Increased Risk Of Acute Myocardial Infarction Research Articles

The association between dairy intake and risk of cardiovascular disease and mortality in patients with stable angina pectoris.

The association of dairy products with cardiovascular disease and mortality risk remains heavily debated. We aimed to investigate the association between intake of total dairy and dairy products and the risk of acute myocardial infarction (AMI), stroke, and cardiovascular and all-cause mortality. We included 1929 patients (80% men, mean age 62 years) with stable angina pectoris from the Western Norway B-vitamin Intervention Trial. Dietary data were obtained via a 169-item food frequency questionnaire. Risk associations were estimated using Cox proportional hazard regression models adjusted for relevant covariates. Non-linear associations were explored visually. The mean (±SD) dairy intake in the study population was 169 ± 108 g/1000 kcal. Median follow-up times were 5.2, 7.8, and 14.1 years for stroke, AMI, and mortality, respectively. Higher intake of total dairy and milk were positively associated with stroke risk [HR (95% CI): 1.14 (1.02, 1.27) and 1.13 (1.02, 1.27), cardiovascular mortality 1.06 (1.00, 1.12) and 1.07 (1.01, 1.13)] and all-cause mortality [1.07 (1.03, 1.11) and 1.06 (1.03, 1.10)] per 50 g/1000 kcal. Higher cheese intake was inversely associated with AMI risk [0.92 (0.83, 1.02)] per 10 g/1000 kcal. Butter was associated with increased AMI risk [1.10 (0.97, 1.24)] and all-cause mortality [1.10 (1.00, 1.20) per 5 g/1000 kcal. Higher dairy and milk consumption were associated with increased risk of mortality and stroke. Cheese was associated with decreased, and butter with increased, risk of AMI. Dairy is a heterogenous food group with divergent health effects and dairy products should therefore be investigated individually.

Lipoprotein(a) as predictor of coronary artery disease and myocardial infarction in a multi-ethnic Asian population

Background and aimsThe role of Lp(a) in multi-ethnic Asian populations with coronary artery disease (CAD) has not been well established. The aims of this study were (i) to investigate whether Lp(a) is a predictor of CAD, and (ii) amongst patients with CAD, to ascertain whether Lp(a) is a predictor of acute myocardial infarction (AMI) and severity of CAD. MethodsWe compared three cardiovascular phenotypes from patients recruited at coronary angiography. CAD was defined as ≥50% coronary artery stenosis and subdivided into a group with AMI history (CAD+AMI+) and a group without (CAD+AMI-). Minimal CAD group (CAD-) was defined as normal or <30% coronary artery stenosis and no AMI. The severity of CAD was defined using the modified Gensini score. ResultsWe studied 2025 patients comprising 94.5% men and 61.4% of Chinese ethnicity. The median Lp(a) level was highest in CAD+AMI+, followed by CAD+AMI- and CAD- (26.2, 20.1, and 15.8 nmol/L respectively). Similarly, the frequency of patients with Lp(a) ≥120 nmol/L were in the same order (11.8%, 9.1% and 2.4%). Lp(a) levels were highest among Asian Indians, followed by Malays and Chinese patients (p < 0.001). Lp(a) levels and Lp(a) ≥120 nmol/L were significant predictors of CAD (Odds ratio (OR) = 1.12 per 10 nmol/L increment, p < 0.001, and OR = 5.41 p = 0.004 respectively). Among patients with CAD, higher Lp(a) levels were associated with increased AMI risk (OR = 1.02 per 10 nmol/L increment, p = 0.024). Lp(a) ≥120 nmol/L was positively associated with CAD severity (p = 0.020). ConclusionsPlasma Lp(a) concentration is a positive predictor of CAD and AMI in a mostly male South East Asian population.

Acute Myocardial Infarction and Daylight Saving Time Transitions: Is There a Risk?

