Invasive Procedures Associated With the Development of Infective Endocarditis.

BACKGROUND: Various invasive medical procedures might induce bacteremia and, hence, act as triggers for infective endocarditis. However, empirical data in humans on the potential dangers of invasive medical procedures in this regard are very sparse. Due to lack of sufficient data, it is currently debated whether the risk for endocarditis with medical procedures is substantial or rather negligible. OBJECTIVES: The purpose of this nationwide case-crossover study was to quantify the excess risk for infective endocarditis in association with invasive medical and surgical procedures. METHODS: The authors identified all adult patients treated for endocarditis in hospitals in Sweden between January 1, 1998, and December 31, 2011. The authors applied a case-crossover design and compared the occurrence of invasive medical procedures 12 weeks before endocarditis with a corresponding 12-week time period exactly 1 year earlier. The authors considered all invasive nondental medical procedures except for those that are likely to be undertaken due to endocarditis or sepsis or due to infections that could possibly lead to endocarditis. RESULTS: The authors identified 7,013 cases of infective endocarditis during the study period. Among others, several cardiovascular procedures, especially coronary artery bypass grafting; procedures of the skin and management of wounds; transfusion; dialysis; bone marrow puncture; and some endoscopies, particularly bronchoscopy, were strongly associated with an increased risk for infective endocarditis. CONCLUSIONS: This study suggests that several invasive nondental medical procedures are associated with a markedly increased risk for infective endocarditis.

Light-moderate alcohol consumption and left ventricular function among healthy, middle-aged adults: the HUNT study.

OBJECTIVES: To investigate the association between alcohol consumption and left ventricular (LV) function in a population with low average alcohol intake. DESIGN, SETTING AND PARTICIPANTS: A total of 1296 healthy participants, free from cardiovascular diseases, were randomly selected from the third wave of the Norwegian HUNT study (2006-2008) and underwent echocardiography. After validation of the inclusion criteria, 30 participants were excluded due to arrhythmias or myocardial or valvular pathology. Alcohol consumption, sociodemographic and major cardiovascular risk factors were assessed by questionnaires and clinical examination in the HUNT3. General linear models were used to analyse the cross-sectional associations between alcohol intake and LV indices. PRIMARY AND SECONDARY OUTCOME MEASURES: LV functional and structural indices were measured with tissue Doppler and speckle tracking echocardiography. RESULTS: We observed no associations between alcohol consumption and multivariable-adjusted LV functional indices. Excluding abstainers who reported regular alcohol consumption 10 years prior to the baseline did not change the results. Alcohol consumption was positively associated with LV mass indices (p<0.01 for linear trend of the means); there was no such association among participants with non-risky drinking characteristics (p=0.67 for linear trend of the means). CONCLUSIONS: We found no clear evidence that light-moderate alcohol consumption is associated with measures of LV function, although our results indicate that consumption, especially when marked by binge drinking, is progressively associated with greater LV mass.

Does Moderate Drinking Increase the Risk of Atrial Fibrillation? The Norwegian HUNT (Nord-Trøndelag Health) Study.

BACKGROUND: Compelling evidence suggests that excessive alcohol consumption increases the risk of atrial fibrillation (AF), but the effect of light-moderate alcohol consumption is less certain. We investigated the association between alcohol consumption within recommended limits and AF risk in a light-drinking population. METHODS AND RESULTS: Among 47 002 participants with information on alcohol consumption in a population-based cohort study in Norway, conducted from October 2006 to June 2008, 1697 validated AF diagnoses were registered during the 8 years of follow-up. We used Cox proportional hazard models with fractional polynomials to analyze the association between alcohol intake and AF. Population attributable risk for drinking within the recommended limit (ie, at most 1 drink per day for women and 2 drinks per day for men without risky drinking) compared with nondrinking was also calculated. The average alcohol intake was 3.8±4.8 g/d. The adjusted hazard ratio for AF was 1.38 (95% confidence interval, 1.06-1.80) when we compared participants consuming >7 drinks per week with abstainers. When we modeled the quantity of alcohol intake as a continuous variable, the risk increased in a curvilinear manner. It was higher with heavier alcohol intake, but there was virtually no association at <1 drink per day for women and <2 drinks per day for men in the absence of risky drinking. The population attributable risk among nonrisky drinkers was 0.07% (95% confidence interval, -0.01% to 0.13%). CONCLUSIONS: Although alcohol consumption was associated with a curvilinearly increasing risk of AF in general, the attributable risk of alcohol consumption within recommended limits among participants without binge or problem drinking was negligible in this population.

