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MI Risk (mi + risk)
Selected AbstractsDrinking pattern and risk of non-fatal myocardial infarction: a population-based case,control studyADDICTION, Issue 3 2004Maurizio Trevisan ABSTRACT Aims Alcohol consumption has been associated with a reduced risk of heart disease incidence and mortality. However, most studies have focused on an average volume per specific time period and have paid little attention to the pattern of drinking. The aim of this study was to examine the association between various drinking patterns and myocardial infarction (MI). Design A population-based case,control study. Methods Participants were 427 white males with incident MI and 905 healthy white male controls (age 35,69 years) selected randomly from two Western New York counties. During computer-assisted interviews detailed information was collected regarding patterns of alcohol consumption during the 12,24 months prior to interview (controls) or MI (cases). Findings Compared to life-time abstainers, adjusted odds ratios (ORs) and 95% confidence interval (CI) for non-current and current drinkers were 0.66 (0.31,1.39) and 0.50 (0.24,1.02), respectively. Daily drinkers exhibited a significantly lower OR (0.41) compared to life-time abstainers. Participants who drank mainly without food had an OR of 1.49 (0.96,2.31) compared to those who drank mainly with food and 0.62 (0.28,1.37) compared to life-time abstainers. Men who reported drinking only at weekends had a significantly greater MI risk [1.91; (1.21,3.01)] compared to men who drank less than once/week, but not compared to life-time abstainers [0.91 (0.40,2.07)]. Conclusions Our results indicate that patterns of alcohol use have important cardiovascular health implications. [source] Drinking Patterns and Myocardial Infarction: A Linear Dose,Response ModelALCOHOLISM, Issue 2 2009Marcia Russell Background:, The relation of alcohol intake to cardiovascular health is complex, involving both protective and harmful effects, depending on the amount and pattern of consumption. Interpretation of data available on the nature of these relations is limited by lack of well-specified, mathematical models relating drinking patterns to alcohol-related consequences. Here we present such a model and apply it to data on myocardial infarction (MI). Methods:, The dose,response model derived assumes: (1) each instance of alcohol use has an effect that either increases or decreases the likelihood of an alcohol-related consequence, and (2) greater quantities of alcohol consumed on any drinking day add linearly to these increases or decreases in risk. Risk was reduced algebraically to a function of drinking frequency and dosage (volume minus frequency, a measure of the extent to which drinkers have more than 1 drink on days when they drink). In addition to estimating the joint impact of frequency and dosage, the model provides a method for calculating the point at which risk related to alcohol consumption is equal to background risk from other causes. A bootstrapped logistic regression based on the dose,response model was conducted using data from a case-control study to obtain the predicted probability of MI associated with current drinking patterns, controlling for covariates. Results:, MI risk decreased with increasing frequency of drinking, but increased as drinking dosage increased. Rates of increasing MI risk associated with drinking dosage were twice as high among women as they were among men. Relative to controls, lower MI risk was associated with consuming < 4.55 drinks per drinking day for men (95% CI: 2.77 to 7.18) and < 3.08 drinks per drinking day for women (95% CI: 1.35 to 5.16), increasing after these cross-over points were exceeded. Conclusions:, Use of a well-specified mathematical dose,response model provided precise estimates for the first time of how drinking frequency and dosage each contribute linearly to the overall impact of a given drinking pattern on MI risk in men and women. [source] Variation in 24 hemostatic genes and associations with non-fatal myocardial infarction and ischemic strokeJOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 1 2008N. L. SMITH Summary., Background:, Arterial thrombosis involves platelet aggregation and clot formation, yet little is known about the contribution of genetic variation in fibrin-based hemostatic factors to arterial clotting risk. We hypothesized that common variation in 24 coagulation,fibrinolysis genes would contribute to risk of incident myocardial infarction (MI) or ischemic stroke (IS). Methods:, We conducted a population-based, case,control study. Subjects were hypertensive adults and postmenopausal women 30,79 years of age, who sustained a first MI (n = 856) or IS (n = 368) between 1995 and 2002, and controls matched on age, hypertension status, and calendar year (n = 2689). We investigated the risk of MI and IS associated with (i) global variation within each gene as measured by common haplotypes and (ii) individual haplotypes and single nucleotide polymorphisms (SNPs). Significance was assessed using a 0.2 threshold of the false discovery rate q -value, which accounts for multiple testing. Results:, After accounting for multiple testing, global genetic variation in factor (F) VIII was associated with IS risk. Two haplotypes in FVIII and one in FXIIIa1 were significantly associated with increased IS risk (all q -values < 0.2). A plasminogen gene SNP was associated with MI risk. All are new discoveries not previously reported. Another 24 tests had P -values < 0.05 and q -values > 0.2 in MI and IS analyses, 23 of which are new and hypothesis generating. Conclusions:, Apart from the association of FVIII variation with IS, we found little evidence that common variation in the 24 candidate fibrin-based hemostasis genes strongly influences arterial thrombotic risk, but our results cannot rule out small effects. [source] Antihypertensives and myocardial infarction risk: the modifying effect of history of drug usePHARMACOEPIDEMIOLOGY AND