Available evidence on the risk of acute myocardial infarction (AMI) in the days after the spring daylight saving time (DST) transition suggests either a modest increase or no risk increase. Partial sleep deprivation and enhanced circadian clock misalignment have been implicated as the underlying mechanisms for increased AMI risk, probably via enhanced thrombo-inflammatory processes and activation of the sympathetic nervous system. Most of the studies, as we suggest as a perspective here, have used potentially inappropriate control periods, including the two post-transitional weeks, because adjustment after the spring DST transition lasts at least four weeks for all chronotypes and probably even beyond this period for late chronotypes. The most plausible conclusions, at the moment, for the risk of AMI after the spring DST transition are: (1) the risk is increased, (2) a relatively modest risk increase could be currently underestimated or in some studies undetected, (3) late chronotypes and/or individuals with high levels of social jetlag (a proxy for circadian clock misalignment) could be more affected by the phenomenon, and (4) underlying pathophysiological mechanisms should be further explored. As a significant part of world’s population continues to be affected by the biannual clock change, the question of increased AMI risk in the post-transitional period remains an intriguing public health issue.

Proton Pump Inhibitor Exposure and Acute Myocardial Infarction Risk: A Nested Cohort Study.

Association of proton pump inhibitor (PPI) exposure with acute myocardial infarction (AMI) risk in the Caucasian population remains under debate. Here, we clarified whether PPI exposure might be related to an increased new-onset AMI risk in an Asian population. Data of 27,624 patients with PPI exposure followed by new-onset AMI development were extracted from Taiwan National Health Insurance Research Database and age- and sex-matched with 27,624 controls with PPIs exposure, but without subsequent AMI and ischemic heart disease development. The amount of PPI exposure was calculated based on the cumulative defined daily dose (cDDD) during the follow-up period. Subsequent AMI risk was measured after adjustments of demographic data and indication of PPI use. AMI risk increased with an increase in PPI exposure: with cDDD ≤ 30 as the reference, the odds ratios (95% confidence intervals) for cDDDs of > 365 was 1.56 (1.45-1.69). All five PPI categories, including pantoprazole, lansoprazole, omeprazole, esomeprazole, and rabeprazole, increased AMI risk. Our study demonstrated long-term or high-dose PPI exposure associated with increased new-onset AMI risk in patients without a history of any ischemic heart disease. The underlying mechanisms of PPI-related cardiovascular effects deserve more investigation.

No effect of plasma trimethylamine N-Oxide (TMAO) and plasma trimethyllysine (TML) on the association between choline intake and acute myocardial infarction risk in patients with stable angina pectoris

Plasma concentrations of trimethylamine N-oxide (TMAO) have been linked to cardiovascular disease (CVD) risk and mortality. TMAO is formed through the bacterial conversion of trimethylamine which is obtained either directly from food, generated from dietary precursors (e.g. choline) or derived from endogenous trimethyllysine (TML) production. In a previous article, we reported an increased risk of acute myocardial infarction with increased total choline intake in patients with stable angina pectoris. Due to the close link between TMAO, TML, choline metabolism and possibly CVD, we investigated whether plasma TMAO and TML modified the effect of total choline intake on acute myocardial infarction (AMI) risk in a post-hoc analysis. We found plasma TMAO and TML do not modify the association between higher dietary choline intake and increased AMI risk. Additionally, this association is not mediated via TMAO. • No effect modification by trimethylamine-N-oxide on the association between choline intake and acute myocardial infarction. • No effect modification by trimethyllysine on the association between choline intake and acute myocardial infarction. • No indirect effect of trimethylamine-N-oxide on the association between choline intake and acute myocardial infarction.