Light-to-moderate drinking and incident heart failure--the Norwegian HUNT study.

BACKGROUND: We analyzed the association between light-to-moderate alcohol intake and the risk of heart failure (HF). METHODS AND RESULTS: We studied 60,665 individuals free of HF who provided information on alcohol consumption in a population-based cohort study conducted in 1995-97 in Norway. Sociodemographic factors, cardiovascular risk factors and common chronic disorders were assessed by questionnaires and/or by a clinical examination. The cohort was followed for a first HF event for an average of 11.2 ± 3.0 years. Mean alcohol consumption was 2.95 ± 4.5 g/day; 1588 HF cases occurred during follow-up. The quantity of alcohol consumption was inversely associated with incident HF in this low-drinking population. The risk was lowest for consumption over three but less than six drinks/week; the multivariate hazard ratio when comparing this category to non-drinkers was 0.67 (95% CI: 0.50-0.92). Among problem drinkers based on CAGE questionnaires, total consumption showed no favorable association with HF, even when overall consumption was otherwise moderate. Excluding former drinkers and controlling for common chronic diseases had minimal effect on these associations. Frequent alcohol consumption, i.e. more than five times/month, was associated with the lowest HF risk; the adjusted hazard ratio comparing this group to alcohol intake less than once/month was 0.83 (95% CI: 0.68-1.03). We found no evidence for a differential effect according to beverage type, nor that the competing risks of death from other causes modified the association. CONCLUSIONS: Frequent light-to-moderate alcohol consumption without problem drinking was associated with a lower HF risk in this population characterized by a low average alcohol intake.

Acute kidney injury after coronary artery bypass grafting and long-term risk of myocardial infarction and death.

BACKGROUND: Acute kidney injury (AKI) after coronary artery bypass grafting (CABG) is associated with early mortality. Its impact on the risk of myocardial infarction (MI) over time and long-term mortality has not been well described. METHODS: We performed a nationwide population-based cohort study in 27,929 patients who underwent a first isolated CABG between 2000 and 2008 in Sweden. Acute kidney injury was divided into three categories based on the absolute increase in postoperative serum creatinine (sCr) concentration compared with the preoperative baseline: stage 1, sCr increase of 0.3 to 0.5mg/dL; stage 2, sCr increase of >0.5 to 1.0mg/dL and stage 3, sCr increase of ≥ 1.0mg/dL. RESULTS: The overall incidence of postoperative AKI was 13%, 6.3% met the criterion for stage 1, 4.3% for stage 2 and 2.3% for stage 3. During a mean follow-up of 5.0 years, there were 2119 (7.6%) MIs and 4679 (17%) deaths. Multivariable adjusted hazard ratios with 95% confidence intervals for MI were 1.35 (1.15 to 1.57), 1.80 (1.53 to 2.13) and 1.63 (1.29 to 2.07), in AKI stages 1, 2 and 3, respectively. The corresponding hazard ratios for all-cause mortality were 1.30 (1.17 to 1.44), 1.65 (1.48 to 1.83) and 2.68 (2.37 to 3.03), respectively. CONCLUSIONS: Our results show that AKI after CABG is associated with an increased long-term risk of MI and death.

Acute kidney injury following coronary artery bypass grafting: early mortality and postoperative complications.

OBJECTIVES: To investigate the prognostic importance of acute kidney injury on early mortality, postoperative stroke, and mediastinitis in patients undergoing a first isolated coronary artery bypass grafting. DESIGN: 7594 patients undergoing coronary artery bypass grafting with information on pre- and postoperative serum-creatinine values were included. Patients were classified using the Acute Kidney Injury Network classification. Odds ratios (OR) for mortality and postoperative complications within 60 days of surgery were calculated after adjustment for confounders separately for stage 1 and for stages 2 and 3 together. RESULTS: 1047 (14%) patients developed acute kidney injury. There were 132 (1.7%) deaths, 103 (1.4%) strokes and 118 (1.6%) cases of mediastinitis during follow-up. Among patients in stage 1 the adjusted odds ratio for death was 4.36 (95% confidence interval 2.83-6.71) and for stage 2 plus 3; 21.5 (12.0-38.6) compared to patients without acute kidney injury. Corresponding OR for stroke were 2.34 (1.43-3.82) and 6.52 (2.97-14.3) and for mediastinitis 2.88 (1.84-4.50) and 4.68 (2.07-10.6), respectively. CONCLUSIONS: Acute kidney injury following coronary artery bypass grafting is related to postoperative mortality, stroke, and mediastinitis. Patients undergoing coronary artery bypass grafting should be assessed for presence of acute kidney injury postoperatively, in order to predict early prognosis.

