A six-year prospective study of 3775 individuals, first examined in 1978, using an original mathematical program of myocardial infarction risk prognosis, is reported. The program is based on an integral assessment of 19 risk factors, each having 4 degrees of severity. The subjects were allocated to one of 3 groups, depending on the prognostic risk score. In the low coronary risk group (2068 people), there was 1 (0.048%) myocardial infarction over 6 years. There were 12 (0.76%) infarctions in the medium risk group (1569 people), and 62 (44.92%) infarctions in the high risk group (138 people). Therefore, the program is capable of identifying a limited (about 4%) population that is going to develop 80% of all myocardial infarctions within the next 5 or 6 years.
BACKGROUND: To do a gender comparison of absolute risk of recurrent myocardial infarction (MI). DESIGN: Registration of all first and second MI amongst Icelandic males and females 1981-1999. METHODS: The whole of Icelandic population, 40-74 years of age. RESULTS: The mean recurrence rate (second attack) for men was 45.7/1000 MI survivors/year and for women 39.0/1000 per year. The male/female (M/F) ratio was 1.17, 95% confidence interval 1.00-1.37, P = 0.05 and did not change significantly with age. The M/F ratio for first MI in comparison was two to seven, lowest in the oldest group. The recurrence rate decreased significantly and similarly in both sexes during the observation period. CONCLUSION: The absolute risk of MI is closely similar amongst both sexes and has decreased similarly suggesting that the same kind of secondary intervention is effective amongst both sexes in a general population.
Active smoking is a well-established risk factor for myocardial infarction, but less is known about the impact of passive smoking, and possible sex differences in risk related to passive smoking. We investigated active and passive smoking as risk factors for myocardial infarction in an 11-year follow-up of 11,762 men and 13,206 women included in the Tromsø Study. There were a total of 769 and 453 incident cases of myocardial infarction in men and women, respectively. We found linear age-adjusted relationships between both active and passive smoking and myocardial infarction incidence in both sexes. The relationships seem to be stronger for women than for men. Age-adjusted analyses indicated a stronger relationship with passive smoking in ever-smokers than in never-smokers. After adjustment for important confounders (body mass index, blood pressure, total cholesterol, HDL cholesterol and physical activity) the associations with active and passive smoking were still statistically significant. Adjusting for active smoking when assessing the effect of passive smoking and vice versa, indicated that the effect of passive smoking in men may be explained by their own active smoking. In women, living with a smoker =30 years after the age of 20 increased the myocardial infarction risk by 40 %, even after adjusting for active smoking. Passive smoking is a risk factor for myocardial infarction on its own, but whereas the effect for men seems to be explained by their own active smoking, the effect in females remains statistically significant.
To measure blood IL-6, IL-10, creatinine levels, calcium, sodium and potassium in blood and saliva, melatonin in urine of patients with acute coronary syndrome without ST segment elevation for the prediction of the clinical course at the post-hospital stage.
The study included 93 patients with complicated (n = 46) and uncomplicated (n = 47) coronary syndrome without ST segment elevation. Blood IL-6, IL-1, creatinine levels, calcium, sodium and potassium in blood and saliva, melatoni n in urine were determined on days 1-3 after hospitalization. 6-hydroxymelatonin was measured by HPLC in urine collected between 23 p.m. and 8 a.m., melatonin i in urine collected between 8 a.m. and 23 p.m.
Complicated coronary syndrome was associated with increased levels of melatonin (night), blood IL-10 and Na, salivary, Na and Ca while the uncomplicated condition with increased blood melatonin (daytime), IL-6, creatinine, Ca, Na, K, and salivary K. 90 patients were followed up within 12 months after discharge. End-points developed in 36 (40%) of them. Logistic analysis yielded variables and 2 logistic regression equations The data on night melatonin +5 and +4 were included in ROC analysis. The night melatonin +5 values over 0.7453 were associated with increased risk of complications in the post-hospital period (6 months) and values of 0.7453 or lower with the enhanced probability of uncomplicated clinical course. Prognostic sensitivity was estimated at 90%, specificity at -54.39%. The night melatonin +4 values over 0.2903 were associated with increased risk of complications in the post-hospital period (12 months) and values of 0.2903 or lower with the enhanced probability of uncomplicated clinical course. Prognostic sensitivity was estimated at 77.8%, specificity at -59.26%.
The night melatonin +5 and +4 models can be used to predict the clinical course of acute coronary syndrome during 6 and 12 months of the post-hospitalization period.