Size-fractionated particulate air pollution and myocardial infarction emergency hospitalization in Shanghai, China

BackgroundFine particulate matter (PM2.5) air pollution has been associated with increased risks of acute myocardial infarction (AMI), but it remains unknown about the potentially differentiated effects of size-fractionated particulate matter on AMI risk. ObjectiveTo identify the specific size ranges that dominate the effects of particulate matter on AMI onset. MethodsWe conducted a time-series study in Shanghai, China from January 2014 to December 2018. We evaluated particle size distribution of 0.01 μm to 2.5 μm from an environmental supersite and AMI emergency hospitalizations from the largest cardiovascular hospital in Shanghai. We used over-dispersed generalized additive models to estimate the associations of size-fractionated particle number concentrations (PNC) with AMI and its types. ResultsWe identified a total of 4720 AMI emergency hospitalizations. PM2.5 was significantly associated with increased AMI risk on the concurrent day. The associations were significant only for PNC < 0.3 μm. For an IQR increase of PNCs for size ranges 0.01–0.03 μm, 0.03–0.05 μm, 0.05–0.10 μm and 0.10–0.30 μm, AMI hospitalizations increased by 6.68% (95% CI: 2.77%, 10.74%), 6.53% (95% CI: 2.08%, 11.17%), 5.78% (95% CI: 0.92%, 10.88%) and 5.92% (95% CI: 1.31%, 10.74%), respectively. The associations of PNC < 0.05 μm remained significant when adjusting for other air pollutants. There were consistently much stronger associations of particles with ST-segment elevation AMI than those with non-ST-segment elevation AMI. ConclusionsThis epidemiological investigation suggested that ultrafine particles, especially those <0.05 μm, may be mainly responsible for the acute AMI risk induced by PM2.5.

Risk of Acute Myocardial Infarction in Patients with Rheumatic Arthritis: A National-Wide Population-Based Cohort Study.

We performed a cohort study to quantify the association between rheumatic arthritis (RA) and acute myocardial infarction (AMI) risk. ICD-9 was used to identify AMI and RA patients, and the Cox proportional hazards model with adjusted confounding factors was used to quantify the risk. The overall risk of AMI for RA patients was an aHR of 1.05 (95% CI 1.01-1.09). We found RA was associated with an increased risk for AMI.

Factors Associated With Excess Myocardial Infarction Risk in HIV-Infected Adults: A Systematic Review and Meta-analysis.

To estimate the pooled relative risk (RR) of incident acute myocardial infarction (AMI) among HIV-infected adults compared with HIV-uninfected controls and explore the contribution of traditional and HIV-related risk factors. Understanding AMI risk and associated risk factors in HIV-infected populations has the potential to inform clinical management and prevention strategies. We systematically identified cohort studies of HIV-infected or HIV-infected and matched uninfected adults reporting AMI incidence rates published up to January 1, 2017. Random-effects meta-analysis models were used to estimate the aggregate RR of AMI by HIV status. Subgroup analysis and meta-regression were used to explore factors affecting risk. Sixteen studies (N = 1,619,690, median age 38.5 years, 78.9% male, mean follow-up of 6.5 years) were included. In pooled analyses of HIV-infected and matched uninfected cohorts (n = 5), HIV-infected individuals had higher AMI incidence rates (absolute risk difference = 2.2 cases per 1000 persons per year) and twice the risk of AMI [RR = 1.96 (1.5-2.6)] compared with matched HIV-uninfected controls. In a multivariate meta-regression, each additional percentage point in the proportion of male participants [odds ratio (OR) = 1.20 (1.14-1.27)] and each additional percentage point in the prevalence of hypertension [OR = 1.19 (1.12-1.27)], dyslipidemia [OR = 1.09 (1.07-1.11)], and smoking [OR = 1.09 (1.05-1.13)] were independently associated with increased AMI risk in HIV-infected adults. Chronic HIV infection is associated with a 2-fold higher AMI risk. Traditional risk factors such as hypertension, dyslipidemia, and smoking are significant contributors to AMI risk among HIV-infected adults and should be aggressively targeted in routine HIV care.

Elevated lipoprotein (a) levels are associated with the acute myocardial infarction in patients with normal low-density lipoprotein cholesterol levels.

