Search

Background: The ratio of transmitral early filling velocity to early diastolic strain rate (E/e'sr) may be a more accurate measure of LV filling pressure then ratio of early filling pressure to early tissue velocity. The aim of the study was to investigate the impact of age, sex, obesity, smoking, hypertension, hypercholesterolemia, diabetes, physical activity level, socioeconomic, and psychosocial status on E/e'sr over a decade. Additionally, the predictive value of ΔE/e'sr on future major adverse cardiovascular events (MACE) has never been explored., Method: The study included 623 participants from the general population, who participated in the 4th and 5th Copenhagen City Heart Study (CCHS4 and CCHS5). Examinations were median 10 years apart. MACE was the composite endpoint of heart failure, myocardial infarction, and all-cause death., Results: Follow-up time was median 5.7 years, and 43 (7%) experienced MACE. Mean age was 51 ± 14 years, and 43% were male. Mean ΔE/e'sr was 2.1 ± 23.0 cm. After multivariable adjustment for demographic, clinical, and biochemistry variables, high age (stand. β-coef. = .24, P < .001) and mean arterial blood pressure (MAP) (stand. β-coef. = .17, P < .001) were significantly associated with an accelerated increase in E/e'sr In multivariable Cox regression, E/e'sr at CCHS5 and ΔE/e'sr were independent predictors of MACE (HR = 1.20, 95% CI [1.01; 1.42] per 10 cm increase for both). ΔE/e'sr did only provide incremental prognostic value to change in left atrial volume index of the conventional diastolic measurements., Conclusion: In the general population, age and MAP were predictors of an accelerated increase in E/e'sr over a decade. E/e'sr at CCHS5 and ΔE/e'sr were independent predictors of future MACE., (© 2021 Wiley Periodicals LLC.)

A decreased glomerular filtration rate (GFR) is a risk factor for cardiovascular disease even after adjustment for conventional risk factors. The myocardial performance index (MPI) is defined as (isovolumetric relaxation time (IVRT) + isovolumetric contraction time (IVCT))/ejection time (ET). It has been shown to be an independent predictor of cardiovascular events. We hypothesized the MPI could prove valuable for assessing cardiac risk in subjects of the general population with decreased estimated GFR (eGFR). MPI was measured in 1915 subjects from a large general population prospective cohort study using color tissue Doppler imaging (TDI) M-mode through the mitral valve. We compared the prognostic capabilities of the MPI between subjects with eGFR ≥ 75 mL/min/1.73 m 2 and subjects with eGFR < 75 mL/min/1.73 m 2 using multivariable adjusted Cox regression models. The composite endpoint was heart failure, myocardial infarction or cardiovascular death. Mean age was 58 years (SD 16.2), 58% were women, 42% had hypertension and 8.3% diabetes. During a median follow-up time of 12.4 years [IQR 10.6-12.7 years] 269 participants reached the combined endpoint. eGFR modified the prognostic capability of MPI (p-value for interaction < 0.001): After multivariable adjustment, MPI remained an independent predictor of the composite endpoint only in participants with eGFR < 75 mL/min/1.73 m 2 : HR 1.18 (95% CI 1.02-1.38), p = 0.03, vs. in subjects with eGFR ≥ 75 mL/min/1.73 m 2 : HR 1.14 (95% CI 0.94-1.39), p = 0.17. These results suggest the MPI could be particularly valuable for identifying elevated cardiac risk in individuals from the general population with decreased eGFR.

Background: While physical activity reduces risk of developing myocardial infarction (MI), it is unknown whether a history of physical activity is also protective of fatal arrhythmia and case-fatality in patients who have suffered an acute MI., Methods: 104,801 individuals included in 2003-2014 in the Copenhagen General Population Study (CGPS), a prospective population-based study with self-reported leisure time physical activity (LTPA) in three categories measured at baseline, were followed until 2014 through national registries. The 1,517 individuals who suffered a first time MI during follow-up constituted the study population. Outcomes were fatal MI, defined as date of death same as date of MI (including out-of-hospital deaths) and 28-day fatality. Through multivariable analyses the association between baseline LTPA and outcomes were assessed adjusted for CVD risk factors., Results: Of 1,517 MI events, 117 (7.7%) were fatal and another 79 (5.6%) lead to death within 28 days. Median time from baseline to MI was 3.6 years (IQR 1.7-5.8). LTPA was associated with lower risk of fatal MI with odds ratios of 0.40 (95% CI: 0.22-0.73) for light and 0.41 (0.22-0.76) for moderate/high LTPA after multivariable adjustment with sedentary LTPA as reference. Age, alcohol-intake, education and smoking were identified as other predictors for fatal MI. We found no association between LTPA and 28-day case fatality., Conclusions: Among individuals with MI, those that have engaged in any light or moderate physical activity were more likely to survive their MI. Results are consistent with effect of exercise preconditioning on risk of fatal arrhythmia., Competing Interests: The authors have declared that no competing interests exist.

