TL;DR: No evidence is found that alcohol consumption before the event had protective effects on AMI, and instead, alcohol consumption increased the risk.
Abstract: Background: Alcohol consumption has been causally related to the incidence of coronary heart disease, but the role of alcohol before the event has not been explored in depth. This s
Regular moderate alcohol consumption without heavy drinking has been shown to be a protective factor for cardiovascular disease including acute myocardial infarction (AMI) in particular [1, 2] .
Other protective factors include regular physical activity and daily consumption of fruits and vegetables, whereas hyperlipidemia, smoking, hypertension, diabetes mellitus and obesity have been identified as major modifiable risk factors for AMI [3, 4] .
Moreover, the results of these controlled studies have been mixed.
As reviewed by McKee and Britton [24] and further sources [1, 2] , a number of possible mechanisms have been discussed in the literature explaining the acute effects of binge drinking on CHD events.
These events might include arrhythmia, ischaemia, and possibly thrombotic processes'.
Study Population and Data Collection
Patients were recruited in three major hospitals in the German-speaking part of Switzerland -a university hospital, a county hospital and a city hospital.
Through collaboration with the staff it was also possible to track all 673 patients who were hospitalized for first time AMI (ICD I21; for detailed definition see below) in the study hospitals between July 26, 2005 and November 15, 2006.
The major reason why not all 673 patients were eligible for interviews was the early relocation of 239 patients (35.5%) within 24 h to another hospital, mainly because of regional responsibility and bed availability.
The interviews were conducted in half of the study population within 38 h after the AMI.
The patients who refused to participate in the interview did not differ in gender distribution with the patients who participated in the interviews, but they were on average 8 years older.
Study Design
The case-crossover methodology used in the present study was introduced by Maclure [33] in the early 1990s to study transient effects on the risk of rare acute events.
An important feature of the case-crossover design is that the control information for each patient is based on his or her own past exposure experience.
The patient was first asked to report time of infarction.
Alcohol consumption in this hazard period was compared with the corresponding time period 1 week prior.
Alcohol Consumption
Participants were asked in detail about their drinking behavior: frequency, including binge drinking, type (e.g. wine, beer, spirits), and amount on a usual drinking occasion in deciliters (dl).
Patients who did not drink at least once a month during the 3 months prior, but drank once a month during some period of their life, were defined as former drinkers.
These categories were used in a landmark study by Jackson et al. [21, 35] , who first examined the short-term influence of alcohol intake on the risk of CHD events via the casecrossover design.
The categories regarding the frequency of binge drinking in the prior year were as follows: never, less than once a month, every month, every week, every day [38] .
Basic Medical Data
Basic medical data were obtained from the medical records of the patients with informed consent.
Information was obtained on the presence of arterial hypertension (documented pressure 1 140/90), hyperlipidemia, diabetes mellitus and prior angina pectoris as well as regular medication before the event.
Further data such as smoking history, weight, height, family history of MI, etc. was asked about in their questionnaire.
The authors study was approved by the responsible cantonal research ethics boards of the participating hospitals.
Statistical Analysis
Conditional logistic regression was used to estimate the odds ratios for alcohol consumption in general and binge drinking, within the time before the AMI compared to the same time span 1 week prior [39] .
Conditional regression tries to answer the question of a causal impact of drinking before the event.
The sample size was determined a priori, in order to detect a difference in proportions of 10% when the proportion of discordant pairs was expected to be 30% and the method analysis was a McNemar's test of equality of paired proportions with a 0.05 two-sided significance level.
Furthermore, the authors compared the usual drinking patterns of their sample with the Swiss Health Survey conducted in the year 2002 [38] .
This sample comprised of 19,706 individuals older than 15 years and living in Switzerland (Swiss or foreign nationality), who were interviewed by phone and 16,141 of whom also completed a written questionnaire.
Description of the Sample
None of the patients had a cardiac rupture, 52% of the patients were hypertensive and 35.6% had the diagnosis of hyperlipidemia.
4% of the sample reported daily drinking, with 3 patients (1.2% of the study group) drinking more than once a day.
Table 3 also provides information about the beverage choice in men and women, mainly wine and beer for men, and wine for women.
Drinking Patterns in the Hazard and Control Period
Drinking moderately in the 12-hour hazard period increased the risk of AMI marginally significant compared with no alcohol consumption (OR 2.3; 95% CI 0.97-5.2).