Elevated lipoprotein (a) [Lp(a)] and coronary artery disease (CAD) risk has been renewed interested in recent years. However, the association between Lp(a) and acute myocardial infarction (AMI) risk in patients with normal low-density lipoprotein cholesterol (LDL-C) levels has yet to been established. A hospital-based observational study including 558 AMI patients and 1959 controls was conducted. Lp(a) level was significantly higher in AMI patients with normal LDL-C levels than that in non-CAD group (median: 134.5 mg/l vs 108 mg/l, P<0.001). According to Lp(a) quartiles (Q1, <51 mg/l; Q2, 51–108 mg/l; Q3, 108–215 mg/l; Q4, ≥215 mg/l), the incidence of AMI increased with the elevated Lp(a) quartiles (P<0.001 and P for trend<0.001). Logistic regression analysis suggested that patients with Q3 and Q4 of Lp(a) values had 1.666 (95%CI = 1.230–2.257, P<0.001) and 1.769 (95%CI = 1.305–2.398, P< 0.001) folds of AMI risk compared with patients with Q1, after adjusting for traditional confounders. Subgroup analyses stratified by gender and age showed that the association only existed in male and late-onset subgroups. In addition, we analyzed the association of Lp(a) with AMI risk in different cut-off values (cut-off 1 = 170 mg/l, cut-off 2 = 300 mg/l). A total of 873 (34.68%) and 432 (17.16%) participants were measured to have higher Lp(a) levels according to cut-off 1 and cut-off 2, respectively. Participants with high Lp(a) levels had 1.418- (cut-off1, 95%CI = 1.150–1.748, P<0.001) and 1.521- (cut-off 2, 95%CI = 1.179–1.963, P< 0.001) folds of AMI risk compared with patients with low Lp(a) levels. The present large-scale study revealed that elevated Lp(a) levels were associated with increased AMI risk in Chinese population with normal LDL-C levels.

Comparative hazards of acute myocardial infarction among hospitalized patients with methamphetamine- or cocaine-use disorders: A retrospective cohort study

BackgroundIt is assumed that recreational use of methamphetamine can trigger acute myocardial infarction (AMI) events, but estimates of longitudinal hazards of AMI among methamphetamine users are lacking. MethodsRetrospective cohort study: Competing-risks analysis was used to estimate time-to-AMI patterns in methamphetamine versus matched appendicitis (population-proxy) and matched cocaine (drug-control) groups. Cohorts were propensity-score-matched using demographic and clinical variables. SettingCalifornia, 1990–2005. ParticipantsCohorts of individuals with no prior or concurrent history of AMI hospitalized with methamphetamine- (n = 73,056), cocaine- (n = 47,726), or appendicitis-related conditions (n = 330,109). MeasurementsICD-9/ICD-10 indications of AMI (ICD-9 410.X; ICD-10 I21.X) in death records or inpatient hospital data. ResultsPatients in methamphetamine cohort were more likely to develop subsequent AMI in comparison to those in matched appendicitis cohort [Hazard ratio (HR): 1.41; 95% CI, 1.23–1.62, p < 0.0001], with increased risk most marked in young methamphetamine users (age 15–34 years; HR: 2.04; 95% CI, 1.63–2.57, p = 0. 0001). Risk was slightly increased vs. that in matched cocaine group (HR: 1.19; 95% CI, 1.02–1.39, p = 0. 029). Individuals in cocaine cohort were also more likely to experience AMI outcome vs. appendicitis cohort (HR: 1.25; 95% CI, 1.08–1.45, p = 0. 0023). ConclusionOur longitudinal data support results of earlier epidemiological studies suggesting that persons with methamphetamine- (or cocaine-) use disorders might have increased AMI risk. However, because of potential study limitations and the unexpectedly modest magnitude of the observed increased AMI hazard, these findings must be considered preliminary and require replication.