Background Animal studies indicate that exercise reduces myocardial damage during myocardial infarction by ischaemic preconditioning. Aim To determine from a prospective cohort study whether the level of leisure time physical activity (LTPA) in humans prior to myocardial infarction could modify the course of myocardial infarction by reducing case fatality and the subsequent risk of heart failure and mortality. Methods A total of 14,223 participants in the Copenhagen City Heart Study were assessed at baseline in 1976-1978; 1,664 later developed myocardial infarction (mean age at myocardial infarction 70.9 years) and were followed through registries until 2013. We explored the association of LTPA assessed before myocardial infarction with the risk of fatal myocardial infarction, heart failure and all-cause mortality after myocardial infarction. Odds ratios (ORs) and hazard ratios (HRs) were estimated by logistic and Cox proportional hazards regression models, adjusted for age at myocardial infarction and other potential confounders. Results A total of 425 (25.5%) myocardial infarctions were fatal. Higher levels of LTPA prior to myocardial infarction were associated with lower case fatality: adjusted ORs (95% confidence interval), with reference to sedentary LTPA were 0.68 (0.51-0.89) for light LTPA and 0.53 (0.38-0.74) for moderate/high LTPA. A total of 360 (29.1%) of the 1,239 myocardial infarction survivors developed heart failure and 1,033 (83.4%) died during follow-up. There was no association between LTPA levels prior to myocardial infarction and the risk of heart failure or all-cause mortality after non-fatal myocardial infarction: adjusted HRs for moderate/high versus sedentary LTPA were 1.06 (0.78-1.45) and 0.90 (0.74-1.08), respectively. Conclusion Individuals who were physically active had lower case fatality of myocardial infarction, but survivors were not protected against subsequent heart failure or mortality.

Background: Cardiovascular disease is 1 of the most common age-related diseases, and also 1 of the most common causes of death in the general population. We tested the hypothesis that visible age-related signs associate with risk of ischemic heart disease (IHD), myocardial infarction (MI), and death in the general population, independent of chronological age., Methods and Results: 10,885 individuals aged 20 to 93 years free of IHD were followed from 1976 through 1978 until June 2011 with 100% complete follow-up. During these 35 years of follow-up, 3401 participants developed IHD and 1708 developed MI. Presence of frontoparietal baldness, crown top baldness, earlobe crease, and xanthelasmata was associated with increased risk of IHD or MI after multifactorial adjustment for chronological age and well-known cardiovascular risk factors. The risk of IHD and MI increased stepwise with increasing number of age-related signs with multifactorially adjusted hazard ratios up to 1.40 (95% confidence interval, 1.20-1.62) for IHD and 1.57 (1.28-1.93) for MI, in individuals with 3 to 4 versus no age-related signs at baseline (P for trend <0.001). In all age groups in both women and men, absolute 10-year risk of IHD and MI increased with increasing number of visible age-related signs., Conclusions: Male pattern baldness, earlobe crease, and xanthelasmata-alone or in combination-associate with increased risk of ischemic heart disease and myocardial infarction independent of chronological age and other well-known cardiovascular risk factors. This is the first prospective study to show that looking old for your age is a marker of poor cardiovascular health.

Physical activity is associated to a lower risk of mortality from all-causes and from coronary heart disease. The long-term effects of changes in physical activity on coronary heart disease are, however, less known. We examined the association between changes in leisure time physical activity and the risk of myocardial infarction (MI), ischemic heart disease (IHD), and all-cause mortality as well as changes in blood pressure in 4,487 men and 5,956 women in the Copenhagen City Heart Study. Physical activity was measured in 1976-1978 and 1981-1983 and participants were followed in nation-wide registers until 2009. Men who decreased physical activity by at least two levels and women who decreased by one level had a higher risk of MI relatively to an unchanged physical activity level (hazard ratio [HR] = 1.74, 95% confidence interval [95% CI]: 1.17-2.60 and HR = 1.30, 95% CI: 1.03-1.65). Similar associations were found for IHD although only significant in women. In all-cause mortality, men who increased physical activity had a lower risk and both men and women who reduced physical activity had a higher risk compared to an unchanged physical activity level. No association between changes in physical activity and blood pressure was observed. Findings from this prospective study suggest that changes in physical activity affect the risk of MI, IHD and all-cause mortality. A decrease in physical activity was associated to a higher risk of coronary heart disease.