18 persons were exposed in terms of moderate drinking in the hazard period and 8 persons were exposed in the control period.
The authors did not find any significant differences regarding binge drinking before AMI, using the international definition of 4 or more for women and 5 or more glasses of alcohol for men (see Method section).
Comparison of Drinking Patterns with the General Population
Patterns of alcohol consumption varied significantly between AMI patients and the general population (likelihood ratio 2 : 40.0; d.f. = 3; p ! 0.001).
The standardized residuals were significant for the categories of abstention and irregular drinking.
In addition, binge drinking occasions were significantly more frequent among AMI patients: both 'less than monthly' (20.7 vs. 10.9%) and 'monthly or more frequent' binge drinking occasions were about twice as prevalent in their study population (6.8 vs. 3.4%).
Both rates had significant standardized residuals of 4.4 and 2.7, respectively.
Discussion
The authors found that drinking alcohol 12 h before the AMI increased the risk for such an event.
Obviously, their study is not without limitations.
As patients from suburban or rural hospitals are often referred to these hospitals for further examinations and therapy, almost half of their study population was based outside the city.
While the chosen design controls for a potential effect of day of the week, the possibility that recall bias is larger for the events of 1 week prior compared to more recent time periods, cannot be excluded.
Given the facts that drinking prior to the event resulted in an increased risk for AMI and that a comparison with the general population of a similar sex and age distribution showed higher rates of previous year heavy drinking occasions in their sample, the hypothesis that heavy drinking occasions lead to an increase in risk for AMI received some support.
TL;DR: Air pollution is an important trigger of myocardial infarction, it is of similar magnitude as other well accepted triggers such as physical exertion, alcohol, and coffee and shows that ever-present small risks might have considerable public health relevance.
Abstract: Findings Of the epidemiologic studies reviewed, 36 provided suffi cient details to be considered. In the studied populations, the exposure prevalence for triggers in the relevant control time window ranged from 0·04% for cocaine use to 100% for air pollution. The reported odds ratios (OR) ranged from 1·05 to 23·7. Ranking triggers from the highest to the lowest OR resulted in the following order: use of cocaine, heavy meal, smoking of marijuana, negative emotions, physical exertion, positive emotions, anger, sexual activity, traffi c exposure, respiratory infections, coff ee consumption, air pollution (based on a diff erence of 30 μg/m³ in particulate matter with a diameter <10 μm [PM10]). Taking into account the OR and the prevalences of exposure, the highest PAF was estimated for traffi c exposure (7·4%), followed by physical exertion (6·2%), alcohol (5·0%), coff ee (5·0%), a diff erence of 30 μg/m³ in PM10 (4·8%), negative emotions (3·9%), anger (3·1%), heavy meal (2·7%), positive emotions (2·4%), sexual activity (2·2%), cocaine use (0·9%), marijuana smoking (0·8%) and respiratory infections (0·6%). Interpretation In view of both the magnitude of the risk and the prevalence in the population, air pollution is an important trigger of myocardial infarction, it is of similar magnitude (PAF 5–7%) as other well accepted triggers such as physical exertion, alcohol, and coff ee. Our work shows that ever-present small risks might have considerable public health relevance.
TL;DR: The authors concluded that the cardioprotective effect of moderate alcohol consumption disappears when, on average, light to moderate drinking is mixed with irregular heavy drinking occasions, even for drinkers whose average consumption is moderate.
Abstract: Contrary to a cardioprotective effect of moderate regular alcohol consumption, accumulating evidence points to a detrimental effect of irregular heavy drinking occasions (>60 g of pure alcohol or > or =5 drinks per occasion at least monthly) on ischemic heart disease risk, even for drinkers whose average consumption is moderate. The authors systematically searched electronic databases from 1980 to 2009 for case-control or cohort studies examining the association of irregular heavy drinking occasions with ischemic heart disease risk. Studies were included if they reported either a relative risk estimate for intoxication or frequency of > or =5 drinks stratified by or adjusted for total average alcohol consumption. The search identified 14 studies (including 31 risk estimates) containing 4,718 ischemic heart disease events (morbidity and mortality). Using a standardized protocol, the authors extracted relative risk estimates and their variance, in addition to study characteristics. In a random-effects model, the pooled relative risk of irregular heavy drinking occasions compared with regular moderate drinking was 1.45 (95% confidence interval: 1.24, 1.70), with significant between-study heterogeneity (I(2) = 53.9%). Results were robust in several sensitivity analyses. The authors concluded that the cardioprotective effect of moderate alcohol consumption disappears when, on average, light to moderate drinking is mixed with irregular heavy drinking occasions.