Association between ABO blood group and acute myocardial infarction

To explore the association between the ABO blood group and the risk of myocardial infarction in Chinese people. We retrospectively recruited 1 988 consecutive patients with acute myocardial infarction (AMI) and 1 856 non-coronary artery disease (non-CAD) subjects who hospitalized in our hospital between January 2013 and December 2013. The clinical features and ABO blood group were analyzed. Blood group distribution was A (27.1%, 539/1 988), B (34.4%, 684/1 988), AB (10.8%, 215/1 988), O (27.7%, 551/1 988) in patients with AMI and A (26.7%, 496/1 856), B(32.2%, 598/1 856), AB(10.8%, 200/1 856), O (30.4%, 564/1 856) in non-CAD group. The single factor analysis showed that blood group O tended to be more common in the non-CAD group than in AMI group (P = 0.06). After adjustment for common cardiovascular risk factors such as age, gender, hypertension, diabetes, smoking and serum cholesterol level, the A, B, and AB blood groups were associated with increased risk of AMI compared with O blood group, and the difference was significant with A blood group (OR = 1.229, 95% CI 1.019-1.482, P = 0.031) and B blood groups (OR = 1.214, 95% CI 1.017-1.449, P = 0.032). In addition, non-O blood group remained significantly associated with the increased risk of AMI than O blood group after logistic regression analysis (OR = 1.223, 95% CI 1.048-1.426, P = 0.01). Our results suggest that non-O blood group is associated with the increased risk of AMI.

The association between spinal cord injury and acute myocardial infarction in a nationwide population-based cohort study.

A spinal cord injury (SCI) retrospective cohort study was derived from the National Health Insurance Research Database of Taiwan. We evaluated risk of acute myocardial infarction (AMI) in patients newly diagnosed with SCI. According to information of the World Health Organization, cardiovascular diseases are the most frequent causes of death in patients with SCI compared with those in the general population. We obtained claims data from the National Health Insurance Research Database for this cohort study. The SCI group comprised 22,197 patients with a diagnosis of SCI. Case and control patients were based on risk-set sampling in a 1:4 ratio, and we excluded patients with a prior diagnosis of AMI. Comorbidities were categorized as the proportion of prior illnesses in the SCI and non-SCI groups. We used the Cox proportion model to explore adjusted hazard ratio (aHR) for developing AMI between case and control patients. Patients with SCI were significantly more likely to exhibit pre-existing illnesses associated with AMI than patients without SCI. Patients with a diagnosis of SCI exhibited significantly higher aHRs for developing AMI than patients without SCI (aHR=1.17; P<0.05). Patients with SCI, compared with patients without SCI, were associated with a subsequent AMI risk (aHR=1.17; P<0.05). Several comorbidities, such as cardiovascular disease (aHR=1.29; P<0.05), chronic obstructive pulmonary disease (aHR=1.51; P<0.05), hypertension (aHR=1.34; P<0.01), and renal disease (aHR=1.76; P<0.05), were associated with an increased AMI risk. Furthermore, T-spine SCI was significantly associated with an AMI risk (aHR=1.38; P<0.05). Patients with as diagnosis of SCI exhibited an increased risk of AMI compared with patients without SCI. These findings have broad implications for surveillance among patients with SCI, and future studies should evaluate whether risk factor modification can decrease AMI risk among patients with SCI. 3.

CD8+ T-cells count in acute myocardial infarction in HIV disease in a predominantly male cohort.

Human Immunodeficiency Virus- (HIV-) infected persons have a higher risk for acute myocardial infarction (AMI) than HIV-uninfected persons. Earlier studies suggest that HIV viral load, CD4+ T-cell count, and antiretroviral therapy are associated with cardiovascular disease (CVD) risk. Whether CD8+ T-cell count is associated with CVD risk is not clear. We investigated the association between CD8+ T-cell count and incident AMI in a cohort of 73,398 people (of which 97.3% were men) enrolled in the U.S. Veterans Aging Cohort Study-Virtual Cohort (VACS-VC). Compared to uninfected people, HIV-infected people with high baseline CD8+ T-cell counts (>1065 cells/mm3) had increased AMI risk (adjusted HR = 1.82, P < 0.001, 95% CI: 1.46 to 2.28). There was evidence that the effect of CD8+ T-cell tertiles on AMI risk differed by CD4+ T-cell level: compared to uninfected people, HIV-infected people with CD4+ T-cell counts ≥200 cells/mm3 had increased AMI risk with high CD8+ T-cell count, while those with CD4+ T-cell counts <200 cells/mm3 had increased AMI risk with low CD8+ T-cell count. CD8+ T-cell counts may add additional AMI risk stratification information beyond that provided by CD4+ T-cell counts alone.

