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In 1968-1969, a population-based sample of Swedish women aged 38-60 years was recruited for a health survey, and 20-year survival was later ascertained from national registries. Occupational and leisure-time physical activity data from the baseline and 6-year follow-up examinations were evaluated in relation to all-cause mortality among 1,405 women who were initially free of major diseases. In comparison with being inactive, the mortality relative risk associated with being somewhat active was 0.28 (95% confidence interval 0.17-0.46) for occupational activity and 0.56 (95% confidence interval 0.39-0.82) for leisure-time activity. Being in the most active occupational or leisure activity category further decreased mortality risk to a minor extent. A within-subject decrease in leisure activity over 6 years was also a significant risk factor for all-cause mortality (relative risk = 2.07, relative to no change), although there was no evidence of a benefit from increasing physical activity levels. Since exclusion of early endpoints did not affect the associations in any significant way, underlying illness is unlikely to have played a major role in these analyses. It is concluded that decreases in physical activity as well as low initial levels are strong risk factors for mortality in women, and that their predictive value persists for many years.

Context Obesity is a risk factor for cardiovascular events. Weight loss might protect against cardiovascular events, but solid evidence is lacking. Objective To study the association between bariatric surgery, weight loss, and cardiovascular events. Design, Setting, and Participants The Swedish Obese Subjects (SOS) study is an ongoing, nonrandomized, prospective, controlled study conducted at 25 public surgical departments and 480 primary health care centers in Sweden of 2010 obese participants who underwent bariatric surgery and 2037 contemporaneously matched obese controls who received usual care. Patients were recruited between September 1, 1987, and January 31, 2001. Date of analysis was December 31, 2009, with median follow-up of 14.7 years (range, 0-20 years). Inclusion criteria were age 37 to 60 years and a body mass index of at least 34 in men and at least 38 in women. Exclusion criteria were identical in surgery and control patients. Surgery patients underwent gastric bypass (13.2%), banding (18.7%), or vertical banded gastroplasty (68.1%), and controls received usual care in the Swedish primary health care system. Physical and biochemical examinations and database cross-checks were undertaken at preplanned intervals. Main Outcome Measures The primary end point of the SOS study (total mortality) was published in 2007. Myocardial infarction and stroke were predefined secondary end points, considered separately and combined. Results Bariatric surgery was associated with a reduced number of cardiovascular deaths (28 events among 2010 patients in the surgery group vs 49 events among 2037 patients in the control group; adjusted hazard ratio [HR], 0.47; 95% CI, 0.29-0.76; P = .002). The number of total first time (fatal or nonfatal) cardiovascular events (myocardial infarction or stroke, whichever came first) was lower in the surgery group (199 events among 2010 patients) than in the control group (234 events among 2037 patients; adjusted HR, 0.67; 95% CI, 0.54-0.83; P Conclusion Compared with usual care, bariatric surgery was associated with reduced number of cardiovascular deaths and lower incidence of cardiovascular events in obese adults.

OBJECTIVE--To examine relations between stressful life events and mortality in middle aged men. DESIGN--Prospective population study. Data on stressful life events, social network, occupation, and other psychosocial factors derived from self administered questionnaires. Mortality data obtained from official registers. SETTING--City of Gothenburg, Sweden. SUBJECTS--752 men from a random population sample of 1016 men aged 50. MAIN OUTCOME MEASURE--Mortality from all causes during seven years9 follow up. RESULTS--Life events which had occurred in the year before the baseline examination were significantly associated with mortality from all causes during seven years9 follow up. Of the men who had experienced three or more events during the past year 10.9% had died compared with 3.3% among those with no life events (odds ratio 3.6; 95% confidence interval 1.5 to 8.5). The association between recent life events and mortality remained true after smoking, self perceived health, occupational class, and indices of social support were controlled for. Many of the deaths were alcohol related, but the number of deaths was too small to allow for analyses of specific causes of death. The association between life events and mortality was evident only in men with low emotional support. CONCLUSION--Stressful life events are associated with high mortality in middle aged men. Men with adequate emotional support seem to be protected.

The role of hyperinsulinemia in the development of hypertension is not well understood, particularly insofar as both conditions relate to obesity. The present analysis examines the hypothesis that hyperinsulinemia, independent of obesity, precedes hypertension and natural blood pressure increases in women. The subjects were 50-year-old women from a prospective population study in Gothenburg, Sweden. Fasting insulin levels were determined at baseline (1968-1969) and were evaluated in relation to subsequent hypertension. Blood pressures were measured at the initial physical examination and at the 6- and 12-year follow-up examinations. The first analysis presented here (n = 278) identified incident cases of hypertension during the 12-year follow-up period, whereas the second analysis (n = 219) examined continuous changes in blood pressure. In both analyses, degree, type, and changes in obesity were considered as possible confounding factors. High fasting insulin values were predictive of subsequent incidence of hypertension over the 12-year follow-up period. Subjects with insulin values above the 75th percentile experienced three times more hypertension than did those below the 25th percentile. There was also a significant association between insulin at baseline and increases in diastolic (but not systolic) blood pressure. The positive relations between fasting insulin, on one hand, and diastolic blood pressure changes and hypertension, on the other, could not be explained by confounding effects of body mass index, waist/hip ratio, or weight gain. These findings are consistent with the hypothesis that fasting insulin levels may be one predisposing factor in the etiology of hypertension.

