blot analyses. Promoter variants were analyzed by transfection/reporter gene assays. We identified 11 genetic variants, two in the 5'-flanking (G-761A, -852/del53 bp), six in exons (R49H, N81N, G93V, S173S, D222Y, P228L) and three in introns (C+29/in3T, C+149/in3T, C+137/in4T). In Belfast, 4890A allele carriers had a risk for MI with an odds ratio (OR) of 1.44 (95% CI 1.12-1.86; P=0.005), the OR for MI associated with the -761G/-4890A haplotype with reference to -761G/-4890C amounting to 2.38 (95% CI 1.23-4.57; P=0.01). Transcript or protein expression of both allelic constructs (4890A and 4890C) did not, however, differ. Conversely, transcriptional activity was significantly elevated (<35%) by -852/del53 bp in THP-1 monocytes compared with the nondeleted promoter (P=0.001); the deletion was observed in one patient with premature MI at the age of 28 years, whose mother had had an MI at the age of 48 years. The association of C4890A with MI in Belfast exclusively, and the presumed absence of its functionality, provides little support for a substantial implication of common ELA2 gene variants in overall MI risk. Whether -852/53del plays a role in cardiovascular pathophysiology or not should be evaluated further.

Molecular Characterization of the Ankle-Link Complex in Cochlear Hair Cells and Its Role in the Hair Bundle Functioning

Several lines of evidence indicate that very large G-protein-coupled receptor 1 (Vlgr1) makes up the ankle links that connect the stereocilia of hair cells at their base. Here, we show that the transmembrane protein usherin, the putative transmembrane protein vezatin, and the PDZ (postsynaptic density-95/Discs large/zona occludens-1) domain-containing submembrane protein whirlin are colocalized with Vlgr1 at the stereocilia base in developing cochlear hair cells and are absent in Vlgr1-/- mice that lack the ankle links. Direct in vitro interactions between these four proteins further support their involvement in a molecular complex associated with the ankle links and scaffolded by whirlin. In addition, the delocalization of these proteins in myosin VIIa defective mutant mice as well as the myosin VIIa tail direct interactions with vezatin, whirlin, and, we show, Vlgr1 and usherin, suggest that myosin VIIa conveys proteins of the ankle-link complex to the stereocilia. Adenylyl cyclase 6, which was found at the base of stereocilia, was both overexpressed and mislocated in Vlgr1-/- mice. In postnatal day 7 Vlgr1-/- mice, mechanoelectrical transduction currents evoked by displacements of the hair bundle toward the tallest stereocilia (i.e., in the excitatory direction) were reduced in outer but not inner hair cells. In both cell types, stimulation of the hair bundle in the opposite direction paradoxically resulted in significant transduction currents. The absence of ankle-link-mediated cohesive forces within hair bundles lacking Vlgr1 may account for the electrophysiological results. However, because some long cadherin-23 isoforms could no longer be detected in Vlgr1-/- mice shortly after birth, the loss of some apical links could be involved too. The premature disappearance of these cadherin isoforms in the Vlgr1-/- mutant argues in favor of a signaling function of the ankle links in hair bundle differentiation.

Effect of Rosiglitazone on the Risk of Myocardial Infarction and Death from Cardiovascular Causes

Rosiglitazone is widely used to treat patients with type 2 diabetes mellitus, but its effect on cardiovascular morbidity and mortality has not been determined. We conducted searches of the published literature, the Web site of the Food and Drug Administration, and a clinical-trials registry maintained by the drug manufacturer (GlaxoSmithKline). Criteria for inclusion in our meta-analysis included a study duration of more than 24 weeks, the use of a randomized control group not receiving rosiglitazone, and the availability of outcome data for myocardial infarction and death from cardiovascular causes. Of 116 potentially relevant studies, 42 trials met the inclusion criteria. We tabulated all occurrences of myocardial infarction and death from cardiovascular causes. Data were combined by means of a fixed-effects model. In the 42 trials, the mean age of the subjects was approximately 56 years, and the mean baseline glycated hemoglobin level was approximately 8.2%. In the rosiglitazone group, as compared with the control group, the odds ratio for myocardial infarction was 1.43 (95% confidence interval [CI], 1.03 to 1.98; P=0.03), and the odds ratio for death from cardiovascular causes was 1.64 (95% CI, 0.98 to 2.74; P=0.06). Rosiglitazone was associated with a significant increase in the risk of myocardial infarction and with an increase in the risk of death from cardiovascular causes that had borderline significance. Our study was limited by a lack of access to original source data, which would have enabled time-to-event analysis. Despite these limitations, patients and providers should consider the potential for serious adverse cardiovascular effects of treatment with rosiglitazone for type 2 diabetes.