Occupational physical activity and 20-year incidence of acute myocardial infarction: results from the Kuopio Ischemic Heart Disease Risk Factor Study

This study aimed to assess the effects of physically demanding work - measured as energy expenditure (EE) during occupational physical activities (OPA) - on risk of acute myocardial infarction (AMI) among men with and without preexisting ischemic heart disease (IHD). The 20-year prospective study examined 1891 middle-aged working men using absolute (kcal/day) and relative (relative aerobic strain and percent oxygen uptake reserve) measures of EE. Linear and quadratic hazard models were explored in Cox regression analyses adjusting for 19 potential confounders and considering interactions with baseline IHD. Relative EE measures were positively associated with 20-year incidence of AMI in linear and quadratic hazard models and interacted with IHD. Each 10% increase of relative aerobic strain increased AMI risk by 18% among men without IHD [hazard ratio (HR) 1.18, 95% confidence interval (95% CI) 1.08-1.28, P=0.001] and by 8% among men with IHD (HR 1.08, 95% CI 0.98-1.20, P=0.129) in fully adjusted linear models. Results for quadratic models and percent oxygen uptake reserve were similar. Absolute EE did not predict AMI. Age, baseline IHD, systolic blood pressure, anti-hypertensive medication, body mass index, blood glucose, low-density lipoprotein cholesterol, cholesterol-lowering medication, mental stress, and smoking were independently associated with AMI, but not income, social support, alcohol, or conditioning leisure-time physical activity. In contrast to absolute EE, relative workload measures that take individual fitness into account were positively associated with AMI incidence among men without IHD. For men with IHD, associations were also positive but weaker possibly due to healthy worker selection effects. These findings provide evidence for a positive association between OPA and AMI among men.

Does childhood misfortune raise the risk of acute myocardial infarction in adulthood?

Whereas most research on acute myocardial infarction (AMI) has focused on more proximal influences, such as adult health behaviors, the present study examines the early origins of AMI. Longitudinal data were drawn from the National Survey of Midlife Development in the United States (N = 3032), a nationally representative survey of men and women aged 25–74, which spans from 1995 to 2005. A series of event history analyses modeling age of first AMI investigated the direct effects of accumulated and separate domains of childhood misfortune as well as the mediating effects of adult health lifestyle and psychosocial factors. Findings reveal that accumulated childhood misfortune and child maltreatment increased AMI risk, net of several adult covariates, including family history of AMI. Smoking fully mediated the effects of both accumulated childhood misfortune and child maltreatment. These findings reveal the importance of the early origins of AMI and health behaviors as mediating factors.

Prehypertension, Hypertension, and the Risk of Acute Myocardial Infarction in HIV-Infected and -Uninfected Veterans

Compared to uninfected people, human immunodeficiency virus (HIV)-infected individuals may have an increased risk of acute myocardial infarction (AMI). Currently, HIV-infected people are treated to the same blood pressure (BP) goals (<140/90 or <130/80 mm Hg) as their uninfected counterparts. Whether HIV-infected people with elevated BP have excess AMI risk compared to uninfected people is not known. This study examines whether the association between elevated BP and AMI risk differs by HIV status. The Veterans Aging Cohort Study Virtual Cohort (VACS VC) consists of HIV-infected and -uninfected veterans matched 1:2 on age, sex, race/ethnicity, and clinical site. For this analysis, we analyzed 81 026 people with available BP data from VACS VC, who were free of cardiovascular disease at baseline. BP was the average of the 3 routine outpatient clinical measurements performed closest to baseline (first clinical visit after April 2003). BP categories used in the analyses were based on criteria of the Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Analyses were performed using Cox proportional hazards regression. Over 5.9 years (median), 860 incident AMIs occurred. Low/high prehypertensive and untreated/treated hypertensive HIV-infected individuals had increased AMI risk compared to uninfected, untreated normotensive individuals (hazard ratio [HR], 1.60 [95% confidence interval {CI}, 1.07-2.39]; HR, 1.81 [95% CI, 1.22-2.68]; HR, 2.57 [95% CI, 1.76-3.76]; and HR, 2.76 [95% CI, 1.90-4.02], respectively). HIV, prehypertensive BP, and hypertensive BP were associated with an increased risk of AMI in a cohort of HIV-infected and -uninfected veterans. Future studies should prospectively investigate whether HIV interacts with BP to further increase AMI risk.