Objective: To compare the cost effectiveness of an amlodipine-based strategy and an atenolol-based strategy in the treatment of hypertension in the UK and Sweden. Design: A prospective, randomised trial complemented with a Markov model to assess long-term costs and health effects. Setting: Primary care. Patients: Patients with moderate hypertension and three or more additional risk factors. Interventions: Amlodipine 5–10 mg with perindopril 4–8 mg added as needed or atenolol 50–100 mg with bendroflumethiazide 1.25–2.5 mg and potassium added as needed Main outcome measures: Cost per cardiovascular event and procedure avoided, and cost per quality-adjusted life-year gained. Results: In the UK, the cost to avoid one cardiovascular event or procedure would be €18 965, and the cost to gain one quality-adjusted life-year would be €21 875. The corresponding figures for Sweden were €13 210 and €16 856. Conclusions: Compared with the thresholds applied by NICE and in the Swedish National Board of Health and Welfare’s Guidelines for Cardiac Care, an amlodipine-based regimen is cost effective for the treatment of hypertension compared with an atenolol-based regimen in the population studied.

Electrocardiographic left ventricular hypertrophy (LVH) is a strong predictor of cardiovascular (CV) morbidity and mortality. However, the predictive value of changes in the magnitude of electrocardiographic LVH criteria during antihypertensive therapy remains unclear.To test the hypothesis that lesser severity of electrocardiographic LVH during antihypertensive treatment is associated with decreased CV morbidity and mortality, independent of blood pressure levels and reduction and treatment modality.Double-blind, randomized, parallel-group study conducted in 1995-2001 among 9193 men and women with hypertension aged 55 through 80 years (mean, 67 years), with electrocardiographic LVH by Cornell voltage-duration product or Sokolow-Lyon voltage criteria and enrolled in the Losartan Intervention For Endpoint Reduction in Hypertension (LIFE) study.Losartan- or atenolol-based treatment regimens, with follow-up assessments for at least 4 (mean, 4.8 [SD, 0.9]) years.Composite end point of CV death, myocardial infarction (MI), or stroke in relation to severity of electrocardiographic LVH determined at baseline and on subsequent electrocardiograms obtained at 1 or more annual revisits.Cardiovascular death, nonfatal MI, or stroke occurred in 1096 patients (11.9%). In Cox regression models controlling for treatment type, baseline Framingham risk score, baseline and in-treatment blood pressure, and severity of baseline electrocardiographic LVH by Cornell product and Sokolow-Lyon voltage, less-severe in-treatment LVH by Cornell product and Sokolow-Lyon voltage were associated with 14% and 17% lower rates, respectively, of the composite CV end point (adjusted hazard ratio [HR], 0.86; 95% confidence interval [CI], 0.82-0.90; P.001 for every 1050-mm x ms [1-SD] decrease in Cornell product; and HR, 0.83; 95% CI, 0.78-0.88; P.001 for every 10.5-mm [1-SD] decrease in Sokolow-Lyon voltage). In parallel analyses, lower Cornell product and Sokolow-Lyon voltage were each independently associated with lower risks of CV mortality (HR, 0.78; 95% CI, 0.73-0.83; P.001; and HR, 0.80; 95% CI, 0.73-0.87; P.001, respectively), MI (HR, 0.90; 95% CI, 0.82-0.98; P=.01; and HR, 0.90; 95% CI, 0.81-1.00; P = .04), and stroke (HR, 0.90; 95% CI, 0.84-0.96; P=.002; and HR, 0.81; 95% CI, 0.75-0.89; P.001).Less-severe electrocardiographic LVH by Cornell product and Sokolow-Lyon voltage criteria during antihypertensive therapy is associated with lower likelihoods of CV morbidity and mortality, independent of blood pressure lowering and treatment modality in persons with essential hypertension. Antihypertensive therapy targeted at regression or prevention of electrocardiographic LVH may improve prognosis.