Levels of intrinsic coagulation factors and the risk of myocardial infarction among men: opposite and synergistic effects of factors XI and XII

AbstractThe role of the intrinsic coagulation system on the risk of myocardial infarction is unclear. In the Study of Myocardial Infarctions Leiden (SMILE) that included 560 men younger than age 70 with a first myocardial infarction and 646 control subjects, we investigated the risk of myocardial infarction for levels of factor XI (factor XIc) and factor XII (factor XIIc). Furthermore, the risks for factor VIII activity (factor VIIIc) and factor IX activity (factor IXc) were assessed. Factor XIc was 113.0% in patients compared with 109.8% in control subjects (difference, 3.2%; 95% CI, 1.1%-5.4%). The risk of myocardial infarction adjusted for age for men in the highest quintile compared with those in the lowest quintile was 1.8-fold increased (ORadj, 1.8; 95% CI, 1.2-2.7). In contrast, factor XIIc among patients with myocardial infarction was lower than in control subjects, respectively, 93.0% and 98.6% (difference, 5.6%; 95% CI, 3.3%-7.9%). The odds ratio of myocardial infarction for men in the highest quintile versus those in the lowest quintile was 0.4 (ORadj, 0.4; 95% CI, 0.2-0.5). The highest risk was found among men with both high factor XIc and low factor XIIc (analyses in tertiles: ORadj, 6.4; 95% CI, 2.2-18.0). Factor VIIIc increased the risk of myocardial infarction although not dose dependently. Factor IXc increased the risk; odds ratio of myocardial infarction for men in the highest quintile versus those in the lowest quintile was 3.2 (ORadj, 3.2; 95% CI, 2.0-5.1). Thus, factors XIc and XIIc have opposite and synergistic effects on the risk of myocardial infarction in men; factor VIIIc and factor IXc increase the risk.

Glycated apolipoprotein B and myocardial infarction

Aims To evaluate the association of serum concentrations of glycated apolipoprotein B (ApoBg) with the incidence of myocardial infarction (MI) in subjects with and without diabetes. Methods The design is a nested case-control study. The cohort included 5632 subjects over 50 years of age attending the clinical laboratories of a small geographic area in southern Italy. After five years, 4563 subjects were traced and 103 had developed MI. We sampled from the cohort two controls for each incident case of MI, frequency matched for sex and diabetes. ApoBg was measured using a monoclonal antibody. Logistic regression was used for statistical analysis of the data. Results ApoBg at baseline was higher in subjects who developed myocardial infarction than in controls in both non-diabetic and diabetic subjects ( t test, P = 0.009 and P = 0.05 respectively). MI odds ratio in the third tertile of ApoBg was 2.01 (95 % CI 0.93–4.33) in non-diabetic and 2.88 (0.85–9.68) in diabetic subjects (chi-square test for trend; non-diabetics P = 0.03, diabetics P = 0.06). Serum triglycerides, cholesterol, HDL and LDL cholesterol, glucose and insulin were not associated with MI ( P > 0.10). Conclusion ApoBg at baseline is directly associated with the development of MI in the following five years in both diabetic and non-diabetic individuals.