Prothrombotic gene polymorphisms and plasma factors in young north Indian survivors of acute myocardial infarction

The aim of this study was to evaluate the association of prothrombotic gene polymorphisms [factor V Leiden (FVL) 1691GA, factor VII (FVII) 10976GA, FVII HVR4, platelet membrane glycoproteins GP1BA 1018CT, GP1BA VNTR, integrin ITGB3 1565TC, integrin ITGA2 807CT and methylenetetrahydrofolate reductase (MTHFR) 677C/T], plasma factors (fibrinogen and homocysteine) and traditional risk factors with acute myocardial infarction (AMI) in 184 patients ≤ 40 years of age and 350 controls (≤ 40 years) from north India. Multiple logistic-regression analysis showed that hypertension (OR 1.9, 95 % CI 1.1-3.8, p = 0.042), diabetes mellitus (OR 10.5, 95 % CI 2.0-56.7, p = 0.006), smoking (OR 7.1, 95 % CI 3.7-13.6, p < 0.001), low socio-economic status (OR 13.5, 95 % CI 2.3-78.4, p = 0.004), high waist-hip ratio (OR 35.6, 95 % CI 11.1-53.7, p < 0.001) and FVL 1691GA (OR 6.0, 95 % CI 1.2-13.4, p = 0.03) were independent risk predictors of AMI in young. Elevated plasma fibrinogen also showed association with increased AMI risk. ITGA2 807C/T polymorphism showed protection against AMI in univariate analysis only, while GP1BA VNTR-ac (OR 0.4, 95 % CI 0.2-0.9, p = 0.033) showed significant protection even after adjusting for age and sex. Multinominal logistic-regression analysis showed gene-gene (GP1BA 1018C/T with GP1BA VNTR and ITGA2 807C/T with ITGB3 1565T/C polymorphisms) and gene-environment interactions (gene polymorphisms with smoking) operating in the occurrence of AMI in young. In conclusion, the role of inherited predisposition to thrombosis in complex, polygenic and multifactorial disease like AMI is limited to certain genetic factors, in combination with environmental factor like smoking.

Risk of new acute myocardial infarction hospitalization associated with use of oral and parenteral non-steroidal anti-inflammation drugs (NSAIDs): a case-crossover study of Taiwan's National Health Insurance claims database and review of current evidence

BackgroundPrevious studies have documented the increased cardiovascular risk associated with the use of some nonsteroidal anti-inflammatory drugs (NSAIDs). Despite this, many old NSAIDs are still prescribed worldwide. Most of the studies to date have been focused on specific oral drugs or limited by the number of cases examined. We studied the risk of new acute myocardial infarction (AMI) hospitalization with current use of a variety of oral and parenteral NSAIDs in a nationwide population, and compared our results with existing evidence.MethodsWe conducted a case-crossover study using the Taiwan's National Health Insurance claim database, identifying patients with new AMI hospitalized in 2006. The 1-30 days and 91-120 days prior to the admission were defined as case and matched control period for each patient, respectively. Uses of NSAIDs during the respective periods were compared using conditional logistic regression and adjusted for use of co-medications.Results8354 new AMI hospitalization patients fulfilled the study criteria. 14 oral and 3 parenteral NSAIDs were selected based on drug utilization profile among 13.7 million NSAID users. The adjusted odds ratio, aOR (95% confidence interval), for risk of AMI and use of oral and parenteral non-selective NSAIDs were 1.42 (1.29, 1.56) and 3.35 (2.50, 4.47), respectively, and significantly greater for parenteral than oral drugs (p for interaction < 0.01). Ketorolac was associated with the highest AMI risk among both of oral and parenteral NSAIDs studied, the aORs were 2.02 (1.00, 4.09) and 4.27 (2.90, 6.29) respectively. Use of oral flurbiprofen, ibuprofen, sulindac, diclofenac, and parenteral ketoprofen were also significantly associated with increased AMI risk. The results of the present study were consistent with the majority of evidence from previous studies.ConclusionsThe collective evidence revealed the tendency of increased AMI risk with current use of some NSAIDs. A higher AMI risk associated with use of parenteral NSAIDs was observed in the present study. Ketorolac had the highest associated risk in both oral and parenteral NSAIDs studied. Though further investigation to confirm the association is warranted, prescribing physicians and the general public should be cautious about the potential risk of AMI when using NSAIDs.

