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Background: Habitual moderate alcohol consumption is associated with a lower risk of acute myocardial infarction (MI), whereas heavy (binge) drinking is associated with higher cardiovascular risk. However, less is known about the immediate effects of alcohol consumption on the risk of acute MI and whether any association differs by beverage type or usual drinking patterns., Methods: We conducted a case-crossover analysis of 3869 participants from the Determinants of Myocardial Infarction Onset Study who were interviewed during hospitalization for acute MI in one of the 64 medical centers across the United States in 1989-1996. We compared the observed number of times that each participant consumed wine, beer, or liquor in the hour preceding MI symptom onset with the expected frequency based on each participant's control information, defined as the number of times the participant consumed alcohol in the past year., Results: Among 3869 participants, 2119 (55%) reported alcohol consumption in the past year, including 76 within 1 hour before acute MI onset. The incidence rate of acute MI onset was elevated 1.72-fold (95% confidence interval [CI] = 1.37-2.16) within 1 hour after alcohol consumption. The association was stronger for liquor than for beer or wine. The higher rate was not apparent for daily drinkers. For the 24 hours after consumption, there was a 14% lower rate (relative risk = 0.86 [95% CI = 0.79-0.95]) of MI compared with periods with no alcohol consumption., Conclusions: Alcohol consumption is associated with an acutely higher risk of MI in the subsequent hour among people who do not typically drink alcohol daily.

The aim of the present study was to explore the association between outbursts of anger and acute myocardial infarction (AMI) risk. Outbursts of anger are associated with an abrupt increase in cardiovascular events; however, it remains unknown whether greater levels of anger intensity are associated with greater levels of AMI risk or whether potentially modifiable factors can mitigate the short-term risk of AMI. We conducted a case-crossover analysis of 3,886 participants from the multicenter Determinants of Myocardial Infarction Onset Study, who were interviewed during the index hospitalization for AMI from 1989 to 1996. We compared the observed number and intensity of anger outbursts in the 2 hours preceding AMI symptom onset with its expected frequency according to each patient's control information, defined as the number of anger outbursts in the previous year. Of the 3,886 participants in the Determinants of Myocardial Infarction Onset Study, 1,484 (38%) reported outbursts of anger in the previous year. The incidence rate of AMI onset was elevated 2.43-fold (95% confidence interval 2.01 to 2.90) within 2 hours of an outburst of anger. The association was consistently stronger with increasing anger intensities (p trend <0.001). In conclusion, the risk of experiencing AMI was more than twofold greater after outbursts of anger compared with at other times, and greater intensities of anger were associated with greater relative risks. Compared with nonusers, regular β-blocker users had a lower susceptibility to heart attacks triggered by anger, suggesting that some drugs might lower the risk from each anger episode., (Copyright © 2013 Elsevier Inc. All rights reserved.)

Background: Acute psychological stress is associated with an abrupt increase in the risk of cardiovascular events. Intense grief in the days after the death of a significant person may trigger the onset of acute myocardial infarction (MI), but this relationship has not been systematically studied., Methods and Results: We conducted a case-crossover analysis of 1985 participants from the multicenter Determinants of Myocardial Infarction Onset Study interviewed during index hospitalization for an acute MI between 1989 and 1994. We compared the observed number of deaths in the days preceding MI symptom onset with its expected frequency based on each patient's control information, defined as the occurrence of deaths in the period from 1 to 6 months before infarction. Among the 1985 subjects, 270 (13.6%) experienced the loss of a significant person in the prior 6 months, including 19 within 1 day of their MI. The incidence rate of acute MI onset was elevated 21.1-fold (95% confidence interval, 13.1-34.1) within 24 hours of the death of a significant person and declined steadily on each subsequent day. The absolute risk of MI within 1 week of the death of a significant person is 1 excess MI per 1394 exposed individuals at low (5%) 10-year MI risk and 1 per 320 among individuals at high (20%) 10-year risk., Conclusions: Grief over the death of a significant person was associated with an acutely increased risk of MI in the subsequent days. The impact may be greatest among individuals at high cardiovascular risk.