Several studies have shown that albuminuria is associated with increased risk for fatal and nonfatal cardiovascular events, independent of conventional risk factors. The partition values for urine albumin-creatinine ratio (UACR) used to identify microalbuminuria have been based on studies that predicted risk in diabetic patients.To determine whether the relation between albuminuria and cardiovascular risk can be used to predict cardiovascular morbidity and mortality in hypertensive patients.Multicenter cohort study derived from a randomized, controlled trial.8206 patients with stage II or III hypertension randomly assigned to double-blind therapy with losartan or atenolol. Follow-up was 39 122 patient-years.Renal glomerular permeability evaluated by UACR.In nondiabetic hypertensive patients with left ventricular hypertrophy, the risk for the composite cardiovascular end point increased continuously as albuminuria increased (P0.001 for trend). There was no specific threshold for increased risk. For every 10-fold increase in UACR, hazard ratios in nondiabetic patients increased as follows: composite end point, by 57% (95% CI, 40.6% to 75.0%); cardiovascular mortality, by 97.7% (CI, 66.5% to 235%); all-cause mortality, by 75.2% (CI, 54.0% to 99.4%); stroke, by 51.0% (CI, 28.8% to 76.9%); and myocardial infarction, by 45% (CI, 19.9% to 75.4%) (P0.001 for all comparisons). Values were similar in diabetic patients, although for myocardial infarction the trend was weaker and not significant.Increased UACR resulted in increasing risk for cardiovascular morbidity and mortality among hypertensive patients with left ventricular hypertrophy. We found no thresholds or plateaus. Risk increases at much lower UACR values than has been reported among diabetic patients.

Cardiovascular morbidity and mortality are reduced by treatment with the angiotensin II AT(1)-receptor antagonist losartan compared with conventional treatment with the beta-blocker atenolol in patients with hypertension and electrocardiogram-defined left ventricular hypertrophy, many of whom had known vascular disease.To determine whether losartan reduces cardiovascular event rates in lower-risk hypertensive patients without clinically evident vascular disease.Subgroup analysis of a randomized trial.The Losartan Intervention for Endpoint reduction in hypertension (LIFE) study.6886 men and women (57% women) 55 to 80 years of age (average, 66 years) with essential hypertension (sitting blood pressure, 160 to 200/95 to 115 mm Hg [average, 174/98 mm Hg]) and electrocardiogram-defined left ventricular hypertrophy who did not have clinically evident vascular disease.Patients were randomly assigned to once-daily double-blind treatment with losartan or atenolol.An end point committee ascertained end points (cardiovascular death, stroke, or myocardial infarction).Blood pressure was reduced similarly by losartan and atenolol. The primary composite end point occurred in 282 losartan-treated patients (17.5 per 1000 patient-years) and 355 atenolol-treated patients (21.8 per 1000 patient-years; relative risk, 0.81 [95% CI, 0.69 to 0.95]; P = 0.008). Cardiovascular death occurred in 103 losartan-treated patients and 132 atenolol-treated patients (relative risk, 0.80 [CI, 0.62 to 1.04]; P = 0.092), stroke (nonfatal and fatal) occurred in 125 losartan-treated patients and 193 atenolol-treated patients (relative risk, 0.66 [CI, 0.53 to 0.82]; P0.001), and myocardial infarction (nonfatal and fatal) occurred in 110 losartan-treated patients and 100 atenolol-treated patients (relative risk, 1.14 [CI, 0.87 to 1.49]; P0.2). New-onset diabetes occurred less often in patients treated with losartan (n = 173) than in patients treated with atenolol (n = 254) (relative risk, 0.69 [CI, 0.57 to 0.84]; P0.001). Benefits of losartan treatment were numerically smaller, but not significantly so, in patients with preexisting vascular disease.In hypertensive patients without clinically evident vascular disease, losartan was more effective than atenolol in preventing cardiovascular morbidity and death, predominantly stroke, independent of blood pressure reduction.

Results Blood pressure was reduced by 28/9 and 28/9 mm Hg in the losartan and atenolol arms. The main outcome was reduced by 25% with losartan compared with atenolol, 25.1 vs 35.4 events per 1000 patient-years (relative risk [RR], 0.75; 95% confidence interval [CI], 0.56-1.01; P=.06, adjusted for risk and degree of ECG-LVH; unadjusted RR, 0.71; 95% CI, 0.53-0.95; P=.02). Patients receiving losartan had reductions in the following without a difference in the incidence of myocardial infarction: cardiovascular mortality (8.7 vs 16.9 events per 1000 patient-years; RR, 0.54; 95% CI, 0.34-0.87; P=.01), nonfatal and fatal stroke (10.6 vs 18.9 events per 1000 patient-years; RR, 0.60; 95% CI, 0.38-0.92; P=.02), new-onset diabetes (12.6 vs 20.1 events per 1000 patient-years; RR, 0.62; 95% CI, 0.40-0.97; P=.04), and total mortality (21.2 vs 30.2 events per 1000 patient-years; RR, 0.72; 95% CI, 0.53-1.00; P=.046). Losartan decreased ECG-LVH more than atenolol (P.001) and was better tolerated. Conclusion These data suggest that losartan is superior to atenolol for treatment of patients with isolated systolic hypertension and ECG-LVH. JAMA. 2002;288:1491-1498 www.jama.com