Vibration exposure and myocardial infarction incidence: the VHEEP case–control study

The main objectives of this study were to assess the risk of contracting first episode of myocardial infarction (MI) subsequent to vibration exposure and to assess a possible exposure-response relationship. The Västernorrland heart epidemiology programme (VHEEP, a part of the Stockholm heart epidemiology programme study) was the source of the data. VHEEP is a population-based case-control study of risk factors for acute MI. Exposure information was collected by questionnaire and vibration exposure was assessed in 218 cases and 257 controls. Relative risks were estimated using odds ratios (ORs) from binary logistic regression. The results show that the OR of acute MI when exposed to vibration was 1.6 (95% CI: 1.1-2.4). It was not possible, however, to determine whether an exposure-response relationship was present. Working entailing vibrating machines is associated with an increased risk for acute MI.

Risk of cardiovascular events and celecoxib: a systematic review and meta-analysis.

To examine whether the increased risk of cardiovascular events with rofecoxib represents a class effect of cyclooxygenase-2 (COX-2) specific inhibitors. Systematic review and meta-analysis of randomized double-blind clinical trials of celecoxib of at least 6 weeks' duration and presented data on serious cardiovascular thromboembolic events. Data sources included six bibliographic databases, the relevant files of the United States Food and Drug Administration, and pharmaceutical company websites. Pooled fixed effects estimates of the odds ratios for risk of cardiovascular events with celecoxib compared with comparator treatment were calculated using the inverse variance weight method. The main outcome measure was myocardial infarction. Four placebo-controlled trials with 4422 patients were included in the primary meta-analysis comparing celecoxib with placebo. The odds ratio of myocardial infarction with celecoxib compared to placebo was 2.26 (95%confidence interval 1.0 to 5.1). For composite cardiovascular events [odd ratio 1.38 (95% CI 0.91 to 2.10)], cardiovascular deaths [OR 1.06 (95% CI 0.38 to 2.95)] and stroke [OR 1.0(95% CI 0.51 to 1.84)] there was no significant increase in risk with celecoxib. The secondary meta-analysis which included a total of six studies (with placebo, diclofenac, ibuprofen, and paracetamol as comparators) of 12 780 patients, showed similar findings with a significant increased risk with celecoxib for myocardial infarction [OR 1.88 (95% CI 1.15 to 3.08)] but not other outcome measures. The available data indicate an increased risk of myocardial infarction with celecoxib therapy, consistent with a class effect for COX-2 specific inhibitors.

Risk of cardiovascular events and celecoxib: a systematic review and meta-analysis

To examine whether the increased risk of cardiovascular events with rofecoxib represents a class effect of cyclooxygenase-2 (COX-2) specific inhibitors. Systematic review and meta-analysis of randomized double-blind clinical trials of celecoxib of at least 6 weeks' duration and presented data on serious cardiovascular thromboembolic events. Data sources included six bibliographic databases, the relevant files of the United States Food and Drug Administration, and pharmaceutical company websites. Pooled fixed effects estimates of the odds ratios for risk of cardiovascular events with celecoxib compared with comparator treatment were calculated using the inverse variance weight method. The main outcome measure was myocardial infarction. Four placebo-controlled trials with 4422 patients were included in the primary meta-analysis comparing celecoxib with placebo. The odds ratio of myocardial infarction with celecoxib compared to placebo was 2.26 (95%confidence interval 1.0 to 5.1). For composite cardiovascular events [odd ratio 1.38 (95% CI 0.91 to 2.10)], cardiovascular deaths [OR 1.06 (95% CI 0.38 to 2.95)] and stroke [OR 1.0(95% CI 0.51 to 1.84)] there was no significant increase in risk with celecoxib. The secondary meta-analysis which included a total of six studies (with placebo, diclofenac, ibuprofen, and paracetamol as comparators) of 12 780 patients, showed similar findings with a significant increased risk with celecoxib for myocardial infarction [OR 1.88 (95% CI 1.15 to 3.08)] but not other outcome measures. The available data indicate an increased risk of myocardial infarction with celecoxib therapy, consistent with a class effect for COX-2 specific inhibitors.