Daylight saving time shifts and incidence of acute myocardial infarction--Swedish Register of Information and Knowledge About Swedish Heart Intensive Care Admissions (RIKS-HIA).

BACKGROUND: Daylight saving time shifts can be looked upon as large-scale natural experiments to study the effects of acute minor sleep deprivation and circadian rhythm disturbances. Limited evidence suggests that these shifts have a short-term influence on the risk of acute myocardial infarction (AMI), but confirmation of this finding and its variation in magnitude between individuals is not clear. METHODS: To identify AMI incidence on specific dates, we used the Register of Information and Knowledge about Swedish Heart Intensive Care Admission, a national register of coronary care unit admissions in Sweden. We compared AMI incidence on the first seven days after the transition with mean incidence during control periods. To assess effect modification, we calculated the incidence ratios in strata defined by patient characteristics. RESULTS: Overall, we found an elevated incidence ratio of 1.039 (95% confidence interval, 1.003-1.075) for the first week after the spring clock shift forward. The higher risk tended to be more pronounced among individuals taking cardiac medications and having low cholesterol and triglycerides. There was no statistically significant change in AMI incidence following the autumn shift. Patients with hyperlipidemia and those taking statins and calcium-channel blockers tended to have a lower incidence than expected. Smokers did not ever have a higher incidence. CONCLUSIONS: Our data suggest that even modest sleep deprivation and disturbances in the sleep-wake cycle might increase the risk of AMI across the population. Confirmation of subgroups at higher risk may suggest preventative strategies to mitigate this risk.

Tea consumption, incidence and long-term prognosis of a first acute myocardial infarction--the SHEEP study.

BACKGROUND & AIMS: Results of previous studies on tea consumption and incidence or prognosis of acute myocardial infarction (AMI) are conflicting. The aim of the present study was to examine the potential role of tea consumption in the previous 12 months in primary and secondary prevention of AMI. METHODS: We studied a total of 1340 individuals with a first non-fatal AMI and 2303 frequency matched control participants on age, gender and hospital catchment area including querying their tea consumption over the previous 12 months. The cohort of AMI cases was then followed for total and cardiac mortality and for non-fatal cardiovascular events with national registers over 8 years. Estimates of relative risks for a first AMI were based on odds ratios from unconditional logistic regression and Cox proportional hazards models were used to examine the prognostic importance of tea consumption in the cohort of cases. RESULTS: The prevalence of daily tea consumption was 20.5% among cases and 21.5% among controls. Tea consumption was associated with a lower risk for a first AMI with adjustment for matching criteria alone, with an odds ratio of 0.78 (95% confidence interval, 0.64-0.95) comparing those who consumed tea daily to those never consuming tea. However, in multivariable adjusted model there was no evidence for an association, the corresponding odds ratio was 1.08(0.86-1.36). There was also no association between tea consumption and cardiac mortality and non-fatal cardiovascular events, with a corresponding adjusted hazard ratio of 0.99(0.77-1.27). CONCLUSIONS: In this epidemiological study, greater tea consumption in the previous year was associated with a lower risk of AMI. However, a clear association between tea consumption and the incidence or prognosis of AMI was not demonstrated, probably because of tea drinkers having a healthier lifestyle.

Childhood appendectomy, tonsillectomy, and risk for premature acute myocardial infarction--a nationwide population-based cohort study.