Objective: Rosiglitazone was found associated with approximately a 43% increase in risk of acute myocardial infarction (AMI) in a two meta-analyses of clinical trials. Our objective is to estimate the magnitude of the association in real-world patients previously treated with metformin., Research Design and Methods: We conducted a nested case control study in British Columbia using health care databases on 4.3 million people. Our cohort consisted of 158,578 patients with Type 2 diabetes who used metformin as first-line drug treatment. We matched 2,244 cases of myocardial infarction (AMI) with up to 4 controls. Conditional logistic regression models were used to estimate matched odds ratios for AMI associated with treatment with rosiglitazone, pioglitazone and sulfonylureas., Results: In our cohort of prior metformin users, adding rosiglitazone for up to 6 months was not associated with an increased risk of AMI compared to adding a sulfonylurea (odds ratio [OR] 1.38; 95% confidence interval [CI], 0.91-2.10), or compared to adding pioglitazone (OR for rosi versus pio 1.41; 95% CI, 0.74-2.66). There were also no significant differences between rosiglitazone, pioglitazone and sulfonylureas for longer durations of treatment. Though not significantly different from sulfonylureas, there was a transient increase in AMI risk associated with the first 6 months of treatment with a glitazone compared to not using the treatment (OR 1.53; 95% CI, 1.13-2.07), Conclusions: In our British Columbia cohort of patients who received metformin as first-line pharmacotherapy for Type 2 diabetes mellitus, further treatment with rosiglitazone did not increase the risk of AMI compared to patients who were treated with pioglitazone or a sulfonylurea. Though not statistically significantly different compared from each other, an increased risk of AMI observed after starting rosiglitazone or sulfonylureas is a matter of concern that requires more research.

Background: The relationship of marijuana use with coronary heart disease, including prognosis among patients with coronary heart disease, is uncertain., Methods: We conducted an inception cohort study of 1913 adults hospitalized with myocardial infarction at 45 US hospitals between 1989 and 1994, with a median follow-up of 3.8 years. We ascertained total mortality according to self-reported marijuana use in the preceding year., Results: A total of 52 patients reported marijuana use during the prior year, and 317 patients died during follow-up. Compared with nonuse, marijuana use less than weekly was associated with a hazard ratio of 2.5 (95% CI, 0.9-7.3). The corresponding hazard ratio for weekly use or more was 4.2 (95% CI, 1.2-14.3). The age- and sex-adjusted hazard ratios associated with any use were 1.9 (95% CI, 0.6-6.3) for cardiovascular mortality and 4.9 (95% CI, 1.6-14.7) for noncardiovascular mortality. In a comparison of 42 marijuana users and 42 other patients matched on propensity scores, there were 6 deaths among marijuana users and one among non-users (log-rank P = .06)., Conclusions: These preliminary results suggest possible hazards of marijuana for patients who survive acute myocardial infarction. Although marijuana use has not been associated with mortality in other populations, it may pose particular risk for susceptible individuals with coronary heart disease.

Objective: To evaluate the effects of patient copayment and coinsurance policies on adherence to therapy with beta-adrenergic blocking agents (beta-blockers) and on the rate of initiation of beta-blocker therapy after acute myocardial infarction (MI) in a population-based natural experiment., Study Design: Three sequential cohorts included British Columbia residents age 66 years and older who initiated beta-blocker therapy during time intervals with full drug coverage (2001), a $10 or $25 copayment (2002), and 25% coinsurance (2003-2004). We used linked data on all prescription drug dispensings, physician services, and hospitalizations. Follow-up of each cohort was 9 months after the policy changes., Methods: We measured the proportion of subjects in each cohort who were adherent to beta-blocker therapy over time, with adherence defined as having >80% of days covered. We also measured the proportion of patients initiating beta-blocker therapy after acute MI. Policy effects were evaluated using multivariable regression., Results: Adherence to beta-blocker therapy was marginally reduced as a consequence of the copayment policy (-1.3 percentage points, 95% confidence interval [CI] = -2.5 , -0.04) or the coinsurance policy (-0.8 percentage points, 95% CI = -2.0, 0.3). The proportion of patients initiating beta-blockers after hospitalization for acute MI remained steady at about 61% during the study period, similar to that observed in a control population of elderly Pennsylvania residents with full drug coverage., Conclusions: Fixed patient copayment and coinsurance policies had little negative effect on adherence to relatively inexpensive beta-blocker therapy, or initiation of beta-blockers after acute MI.