Insulin Sensitizing Pharmacotherapy for Prevention of Myocardial Infarction in Patients With Diabetes Mellitus

Type 2 diabetes mellitus and insulin resistance are associated with an increased risk of myocardial infarction (MI). Although differences exist in insulin sensitization among oral hypoglycemic drugs, it is unclear whether these differences translate into a differential risk of MI and whether differences exist among these drugs. We conducted a case-control study of first MI in a 5-county area during a 56-month period. The patients were those with type 2 diabetes mellitus hospitalized with a first MI and the controls were those with diabetes mellitus randomly selected from the same geographic area. Information on medication use and other clinical data were obtained by telephone interview. After adjustment for all confounders, the odds ratio for MI for current monotherapy with thiazolidinedione and monotherapy with metformin compared with monotherapy with sulfonylurea was 0.33 (95% confidence interval 0.12 to 0.92, p = 0.03) and 0.48 (95% confidence interval 0.27 to 0.82, p = 0.01), respectively. The addition of a thiazolidinedione, but not metformin, to sulfonylurea monotherapy was associated with a significant reduction in MI risk compared with sulfonylurea therapy alone. In conclusion, the use of insulin-sensitizing drugs is associated with a significantly reduced risk of MI compared with sulfonylurea use, and the addition of a thiazolidinedione to sulfonylurea monotherapy is associated with a lower risk of MI.

The association between homocysteine and myocardial infarction is independent of age, sex, blood pressure, cholesterol, smoking and markers of inflammation: the Glasgow Myocardial Infarction Study

Homocysteine is associated with both myocardial infarction and arterial wall inflammation. To establish whether homocysteine is associated with myocardial infarction after adjusting for age, sex, the major cardiovascular risk factors and inflammatory risk predictors (fibrinogen, C-reactive protein and interleukin-6). A case-control study, using 364 myocardial infarction cases drawn from the north Glasgow MONICA study, 3-9 months after their event, and 383 controls drawn from the general population of the same geographical area. The odds ratio for myocardial infarction increased progressively across the four quarters of the homocysteine distribution, after adjusting for only age and sex or for the full adjustment (age, sex, smoking, systolic blood pressure, total cholesterol, fibrinogen, C-reactive protein and interleukin-6). The odds ratios produced by the two adjustments were similar. Comparing the top quarter with the bottom quarter of homocysteine, the odds ratio was 2.21 (95% confidence interval: 1.30-3.76) after the full adjustment. The odds ratio for a 5 micromol/l increase in homocysteine was 1.12 (95% confidence interval: 1.01-1.24) after the full adjustment. This study suggests that homocysteine has an effect on cardiovascular risk over and above that of inflammatory markers and the major cardiovascular risk factors.

Heart Disease and Dementia: A Population-based Study

There are conflicting reports on the possible positive association between coronary disease and dementia. The objectives of this study were to examine the association between coronary disease, as measured by myocardial infarction and cardiac death, and dementia in a population-based study. By use of the record-linkage system of the Rochester Epidemiology Project, 916 cases of dementia and 916 age (+/-1 year)- and sex-matched controls were identified in Rochester, Minnesota, between 1985 and 1994. From the same population, the authors identified all subjects who experienced a myocardial infarction (defined using standardized criteria) during the period 1979-1998. For myocardial infarction occurring prior to the index year of dementia, the authors used conditional logistic regression (case-control analysis), while for myocardial infarction and death occurring after the index year, they used competing risk survival analysis to account for informative censoring (cohort analysis). Before the index year, the odds ratio for myocardial infarction among cases with dementia compared with controls was 1.00 (95% confidence interval (CI): 0.62, 1.62; p = 1.00). After the index year, patients with dementia had a 46% decreased risk of subsequent myocardial infarction (hazard ratio = 0.54, 95% CI: 0.36, 0.82; p = 0.004) and an 18% decreased risk of cardiac death (hazard ratio = 0.82, 95% CI: 0.70, 0.95; p = 0.010). There was no evidence of a positive association between dementia and preceding myocardial infarction, while there was a decreased risk of myocardial infarction and cardiac death following dementia.