AIMS: Although inflammation contributes to cardiovascular disease, the associations of appendectomy and tonsillectomy, which remove mucosa-associated lymphoid tissue, with risk of acute myocardial infarction (AMI) are unknown. Our aim was to assess the association between these operations performed in childhood and AMI risk later in life. METHODS AND RESULTS: We conducted a prospective matched cohort study among all Swedish residents born between 1955 and 1970. A national register identified all appendectomies and tonsillectomies. For each patient undergoing appendectomy or tonsillectomy, we randomly selected five controls without the history of the respective operation, matched on sex, age, and county of residence. Participants were followed for fatal and non-fatal AMI for an average of 23.5 years. Because appendiceal and tonsillar tissues have reduced function after adolescence, our primary analyses were restricted to individuals below age 20 at the time of surgery (54 449 appendectomies and 27 284 tonsillectomies). We derived hazard ratios (HRs) from proportional hazard models adjusted for parental occupation and parental history of AMI. Operations before 20 years of age were associated with an increased risk for AMI (417 and 216 events in the appendectomy and tonsillectomy datasets, respectively), with adjusted HRs of 1.33 [95% confidence interval (CI), 1.05-1.70] for appendectomy and 1.44 (95% CI, 1.04-2.01) for tonsillectomy. This association was graded, with the highest risk among those undergoing both procedures, and generally similar among both males and females. Appendectomy and tonsillectomy performed at or above 20 years of age were not associated with the risk of AMI. CONCLUSIONS: We found a higher risk of AMI related to surgical removal of the tonsils and appendix before age 20. These results are consistent with the hypothesis that subtle alterations in immune function following these operations may alter the subsequent cardiovascular risk, but further studies are needed to confirm these findings and to explore possible mechanisms.

Early-onset depression, anxiety, and risk of subsequent coronary heart disease: 37-year follow-up of 49,321 young Swedish men.

OBJECTIVES: The purpose of this study was to investigate the long-term cardiac effects of depression and anxiety assessed at a young age, when reverse causation is not feasible. BACKGROUND: Most prospective studies found a relatively strong association between depression and subsequent coronary heart disease (CHD). However, almost exclusively, only middle-age or older participants were examined, and subclinical atherosclerosis might contribute to the observed association. The prospective association between anxiety and CHD was less evident in previous studies and has been subjected to similar methodological concerns on the possibility for a reverse causation. METHODS: In a nationwide survey, 49,321 young Swedish men, 18 to 20 years of age, were medically examined for military service in 1969 and 1970. All the conscripts were seen by a psychologist for a structured interview. Conscripts reporting or presenting any psychiatric symptoms were seen by psychiatrists. Depression and anxiety was diagnosed according to International Classification of Diseases-8th Revision (ICD-8). Data on well-established CHD risk factors and potential confounders were also collected (i.e., anthropometrics, diabetes, blood pressure, smoking, alcohol consumption, physical activity, socioeconomic position, family history of CHD, and geographic area). Participants were followed for CHD and for acute myocardial infarction for 37 years. RESULTS: Multiadjusted hazard ratios associated with depression were 1.04 (95% confidence interval [CI]: 0.70 to 1.54), 1.03 (95% CI: 0.65 to 1.65), for CHD and for acute myocardial infarction, respectively. The corresponding multiadjusted hazard ratios for anxiety were 2.17 (95% CI: 1.28 to 3.67) and 2.51 (95% CI: 1.38 to 4.55). CONCLUSIONS: In men, aged 18 to 20 years, anxiety as diagnosed by experts according to ICD-8 criteria independently predicted subsequent CHD events. In contrast, we found no support for such an effect concerning early-onset depression in men.

Anger expression and prognosis after a coronary event in women.

BACKGROUND: Suggestive evidence supports that anger is associated with increased cardiovascular morbidity and mortality. However, the knowledge regarding the impact of anger on prognosis after a coronary event, especially among women is limited. We investigated whether anger expression increases the risk of recurrent events in women with coronary heart disease (CHD). METHODS: Women (n=203) hospitalized for an acute cardiac event were assessed for the four scales of the Framingham Anger Questionnaire, demographic, biomedical and lifestyle factors and were followed for 6.4+/-1 years for total mortality and the combination of cardiovascular death and non-fatal acute myocardial infarction (AMI). RESULTS: After adjustment for confounders such as age, inclusion diagnosis and smoking in the proportional hazard models the tendency to suppress angry feelings was associated with the combination of cardiac death and recurrent AMI (hazard ratio (HR): 1.19, 95% confidence interval (CI): 0.99-1.42) and with all-cause mortality (HR:1.29, 95% CI: 1.03-1.60). Each unit increase in the outward expression of anger increased by 42% the risk for cardiac death or a new AMI (95% CI: 1.01-2.00). Among the potential biological mediators only inflammatory markers attenuated somewhat the relationship. Anger symptoms and discussion of anger were not related to prognosis. CONCLUSIONS: The outward expression and the suppression of anger seem to be associated with prognosis in women with CHD. Future studies need to confirm these findings and to test whether behavioural intervention programs aiming to reduce detrimental anger behaviour in women can influence CHD prognosis.