TL;DR: The purpose of this review is to bring together the evidence of the association between several triggers and cardiovascular outcomes and to discuss the common underlying pathophysiology of these triggers.
Abstract: In addition to the impact of long-term stressors such as sedentary lifestyle and long-term exposure to high levels of air pollution, many studies have shown that there is an increased risk of acute cardiovascular events immediately after behavioral, psychosocial, and environmental triggers.1–8 After the landmark study documenting the increased rates of myocardial infarction (MI) related to the 1981 earthquake in Athens9 and the description of the circadian variation in the incidence of MI by Muller et al,10 various studies documented the frequency of potential triggers in the period immediately preceding MI onset.
Although the observational studies examining physical, psychological, and chemical triggers of acute cardiovascular events are not without limitations, studies continue to show that short-term exposures appear to play a role in the occurrence of cardiovascular events. These triggers have been discussed in previous reviews,1–8 with a general consensus that different preventive strategies may be appropriate for particular triggers. The purpose of this review is to bring together the evidence of the association between several triggers and cardiovascular outcomes and to discuss the common underlying pathophysiology of these triggers.
Rather than leading to slowly progressive atherosclerosis, triggers represent the final step in the pathophysiological process leading to cardiovascular outcomes among susceptible individuals, such as those with vulnerable atherosclerotic plaque, chronic atherosclerotic disease, disorders of the cardiac conduction system, and microvascular disease. In the presence of a vulnerable atherosclerotic plaque, chemical, physical, and psychological stressors may trigger transient vasoconstrictive and prothrombotic effects that ultimately cause plaque disruption and thrombosis. Even in the absence of an occlusive thrombus, triggers may lower the threshold for cardiac electric instability and increase cardiac sympathetic activation via centrally mediated release of catecholamines, thereby evoking primary ventricular fibrillation and sudden cardiac death.11 Figure 1 depicts several potential …
TL;DR: Although the observational studies examining physical,psychological, and chemical triggers of acute cardiovascularevents are not without limitations, studies continue to show that short-term exposures appear to play a role in theoccurrence ofcardiovascular events.
Abstract: various studies documentedthe frequency of potential triggers in the period immediatelypreceding MI onset.Although the observational studies examining physical,psychological, and chemical triggers of acute cardiovascularevents are not without limitations, studies continue to showthat short-term exposures appear to play a role in theoccurrenceofcardiovascularevents.Thesetriggershavebeendiscussed in previous reviews,
TL;DR: There appears to be a consistent finding of an immediately higher cardiovascular risk following any alcohol consumption, but, by 24 hours, only heavy alcohol intake conferred continued risk.
Abstract: Background—Although considerable research describes the cardiovascular effects of habitual moderate and heavy alcohol consumption, the immediate risks following alcohol intake have not been well characterized. Based on its physiological effects, alcohol may have markedly different effects on immediate and long-term risk. Methods and Results—We searched CINAHL, Embase, and PubMed from inception to March 12, 2015, supplemented with manual screening for observational studies assessing the association between alcohol intake and cardiovascular events in the following hours and days. We calculated pooled relative risks and 95% confidence intervals for the association between alcohol intake and myocardial infarction, ischemic stroke, and hemorrhagic stroke using DerSimonian and Laird random-effects models to model any alcohol intake or dose–response relationships of alcohol intake and cardiovascular events. Among 1056 citations and 37 full-text articles reviewed, 23 studies (29 457 participants) were included. M...
TL;DR: Abnormal lipids, smoking, hypertension, diabetes, abdominal obesity, psychosocial factors, consumption of fruits, vegetables, and alcohol, and regular physical activity account for most of the risk of myocardial infarction worldwide in both sexes and at all ages in all regions.