Results from recent studies on the effects of beta1-blockade in patients with heart failure demonstrated a 34% reduction in total mortality. However, the effect of beta1-blockade on the frequency of hospitalizations, symptoms, and quality of life in patients with heart failure has not been fully explored.To examine the effects of the beta1-blocker controlled-release/extended-release metoprolol succinate (metoprolol CR/XL) on mortality, hospitalization, symptoms, and quality of life in patients with heart failure.Randomized, double-blind controlled trial, preceded by a 2-week single-blind placebo run-in period, conducted from February 14, 1997, to October 31, 1998, with a mean follow-up of 1 year.Three hundred thirteen sites in 14 countries.Patients (n = 3991) with chronic heart failure, New York Heart Association (NYHA) functional class II to IV, and ejection fraction of 0.40 or less who were stabilized with optimum standard therapy.Patients were randomized to metoprolol CR/XL, 25 mg once per day (NYHA class II), or 12.5 mg once per day (NYHA class III or IV), titrated for 6 to 8 weeks up to a target dosage of 200 mg once per day (n = 1990); or matching placebo (n = 2001).Total mortality or any hospitalization (time to first event), number of hospitalizations for worsening heart failure, and change in NYHA class, by intervention group; quality of life was assessed in a substudy of 741 patients.The incidence of all predefined end points was lower in the metoprolol CR/XL group than in the placebo group, including total mortality or all-cause hospitalizations (the prespecified second primary end point; 641 vs 767 events; risk reduction, 19%; 95% confidence interval [CI], 10%-27%; P.001); total mortality or hospitalizations due to worsening heart failure (311 vs 439 events; risk reduction, 31%; 95% CI, 20%-40%; P.001), number of hospitalizations due to worsening heart failure (317 vs 451; P.001); and number of days in hospital due to worsening heart failure (3401 vs 5303 days; P.001). NYHA functional class, assessed by physicians, and McMaster Overall Treatment Evaluation score, assessed by patients, both improved in the metoprolol CR/XL group compared with the placebo group (P = .003 and P = .009, respectively).In this study of patients with symptomatic heartfailure, metoprolol CR/XL improved survival, reduced the need for hospitalizations due to worsening heart failure, improved NYHA functional class, and had beneficial effects on patient well-being.

Methods: We used data from the randomised, placebo-controlled Anglo-Scandinavian Cardiac Outcomes Trial-Lipid Lowering Arm (ASCOT-LLA) to conduct a prespecified comparison of the lipid-lowering efficacy of statin therapy among hypertensive participants from different ethnic groups in the UK and Ireland. The effects of atorvastatin (10mg daily) and placebo on fasting plasma lipid profiles were compared in matched groups of Whites and Blacks (of African-Caribbean or African origin) and Whites and South Asians (from the Indian subcontinent), adjusting for placebo effect.

Background: Long-term safety is an important consideration in the selection and use of drugs, such as lipid-lowering agents, that are prescribed to reduce the risk of clinical events during long periods. Methods: The Scandinavian Simvastatin Survival Study was designed to evaluate the effects of cholesterol lowering with simvastatin on mortality and morbidity in patients with coronary heart disease. The 4444 patients aged 35 to 70 years (mean, 58.9 years) with angina pectoris or previous myocardial infarction and serum cholesterol levels of 5.5 to 8.0 mmol/L (213-310 mg/dL) receiving a lipid-lowering diet were randomly assigned to take double-blind treatment with simvastatin, 20 to 40 mg once daily, or placebo. In addition to previously reported end-point events, detailed clinical and laboratory safety data were collected during a median follow-up period of 5.4 years (range in survivors, 4.9-6.2 years). Results: The only clearly drug-related serious adverse event during the 5.4-year median follow-up period was a single reversible case of myopathy. The frequencies of persistent elevations of hepatic aminotransferase levels above 3 times the upper limit of normal and of nonviral hepatitis in the simvastatin and placebo treatment groups were not significantly different. Examination of the lens showed no between-group differences, and no previously unrecognized adverse effects of the drug were observed. There were no significant between-group differences in adverse events in any body system. In particular, the frequency of adverse events related to the central nervous system was similar in both groups. Conclusion: The safety profile of simvastatin, 20 to 40 mg daily, over 5 years was excellent. Arch Intern Med. 1996;156:2085-2092