Objectives: We compared the ability of very high levels of nonfasting cholesterol and triglycerides to predict risk of myocardial infarction and total mortality., Design: Prospective study from 1976 to 1978 until 2007., Setting: Danish general population., Participants: Randomly selected population of 7581 women and 6391 men, of whom 768 and 1151 developed myocardial infarction and 4398 and 4416 died, respectively. Participation rate was 72%, and follow-up was 100% complete. Less than 2% of participants were taking lipid-lowering therapy., Results: Compared to women with cholesterol <5 mmol L(-1) , multivariate-adjusted hazard ratios for myocardial infarction ranged from 1.3 [95% confidence interval (CI): 0.9-1.8] for a cholesterol level of 5.0-5.99 mmol L(-1) to 2.5 (95%CI: 1.6-4.0) for cholesterol ≥ 9 mmol L(-1) (trend: P < 0.0001). Compared with women with nonfasting triglycerides <1 mmol L(-1) , hazard ratios for myocardial infarction ranged from 1.5 (95%CI: 1.2-1.8) for triglycerides of 1.0-1.99 mmol L(-1) to 4.2 (95%CI: 2.5-7.2) for triglycerides ≥ 5 mmol L(-1) (p<0.0001). In men, corresponding hazard ratios ranged from 1.2 (95%CI: 1.0-1.5) to 5.3 (95%CI: 3.6-8.0) for cholesterol (P < 0.0001) and from 1.3 (95%CI: 1.0-1.6) to 2.1 (95%CI: 1.5-2.8) for triglycerides (P < 0.0001). Increasing cholesterol levels were not consistently associated with total mortality in women (trend: P = 0.39) or men (P = 0.02). By contrast, compared with women with triglycerides <1 mmol L(-1) , multivariate-adjusted hazard ratios for total mortality ranged from 1.1 (95%CI: 1.0-1.2) for triglycerides of 1.0-1.99 mmol L(-1) to 2.0 (95%CI: 1.5-2.9) for triglycerides ≥5 mmol L(-1) (trend: P < 0.0001); corresponding hazard ratios in men ranged from 1.1 (95%CI: 1.0-1.2) to 1.5 (95%CI: 1.2-1.7) (P < 0.0001)., Conclusions: Stepwise increasing levels of nonfasting cholesterol and nonfasting triglycerides were similarly associated with stepwise increasing risk of myocardial infarction, with nonfasting triglycerides being the best predictor in women and nonfasting cholesterol the best predictor in men. Even more surprisingly, only increasing levels of nonfasting triglycerides were associated with total mortality, whereas increasing cholesterol levels were not., (© 2010 The Association for the Publication of the Journal of Internal Medicine.)

Background: More attention has been paid to psychosocial conditions as possible risk factors for cardiovascular disease (CVD) and the impact of accumulated major life events (MLE) on the development of CVD has received little attention., Design: The aim of this study was to explore the influences of MLE on CVD risk in a large cohort study., Methods: The study population consisted of 9542 randomly selected adults free of CVD examined in the Copenhagen City Heart Study in 1991-1994 and followed up for CVD defined as myocardial infarction or ischaemic stroke until 2001. MLE were analysed using an 11-item questionnaire and hazard ratios (HR) were calculated using the Cox proportional hazards model., Results: During follow-up there were 443 myocardial infarctions (MI) and 350 ischaemic strokes. Financial problems in both childhood and adulthood were associated with risk of stroke with an HR of 1.71 (95% CI: 1.29-2.26) and 1.60 (1.12-2.30), respectively. Accumulation of MLE was also associated with risk of stroke with HR reaching a maximum of 1.41 (95% CI: 1.06-1.90) for more than one event in childhood and 1.49 (95% CI: 1.09-2.04) for more than one event in adulthood. MLE accumulated over a life course showed a dose-response relationship with stroke. Associations were somewhat attenuated by adjustment for vital exhaustion suggesting a mediating role, but not by adjustment for behavioural risk factors. There were no associations between MLE and MI., Conclusion: In this population-based cohort study, we found that MLE conveyed a moderately increased risk of stroke partly mediated through vital exhaustion. We found no association between MLE and the risk of MI.