Abstract: Summary Background Although more than 80% of the global burden of cardiovascular disease occurs in low-income and middle-income countries, knowledge of the importance of risk factors is largely derived from developed countries. Therefore, the effect of such factors on risk of coronary heart disease in most regions of the world is unknown. Methods We established a standardised case-control study of acute myocardial infarction in 52 countries, representing every inhabited continent. 15 152 cases and 14 820 controls were enrolled. The relation of smoking, history of hypertension or diabetes, waist/hip ratio, dietary patterns, physical activity, consumption of alcohol, blood apolipoproteins (Apo), and psychosocial factors to myocardial infarction are reported here. Odds ratios and their 99% CIs for the association of risk factors to myocardial infarction and their population attributable risks (PAR) were calculated. Findings Smoking (odds ratio 2·87 for current vs never, PAR 35·7% for current and former vs never), raised ApoB/ApoA1 ratio (3·25 for top vs lowest quintile, PAR 49·2% for top four quintiles vs lowest quintile), history of hypertension (1·91, PAR 17·9%), diabetes (2·37, PAR 9·9%), abdominal obesity (1·12 for top vs lowest tertile and 1·62 for middle vs lowest tertile, PAR 20·1% for top two tertiles vs lowest tertile), psychosocial factors (2·67, PAR 32·5%), daily consumption of fruits and vegetables (0·70, PAR 13·7% for lack of daily consumption), regular alcohol consumption (0·91, PAR 6·7%), and regular physical activity (0·86, PAR 12·2%), were all significantly related to acute myocardial infarction (p<0·0001 for all risk factors and p=0·03 for alcohol). These associations were noted in men and women, old and young, and in all regions of the world. Collectively, these nine risk factors accounted for 90% of the PAR in men and 94% in women. Interpretation Abnormal lipids, smoking, hypertension, diabetes, abdominal obesity, psychosocial factors, consumption of fruits, vegetables, and alcohol, and regular physical activity account for most of the risk of myocardial infarction worldwide in both sexes and at all ages in all regions. This finding suggests that approaches to prevention can be based on similar principles worldwide and have the potential to prevent most premature cases of myocardial infarction.
TL;DR: Significant differences in the relation of psychosocial factors to risk of myocardial infarction in 24767 people from 52 countries were found, suggesting that approaches aimed at modifying these factors should be developed.
Abstract: Summary Background Psychosocial factors have been reported to be independently associated with coronary heart disease. However, previous studies have been in mainly North American or European populations. The aim of the present analysis was to investigate the relation of psychosocial factors to risk of myocardial infarction in 24767 people from 52 countries. Methods We used a case-control design with 11119 patients with a first myocardial infarction and 13648 age-matched (up to 5 years older or younger) and sex-matched controls from 262 centres in Asia, Europe, the Middle East, Africa, Australia, and North and South America. Data for demographic factors, education, income, and cardiovascular risk factors were obtained by standardised approaches. Psychosocial stress was assessed by four simple questions about stress at work and at home, financial stress, and major life events in the past year. Additional questions assessed locus of control and presence of depression. Findings People with myocardial infarction (cases) reported higher prevalence of all four stress factors (p vs 12·2% [1659]; odds ratio 1·33 [99% CI 1·19–1·48]). Stressful life events in the past year were also more frequent in cases than controls (16·1% [1790] vs 13·0% [1771]; 1·48 [1·33–1·64]), as was depression (24·0% [2673] vs 17·6% [2404]; odds ratio 1·55 [1·42–1·69]). These differences were consistent across regions, in different ethnic groups, and in men and women. Interpretation Presence of psychosocial stressors is associated with increased risk of acute myocardial infarction, suggesting that approaches aimed at modifying these factors should be developed. Published online September 3, 2004 http://image.thelancet.com/extras/04art8002web.pdf
TL;DR: 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 and self-matching of cases eliminates the threat of control-selection bias and increases efficiency.
Abstract: 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.
TL;DR: Improved understanding of the mechanisms by which heavy physical exertion triggers the onset of myocardial infarction and the manner in which regular exertion protects against it would facilitate the design of new preventive approaches.
Abstract: Background Despite anecdotal evidence suggesting that heavy physical exertion can trigger the onset of acute myocardial infarction, there have been no controlled studies of the risk of myocardial infarction during and after heavy exertion, the length of time between heavy exertion and the onset of symptoms (induction time), and whether the risk can be modified by regular physical exertion. To address these questions, we collected data from patients with confirmed myocardial infarction on their activities one hour before the onset of myocardial infarction and during control periods. Methods Interviews with 1228 patients conducted an average of four days after myocardial infarction provided data on their usual annual frequency of physical activity and the time, type, and intensity of physical exertion in the 26 hours before the onset of myocardial infarction. We compared the observed frequency of heavy exertion (6 or more metabolic equivalents) with the expected values using two types of self-matched analys...
