Nikulás Sigfússon

Unrecognized Myocardial Infarction: Epidemiology, Clinical Characteristics, and the Prognostic Role of Angina Pectoris: The Reykjavik Study

The clinical manifestations of coronary heart disease vary considerably. Since it was first described by James B. Herrick in 1912, clinically unrecognized myocardial infarction [1] has been extensively researched and debated. Epidemiologic studies have shown that silent, atypical, or unrecognized myocardial infarctions constitute between 20% and 60% of all myocardial infarctions [2-7]. Unrecognized myocardial infarction is diagnosed objectively using thallium perfusion imaging, radionuclide angiography, or echocardiography; it is most often diagnosed from typical, unequivocal changes on the electro-cardiogram of a patient with symptoms so atypical that neither patient nor physician recognizes the problem as an infarction. Atypical and silent myocardial infarction have traditionally been grouped together as unrecognized myocardial infarction. Patients with silent myocardial infarction seemingly have no symptoms. Half of all patients with unrecognized myocardial infarction recall no symptoms and have therefore had silent myocardial infarctions; the remainder have had atypical myocardial infarctions [8, 9]. Silent myocardial ischemia as an important manifestation in patients with coronary heart disease has been studied in recent decades and clearly affects prognosis unfavorably [10, 11]. Because the prognosis for patients with unrecognized myocardial infarction seems to be as serious as that for patients with recognized myocardial infarction [12, 13], practicing physicians face considerable diagnostic and therapeutic challenges when dealing with the many patients with this condition. Not only is it difficult to choose methods with which to identify these patients, it is also difficult to make decisions about secondary prevention and medical treatment. Detailed knowledge about this disease entity is therefore important and must include a thorough understanding of which patient subgroups are especially vulnerable. We report the results of a long-term study of a population-based cohort participating in the Reykjavik Study. Our purpose was to determine the incidence, prevalence, and prognosis associated with unrecognized myocardial infarction. We evaluated the risk factor profile for patients with unrecognized myocardial infarction compared with that of patients with recognized myocardial infarction, as well as the prognostic role of angina pectoris in persons with unrecognized myocardial infarction. Methods The design of the Reykjavik study has been described previously [6], and only a brief description is included here. The study is a large population-based cohort study that started in 1967. Men living in the Reykjavik area who were born between 1907 and 1934 were invited to participate. The study has been conducted in several stages: 1967-1968, 1970-1971, 1974-1975, 1979-1980, and 1983-1987. The response rate has varied from 64% to 75%. Since 1969, women have also participated in the study, but their results will be the subject of a separate report. Each participant answered a questionnaire that included the Rose chest pain questionnaire used by the London School of Hygiene and Tropical Medicine [14]; was examined by a physician; and had a standardized 12-lead electrocardiogram recorded and evaluated according to the Minnesota Code [15]. A total of 9141 men participated in the study at least once. Since 1981, data on the incidence of myocardial infarction have been collected as part of the World Health Organization MONICA Project [16]. Hospital records for persons who had had myocardial infarctions before 1981 were reviewed and evaluated according to criteria used in the MONICA study. Causes of death were determined from all death certificates from the start of the study until 31 December 1987. All autopsy records were also reviewed (autopsy rate, 55%). Diagnostic categories were defined as follows: 1. Recognized myocardial infarction: Patients who fulfilled the MONICA criteria for definite myocardial infarction [16] were placed in this category. These criteria include electrocardiographic changes (Minnesota codes 1.1.1-1.2.8); typical, atypical, or inadequately described symptoms together with probable electrocardiographic changes and abnormal enzyme levels; and typical symptoms and abnormal enzyme levels with ischemic or noncodable electrocardiographic results. 2. Unrecognized myocardial infarction: Participants in this category had no history or symptoms of heart attack but had electrocardiographic changes that fulfilled the criteria for definite myocardial infarction results (Minnesota codes 1.1.1-1.2.8). 3. Angina pectoris with electrocardiographic manifestations of myocardial ischemia: Participants who fulfilled the Rose questionnaire criteria for angina pectoris and who had either ischemic electrocardiographic results (Minnesota codes 1.3.1-1.3.6, 4.1-4.4, 5.1-5.4) or normal resting electrocardiographic results with a positive exercise stress test result ( 0.2 mV horizontal or down-sloping ST depression) were placed in this category. 