Men aged 40-64 years with mild to moderate hypertension [diastolic blood pressure (DBP) 100-130 mmHg] were randomized to treatment with a diuretic (n = 3272) or a beta-blocker (n = 3297), with additional drugs if necessary, to determine whether a beta-blocker based treatment differs from thiazide diuretic based treatment with regard to the prevention of coronary heart disease (CHD) events and death. Patients with previous CHD, stroke or other serious diseases, or with contraindications to diuretics or beta-blockers were excluded. If normotension (DBP less than 95 mmHg) was not achieved by monotherapy, other antihypertensive drugs were added, but the two basic drugs were not crossed over. Patients were assessed at 6-monthly intervals. The mean follow-up for end-points was 45.1 months. Blood pressure (BP) side effects and end-points were recorded in a standardized manner. Entry characteristics and the BP reduction achieved were very similar in both treatment groups. All analyses were made on an intention-to-treat basis. The incidence of CHD did not differ between the two treatment groups. The incidence of fatal stroke tended to be lower in the beta-blocker treated group than in the diuretic treated group. Total mortality and the total number of end-points were similar in both groups. The percentage of patients withdrawn due to side effects was similar, whereas the number of reported symptoms, according to a questionnaire, was higher for patients on beta-blockers. The incidence of diabetes did not differ between the two groups. Subgroup analyses did not detect a difference in the effect of beta-blockers compared with diuretics in smokers as opposed to non-smokers, and beta-blockers also had the same effects as diuretics in the quartile with the highest predicted risk for CHD. Beta-blockers and thiazide diuretics were approximately equally well tolerated. The two drugs had a similar BP reducing effect although additional drugs had to be given more often in the diuretic group. Antihypertensive treatment based on a beta-blocker or on a thiazide diuretic could not be shown to affect the prevention of hypertensive complications, including CHD, to a different extent.

A random population sample of middle-aged men from the Primary Prevention Trial was followed for 11.3 years from a first screening when different factors known to be associated with coronary artery disease (CAD) were analyzed. Men with uncomplicated angina pectoris (AP) (n = 167) derived from this population had an incidence of fatal and nonfatal CAD events 3 times higher than that of men without AP or myocardial infarction (n = 5,774). Men with myocardial infarction with or without AP had an incidence of CAD events 7 to 8 times higher than that of men without AP or myocardial infarction. Similar differences were found for new cases of uncomplicated AP (n = 128) and myocardial infarction detected at a second screening after 4 years and followed for 7.3 years. Pooled data from this series of men with uncomplicated AP showed the following factors to be associated in multivariate analysis with nonfatal or fatal CAD endpoints during follow-up: elevated serum cholesterol, elevated blood pressure, smoking and attack score. The risk increase associated with the first 3 factors was similar to the general population. These findings indicate that the same factors affecting prognosis after a first appearance of AP affect similarly patients with myocardial infarction and clinically healthy subjects. Preventive measures against these risk factors seem to be of similar importance among patients with AP, post-infarct patients and healthy subjects.

The effect of metoprolol on mortality was compared with that of placebo in a double-blind randomised trial in patients with definite or suspected acute myocardial infarction. Treatment with metoprolol or placebo started as soon as possible after the patient's arrival in hospital and was continued for 90 days. Metoprolol was given as a 15 mg intravenous dose followed by oral administration of 100 mg twice daily. 1395 patients (697 on placebo and 698 on metoprolol) were included in the trial. Definite acute myocardial infarction developed in 809 and probable infarction in 162. Patients were allocated to various risk groups and within each group patients were randomly assigned to treatment with metoprolol or placebo. There were 62 deaths in the placebo group (8·9%) and 40 deaths in the metoprolol group (5·7%), a reduction of 36% (p

The suitability of nematic phenylcyclohexanes and cyclohexylcyclohexanes as solvents for linear dichroism measurements has been investigated. Especially the cyclohexylcyclohexanes orient solute molecules very well and they are broadly applicable, because their absorption edge lies below 200 nm.

The properties of 709 strains of Escherichia coli isolated from feces of healthy schoolchildren were compared with those of 115 strains from the urine of girls with asymptomatic bacteriuria (ABU) detected in a screening program. These fecal strains were also compared with 45 strains that caused asymptomatic reinfections and 10 that caused symptomatic reinfections in the same group of girls. Typing of O antigen was done by direct bacterial agglutination, and K typing was done with a serum agar technique. Hemolytic capacity was assessed in solid medium. Sensitivity to the bactericidal effect of normal serum and minimal inhibitory concentrations of ampicillin were also determined. The strains isolated from girls who had reinfections of ABU were found to be a random sample of the fecal flora, but the strains from children with symptomatic reinfection were not. Strains from index patients with ABU differed from the other groups in a way that was indicative of adaptive changes in the structure of cell envelopes.