TL;DR: It is concluded that depression predicts the development of CHD in initially healthy people and the stronger effect size for clinical depression compared to depressive mood points out that there might be a dose-response relationship between depression and CHD.
Abstract: Objective: To review and quantify the impact of depression on the development of coronary heart disease (CHD) in initially healthy subjects. Data sources: Cohort studies on depression and CHD were searched in MEDLINE (1966–2000) and PSYCHINFO (1887–2000), bibliographies, expert consultation, and personal reference files. Data selection: Cohort studies with clinical depression or depressive mood as the exposure, and myocardial infarction or coronary death as the outcome. Data extraction: Information on study design, sample size and characteristics, assessment of depression, outcome, number of cases, crude and most-adjusted relative risks, and variables used in multivariate adjustments were abstracted. Data synthesis: Eleven studies met the inclusion criteria. The overall relative risk [RR] for the development of CHD in depressed subjects was 1.64 (95% confidence interval [CI]=1.29–2.08, p p p =0.02). Conclusion: It is concluded that depression predicts the development of CHD in initially healthy people. The stronger effect size for clinical depression compared to depressive mood points out that there might be a dose-response relationship between depression and CHD. Implications of the findings for a broader bio-psycho-social framework are discussed.
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"Patterns of alcohol consumption and..." refers background in this paper
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Q1. What are the contributions mentioned in the paper "Patterns of alcohol consumption and acute myocardial infarction: a case-crossover analysis" ?
This study tested the hypothesis that heavy drinking ( binge drinking ) increases the risk of subsequent acute myocardial infarctions ( AMI ), whereas light to moderate drinking occasions decrease the risk. In a recent study of alcohol drinking patterns and myocardial infarction ( MI ) in women, those who drank at least once a month in a way that ‘ their speech was slurred or they became unsteady on their feet ’, a behavior classified as ‘ intoxication ’, had nearly a threefold risk of MI when compared to lifetime abstainers. Based on these epidemiological findings, this study tested the hypothesis that heavy drinking occasions ( binge drinking ) increase the risk of subsequent AMI, whereas light to moderate drinking occasions decrease the risk. Through collaboration with the staff it was also possible to track all 673 patients who were hospitalized for first time AMI ( ICD I21 ; for detailed definition see below ) in the study hospitals between July 26, 2005 and November 15, 2006. The authors used the following definition of AMI which is compatible with the national register for Acute Myocardial Infarction in Switzerland ( AMIS-plus database ): symptoms and/or ECG changes compatible with acute coronary syndrome and with the enzymes creatine kinase or creatine kinase-muscle brain at least twice the upper limits of normal. As a result, the study group consisted of 250 patients. The authors arranged with the hospitals that patients were not to be interviewed on their first day in hospital, in order to not disturb medical examinations, and in consideration of the patients with recent major complications. The other exclusion criteria were: no domicile in Switzerland ( tourists ) ( 5 persons, 0. 7 % ) ; insufficient skills in German language ( 29, 4. 3 % ) ; mental or physical inability to participate in an interview ( e. g. cerebral damages, dementia, aphasia, hypoxia, patient too confused ) ( 55 persons, 8. 2 % ) or death after admission ( 12, 1. 8 % ), involvement in another interview study ( 17 persons, 2. 5 % ) or other ( e. g. the patient left the hospital without official discharge ) ( 4 persons, 0. 6 % ). The interviews were conducted in half of the study population within 38 h after the AMI. 55 % of the patients were referred directly to the study hospital and 45 % were transferred from another hospital to the study hospital. The case-crossover methodology used in the present study was introduced by Maclure [ 33 ] in the early 1990s to study transient effects on the risk of rare acute events. Com/ear Gerlich/Krämer/Gmel/Maggiorini/ Lüscher/Rickli/Kleger/Rehm Eur Addict Res 2009 ; 15:143–149 144 discussed heavy acute alcohol intake as a potential trigger for AMI [ 16–19 ], but only a few studies in the literature have systematically investigated the effect of alcohol exposure shortly before CHD events using a case-crossover or case-control design [ 20–22 ]. As reviewed by McKee and Britton [ 24 ] and further sources [ 1, 2 ], a number of possible mechanisms have been discussed in the literature explaining the acute effects of binge drinking on CHD events. Kauhanen et al. [ 25 ] suggested that ‘ heavy acute intake of beer may involve acute triggers of severe pathophysiological events in the myocardium or the coronary arteries, or both.