4. Angina pectoris with normal resting electrocardiographic results: Participants with normal resting electrocardiographic results who either had normal exercise test results or had had no exercise test were assigned to this category if Rose questionnaire results indicated angina pectoris and if the examining physician could confirm the diagnosis. 5. Angina pectoris by the Rose questionnaire only: Participants fulfilling the Rose questionnaire criteria for angina pectoris, if their electrocardiograms did not indicate ischemia and the investigating physician could not confirm the diagnosis, were placed in this category. 6. No coronary heart disease: Participants in this category had no history or electrocardiographic manifestations of myocardial infarction. Patients were classified as having recognized myocardial infarction (category 1) on the basis of hospital records. Classification into the other diagnostic categories, including that of unrecognized myocardial infarction, was based on data collected at set intervals when patients attended the study clinic. Statistical Methods Three designs were used. In the first, a cross-sectional study, logistic regression was used to compute the prevalence odds of unrecognized myocardial infarction as a function of age and calendar year. It was also used to estimate the dependence of unrecognized and recognized myocardial infarction on simultaneous values of measured variables. In the second design, a prospective study, Poisson regression was used to compute the incidence of unrecognized myocardial infarction as a function of age and calendar year. It was also used to compute the predictive power of the measured variables for future unrecognized and recognized myocardial infarction. In these computations, consecutive visits were paired and each pair was used; pairs of visits were excluded if myocardial infarction had been diagnosed during the former visit. The risk period was the time elapsed between two visits (3 to 6 years), and age was the participants age halfway between the visits. In the third design, a prospective study of survival, Cox regression was used to estimate the simultaneous predictive power for risk for death (cause-specific or from all causes). -coefficients were calculated to investigate the prognostic value of risk factors and to form a composite score for individual persons. The composite risk score was the product sum of -coefficients and values of risk factors. Significance testing was two-sided and based on a 5% probability level. The software package used was EGRET (Epidemiologic Graphics, Estimation and Testing) [17]. Results Prevalence and Incidence The overall prevalence of unrecognized myocardial infarction in the first stage of the study was 0.5% in 1968 and 0.4% in 1971, and it increased in later stages of the study. In 1975 and 1980 it was 1.0% and 1.3%, respectively, and in the last stage, in 1986, it was 2.8%. To adjust for changes in age in the participants during the study period, we used logistic regression in which the prevalence odds were modeled as a function of age and either stage number or calendar year. As shown in Figure 1, prevalence increased steeply after age 60 years; it was 0.5% at age 50 years but exceeded 5% at age 75 years. The odds ratio per year was 1.10 (95% CI, 1.07 to 1.12). There was no significant time trend when the computation of prevalence was limited to the first visit of each participant, thus eliminating the bias introduced by the diagnosis of the previously unrecognized infarction. Figure 1. The prevalence of unrecognized myocardial infarction as a function of age. The incidence rate was obtained from the prospective study using a Poisson regression. The only explanatory variables tried at this stage were age, age squared, and calendar time. The incidence rate did not depend significantly on calendar time. Figure 2 shows that incidence was almost zero before age 40 years and increased steeply from age 40 years to age 60 years, at which it exceeded 300 per year per 100 000 persons. After age 65 years, the incidence rate decreased with age. The odds ratio for age (per year) was 2.06 (CI, 1.23 to 3.46); for age squared it was 0.994 (CI, 0.990 to 0.999). This was a significant (P < 0.05) contribution by age squared to the explanation of the incidence rate and indicated a decrease in the incidence rate of unrecognized myocardial infarction after age 65 years (Figure 2). Figure 2. Incidence of unrecognized myocardial infarction as a function of age. Risk Factor Profile Table 1 compares the mean values of some of the baseline characteristics of the cohort that had unrecognized myocardial infarction with those of the cohort that had recognized myocardial infarction. Although more participants with recognized than with unrecognized myocardial infarction were treated for high blood pressure and diabetes mellitus, the differences were not significant. Age and cholesterol, triglycer