In a longitudinal population study of Swedish men aged 50 at entry the relationships between a number of variables on the one hand and the systolic blood pressure at the start of the study and the subsequent systolic blood pressure change on the other were analyzed. Weight, skinfold, mother's death from cardiovascular disease, systolic blood pressure at work and scrum protein were all significantly correlated with both the initial pressure level and the subsequent pressure change, implying that they are either causal factors for blood pressure increase or have the same cause as the blood pressure increase. Blood glucose, serum lipids, haematocrit, pulse rate, eyeground features, heart volume, smoking habits, serum transaminase and a number of other factors were correlated with the initial pressure level only, implying that they are probably not causing the pressure change. Alcohol consumption, stress, coffee consumption, occupation and other variables were neither related to the initial blood pressure level nor to the blood pressure change

In the Gothenburg primary prevention study 7083 middle aged men were classified into five categories by occupational state. A retrospective analysis of the data showed that low occupational class was associated with slight increases in smoking rates, systolic blood pressure, serum cholesterol concentration, body mass index, and heart rate. Alcohol abuse was strongly associated with low occupational class. After a mean of 11.8 years' follow up the incidence of coronary heart disease was found to be strongly and inversely related to occupational class. For death from coronary heart disease this association fell just below significance when other risk factors were taken into account, but the inverse association between non-fatal myocardial infarction and occupational class persisted even in multivariate analysis. A weak but independent inverse relation was found between occupational class and fatal cancer. Mortality from all causes in the lowest occupational class was 12% compared with 6% in the highest class, and this difference could only partly be explained by other factors. After 10 years a sub-sample of the men were examined again. Risk factors had decreased in all occupational classes, but the changes in risk were not associated with occupational class. Social class, defined by occupation, in Sweden is clearly related to the incidence of coronary heart disease.

A longitudinal population study of 1,462 women, aged 38-60 years at entry, was begun in Gothenburg, Sweden, in 1968-1969. This paper deals with the first 12-year follow-up period. In univariate analysis, peak expiratory flow showed a significant negative correlation with the 12-year incidences of myocardial infarction, electrocardiographic changes suggesting ischemic heart disease, stroke, and death. The association with incidence of myocardial infarction, stroke, and death remained in multivariate analysis, and was independent of age, body height, body mass index, adipose tissue distribution, chest deformity, history of pulmonary disease, smoking habit, serum cholesterol concentration, serum triglyceride concentration, systolic blood pressure, diabetes, and physical activity. The findings indicate that measuring peak expiratory flow is a simple procedure to identify women with an increased risk of cardiovascular disease or death. It seems urgent to find out what preventive measures might be taken as a consequence of these observations.

In a large primary prevention trial among middle-aged men in Gothenburg, Sweden, register data were used to establish marital status, alcohol abuse, and economic problems for nearly all of the study population in 1970-1973. Married men had a higher participation rate in the examinations for the trial than non-married men, with non-married alcoholic men having the lowest participation rates. Among the participants, 26% of divorced men, but only 5% of married men were registered with the social authorities for alcohol problems. Serum cholesterol, body mass index, and diabetes were not associated with marital status, but smoking was more common among widowers and divorced men. Nonfatal myocardial infarction was not related to marital status among participants, after a mean follow-up of 11.8 years. Death from coronary heart disease was more common in non-married men in univariate analysis, but not when other risk factors were taken into consideration. In participants, married men had a mortality rate of 9%, compared with 20% for divorced men. After adjustment for other risk factors, including registration for alcohol problems, smoking, and occupational class, the association between marital status and total mortality was still highly significant. Among nonparticipants in the trial, 13% of married men were registered for alcohol problems, compared with 41% of divorced men. Nonparticipants had higher all-cause mortality, 18% for married men and 33% for divorced men.

The purpose of the trial was to analyze whether supervised physical training could reduce death and nonfatal reinfarction in a nonselected series of postinfarct patients. All patients born in 1913 and later, who were hospitalized for a myocardial infarction during 1968–1970 in Goteborg Sweden, were randomized to a training group (158 patients) and a control group (157 patients). Other treatment was exactly the same and standardized for the two groups. Twenty-seven percent were excluded from training. Training started 3 months after the infarct and was scheduled for three times a week. The training group had higher physical working capacity after 1 yr than the control group. Blood pressure was lower, but there was no differences in blood lipids. During 4 yr of follow-up, 28 patients died in the training group and 35 in the control group. The numbers of nonfatal reinfarcts were 25 and 28, respectively. Within the training group patients adhering to the program had lower mortality than those who did not, but the former also had lower initially predicted risk of dying. A special analysis of patients who attended the training program in comparison to matched controls also showed a lower mortality. No differences in mortality between the training group and the control group were statistically significant, however.