Context: Elevated nonfasting triglycerides indicate the presence of remnant lipoproteins, which may promote atherosclerosis., Objective: To test the hypothesis that very high levels of nonfasting triglycerides predict myocardial infarction (MI), ischemic heart disease (IHD), and death., Design, Setting, and Participants: A prospective cohort study of 7587 women and 6394 men from the general population of Copenhagen, Denmark, aged 20 to 93 years, followed up from baseline (1976-1978) until 2004., Main Outcome Measures: Hazard ratios (HRs) for incident MI, IHD, and total death according to baseline nonfasting triglyceride level categories of 1 to 1.99 mmol/L (88.5-176.1 mg/dL), 2 to 2.99 mmol/L (177.0-264.6 mg/dL), 3 to 3.99 mmol/L (265.5-353.0 mg/dL), 4 to 4.99 mmol/L (354.0-441.6 mg/dL), and 5 mmol/L or more (> or =442.5 mg/dL) vs triglyceride levels of less than 1 mmol/L (<88.5 mg/dL)., Results: With increasing levels of nonfasting triglycerides, levels of remnant lipoprotein cholesterol increased. During a mean follow-up of 26 years, 1793 participants (691 women and 1102 men) developed MI, 3479 (1567 women and 1912 men) developed IHD, and 7818 (3731 women and 4087 men) died. For MI, among women, the age-adjusted HRs and multifactorially adjusted HRs (aHRs) for each respective category per 1-mmol/L increase in nonfasting triglyceride levels were 2.2 (aHR, 1.7), 4.4 (aHR, 2.5), 3.9 (aHR, 2.1), 5.1 (aHR, 2.4), and 16.8 (aHR, 5.4); for both, P for trend < .001. For MI, among men, the values were 1.6 (aHR, 1.4), 2.3 (aHR, 1.6), 3.6 (aHR, 2.3), 3.3 (aHR, 1.9), and 4.6 (aHR, 2.4); for both, P for trend < .001. For IHD, among women, the values were 1.7 (aHR, 1.4), 2.8 (aHR, 1.8), 3.0 (aHR, 1.8), 2.1 (aHR, 1.2), and 5.9 (aHR, 2.6); for both, P for trend < .001. For IHD, among men, the values were 1.3 (aHR, 1.1), 1.7 (aHR, 1.3), 2.1 (aHR, 1.3), 2.0 (aHR, 1.2), and 2.9 (aHR, 1.5); P for trend < .001 for age-adjusted and P for trend = .03 for multifactorially adjusted. For total death, among women, the values were 1.3 (aHR, 1.3), 1.7 (aHR, 1.6), 2.2 (aHR, 2.2), 2.2 (aHR, 1.9), and 4.3 (aHR, 3.3); for both, P for trend < .001. For total death, among men, the values were 1.3 (aHR, 1.2), 1.4 (aHR, 1.4), 1.7 (aHR, 1.5), 1.8 (aHR, 1.6), and 2.0 (aHR, 1.8); for both, P for trend < .001., Conclusion: In this general population cohort, elevated nonfasting triglyceride levels were associated with increased risk of MI, IHD, and death in men and women.

Objective: Zinc Finger Protein 202 (ZNF202) is a transcriptional repressor of genes affecting the vascular endothelium as well as lipid metabolism. A phenotype associated with genetic variation in ZNF202 is presently unknown. We tested the hypothesis that a common variant in ZNF202, A154V, predicts risk of ischemic heart disease (IHD), myocardial infarction (MI), and ischemic cerebrovascular disease (ICVD)., Methods and Results: We conducted a prospective study of more than 9000 individuals from the general population with 24 years follow-up. In women, age-adjusted hazard ratios in heterozygotes and homozygotes versus non-carriers were 1.2 (95% CI: 1.0-1.5, P = 0.04) and 1.5 (1.1-2.1, P = 0.007) for IHD, 1.5 (1.1-2.1; P = 0.01) and 1.7 (1.1-2.8, P = 0.02) for MI, and 1.3 (1.0-1.8, P = 0.07) and 1.3 (0.8-2.1; P = 0.33) for ICVD. Adjustments for lipids and lipoproteins did not alter these hazard ratios substantially. Genotype did not predict risk in men. Finally, results for IHD were borderline significant (P = 0.06) in an independent case-control study including 933 patients and 8068 controls., Conclusion: This is the first study to suggest that ZNF202 could be a new candidate gene for IHD and MI in the general population.