The CC genotype of the angiotensin II type I receptor gene independently associates with acute myocardial infarction in a Tunisian population

Acute myocardial infarction (AMI) is a multifactorial disease influenced by environmental and genetic factors. The aim of this study was to assess the association of angiotensin II type 1 receptor (ATR1) gene polymorphisms with AMI as well as to evaluate the role of serum angiotensin-converting enzyme (ACE) activity and that of cardiac troponin I (cTnI) in Tunisian AMI patients. One hundred and eighteen AMI patients were compared to 150 healthy controls. ATR1 genotypes were determined by polymerase chain reaction restriction fragment length polymorphism (PCR-RFLP). The ATR1 A1166C polymorphism was significantly associated with AMI (p = 0.024). CC genotype and C allele frequencies were associated with increased AMI risk [CC vs. AC and AA: OR = 2.06; p = 0.045; 95 % CI (1.02-4.18); C vs. A: OR = 1.68; p = 0.004; 95 % CI (1.17-2.41)]. By multivariate logistic regression analysis, CC genotype, hypertension, diabetes, serum ACE activity and peak-cTnI were significant independent predictors of AMI. Increased serum ACE activity and cTnI peak levels were associated with the CC genotype in AMI patients. In conclusion, the ATR1 A1166C polymorphism is associated with AMI and the CC genotype associated with increased ACE activity and cTnI levels appear to predispose for AMI risk.

Indices of central and peripheral body fat: association with non-fatal acute myocardial infarction

The majority of the studies have focused on the effect of general and central fat on coronary risk, neglecting the potential role of peripheral body fat. To assess the effect of surrogate measures for general, central and peripheral body fat on the occurrence of non-fatal acute myocardial infarction (AMI). Population-based case-control study; cases were patients aged >or=40 years consecutively hospitalized with an incident AMI (n=653), and controls were community participants without previous AMI, selected randomly from the hospitals' catchment area population (n=1713). Body mass index (BMI), waist circumference (WC), hip circumference and a skinfolds composite index to estimate the proportion of peripheral subcutaneous fat in the arms were ascertained. Associations were summarized with odds ratios (OR) and 95% confidence intervals (95% CI), obtained from unconditional logistic regression with adjustment for the main confounders. WC, and in particular waist-to-hip ratio (WHR), had strong direct associations with AMI risk. Peripheral subcutaneous fat was inversely associated with AMI in women, but directly in men. Using principal component analysis, three uncorrelated factors were identified representing different patterns of fat distribution: (1) generalized fat, with high BMI and high WC; (2) central fat, with high WC and WHR; and (3) peripheral subcutaneous fat. The first factor showed no significant association with AMI, but the second factor increased AMI risk in each sex (upper vs lower fourth: OR 12.2, 95% CI 5.34-27.9 in women; OR 25.0, 95% CI 14.0-44.7 in men). In contrast, the third factor was inversely associated with AMI in women (upper vs lower fourth: OR 0.59, 95% CI 0.36-0.96) and directly associated in men (OR 2.45, 95% CI 1.69-3.55; P-value for sex interaction<0.001). Central fat was associated with increased risk of AMI in women and men, while the peripheral subcutaneous fat index predicted a lower risk of AMI in women and a higher risk in men.