DRUG SAFETY, Issue 4 2001Chantal Bourgault PhD Abstract Purpose Confounding by indication is common in observational studies of outcomes that treatment is intended to affect. In light of the stepped-care approach to hypertension management, we reexamined the controversy around myocardial infarction (MI) risk in relation to antihypertensive agents by considering past drug history both as a confounder and as an effect modifier. Methods Case,control design nested within a cohort of 19,501 adults initiating therapy with angiotensin-converting enzyme inhibitors (ACEI), calcium channel blockers (CCB) or ,-blockers in Saskatchewan (1990,93) and followed up to 1997. MI cases were identified using death certificates and hospital discharge diagnoses (ICD-9 410). Four controls were matched to each case to account for duration and timing of follow-up. Results 812 MI cases were identified, of which 26% were fatal. At first, current use of CCB and ACEI (versus ,-blockers) appeared to be associated with an increased risk of MI (RR,=,2.2; 95% CI,=,1.8,2.7 and RR,=,1.3; CI,=,1.0,1.6 respectively). Adjustment for drug use history attenuated both associations (RR,=,1.6; CI,=,1.1,2.2 and RR,=,1.0; CI,=,0.7,1.4). Moreover, the risk for CCB use disappeared when restricted to patients who had already used these agents in the past (RR,=,1.1; CI,=,0.77,1.7) whereas a high risk of MI for ACEI was found in digoxin users (RR,=,9.4; CI,=,3.2,27.5). Conclusion Past drug history can be both a confounder and an effect modifier in observational studies. We found adjustment for medication history to attenuate the associations between antihypertensive agents and MI risk. In addition, the estimates significantly varied across drug history profiles thus suggesting the presence of preferential prescribing of specific drug classes to high-risk patients. Copyright © 2001 John Wiley & Sons, Ltd. [source] Cholesteryl Ester Transfer Protein (CETP) Genetic Variation and Early Onset of Non-Fatal Myocardial InfarctionANNALS OF HUMAN GENETICS, Issue 6 2008V. Meiner Summary Although Cholesteryl Ester Transfer Protein (CETP) mediates the transfer of cholesteryl esters and triglycerides between lipoprotein particles and thus plays a crucial role in reverse cholesterol transport, the association of variations in the CETP gene with acute myocardial infarction (MI) remains unclear. In this study we examined whether common genetic variation in the CETP gene is related to early-onset non-fatal MI risk in a population-based case-control study from western Washington State. Genotyping for the CETP ,2708 G/A, ,971 A/G, ,629 A/C, Intron-I TaqI G/A and exon-14 A/G (I405V) SNPs was performed in 578 cases with first acute non-fatal MI and in 666 demographically similar controls, free of clinical cardiovascular disease, identified randomly from the community. In-person interviews and non-fasting blood specimens provided data on coronary heart disease risk factors. In men, there was little evidence for an association between single SNPs and MI risk, but in women the age- and race-adjusted OR was found to be significant in 4 out of the 5 CETP single variants. Haplotype analysis revealed two haplotypes associated with MI risk among men. As compared to men homozygous for the most common haplotype D (,2708 G, ,971 G, ,629 C, TaqI G and exon-14 A), the fully-adjusted multiplicative model identified haplotype G (,2708 G, ,971 A, ,629 A, TaqI G and exon-14 G) was associated with a 4.0-6.0-fold increased risk of MI for each additional copy; [95%CI 2.4,14.8] and haplotype B (,2708 G, ,971 G, ,629 A, TaqI A and exon-14 A) showed a significant decreased risk for early onset MI [OR = 0.18; 95%CI 0.04 , 0.75]. An evolutionary-based haplotype analysis indicated that the two haplotypes associated with the MI risk are most evolutionarily divergent from the other haplotypes. Variation at the CETP gene locus is associated with the risk of early-onset non-fatal MI. This association was found to be independent of HDL-C levels. These data and the sex-specific findings require confirmation in other populations. [source] Psoriasis and risk of incident myocardial infarction, stroke or transient ischaemic attack: an inception cohort study with a nested case,control analysisBRITISH JOURNAL OF DERMATOLOGY, Issue 5 2009Y.B. Brauchli Summary Background, Systemic inflammation may increase the risk for cardiovascular diseases in patients with psoriasis, but data on this risk in patients with early psoriasis are scarce. Objectives, To assess and compare the risk of developing incident myocardial infarction (MI), stroke or transient ischaemic attack (TIA) between an inception cohort of patients with psoriasis and a psoriasis-free population. Methods, We conducted an inception cohort study with a nested case,control analysis within the U.K.-based General Practice Research Database. The study population encompassed 36 702 patients with a first-time recorded diagnosis of psoriasis 1994,2005, matched 1 : 1 to psoriasis-free patients. We assessed crude incidence rates (IRs) and applied conditional logistic regression to obtain odds ratios (ORs) with 95% confidence intervals (CIs). Results, Overall, the IRs of MI (n = 449), stroke (n = 535) and TIA (n = 402) were similar among patients with or without psoriasis. However, the adjusted OR of developing MI for patients with psoriasis aged < 60 years was 1·66 (95% CI 1·03,2·66) compared with patients without psoriasis, while the OR for patients aged , 60 years was 0·99 (95% CI 0·77,1·26). The adjusted ORs of developing MI for patients of all ages with , 2 or > 2 prescriptions/year for oral psoriasis treatment were 2·48 (95% CI 0·69,8·91) and 1·39 (95% CI 0·43,4·53), with a similar finding for stroke and TIA. Conclusions, The risk of developing a cardiovascular outcome was not materially elevated for patients with early psoriasis overall. In subanalyses, however, there was a suggestion of an increased (but low absolute) MI risk for patients with psoriasis aged < 60 years, mainly with severe disease. [source] | ||||||||||