Study Objective: To determine risk of myocardial infarction (MI) and all cause mortality associated with light smoking and inhalation habits in men and women., Design: Prospective cohort study with follow up of MI and all cause mortality through record linkage., Setting: The Copenhagen City Heart Study, a cardiovascular study based on a sample of the general population established in 1976., Participants: 6505 women and 5644 men followed up until 1998 for first MI and for death from all causes., Main Results: During follow up 476 women and 872 men suffered a MI whereas 2305 women and 2883 men died. After adjusting for major cardiovascular risk factors there was a dose-response relation between smoking with and without inhaling and both MI and all cause mortality. Among inhaling smokers significantly increased risks were found in women at a consumption of only 3-5 grams of tobacco per day with relative risks (RR) of MI and all cause mortality of 2.14 (95% CI 1.11 to 4.13) and 1.86 (95% CI 1.37 to 2.51), respectively. In men increased risks were seen when smoking 6-9 grams per day with RR of MI and all cause mortality of 2.10 (95% CI 1.40 to 3.14) and 1.76 (95% CI 1.39 to 2.23), respectively. Risks were also increased in non-inhaling smokers, although in men only significantly so for all cause mortality. After adjusting for inhalation and quantity smoked, cigarette smokers had a higher risk of all cause mortality (RR 1.16 (95% CI 1.07 to 1.26)) but not of MI (RR 1.11 (95% CI 0.95 to 1.30)). The RR associated with smoking were significantly higher in women than in men for both MI and all cause mortality., Conclusions: Smoking as little as 3-5 grams of tobacco per day or not inhaling the smoke was shown to carry a significantly increased risk of developing MI and of all cause mortality with higher RR found in women than in men. The study emphasises the importance of recognising that even very limited tobacco consumption has detrimental health effects.

Background: The M235T and T174M angiotensinogen mutations have been linked to increased risk for ischemic heart and cerebrovascular disease., Objective: To determine whether angiotensinogen mutations are associated with ischemic heart disease, myocardial infarction, and ischemic cerebrovascular disease., Design: Six case-control studies from the Copenhagen City Heart Study., Setting: Copenhagen, Denmark., Participants: Participants in the Copenhagen City Heart Study and patients from the same hospital with ischemic heart disease (n = 866 and n = 943, respectively), myocardial infarction (n = 519 and n = 493, respectively), or ischemic cerebrovascular disease (n = 489 and n = 434, respectively) and 7975 controls without these conditions., Measurements: Genotypes for the M235T and T174M angiotensinogen mutations were compared between controls and Copenhagen City Heart Study participants with ischemic heart disease, myocardial infarction, and cerebrovascular disease (studies 1a, 1b, and 1c) and patients from Copenhagen University Hospital with the same conditions (studies 2a, 2b, and 2c)., Results: Relative allele frequencies of 235T and 174M in the general population were 0.41 and 0.12, respectively. Genotype was not associated with increased risk for ischemic heart or ischemic cerebrovascular disease in studies of either mutation alone or combined in women or men. Among compound heterozygotes (235MT /174TM ), women in case-control study 2a had decreased risk for ischemic heart disease in age-adjusted analysis; however, this decreased risk was not seen in multifactorial-adjusted or matched analyses, in men, or in case-control study 1a. Among double homozygotes (235TT /174MM ), women in case-control study 2b had increased risk for myocardial infarction in matched analysis; however, this increased risk was not seen in age- or multifactorial-adjusted analyses, in men, or in case-control study 1b. Among single homozygotes (235TT /174TT ), men in case-control study 2b had increased risk for myocardial infarction in multifactorial-adjusted and matched analyses. This risk was not present in age-adjusted analysis, in women, or in case-control study 1b. In addition, male single homozygotes had decreased risk for ischemic cerebrovascular disease in case-control study 2c in age- and multifactorial-adjusted analyses, but this finding was not seen in matched analysis, in women, or in case-control study 1c., Conclusions: In six large case-control studies, the M235T and T174M angiotensinogen mutations were not consistently associated with increased (or decreased) risk for ischemic heart disease, myocardial infarction, or ischemic cerebrovascular disease. Statistically significant associations may represent chance findings rather than real phenomena.