Increased risk and worse prognosis of myocardial infarction in patients with prior hospitalization for epilepsy--the Stockholm Heart Epidemiology Program.

The association of epilepsy with risk of acute myocardial infarction (AMI) remains uncertain, and its association with myocardial infarction prognosis has not been evaluated. In this study, we performed a population-based case-control study that included 1799 cases with first AMI and 2339 controls, frequency matched by age, sex and hospital catchment area. A history of epilepsy was identified using the Swedish hospital discharge registry. Information on lifestyle and biomarkers was determined from questionnaires and standardized clinic examinations. The cohort of cases was followed for 8 years to evaluate the relationship between epilepsy and post AMI prognosis. A diagnosis of epilepsy was associated with higher risk of incident AMI, with an odds ratio (OR) of 4.92 [95% confidence interval (CI) 2.34-10.31] after adjustment for age, gender, hospital catchment area, and education. There was a graded positive relation between number of hospitalizations for epilepsy and risk of AMI. Adjustment for smoking and levels of tissue plasminogen activator (tPA)/plasminogen activator inhibitor 1 (PAI-1) complex, von Willebrand factor and homocysteine weakened, and adjustment for high-density lipoprotein (HDL) and fibrinogen strengthened, the relationship between epilepsy and AMI. The OR for epilepsy was 4.83 (95% CI 1.62-14.43) when age, gender, hospital catchment area, education and established, clinically relevant AMI risk factors, i.e. diabetes mellitus, smoking, hypertension, physical activity, obesity, high-density lipoprotein, total cholesterol and alcohol consumption were simultaneously controlled for. Epilepsy was also associated with AMI prognosis. Multivariable adjusted hazard ratios for total and cardiac mortality and for a combined outcome of cardiac death and non-fatal reinfarction, heart failure and stroke during follow up, were 1.95 (0.70-5.43), 3.49 (1.05-11.65) and 2.39 (1.16-4.90), respectively. We conclude that epilepsy might be a risk and an adverse prognostic factor for AMI. Smoking and increase in the level of homocysteine, tPA/PAI-1 complex and von Willebrand factor are candidate mechanisms linking epilepsy to increased AMI risk. Physicians should be aware of the potential cardiovascular implications of epilepsy.

Coffee consumption and mortality after acute myocardial infarction: the Stockholm Heart Epidemiology Program.

BACKGROUND: Cohort studies have suggested little effect of coffee consumption on risk of acute myocardial infarction. The effect of coffee consumption on prognosis after myocardial infarction is uncertain. METHODS: In a population-based inception cohort study, we followed 1,369 patients hospitalized with a confirmed first acute myocardial infarction between 1992 and 1994 in Stockholm County, Sweden, as part of the Stockholm Heart Epidemiology Program. Participants reported usual coffee consumption over the preceding year with a standardized questionnaire distributed during hospitalization and underwent a health examination 3 months after discharge. Participants were followed for hospitalizations and mortality with national registers through November 2001. RESULTS: A total of 289 patients died during follow-up. Compared with intake of <1 cup per day, coffee consumption was inversely associated with mortality, with multivariable-adjusted hazard ratios of 0.68 (95% confidence interval [CI] 0.45-1.02) for 1 to <3 cups, 0.56 (95% CI 0.37-0.85) for 3 to <5 cups, 0.52 (95% CI 0.34-0.83) for 5 to <7 cups, and 0.58 (95% CI 0.34-0.98) for > or =7 cups per day (P trend .06). Coffee intake was not associated with hospitalization for congestive heart failure or stroke. Candidate lipid and inflammatory biomarkers did not appear to account for the observed inverse association with mortality. CONCLUSIONS: Self-reported coffee consumption at the time of hospitalization for myocardial infarction was inversely associated with subsequent postinfarction mortality in this population with broad coffee intake. If confirmed in other settings, identification of relevant mechanisms could lead to an improved prognosis for survivors of acute myocardial infarction.