Predictive value of apolipoproteins in a prospective survey of coronary artery disease in men

Some studies have suggested that measurements of apolipoproteins may be valuable in the clinical assessment of susceptibility to coronary artery disease, over and above the lipoprotein lipids. Only a few of these studies have been prospective in nature and further knowledge is therefore needed to clarify the issue. The independent prognostic value of apolipoproteins (apo-B, apo-AI and apo[a]) with regard to coronary artery disease was estimated from a prospective survey among 1,332 randomly selected Icelandic men, aged 45 to 72 years, participating in a health survey from 1979 to 1981. The group was followed for 8.6 years, and during that period 104 men had fatal or nonfatal myocardial infarction. The Coxs proportional hazards model was used to estimate the significance of independent variables. The results of multivariate analysis showed that apo(a) was a significant independent risk factor (odds ratio 1.22 for 1 SD), but apo-AI was a stronger negative risk factor (odds ratio 0.70 for 1 SD). Apo-B was a highly significant risk factor in a univariate analysis, but not in a multivariate analysis when serum cholesterol was included. Previous population surveys in Iceland have confirmed the importance of cigarette smoking, cholesterol, triglycerides and blood pressure as risk factors for coronary artery disease. The present results illustrate additional importance of apo-AI and apo(a) concentrations in predicting coronary artery disease among Icelandic men, whereas apo-B did not contribute anything further to the prediction than serum total cholesterol.

Epidemiology of Dupuytren's disease: Clinical, serological, and social assessment. The Reykjavik Study

Dupuytrens disease or palmar fibromatosis is a common disabling hand disorder, mainly confined to Caucasians of northwestern European origin. The prevalence of Dupuytrens disease and possible risk factors related to the disease were evaluated in a random sample of 1297 males and 868 females, aged 46 to 74 years. Blood samples were collected and biochemical parameters were evaluated. The possible relation between the disease and clinical, social, and biochemical parameters were estimated with age-adjusted univariate logistic regression analysis. Altogether 19.2% of the males and 4.4% of the female participants had clinical signs of Dupuytrens disease. The prevalence increased with age, from 7.2% among males in the age group 45-49 years up to 39.5% in those 70-74 years old. The more severe form of the disease, finger contractures, was found in 5.0% of the men and 1.4% had required operation, while this was rarely seen among women. In men elevated fasting blood glucose (P < 0.04), low body weight, and body mass index were significantly correlated with the presence of the disease (P < 0.001). Dupuytrens disease was common among heavy smokers (P = 0.02) and those having manual labor as occupation (P = 0.018). These results show that Dupuytrens disease is common in the Icelandic population and occupation and lifestyle seem to be related to the disease.

Do Lipids, Blood Pressure, Diabetes, and Smoking Confer Equal Risk of Myocardial Infarction in Women as in Men? the Reykjavik Study

Background Studies on coronary risk factors in men and women are mainly based on mortality data and few compare results of both sexes with consistent study design and diagnostic criteria. This study assesses the major risk factors for coronary events in men and women from the Reykjavik Study. Design Within a prospective, population-based cohort study individuals without history of myocardial infarction were identified and the relative risk of baseline variables was assessed in relation to verified myocardial infarction or coronary death during follow-up. Methods Of the 9681 women and 8888 men who attended risk assessment from 1967–1991, with follow-up period of up to 28 years, 706 women and 1700 men suffered a non-fatal myocardial infarction or coronary death. Results Serum cholesterol was a significant risk factor for both sexes, with hazard ratios (HR) decreasing with age. Systolic blood pressure was a stronger risk factor for women as was ECG-confirmed left ventricular hypertrophy (women HR 2.89, 95% confidence interval [CI] 1.67–5.01; men HR 1.11 [CI 0.86–1.43]). Fasting blood glucose ≥6.7 mmol/L identified significantly higher risk for women (HR 2.65) than men (HR 2.08) as did self-reported diabetes. Triglyceride risk was significantly higher for women and decreased significantly with age. Smoking increased risk two- to five-fold, increasing with dose, for women, which was significantly higher than the doubling in risk for men. Conclusions This large study of the major risk factors compared between the sexes demonstrates similar relative risk of myocardial infarction associated with cholesterol for both sexes, however, the relative risk is higher in women for many other risk factors such as smoking, diabetes, elevated triglycerides and left ventricular hypertrophy.