Objective: To compare risk of myocardial infarction associated with smoking in men and women, taking into consideration differences in smoking behaviour and a number of potential confounding variables., Design: Prospective cohort study with follow up of myocardial infarction., Setting: Pooled data from three population studies conducted in Copenhagen., Subjects: 11,472 women and 13,191 men followed for a mean of 12.3 years., Main Outcome Measures: First admission to hospital or death caused by myocardial infarction., Results: 1251 men and 512 women had a myocardial infarction during follow up. Compared with non-smokers, female current smokers had a relative risk of myocardial infarction of 2.24 (range 1.85-2.71) and male smokers 1.43 (1.26-1.62); ratio 1.57 (1.25-1.97). Relative risk of myocardial infarction increased with tobacco consumption in both men and women and was higher in inhalers than in non-inhalers. The risks associated with smoking, measured by both current and accumulated tobacco exposure, were consistently higher in women than in men and did not depend on age. This sex difference was not affected by adjustment for arterial blood pressure, total and high density lipoprotein cholesterol concentrations, triglyceride concentrations, diabetes, body mass index, height, alcohol intake, physical activity, and level of education., Conclusion: Women may be more sensitive than men to some of the harmful effects of smoking. Interactions between components of smoke and hormonal factors that may be involved in development of ischaemic heart disease should be examined further.

To investigate a possible relation between aging signs such as graying of the hair, baldness, and facial wrinkling and myocardial infarction (MI), we analyzed data from The Copenhagen City Heart Study. During the 12-year follow-up, 750 cases of first-time MI were observed. After statistical adjustment for possible confounders, we found a correlation between graying of the hair, facial wrinkling, and frontoparietal baldness and crown-top baldness and MI in men. For example, the relative risk was 1.4 (95% CI, 0.9 to 2.0) for men with moderately gray hair compared with men with no gray hair and 1.9 (1.2 to 2.8) for men with completely gray hair (p < 0.001). With regard to gray hair, a similar although weaker and not statistically significant trend was seen in women. We conclude that, in addition to established coronary risk factors, aging signs like graying of the hair, male baldness, and facial wrinkling indicate an additional risk of MI.

The relationship of ventilatory function to cardiovascular events was studied in 12,511 men and women, enrolled in 1976-1978 in a prospective population study. Until the end of 1983, 388 subjects died because of a cardiovascular disease, 133 died within 30 days of developing myocardial infarction (fatal myocardial infarction), while 238 had a non-fatal myocardial infarction. Cox proportional hazards models were employed for the analysis. In the models including tobacco smoking, cholesterol level, blood pressure, diabetes mellitus and body-mass index as covariates, forced expiratory volume in one second in percentage of predicted (FEV1% pred), forced vital capacity in percentage of predicted (FVC% pred), and the ratio between FEV1 and FVC (FEV1/FVC) were significantly related to the risk of cardiovascular death, e.g. compared with subjects with FEV1% pred or FVC% pred greater than or equal to 80 the risk of death from cardiovascular disease among subjects with FEV1% pred or FVC% pred less than 60 was approximately twice as high. There was a nonsignificant trend towards an increased risk of fatal myocardial infarction with reduction of FVC% pred, but in general the regression models did not show consistent relationship between lung function impairment and risk of myocardial infarction. In the regression models, which only included age and sex as covariates, reduced FVC% pred and FEV1% pred were significantly related to both cardiovascular mortality and to fatal myocardial infarction, but not to the non-fatal infarction, whereas the FEV1/FVC ratio was not related to fatal or to non-fatal myocardial infarction.(ABSTRACT TRUNCATED AT 250 WORDS)

When analyzing risk factors for first acute myocardial infarction in the Copenhagen City Heart Study, a large prospective population study of 20,000 men and women, smoking was found to influence risk significantly in a dose-dependent manner, the risk increasing 2% to 3% for each gram of tobacco smoked daily. Risk was particularly associated with inhalation, the risk for inhalers being almost twice that of noninhalers. No difference in risk could be demonstrated between various types of tobacco (pipe, cigar/cheroots, or plain and filtered cigarettes). The risk seemed associated with current smoking only, inasmuch as the duration of the smoking habit was not important. Ex-smokers had the same risk as those who had never smoked regardless of duration of smoking and time elapsed since quitting. Relative excess risk was significantly higher in female smokers than in male smokers, and daily alcohol intake appeared to have some protective effect on the risk of first acute myocardial infarction among heavy smokers.