Background: As medication spending grows, Medicare Part D will need to adapt its coverage policies according to emerging evidence from a variety of insurance policies. We sought to evaluate the consequences of copayment and coinsurance policies on the initiation of statin therapy after acute myocardial infarction and adherence to therapy in statin initiators using a natural experiment of all British Columbia residents aged 66 years and older., Methods and Results: Three consecutive cohorts that included all patients who began statin therapy during full drug coverage (2001), coverage with a $10 or $25 copay (2002), and coverage with a 25% coinsurance benefit (2003-2004) were followed up with linked healthcare utilization data (n=51,561). Follow-up of cohorts was 9 months after each policy change. Adherence to statin therapy was defined as > or = 80% of days covered. Relative to full-coverage policies, adherence to new statin therapy was significantly reduced, from 55.8% to 50.5%, under a fixed copayment policy (-5.4% points; 95% CI, -6.4% to -4.4%) and the subsequent coinsurance policy (-5.4% points; 95% CI, -6.3% to -4.4%). An uninterrupted increase in the proportion of patients initiating statin therapy after an acute myocardial infarction (1.7% points per quarter) was observed over the study period, similar to a Pennsylvania control population with full coverage. Sudden changes to full out-of-pocket spending, similar to Medicare's Part D "doughnut hole," almost doubled the risk of stopping statins (adjusted odds ratio, 1.94, 95% CI, 1.82 to 2.08)., Conclusions: Fixed patient copayment and coinsurance policies have negative effects on adherence to statin lipid-lowering drug therapy but not on their initiation after myocardial infarction.

Background: Tea consumption is associated with lower post-infarct mortality among patients with acute myocardial infarction. We previously found preliminary evidence that tea consumption may also be associated with lower risk of infarct-related ventricular arrhythmias., Methods: Between 1989 and 1996, 3882 subjects with AMI were enrolled in the two phases of the Determinants of Myocardial Infarction Onset Study a median of four days after admission. Trained interviewers assessed self-reported usual tea and coffee consumption during the year prior to infarction with a standardized questionnaire. We examined the prevalence of ventricular arrhythmias in the two phases of the study separately and together., Results: Among the 1912 patients with complete information in the first phase, the prevalence of ventricular arrhythmias was 16% among abstainers from tea, 11% among moderate tea drinkers (<14 cups per week), and 14% among heavier tea drinkers (> or =14 cups per week) (p homogeneity = 0.03). Among the 1791 patients with comparable information in the second phase, the corresponding prevalence rates were 11%, 8%, and 8%, respectively (p = 0.06). When the phases were combined, the adjusted odds ratios for VA were 0.7 (95% confidence interval, 0.6-0.9) among moderate tea drinkers and 0.9 (95% confidence interval, 0.7-1.2) among heavier tea drinkers. The findings were of similar direction for both ventricular tachycardia and fibrillation. In contrast, there was higher risk of VA with increasing coffee intake (odds ratio for >14 cups per week 1.3; 95% confidence interval, 1.0-1.7; p trend 0.02)., Conclusions: Moderate tea intake is associated with a lower prevalence, and higher coffee intake with a slightly higher prevalence, of ventricular arrhythmias among patients hospitalized with acute myocardial infarction. If the association with tea intake is confirmed, it may suggest new approaches to prevention of ischemia-related arrhythmias.