Daily stress and social support among women with CAD: results from a 1-year randomized controlled stress management intervention study.

BACKGROUND: Psychosocial stress may play a causative role in development and progression of coronary artery disease (CAD). PURPOSE: We investigated the effects of a 1-year stress management program on daily stress behavior and social support among female CAD patients. METHOD: Women, 247 (

Financial strain predicts recurrent events among women with coronary artery disease.

BACKGROUND: Although a number of epidemiological studies have found an association between socioeconomic status (SES) indices such as income and education and coronary morbidity and mortality, few have looked at health consequences arising from actually experiencing financial shortcomings. The objective of the present study was to examine whether financial strain predicts recurrent coronary artery disease (CAD) events among women with established CAD. METHODS: Two hundred two women (mean age 62+/-9 years) hospitalized for an acute coronary event were followed over a period of 3.5 years. Demographic, socioeconomic, lifestyle-related, psychosocial and biological characteristics were obtained by means of questionnaires and clinical examination. Data on recurrent cardiac events were collected from the Swedish discharge and death registers. RESULTS: Women experiencing financial strain over the past year had an increased risk for recurrent events, i.e. the combination of all-cause mortality, new acute myocardial infarction and unstable angina pectoris during the follow-up with an unadjusted hazard ratio (HR) of 3.2 (95% CI 1.6-6.6), and a HR of 2.76 (95% CI 1.02-7.50) after controlling for education, household income, age, cohabiting status, inclusion diagnosis and rehabilitation therapy. Adjustment for potential mediators, i.e. psychosocial factors, lipids, diabetes mellitus, smoking, body-mass index, blood pressure, physical activity, alcohol consumption, participation in other cardiac rehabilitation programs did not alter the results significantly. CONCLUSIONS: Financial strain was a predictor for recurrent events among women with CAD, independently of commonly used SES indicators such as education and household income. Future studies will have to explore the mechanism behind this association.

Income and recurrent events after a coronary event in women.

Strong evidence supports the existence of a social gradient in poor prognosis in patients with coronary heart disease (CHD). However, knowledge regarding what factors may explain this relationship is limited. We aimed to analyze in women CHD patients the association between personal income and recurrent events and to determine whether lifestyle, biological and psychosocial factors contribute to the explanation of this relationship. Altogether 188 women hospitalized for a cardiac event were assessed for personal income, demographic factors, lipids, inflammatory markers, cortisol, creatinine, lifestyle and psychosocial factors, i.e. alcohol consumption, smoking habits, body-mass index, depressive symptoms, anxiety, vital exhaustion, availability of social interaction, hostility and anger-related characteristics and were followed for cardiovascular death and recurrent acute myocardial infarction (AMI). During the 6-year follow-up 18 patients deceased and 31 experienced cardiovascular death or non-fatal AMI. After adjustment for confounders, patients with medium and high income had lower risk for recurrent events relative to those with low income (HR (95% CI): 0.38 (0.15-0.97) and 0.39 (0.17-0.93), respectively). Controlling for smoking reduced by 12.8% the risk for recurrent events associated with high versus low income, while adjusting for depression decreased the risk for middle versus low income by 13.5%. Anger symptoms explained 16.7% of the risk for recurrent events associated with middle versus low income and 10.2% of the risk for high versus low income. We suggest that in women with CHD low income is associated with recurrent events and that smoking, depressive symptomatology and anger symptoms may contribute to the explanation of this relationship.

Alcohol and long-term prognosis after a first acute myocardial infarction: the SHEEP study.