The Copenhagen City Heart Study is a prospective cardiovascular population study designed to evaluate incidence of, and risk factors for, cardiovascular disease. A random sample, comprising approximately 20,000 people, were invited to participate. Initial information about potential risk factors was collected during 1976-78 (attendance rate 74%); data about 389 new cases of first acute myocardial infarction (AMI) was obtained from a second survey in 1981-83, as well as from hospital and death registers up to 31 December 1983. The average observation period was 6.5 years. Cox's regression model was used for data analysis. Some 'basic' factors, namely age, sex, family history of AMI, early parental death, height, earlobe crease, length of school education, income and living alone or with a partner were dealt with in a previous paper and are among the potential risk factors for AMI included in the Copenhagen City Heart Study. In this analysis we also include life-style characteristics, some biological traits and disease conditions. An increased risk for first AMI among smokers was graded: the estimated relative risk (ERR) for heavy smokers consuming more than 29g tobacco per day was 2.8 relative to non-smokers. Alcohol intake of five or more drinks per day was associated with a decreased risk, an ERR of 0.6 relative to those who did not drink alcohol daily. Physical inactivity during work but not at leisure was associated with increased risk (ERR 1.4) as was body mass index where the risk was mediated mainly through blood pressure and plasma triglycerides. Oral contraception was not associated with an increased risk, whereas with diabetes the risk increased (the ERR for diabetes being 1.8). Plasma cholesterol above the level of approximately 7 mmol l-1 proportionally increased risk; the ERR in the 1.5% with the highest level was 3.7. A low triglyceride level was associated with low risk; the ERR in the fifth of the study population with the lowest level was 0.6. Elevated blood pressure also proportionally increased risk. Subjects on antihypertensive drug treatment had higher risk than non-treated subjects with similar blood pressure. The effect of socioeconomic factors described in the previous paper was not mediated through their influence on the risk factors included in the present analysis.

The Copenhagen City Heart Study was designed to evaluate the incidence of and risk factors for cardiovascular disease. Information about potential risk factors was collected from 14,223 persons during an initial examination (1976-78) (attendance rate 74%). Information about new cases of acute myocardial infarction (AMI) was obtained from a second examination (1981-83), hospital registries and death registries up to December 31st 1983. This article deals with 'basic' risk factors, namely age, sex, some factors presumably of genetic character (family history of AMI, early parental death, height and earlobe crease) and social factors such as length of school education, income and marital status. The Cox regression model was used. As expected, the risk of first AMI increased with age and was highest among males. Earlobe crease and family history of AMI were found to be significant risk factors, the relative risk being 1.4 for both. No effect was found of early parental death and height. Low grade of education was associated with a higher risk, significantly so only in women, the relative risk being 1.7. Low income carried an increased risk, particularly for females. Cohabitation carried a higher risk, most pronounced in the low income group. Approximately half the effect of education was exerted through its influence on income and marital status.

A number of studies have reported hyperoestrogenaemia in men surviving an acute myocardial infarction (AMI). This has led to speculations that hyperoestrogenaemia might be a coronary risk factor. It is not clear why plasma levels of oestrogens should be elevated in coronary heart disease. To ascertain whether hyperoestrogenaemia might be present before the onset of a myocardial infarction, we performed a prospective study in 252 men above the age of forty who within the following 5 years suffered an AMI and, as controls, 526 men matched for age and coronary risk factors and 329 randomly selected men. Mean plasma concentrations of oestradiol and oestrone did not differ significantly between the groups. This suggests that hyperoestrogenaemia is not a coronary risk factor and thus, if present after the AMI, is more likely develop concurrently with the myocardial infarction.

Hearing for pure tone air-conduction in a sample of women survivors of myocardial infarction (MI) and a random sample of women living in Copenhagen has been examined. For both groups we found that the hearing decreases with age, but the MI survivors at all frequencies have the poorest hearing compared with the random sample. There was no difference between the two groups as regards smoking habits or blood pressure. The noise exposure in the two groups was also the same. There was a significant difference in the mean values of s-cholesterol between the two groups, but we found no correlation between s-cholesterol and hearing in the random sample. Our study supports the hypothesis that MI survivors are more biologically aged than age-matched controls.