Daily Intake of Magnesium and Calcium From Drinking Water in Relation to Myocardial Infarction

A decreased risk for cardiovascular disease has been related to the hardness of drinking water, particularly high levels of magnesium. However, the evidence is still uncertain, especially in relation to individual intake from water. We used data from the Stockholm Heart Epidemiology Program, a population-based case-control study conducted during 1992-1994, to study the association between myocardial infarction and the daily intake of drinking water magnesium and calcium. Our analyses are based on 497 cases age 45-70 years, and 677 controls matched on age, sex, and hospital catchment area. Individual data on magnesium, calcium, and hardness of the domestic drinking water were assessed from waterwork registers or analyses of well water. After adjustment for the matching variables and smoking, hypertension, socioeconomic status, job strain, body mass index, diabetes, and physical inactivity, the odds ratio for myocardial infarction was 1.09 (95% confidence interval = 0.81-1.46) associated with a tap water hardness above the median (>4.4 German hardness degrees) and 0.88 (0.67-1.15) associated with a water magnesium intake above the median (>1.86 mg/d). There was no apparent sign of any exposure-response pattern related to water intake of magnesium or calcium. This study does not support previous reports of a protective effect on myocardial infarction associated with consumption of drinking water with higher levels of hardness, magnesium, or calcium.

Patients Exposed to Rofecoxib and Celecoxib Have Different Odds of Nonfatal Myocardial Infarction

Studies have postulated that cyclooxygenase-2 (COX-2) selective inhibitors affect cardiovascular risk through various mechanisms. Some of these mechanisms could increase risk (for example, inhibition of prostacyclin production), and some could decrease risk (for example, inhibition of inflammation). To determine the effect of COX-2 inhibitors on risk for nonfatal myocardial infarction (MI). Case-control study. 36 hospitals in a 5-county area. 1718 case-patients with a first, nonfatal MI admitted to these hospitals and 6800 controls randomly selected from the same counties. Self-reported medication use assessed through telephone interviews. The adjusted odds ratio for MI among celecoxib users, relative to persons who did not use nonaspirin nonsteroidal anti-inflammatory drugs (NSAIDs), was 0.43 (95% CI, 0.23 to 0.79) compared with 1.16 (CI, 0.70 to 1.93) among rofecoxib users. The use of rofecoxib was associated with a statistically significant higher odds of MI compared with the use of celecoxib (adjusted odds ratio for rofecoxib vs. celecoxib, 2.72 [CI, 1.24 to 5.95]; P = 0.01). Nonselective NSAIDs were associated with a reduced odds of nonfatal MI relative to nonusers. Comparisons of COX-2 inhibitors with nonselective NSAIDs were the following: rofecoxib versus naproxen (odds ratio, 3.39 [CI, 1.37 to 8.40]) and celecoxib versus ibuprofen or diclofenac (odds ratio, 0.77 [CI, 0.40 to 1.48]). The possibility of recall bias and uncontrolled confounding in this observational study limit the ability to make definitive conclusions. The association of celecoxib with a lower odds of MI could have occurred by chance. Only about 50% of eligible participants completed telephone interviews. Celecoxib and rofecoxib were associated with different odds of MI. Cardiovascular effects among the COX-2 inhibitors seem different, but further studies, preferably randomized trials, are needed to fully understand the spectrum of effects of COX-2 inhibitors and potential differences among them.

Dutch women with a low birth weight have an increased risk of myocardial infarction later in life: a case control study

BackgroundTo investigate whether low birth weight increases the risk of myocardial infarction later in life in women.MethodsNationwide population-based case-control study. Patients and controls: 152 patients with a first myocardial infarction before the age of 50 years in the Netherlands. 568 control women who had not had a myocardial infarction stratified for age, calendar year of the index event, and area of residence.ResultsBirth weight in the patient group was significantly lower than in control women (3214 vs. 3370 gram, mean difference -156.3 gram (95%CI -9.5 to -303.1). The odds ratio for myocardial infarction, associated with a birth weight lower than 3000 gram (20th percentile in controls) compared to higher than 3000 gram was 1.7 (95%CI 1.1–2.7), while the odds ratio for myocardial infarction for children with a low birth weight (< 2000 g) compared to a birth weight ≥ 2000 g was 2.4 (95%CI 1.0 – 5.8). Both figures did not change after adjustment for putative confounders (age, education level, body mass index, waist-hip ratio, hypertension, diabetes, hypercholesterolemia, smoking, and family history of cardiovascular disease).ConclusionsLow birth weight is associated with an increased risk of myocardial infarction before age of 50 in Dutch women.