The Skaraborg Hypertension Project was undertaken in 1977-1981, and 1428 male and 1812 female hypertensives aged 40-69 years were involved at hypertension out-patient clinics in primary health care. Their long-term risk of acute myocardial infarction during a follow-up of 8.3 years was compared to that of age- and sex-matched controls drawn from the census register at the beginning of surveillance and to normotensive untreated controls identified in a population survey in 1977. Relative risks (with a 95% confidence interval) for acute myocardial infarction morbidity compared to the population was 0.99 (0.78, 1.25) in men and 1.36 (0.95, 1.94) in women. Corresponding figures for acute myocardial infarction mortality were 0.97 (0.68, 1.38) and 1.15 (0.67, 1.99). With normotensive controls used as reference and adjusting for smoking habits and body mass index, the relative risks for acute myocardial infarction morbidity were 1.48 (1.12, 1.98) in men and 2.34 (1.43, 3.85) in women, and for acute myocardial infarction mortality 1.66 (1.07, 2.57) and 1.71 (0.84, 3.48), respectively. Treated hypertension is a weak risk factor for acute myocardial infarction in unselected hypertensive patients.
Studies have related air pollution to myocardial infarction (MI) events over days or weeks, with few data on very short-term risks. We studied risk of ST-segment elevation MI (STEMI) within hours of exposure to air pollution while adjusting for weather.
We performed a case-crossover study of STEMI cases in Stockholm, Sweden (Jan 2000-June 2014) based on SWEDEHEART. Exposures during hazard periods up to 24?h prior to admission were compared to bidirectionally sampled control periods. Risks attributable to sulphur dioxide (SO2), nitrogen dioxide (NO2), ozone and particulate pollutants (PM2.5, PM10) were studied in conditional logistic regression models for interquartile range increments.
Risk of STEMI (n?=?14,601) was associated with NO2 (strongest at 15-h lag) and with PM2.5 (strongest at 20-h lag), in single-pollutant models adjusting for air temperature and humidity (NO2: odds ratio (OR; 95% confidence interval) 1.065 (1.031-1.101); PM2.5: 1.026 (1.001-1.054)). After adjusting models for atmospheric pressure (significantly associated with STEMI risk at 14-24-h lags), NO2 remained highly statistically significant (1.057 (1.022-1.094)) but not PM2.5 (1.024 (0.997-1.052)). No associations were seen for SO2, ozone or PM10.
Risk of STEMI rises within hours of exposure to air pollutants, with strongest impact of NO2. These findings are complementary to earlier reports which have not acknowledged widely the importance of very short-term fluctuations in air pollution.
OBJECTIVES: Little is known about the possible influence of different kinds of alcohol drinking pattern on the risk of acute myocardial infarction. In this study the association between average daily alcohol consumption, as well as large intakes of alcohol on single occasions, and myocardial infarction incidence was investigated. DESIGN: A case referent analysis nested within a prospective cohort study. SETTING: Incident cases of myocardial infarction were identified by using hospital discharge data and deaths. Referents were selected from the study population through a stratified random sample. SUBJECTS: Individuals of the Swedish Twin Register below 75 years of age living in a region of 10 Swedish counties in 1972-1981 or in Stockholm County in 1972-1987. MAIN OUTCOME MEASURE: Incidence of acute myocardial infarction. RESULTS: No difference in myocardial infarction incidence was found between former alcohol drinkers and lifelong abstainers. For men, drinkers had a 40% lower incidence than non-drinkers, as did those with a drinking pattern involving a large intake on single occasions. Women had on average a very low level of alcohol consumption and there were only small differences in incidence of myocardial infarction between drinkers and non-drinkers. An increased incidence was indicated for women reporting some-times drinking comparatively large amounts of alcohol on single occasions. CONCLUSIONS: The results support the suggestion that low and moderate alcohol consumption is protective for myocardial infarction. A drinking pattern involving a large intake of alcohol on single occasions did not seem to substantially influence myocardial infarction incidence except possibly for women with an overall very low level of consumption.
The consequences of alcoholic intemperance and economic problems on CHD mortality and morbidity were studied among the participants in a large primary preventive trial. Official register data were used. Subjects registered with the Board of Social Welfare were categorised with respect to increasing load of alcoholic intemperance. Non-fatal CHD was not related to alcoholic problems. Fatal CHD, on the other hand, was strongly associated with registration for intemperance. This was especially pronounced for cases dying suddenly from CHD. A multivariate analysis was performed, controlling for smoking, systolic blood pressure and serum cholesterol, which showed that the association between intemperance and fatal CHD was independent of these factors.