The Primary Preventive Trial in Göteborg, Sweden, a study of a random population sample of middle-aged men, made it possible to analyse the risk factor pattern cross-sectionally in 166 men with uncomplicated angina pectoris (AP) and compare with 5735 men without angina pectoris or myocardial infarction (MI). A prospective analysis was also performed concerning the risk factor pattern in 128 cases with uncomplicated AP and 34 cases with complicated AP (following an MI) respectively, appearing during a follow-up time of 4 years. At cross-sectional analysis, uncomplicated AP was related to elevated serum cholesterol, elevated systolic and diastolic blood pressure, increased relative body weight, smoking, diabetes mellitus, low physical activity during leisure time, dyspnea and mental stress. However at multivariate, prospective analysis only dyspnea, stress, diabetes mellitus and increased relative body weight were predictors for uncomplicated AP. In contrast, elevated serum cholesterol, high blood pressure, smoking, and high physical activity at work were predictors for complicated AP. Possible reasons for the apparent risk factor differences and different mechanisms in AP and MI are discussed.

Mortality from coronary heart disease (CHD) increased among Swedish men between 1968 and 1981, but after that, began to decline. CHD mortality in women decreased slightly, mostly among older women. From 1980, the incidence of non-fatal myocardial infarction (MI) started to decrease among men. Among middle-aged women, however, there was a significantly increased incidence. Mortality during the two years following hospital discharge decreased both in men and women between 1968 and 1985 in Gothenburg. Between one-sixth and one-fifth of major CHD events occur among patients with previous MI or angina pectoris. Serum cholesterol and smoking habits increased among middle-aged men from 1963 to 1973, but decreased thereafter. Blood pressure decreased, and the percentage of people on treatment increased. Blood pressure and serum cholesterol decreased among middle-aged women, but smoking and triglycerides increased. These different trends might explain an increasing CHD incidence among younger women but decreasing incidence and mortality among older women.

The prevalence of primary risk factors, previous medical history, and physical activity were assessed among 262 women and 1259 men who suffered a first nonfatal myocardial infarction between 1968 and 1977 in Göteborg, Sweden. The probability of suffering a myocardial infarction based on the conventional factors cholesterol level, systolic blood pressure and smoking habits was estimated in both sexes by means of a multiple risk function. Comparisons between sexes were made with age alone and age and estimated primary risk as confounders. Survival rate and reinfarction rate were calculated for a 5-year period of follow-up. Women with infarctions had higher serum cholesterol levels (p less than 0.001) and higher blood pressure values (p less than 0.001) but were less often smokers than men (p less than 0.001). The female patients also reported chest pain and dyspnea on exertion, and low physical activity both at work and during leisure time significantly more often than men; these differences remained after controlling for estimated primary risk. An overrepresentation of hypertension and diabetes prior to myocardial infarction was found among women below 45 years of age compared with men. A high frequency of women in this age group was also on sick leave or disability pension at onset of myocardial infarction, suggesting that mainly women with several risk factors including socioeconomic factors suffer an infarction at this age. No similar and consistent differences were found between women and men of older ages. The cumulative 5-year survival rate was 80% in women and 81% in men. Below age 45 the survival rate was lower among women than men (p less than 0.01). No sex difference was found in the recurrence rate of nonfatal reinfarctions. This indicates that once women have suffered a myocardial infarction they are exposed to at least as high a risk as men.

Representative population samples of middle-aged women (1462 participants, a participation rate of 90.1%) were followed from 1968-1969 for 10 years with respect to morbidity and mortality from myocardial infarction, stroke and all causes of death. The same sample (1302 participants, 80.3%) was studied in 1974-1975. Data on the incidences of angina pectoris, intermittent claudication and hypertension in these women during the 6-year interval were analyzed. Obesity as a premorbid characteristic was estimated by weight index and sum of triceps and subscapsular skinfold thicknesses. The overall trends between weight index and the incidences of myocardial infarction and angina pectoris were weak, while there were excess frequencies in the top quintiles, indicating that only marked obesity constitutes an increased risk. The incidence of hypertension was positively correlated to both indices of obesity. The death rate irrespective of cause was negatively correlated to the sum of skinfolds but was not correlated to the weight index. The death rate from myocardial infarction seemed to be correlated to both obesity indices.