A marked decline in the prevalence and incidence of intermittent claudication in icelandic men 1968–1986: A strong relationship to smoking and serum cholesterol—The Reykjavik study

The epidemiology of peripheral vascular disease has been studied much less extensively than the epidemiology of coronary heart disease (CHD). The prospective Reykjavik Study gave an opportunity to monitor secular trends from 1968 to 1986 of clinical intermittent claudication (IC) amongst Icelandic males, aged 34-80 and to assess the importance of possible risk factors. Both prevalence and incidence of IC decreased sharply after 1970 in all age groups, and this decline occurred a few years earlier than the decline of CHD in Iceland. The only significant risk factors for intermittent claudication, in addition to age, were smoking which increased the risk of IC 8- to 10-fold and serum cholesterol level. Approximately one-half of the striking decline in the incidence of IC can be explained by decreased smoking and cholesterol levels amongst Icelandic men. A follow-up study verified that IC patients stood twice the risk of cardiovascular and total mortality as non-IC patients, indicating that IC is a high risk group which should receive all possible preventive measures.

Decline in ischaemic heart disease in Iceland and change in risk factor levels

OBJECTIVE--To monitor trends in mortality and morbidity due to ischaemic heart disease and compare these with observed levels of risk factors from population surveys. DESIGN--Analysis of trends in death rates from ischaemic heart disease in Iceland compared with expected rates computed from population surveys. Risk factor levels together with beta factors obtained from Coxs regression analysis were used to compute expected death rates. Trends in morbidity due to acute myocardial infarction were assessed and secular trends in dietary consumption compared with trends in cholesterol concentrations. SETTING--Reykjavik, Iceland (total population 250,000; over half the population live in Reykjavik). SUBJECTS--12,814 randomly selected residents in the Reykjavik area aged 45-64 (6623 men, 6191 women; 72% and 80% of those invited). MAIN OUTCOME MEASURES--Age adjusted rates of myocardial infarction and deaths from ischaemic heart disease. Expected risk from risk factor levels (smoking, total serum cholesterol concentration, systolic blood pressure) at each unique survey visit. RESULTS--Mortality from ischaemic heart disease has decreased by 17-18% since 1970. During 1981-6 the myocardial infarction attack rate in men under 75 decreased by 23%. A decrease occurred in the level of all three major risk factors after 1968. The fall in the serum cholesterol concentration coincided with a reduction in consumption of dairy fat and margarine. The calculated reduction in risk for the age group 45-64 was about 35%, which was closely similar to the observed decrease in mortality due to ischaemic heart disease in that age group. CONCLUSION--The reduction in mortality from ischaemic heart disease was substantially due to a decreased incidence of myocardial infarction and could be attributed largely to the reduction in risk factors.

Silent ST-T changes in an epidemiologic cohort study—A marker of hypertension or coronary heart disease, or both: The Reykjavik study