Mannan binding lectin as an adjunct to risk assessment for myocardial infarction in individuals with enhanced risk

Inflammation can predispose to myocardial infarction (MI), and mannan binding lectin (MBL) promotes phagocytic clearance of inflammatory agents, but the predictive value of MBL levels for MI is not known. MBL was analyzed in subgroups of the population-based Reykjavik study, a cohort of 19,381 participants recruited from 1967. MBL levels were very stable over time (self correlation: 0.86). In a cross-sectional group from the original cohort (n = 987), high MBL (>1,000 μg/L) was associated with a greatly lowered odds ratio for MI (0.64, P < 0.001). To verify this finding, a nested case control sample (n = 1,309) was randomly selected from the cohort. High MBL at recruitment was also associated with decreased MI risk in this follow-up group, but to a lesser extent and not significant for the whole group, smokers, or hypertensive individuals. However, high MBL was as in the cross-sectional group, associated with greatly decreased MI risk in diabetic (P = 0.02) or hypercholesterolemic individuals (P = 0.004). This also applied to raised erythrocyte sedimentation rate (P = 0.007). Diabetic patients with high MBL did not have a higher MI risk than nondiabetic individuals. Our findings indicate that high MBL may predict decreased likelihood of MI, particularly in diabetics, and are consistent with the possibility that MBL may promote clearance of atherogenic agents.

Antidepressants and risk of first-time hospitalization for myocardial infarction: A population-based case-control study

Several studies have found an increased risk of myocardial infarction among depressed patients. Selective serotonin reuptake inhibitors (SSRIs) appear to lack the arrhythmic adverse effects of tricyclic antidepressants, and are thought to inhibit platelet aggregation. We examined whether use of different antidepressant classes is associated with a lower risk of first-time hospitalization for myocardial infarction, as compared with nonuse. We identified 8887 cases of first-time hospitalization for myocardial infarction and 88,862 age- and sex-matched population-based controls during 1994-2002, using data from North Jutland County, Denmark. Cases and controls were stratified according to history of cardiovascular disease. All prescriptions for antidepressants before hospitalization for myocardial infarction were identified using a prescription database. Conditional logistic regression was used to estimate odds ratios of myocardial infarction associated with antidepressant use, adjusted for possible confounding factors. In patients with a history of cardiovascular disease, we found indications of a lower risk of myocardial infarction among those who used SSRIs (adjusted odds ratio [OR] = 0.85; 95% confidence interval [CI]: 0.62 to 1.16), nonselective serotonin reuptake inhibitors (adjusted OR = 0.83; 95% CI: 0.50 to 1.38), and other antidepressants (adjusted OR = 0.55; 95% CI: 0.31 to 0.97). There were no such associations among persons without a history of cardiovascular disease. Antidepressant use may be associated with a decreased risk of hospitalization for myocardial infarction among persons with a history of cardiovascular disease, although it remains uncertain whether there are differences by class of antidepressant.