Background: Moderate drinkers have a lower risk of mortality after myocardial infarction (MI). Although binge drinking has been associated with a higher risk of MI in some studies, its relation to prognosis after MI is uncertain., Methods and Results: In a prospective, inception cohort study conducted at 45 US hospitals, 1935 patients hospitalized with a confirmed MI between 1989 and 1994 underwent detailed personal interviews. Patients reported their usual frequency of binge drinking of beer, wine, and liquor, defined as intake of 3 or more drinks within 1 to 2 hours, and were followed up for mortality for a median of 3.8 years. Of 1919 eligible patients, 250 (94% men) reported binge drinking during the prior year, and a total of 318 patients died during follow-up. Binge drinkers had a 2-fold higher risk of mortality than drinkers who did not binge (hazard ratio, 2.0; 95% confidence interval, 1.3 to 3.0). A comparison of 192 binge drinkers and 192 other patients matched on propensity scores yielded a similar result. The association between binge drinking and total mortality tended to be similar among patients whose usual alcohol intake was light or heavier and for binge drinkers who consumed beer, wine, or liquor. Usual alcohol intake was inversely associated with mortality, but binge drinking completely attenuated this relation., Conclusions: Our results suggest that alcohol consumption may be linked to potential hazards among patients who survive acute MI. Although moderate intake has been associated with lower mortality, binge drinking, even among light drinkers, appears to be associated with 2-fold higher mortality.

Sexual intercourse is a rare trigger of acute myocardial infarction (MI). In the 2 hours after intercourse, the risk for MI is increased twofold to fourfold. However, there is limited information on the risk for MI after intercourse in men receiving treatment for erectile dysfunction. This study aimed to evaluate whether the use of sildenafil citrate in men with erectile dysfunction is associated with the triggering of acute MI. A self-matched case-crossover approach was used to evaluate the incidence of MI in men enrolled in 80 clinical trials of sildenafil at sites worldwide from 1993 to 2000. The risk for MI was assessed during 2 hazard periods: within 24 and within 6 hours after the ingestion of sildenafil. Relative risk was estimated using the Mantel-Haenszel estimator for sparse person-time data. A total of 69 MIs were observed during >11,000 person-years of exposure to sildenafil. The mean time between the last dose of sildenafil and the onset of MI was 14 +/- 2.9 days. The relative risk for MI was 0.80 (95% confidence interval [CI] 0.52 to 1.26) within 24 hours after taking sildenafil and 0.79 (95% CI 0.33 to 1.87) within 6 hours after taking sildenafil. In conclusion, these data indicate that sildenafil was not associated with short-term risk for MI and are consistent with the growing body of evidence that sildenafil use is not associated with an increased risk for cardiovascular events.

Background: Previous studies have generally suggested no effect of coffee consumption on the risk of acute myocardial infarction. The effect of coffee consumption on prognosis after acute myocardial infarction is uncertain., Methods: In an inception cohort study, we observed 1935 patients who were hospitalized with a confirmed acute myocardial infarction between 1989 and 1994 at 45 community hospitals and tertiary care centers in the United States, as part of the Determinants of Myocardial Infarction Onset Study. Trained interviewers assessed self-reported caffeinated coffee consumption before infarction with a standardized questionnaire. We analyzed survival censored at December 31, 1995, using Cox proportional hazards regression., Results: Of the 1902 patients for whom we had information on coffee intake, 315 (17%) died during a median follow-up period of 3.8 years. Coffee drinkers tended to be men, younger, and free of comorbidity, and they were more likely to be current smokers. Coffee consumption was not associated with an overall change in long-term post-infarction mortality rate. However, we did observe an unexpected and unexplained variation in the association between coffee consumption and mortality with time, with an apparent inverse association in the first 90 days after infarction., Conclusions: Self-reported coffee consumption has no overall association with post-infarction mortality. The unexpected time variation in the effect of coffee intake requires evaluation in other studies.

We assessed educational attainment and complications during hospitalization in 3,882 patients with acute myocardial infarction for the Determinants of Myocardial Infarction Onset Study. Educational attainment had a graded, inverse association with prevalence of congestive heart failure (CHF) during hospitalization, with the lowest prevalence among patients who attended college (odds ratio 0.75; 95% confidence interval, 0.57 to 0.99; p for trend 0.02), with similar findings among men, women, whites, and blacks.