In a double-blind randomized trial, 1,395 patients with suspected acute myocardial infarction (MI) were investigated to evaluate the possibility of limiting indirect signs of the size and severity of acute MI with the beta 1-selective adrenoceptor antagonist metoprolol. Metoprolol (15 mg) was given intravenously and followed by oral administration for 3 months (200 mg daily). Placebo was given in the same way. The size of the MI was estimated by heat-stable lactate dehydrogenase (LD[EC 1.1.1.27]) analyses and precordial electrocardiographic mapping. Lower maximal enzyme activities compared with placebo were seen in the metoprolol group (11.1 +/- 0.5 mukat X liter-1) when the patient was treated within 12 hours of the onset of pain (13.3 +/- 0.6 mukat X liter-1; n = 936; p = 0.009). When treatment was started later than 12 hours, no difference was found between the 2 groups. Enzyme analyses were performed in all but 20 patients (n = 1,375). Precordial mapping with 24 chest electrodes was performed in patients with anterior wall MI. The final total R-wave amplitude was higher and the final total Q-wave amplitude lower in the metoprolol group than in the placebo group. Patients treated with metoprolol less than or equal to 12 hours also showed a decreased need for furosemide, a shortened hospital stay, and a significantly reduced 1-year mortality compared with the placebo group, whereas no difference was observed among patients treated later on. After 3 months, however, there was a similar reduction in mortality among patients in whom therapy was started less than or equal to 12 hours and greater than 12 hours after the onset of pain. The results support the hypothesis that intravenous metoprolol followed by oral treatment early in the course of suspected myocardial infarction can limit infarct size and improve long-term prognosis.

Beta-blocking drugs may be more effective than saluretic diuretics in reducing the total mortality and incidence of myocardial infarction, sudden death and stroke in middle-aged men with mild to moderate hypertension. To test this hypothesis, an international multicenter, randomized study is in progress, and its design and some early results are presented here. It is probable that 4,000–5,000 men will need to be enrolled for five years to show a statistically significant difference between treatments. Identical control of blood pressure in the two treatment groups is mandatory, and has been achieved using a fixed therapeutic schedule. The ongoing study will be completed during 1985–1990.

A stepwise bicycle exercise test up to maximum was performed in a random population sample of 793 Swedish men, all aged 54 years. High respiratory rate during exercise characterized those who later suffered myocardial infarction (MI) or sudden coronary death (SD). In addition to high cholesterol, high blood pressure (BP), and smoking, low maximal performance, but not ST changes during exercise, increased the risk of MI + SD also in multivariate analysis. Pulse rate, systolic BP at both submaximal and maximal work load were positively correlated with the initial blood pressure level. BP at these work loads was also positively correlated with subsequent BP increase.

Among 262 women with a first myocardial infarction discharged alive from hospital in Goteborg, Sweden between 1968 and 1977, 161 (61%) were smokers at the time of infarction. Postinfarction smoking was established after three months. In relation to smoking status three months after the infarction, subsequent survival and reinfarction rate were calculated by comparing those who smoked before infarction and later stopped (52%) with those who continued to smoke after the infarction (48%). There were no differences in preinfarction characteristics between quitters and continuing smokers. Women who stopped smoking after the infarction had higher serum enzymes during the acute phase than those who continued to smoke. The cumulative five-year survival rate was 85% among those who stopped smoking compared to 73% among those who continued to smoke (p less than 0.05). No significant difference was found in the cumulative reinfarction rate between the two groups with different smoking habits.

Total mortality and cardiovascular disease (CVD) mortality and morbidity during 10 years of follow-up in relation to systolic blood pressure (SBP) at entry were compared between a random sample of 7455 men, aged 47-54 years at entry, in whom multifactorial risk-factor intervention including intense efforts to detect and treat hypertension had been performed [the Primary Prevention Trial (PPT)], and a similar population (from an observational study) in which intervention, on CVD risk factors was kept to a minimum (the Study of Men Born in 1913). Total mortality, CVD mortality, coronary heart disease (CHD) and stroke incidence increased with SBP in both populations, but levelled off above the cut-off point for antihypertensive treatment in the population subjected to multifactorial CVD risk factor intervention. In this population total mortality was reduced by 30%, CVD mortality by 37%, CHD morbidity by 13% and stroke morbidity by 30% above the cut-off point for blood pressure intervention compared with the incidence predicted from the observational study. These findings indicate that multifactorial intervention, and especially antihypertensive treatment, have preventive effects in the hypertensive part of the middle-aged male population.

In this study covering more than 150,000 person-years from women younger than 55 years of age, 61 survived a first acute myocardial infarction (AMI). Of these, 59 were compared with a random sample from the same population regarding serum lipids and apolipoproteins (apo) A-I, A-II, B, and E, as well as several other cardiovascular risk factors. Mean values of serum cholesterol, triglycerides, apo B, and apo E were significantly higher and high density lipoprotein cholesterol and apo A-I were significantly lower among patients with infarction than among controls. Those who sustained and survived an AMI more often had a history of hypertension and of tobacco smoking than did the controls. Cigarette smoking, a history of hypertension, age, high serum triglycerides and apo E, as well as low levels of apo A-I, were independently and significantly associated with infarction. Sixty percent of the cases and 11% of the controls were distributed in the highest quartile of risk. A major contribution to the association with AMI was accounted for by the conventional risk factors, cigarette smoking and hypertension, as well as high serum triglycerides. In this group of relatively young women, high serum triglycerides were strongly associated with infarction, while levels of serum cholesterol were not.