CONTEXT: Few studies have investigated the relation between alcohol consumption, former drinking, and prognosis after an acute myocardial infarction (AMI), particularly for non-fatal outcomes. OBJECTIVE: To investigate the prognostic importance of drinking habits among patients surviving a first AMI. DESIGN, SETTINGS, AND PATIENTS: A total of 1346 consecutive patients between 45-70 years with a first non-fatal AMI underwent a standardized clinical examination and were followed for over 8 years. MAIN OUTCOME MEASURES: Total and cardiac mortality and hospitalization for non-fatal cardiovascular disease in relation to individual alcoholic beverage consumption at the time of AMI and 5 years before inclusion, assessed by a standardized questionnaire administered during hospitalization. RESULTS: We recorded 267 deaths, and 145 deaths from cardiac causes, during the follow-up period. After adjustment for several potential confounders, hazard ratios for total and cardiac mortality were 0.77 (0.51-1.15) and 0.61 (0.36-1.02) for those drinking >0-<5 g per day, 0.77 (0.50-1.18) and 0.62 (0.36-1.07) for those drinking 5-20 g per day, and 0.89 (0.56-1.40) and 0.69 (0.38-1.25) for those drinking over 20 g per day. Risk of hospitalization for recurrent non-fatal AMI, stroke, or heart failure generally showed a similar pattern to that of total and cardiac mortality. Recent quitters at the time of AMI had a hazard ratio of 4.55 (2.03-10.20) for total mortality. Measures of insulin sensitivity appeared to be the strongest mediators of this association. CONCLUSIONS: Moderate alcohol drinking might have beneficial effects on several aspects of long-term prognosis after an AMI. Our findings also highlight that former drinkers should be examined separately from long-term abstainers. The potential mechanisms that underlie this association still need to be elucidated.

Inflammation a possible link between economical stress and coronary heart disease.

OBJECTIVE: To assess the relationship between economical stress, as an indicator of SES, and inflammation in women patients with coronary heart disease (CHD). DESIGN: a cross-sectional study. SETTING AND PARTICIPANTS: Two hundred and thirteen women patients recruited from two hospitals in Stockholm, Sweden; mean age 63+/-8, range 35-75 years, hospitalised for acute myocardial infarction, coronary angioplasty or bypass surgery between 1996 and 2000, examined in a stable phase, 1 year and 5 months (+/-2.5 months) after the index event. MAIN OUTCOME MEASURES: Economical stress, and other SES indicators were assessed by questionnaires. Levels of high-sensitivity C-reactive protein (CRP) were measured by nephelometry and the concentrations of interleukin-6 (Il-6) and interleukin-1 receptor antagonist (Il-1ra) were determined by enzyme-linked immunoassay. RESULTS: After controlling for the potential confounders, i.e. treatment, menstruational, marital and education status in addition to age, patients having economical stress showed higher levels of hsCRP (2.79 vs. 1.83 mg/l, p=0.04), Il-6 (3.12 vs. 2.38 mg/l, p=0.015) and Il-1ra (599 vs. 456 mg/l, p=0.02). The association persisted after controlling for other measures of economical status, like personal and household income. According to our mediational analyses, lifestyle variables, especially BMI, could partly explain the observed association. CONCLUSION: High economical stress was associated with higher Il-6, CRP and Il-1ra levels in women with stable CHD. The direction of causality cannot be inferred from such a cross-sectional study however, our results raise the possibility that increased inflammatory activity is a mediator for the effect of economical stress on adverse outcomes after a coronary event.

Work and marital status in relation to depressive symptoms and social support among women with coronary artery disease.

BACKGROUND: Work and marital status have been shown to be associated with health outcome in women. However, the effect of employment and marriage on psychosocial functioning has been studied predominantly in healthy subjects. We investigated whether work and marital status are associated with depressive symptoms, social support, and daily stress behavior in women with coronary artery disease (CAD). METHODS: Data of 105 women with CAD and of working age were analyzed. General linear models were used to determine the association between work and marital status and depressive symptoms, social support, and daily stress behavior. RESULTS: Women who were working at the time of measurement had lower levels of depressive symptoms (7.0 +/- 1.2 vs. 12.1 +/- 0.9, p < 0.01) and higher levels of social support (21.6 +/- 1.0 vs. 18.9 +/- 0.7, p = 0.03) than the nonworking women, whereas marital status was not related to any of the outcome variables. Results were similar after adjusting for potential confounders, that is, age, education, self-reported health, and risk factors for CAD. There was no significant interaction between marital status and working status on depressive symptoms, social support, or daily stress behavior. CONCLUSIONS: In women with CAD, all <65 years of age, after a cardiac event, patients working had lower levels of depressive symptoms and a better social integration than those not working, regardless of reason for being nonemployed. Daily stress behavior, depression, and social support did not differ between cohabiting and not cohabiting women. Future interventions should take into consideration that women with CAD who are unemployed may have a higher risk for depression and social isolation and, therefore, poor clinical outcomes.