Gender Dependent Association of Thrombospondin-4 A387P Polymorphism With Myocardial Infarction

To the Editor: A recently identified novel missense variant of TSP-4, A389P (29926 G>C) was correlated with premature myocardial infarction (MI) by an exploratory genetic association study on 184 MI patients from the American population.1 In this study, the TSP-4 387P allele showed the strongest association, with an adjusted odds ratio for MI of 1.89 ( P =0.002 adjusted for covariates) for individuals carrying the 387P allele. This was replicated by the same group using a larger number of patients.2 An in vitro functional study of the TSP-4 A387P substitution provided further evidence in support of a proatherogenic effect. The TSP-4 A387P substitution was shown to have a gain of function effect leading to suppression of endothelial cell adhesion and proliferation.3 The TSP-4 A387P variant also shows ethnic distribution differences. The TSP-4 387P allele showed a dramatically lower prevalence in Asian Chinese populations compared with whites (3.8% versus 19.6 to 23.2%) and failed to associate with coronary artery disease (CAD) or MI in the studied populations.4–5 Interestingly, in a more recent investigation, the TSP-4 variant 387P allele was significantly associated with reduced risk, rather than increased risk, for premature MI (OR=0.43, 0.22 to 0.85) in Netherlands whites.6 Therefore, the true effect of TSP-4 A387P in MI remains unknown. We believe that the contradictory results may be caused by either population genetic mixture or the effects of different modifiers for the TSP-4387P allele among the different ethnic populations. We examined the TSP-4 A387P variant as part of our study to explore potential gene variants as risk factors for MI and the effect of interaction between different variants on MI. …

Exposure to Traffic and the Onset of Myocardial Infarction

An association between exposure to vehicular traffic in urban areas and the exacerbation of cardiovascular disease has been suggested in previous studies. This study was designed to assess whether exposure to traffic can trigger myocardial infarction. We conducted a case-crossover study in which cases of myocardial infarction were identified with the use of data from the Cooperative Health Research in the Region of Augsburg Myocardial Infarction Registry in Augsburg, in southern Germany, for the period from February 1999 to July 2001. There were 691 subjects for whom the date and time of the myocardial infarction were known who had survived for at least 24 hours after the event, completed the registry's standardized interview, and provided information on factors that may have triggered the myocardial infarction. Data on subjects' activities during the four days preceding the onset of symptoms were collected with the use of patient diaries. An association was found between exposure to traffic and the onset of a myocardial infarction within one hour afterward (odds ratio, 2.92; 95 percent confidence interval, 2.22 to 3.83; P<0.001). The time the subjects spent in cars, on public transportation, or on motorcycles or bicycles was consistently linked with an increase in the risk of myocardial infarction. Adjusting for the level of exercise on a bicycle or for getting up in the morning changed the estimated effect of exposure to traffic only slightly (odds ratio for myocardial infarction, 2.73; 95 percent confidence interval, 2.06 to 3.61; P<0.001). The subject's use of a car was the most common source of exposure to traffic; nevertheless, there was also an association between time spent on public transportation and the onset of a myocardial infarction one hour later. Transient exposure to traffic may increase the risk of myocardial infarction in susceptible persons.

High serum antibody levels to Porphyromonas gingivalis predict myocardial infarction

An association between coronary heart disease (CHD) and clinically diagnosed periodontitis has been found in several epidemiological studies. However, seroepidemiologic evidence based on prospective data on this association is totally lacking. The aim of the study was to investigate serum antibodies to major periodontal pathogens for their prediction of myocardial infarction (MI) in men free of CHD at baseline. Cases and controls were ascertained from a random population sample of 4255 men aged 30 to 59 years at baseline. The study cases included 63 men with nonfatal MI or coronary death within the follow-up time of 10 years. Age-matched control subjects (n=63) were randomly chosen from the same cohort. Serum antibody levels to two major periodontopathogenic bacteria, Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis, were determined. There was no significant association between the risk for MI and IgG- or IgA-class antibody levels to A. actinomycetemcomitans or IgG-class antibody levels to P. gingivalis. However, a high P. gingivalis IgA-class antibody level predicted MI independently of classical cardiovascular risk factors. The risk for MI increased by increasing quartiles of antibody levels (P for the trend 0.021). Compared with the first quartile, the multivariate odds ratios of MI in the second, third and fourth quartiles were 2.47 (95% CI 0.75-8.11), 3.30 (1.03-10.58) and 3.99 (1.22-13.10), respectively. The study provides serological evidence that an infection caused by the periodontal pathogen, P. gingivalis, increases the risk for MI.