OBJECTIVES We sought to evaluate the prognostic value and clinical characteristics associated with electrocardiographic (ECG) ST-T changes among men without other manifestations of coronary heart disease. BACKGROUND Recent achievements in secondary prevention and treatment of coronary heart disease have highlighted the importance of early diagnosis of both symptomatic and silent forms of the disease. The prognostic and clinical importance of ST-T changes in men with no other manifestations of coronary heart disease is still unclear. Do they reflect silent coronary heart disease or hypertension, or both, and what is their independent contribution to prognosis? METHODS The subjects were 9,139 men born in the years 1907 to 1934 and followed up for 4 to 24 years. On initial visit they were assigned to different categories of coronary heart disease on the basis of Rose chest pain questionnaire, hospital records, 12-lead ECG, history and physical examination. RESULTS The prevalence of silent ST-T changes among men without overt coronary heart disease was strongly influenced by age, increasing from 2% at age 40 years to 30% at age 80 years. Men with such ST-T changes were older and had higher serum triglyceride levels and worse glucose tolerance than men without such changes or other evidence of coronary heart disease. Their blood pressure was higher, and they more often had an enlarged heart or left ventricular hypertrophy and more often took antihypertensive medication, digitalis or diuretic drugs. Serum cholesterol levels were not different between the two groups. After adjustment for other risk factors, these silent ST-T changes had a risk ratio of 2.0 for death from coronary heart disease and 1.6 for subsequent myocardial infarction or angina pectoris. CONCLUSIONS Silent ST-T changes that are ischemic by the Minnesota code are probably both a marker of silent coronary heart disease and high blood pressure. They define a distinct group of patients with highly abnormal risk factor profile. Although not specific for coronary heart disease and often transient, they are associated with the development of every clinical manifestation of coronary heart disease and are independent predictors of reduced survival.

Effects of leisure-time physical activity and ventilatory function on risk for stroke in men: the Reykjavík Study.