Background: Some studies have suggested that tea consumption may be associated with lower mortality among individuals with cardiovascular disease, but the effects of tea consumption on mortality after acute myocardial infarction are unknown., Methods and Results: As part of the Determinants of Myocardial Infarction Onset Study, we performed a prospective cohort study of 1900 patients hospitalized with a confirmed acute myocardial infarction between 1989 and 1994, with a median follow-up of 3.8 years. Trained interviewers assessed self-reported usual weekly caffeinated tea consumption during the year before infarction with a standardized questionnaire. We compared long-term mortality according to tea consumption using Cox proportional hazards regression. Of the 1900 patients, 1019 consumed no tea (nondrinkers), 615 consumed <14 cups per week (moderate tea drinkers), and 266 consumed 14 or more cups per week (heavy tea drinkers). Compared with nondrinkers, age- and sex-adjusted mortality was lower among moderate tea drinkers (hazard ratio, 0.69; 95% CI, 0.53 to 0.89) and heavy tea drinkers (hazard ratio, 0.61; 95% CI, 0.42 to 0.86). Additional adjustment for clinical and sociodemographic characteristics did not appreciably alter this association (hazard ratio, 0.72; 95% CI, 0.55 to 0.94 for moderate tea drinkers; hazard ratio, 0.56; 95% CI, 0.37 to 0.84 for heavy tea drinkers). The association of tea and mortality was similar for total and cardiovascular mortality., Conclusions: Self-reported tea consumption in the year before acute myocardial infarction is associated with lower mortality after infarction.

A case-control design involving only cases may be used when brief exposure causes a transient change in risk of a rare acute-onset disease. The design resembles a retrospective nonrandomized crossover study but differs in having only a sample of the base population-time. The average incidence rate ratio for a hypothesized effect period following the exposure is estimable using the Mantel-Haenszel estimator. The duration of the effect period is assumed to be that which maximizes the rate ratio estimate. Self-matching of cases eliminates the threat of control-selection bias and increases efficiency. Pilot data from a study of myocardial infarction onset illustrate the control of within-individual confounding due to temporal association of exposures. Am J Epidemioi 1991:133:144-53. [ABSTRACT FROM AUTHOR]

Large health care databases are used extensively for pharmacoepidemiologic studies. Unique methodological issues arise when applying self-controlled designs (i.e., using within-person comparisons) for active surveillance of newly marketed drugs. We use 3 examples to illustrate bias related to population-level exposure time trends when using outcome-indexed self-controlled (i.e., case-crossover) designs for active surveillance and evaluate the ability of the case-time-control design to adjust for bias from population-level exposure time trends. We mimicked active surveillance by conducting sequential analyses after market entry for 3 medications and outcomes (valdecoxib for myocardial infarction (MI), aripiprazole for MI, and telithromycin for acute liver failure) using Medicaid Analytic eXtracts (from all 50 US states, 2000–2006). The case-crossover exposure odds ratio (EOR) in the months immediately following valdecoxib market entry implausibly suggested a 12-fold higher risk of MI during exposed time relative to unexposed time; among age-, sex-, and time-matched controls, the corresponding EOR of 4.5 indicated strong population-level exposure time trends. Over subsequent monitoring periods, case-crossover EORs rapidly dropped to 1.4. Adjustment for bias from population-level exposure time trends with the case-time-control analysis resulted in more consistent associations between valdecoxib and MI across sequential monitoring periods. Similar results were observed in each example. Strong population-level exposure time trends can bias case-crossover studies conducted among “first-wave” users of newly marketed medications. Suggested strategies can help assess and adjust for population-level exposure time trends. [ABSTRACT FROM PUBLISHER]

Deals with a study which determined the effect of diabetes on long-term survival after acute myocardial infarction. Research design and methods; Association between diabetes and mortality; Comparison between diabetes and previous myocardial infarction; Results and conclusions.

A letter to the editor is presented in response to the article on alcohol intake and risk of myocardial infarction by J. Michael Gaziano and colleagues in the December 16, 1993 issue.

Evaluates sex-related differences in the survival rates of patients who were hospitalized for acute myocardial infarction in the past. Key issues of interest; Analysis of pertinent topics and relevant issues; Implications on cardiology.