Physical activity has been found to confer favorable changes on many cardiovascular risk factors and to reduce risk for cardiovascular disease and cancer (1). Although information on the benefits of physical activity with respect to stroke is limited, several studies have reported that physical inactivity is associated with increased risk for stroke, and a few studies have shown that leisure-time physical activity has a protective effect (2-7). Impaired ventilatory function reportedly predicts fatal stroke (7), but limited information is available on the nature of this association (8). We report on risk for stroke and its association with leisure-time physical activity and ventilatory function among men in a long-term, population-based cohort study. This study design allows thorough accounting for numerous confounders. Methods Study Sample The Reykjavk Study is a prospective cardiovascular population study that started in 1967. The plan of the study and selection criteria have been described in detail elsewhere (9, 10). The current report includes 4484 men without a history of stroke who participated in the fourth (1979 to 1981) or fifth (1985 to 1987) stage of the study. Participants attended the study clinic in the morning after a 10-hour fast. Height, weight, and supine blood pressure were measured. Blood samples, including one used for a 90-minute glucose tolerance test, were drawn (9). Spirometry was done by using a Vitalograph spirometer (Vitalograph, Ltd., Buckingham, United Kingdom). The mean of the highest two of three FEV1 measurements and corresponding measurements of FVC were recorded. Patients were considered to have hypertension if their blood pressure was at least 160/95 mm Hg or if they were being treated for hypertension. At study entry, each participant completed a written questionnaire on health and social factors (9), including yes/no questions on regular leisure-time physical activity at any time during adult life and for the age periods 20 to 29, 30 to 39, 40 to 49, and 50 to 59 years. Respondents who reported participation in regular physical activity were asked to indicate the number of hours per week ( 5 or 6; winter or summer) and the type of activity (walking, swimming, aerobics, golf, or bicycling [group A] or jogging, track and field, ball games, tennis, judo, or other vigorous activity [group B]). Through computerized medical records, we identified patients hospitalized for stroke that had been assigned the International Classification of Diseases, Ninth Revision, diagnostic codes 430 to 434 or 436. All hospital records and reports of computed tomography of the brain were reviewed and verified by one of the authors. Fatal strokes for which the patient was not hospitalized were identified from death certificates. Because outpatient management of acute, nonfatal stroke in Iceland is uncommon, we did not include events for which patients were not hospitalized. Complete follow-up of the study sample was achieved through the unique personal identification number used by the Icelandic National Registry. First stroke or survival to 31 December 1993 was the outcome measure. Stroke was defined according to the World Health Organization criteria and was classified as fatal or nonfatal and as hemorrhagic or ischemic (11). Statistical Analysis We first examined the association between each variable and stroke while adjusting for age. Cox regression was used to analyze the association of patient characteristics with the incidence of the first fatal or nonfatal stroke, and 95% CIs were calculated. Physical activity and hypertension were treated as yes/no variables. Physical activity was grouped into relative intensity categories: low intensity (activities in category A) and high intensity (activities in category B). The continuous variables considered are given in Table 1. Smoking was treated as a three-level variable, and FEV1 and FVC were treated as five-level variables. Confounding was tested by adding variables into a multivariable model. Multivariable hazard analysis was performed by backward elimination of baseline variables. To test interaction, we added terms that were formed by products between each pair of variables remaining in the multivariable model, one at a time. The software package used was SPIDA (12). Table 1. Baseline Characteristics and Risk for Stroke in 4484 Men Results During a follow-up that lasted as long as 14.5 years (mean SD, 10.6 3.6 years), 249 of the 4484 men (5.6%) sustained a stroke (205 [82%] ischemic strokes and 44 [18%] hemorrhagic strokes). Computed tomography of the brain confirmed 158 (72%) of the ischemic strokes and 35 (79.5%) of the hemorrhagic strokes. The mean age at the time of stroke was 70.1 years. Fatal stroke occurred in 62 (6.7% [95% CI, 5% to 9%]) of the 901 men who died during follow-up. Baseline mean values, frequencies, and an age-adjusted univariable risk analysis for total and ischemic stroke were calculated (Table 1). After adjustment for age and smoking, a reduced risk for stroke was associated with leisure-time physical activity after 40 years of age. This finding was significant for both total and ischemic stroke. Quintiles of FVC from highest ( 4.66 L) to lowest (<3.29 L) were analyzed. The relative risk for ischemic stroke was 80% greater in the lowest quintile than in the highest (P<0.01). Similar results were obtained for FEV1. The quotient between FEV1 and FVC had no predictive power on risk for stroke; this finding suggested that there is no trend in stroke risk for obstructive compared with restrictive pulmonary conditions. The results from multivariable analysis (Table 2) show that leisure-time physical activity after 40 years of age is associated with a reduced risk for ischemic stroke (relative risk, 0.62 [CI, 0.40 to 0.97]); after adjustment for other variables shown in Table 2, risk for ischemic stroke was also reduced for former tobacco smokers (relative risk, 0.62; P=0.03). Table 2. Multivariable Analysis of Risk for Stroke in 4484 Men Increased risk for stroke was associated with older age, current smoking, hypertension, high body mass index, and the lowest pulmonary function quintile. No interaction term had predictive power at the 5% level for total or ischemic stroke. Finally, we performed a separate analysis of the 158 ischemic strokes verified by computed tomography. A univariable analysis for leisure-time physical activity after 40 years of age, adjusted for age and smoking, showed a statistically significant reduction in risk for stroke (relative risk, 0.62 [CI, 0.40 to 0.95]). This analysis also showed an increased risk for stroke among patients in the lowest quintile of pulmonary function (relative risk, 2.0 [CI, 1.06 to 3.78]). The multivariable analysis showed a similar point estimate for the relative risk; however, the CIs were broader and the association was no longer statistically significant for leisure-time physical activity after 40 years of age (relative risk, 0.67 [CI, 0.43 to 1.04]) and for FEV1 in the lowest quintile (relative risk, 1.69 [CI, 0.89 to 3.19]). Serum cholesterol level was not a risk factor for total or ischemic stroke; neither cholesterol quartiles nor a cholesterol level greater than 8 mmol/L (308 mg/dL) indicated a risk association (data not shown). Discussion The principal findings of our study are the apparent protective effect of regular, continued leisure-time physical activity in middle-aged men and the detrimental effect of diminished pulmonary function on the risk for ischemic stroke. The reduced risk for stroke associated with leisure-time physical activity has been observed in several studies (2-6). The Honolulu Heart Program (2) found that physical activity among older nonsmokers reduced the risk for thromboembolic stroke and that physical activity protected against hemorrhagic stroke. Our study did not suggest the latter finding. The Manhattan Stroke Study (4) found a meaningful protective effect of leisure-time physical activity on risk for ischemic stroke and calculated a dose-response relation for intensity of physical activity. This was also not demonstrated in our study; the greatest benefit seemed to be associated with low-intensity sports (such as walking and swimming), although the difference between activity groups was not statistically significant. The important factor associated with the protective effect seems to be regular physical activity maintained into ages at which the risk for stroke increases. Physical activity has complex physiologic effects. It causes favorable changes in the lipoprotein profile (1, 13) and may reduce thrombotic potential through enhanced fibrinolytic activity and reduced platelet adhesiveness (14, 15). Recently, a high level of cardiorespiratory fitness was shown to be associated with reduced risk for impaired fasting glucose and type 2 diabetes, probably through favorable effects on insulin resistance (16). The recently reported apparent slowdown of the reduction in stroke mortality in the United States, related in part to obesity (17, 18), may also be related to the sedentary lifestyle of industrial and modernized society rather than to trends in hypertension and smoking. Endurance training leads to substantial respiratory changes. The magnitude of these adaptations largely depends on the persons fitness and various aspects of physical training (1). Impaired pulmonary function is an obvious obstacle to physical training and leisure time physical activity and may contribute to the association between reduced pulmonary function and impaired physical fitness. The relation between stroke risk and pulmonary function after correction for tobacco smoking is notable. Both FEV1 and FVC are composite indicators; genetic factors probably interact with environmental factors, and the two measures are strongly associated with physical fitness (19). Our study found no association between hematocrit and stroke (data not shown); thus, polycythemia

Predominance of aortic calcification as an atherosclerotic manifestation in women: The Reykjavík study

Since 1967 the Reykjavík study has monitored coronary artery disease and its risk factors in randomly selected cohorts. From 1979 to 1984, 3246 men and 3545 women aged 45-74 years were studied. Routine biplane chest X rays were assessed by a radiologist who noted the presence or absence of aortic calcification (AC), but had no detailed knowledge of the subjects. Overall, AC was diagnosed in 283 (8%) women, but in only 54 of the men (1.7%). In the women, the prevalence of AC increased from 2.0% at age 45-49 years to 17.1% at the age of 70-74 years, while in men it was 0 and 8.3%, respectively. In women, multivariate analysis of risk factors showed AC to be positively related to systolic and negatively related to diastolic blood pressure, indicating a potential relation to pulse pressure. Furthermore, AC was independently associated with age, drug treatment for hypertension, nonfasting blood sugar, use of antidiabetic drugs, total serum cholesterol levels, and the amount of smoking. Too few men had AC for multivariate assessment of risk factors. In addition, in women AC was also related to a previous myocardial infarction (p < 0.05), mortality from coronary artery disease (p < 0.01), and the presence of intermittent claudication (p < 0.01). In men, however, AC was related only to total mortality (p < 0.05). Thus, these data show AC to be more prevalent in women, independently associated with recognized atherosclerotic risk factors, and a potential marker for coronary and peripheral artery disease.

Prevalence of iron deficiency and iron overload in the adult icelandic population

The aim of this cross-sectional study was to estimate the prevalence of iron deficiency and overload in the adult population in Iceland, a developed Scandinavian country. The study population consisted of 4240 individuals aged 25-74 years randomly selected from the national roster. Basic hematological, S-iron, S-total iron binding capacity (TIBC), and S-ferritin measurements were obtained on 2588 individuals (61.0%). The results indicated unusually large iron stores in the adult Icelandic population and significantly larger iron stores in the rural compared to the urban population. Iron deficiency was rare except in urban premenopausal women, where 1 in 4 showed evidence of iron deficiency and 3.2% had iron deficiency anemia. Seven patients with hereditary hemochromatosis were identified from a subgroup of 1887 subjects, resulting in a prevalence of 0.37%. Two of the hereditary hemochromatosis patients had been gastrectomized. Measures to improve the iron balance in urban premenopausal women cannot therefore include increased iron fortification of food but must be more directed towards the target group.