Biomedical subjects

Jacqueline C M Witteman

Publications and source records attributed to Jacqueline C M Witteman.

At least 19 recordsLinked to original sources

PubMed2006

C-reactive protein levels, variation in the C-reactive protein gene, and cancer risk: the Rotterdam Study.

PURPOSE: It remains unclear if inflammation itself may induce cancer, if inflammation is a result of tumor growth, or a combination of both exists. The aim of this study was to examine whether C-reactive protein (CRP) levels and CRP gene variations were associated with an altered risk of colorectal, lung, breast, or prostate cancer. PATIENTS AND METHODS: A total of 7,017 participants age > or = 55 years from the Rotterdam Study were eligible for analyses. Mean follow-up time was 10.2 years. High-sensitivity CRP measurements were performed to identify additional values of 0.2 to 1.0 mg/L compared with standard procedures. Genotypes of the CRP gene were determined with an allelic discrimination assay. RESULTS: High levels (> 3 mg/L) of CRP were associated with an increased risk of incident cancer (hazard ratio, 1.4; 95% CI, 1.1 to 1.7) compared with persons with low levels (< 1 mg/L), even after a potential latent period of 5 years was introduced. Although CRP seems to affect several cancer sites, the association was strongest for lung cancer (hazard ratio, 2.8; 95% CI, 1.6 to 4.9). A CRP single nucleotide polymorphism associated with decreased CRP levels was associated with an increased lung cancer risk of 2.6 (95% CI, 1.6 to 4.4) in homozygous carriers. CONCLUSION: Baseline CRP levels seem to be a biomarker of chronic inflammation preceding lung cancer, even after subtracting a 5-year latent period. Furthermore, CRP gene variation associated with low CRP blood levels was relatively common in patients with lung cancer. Both chronic inflammation and impaired defense mechanisms resulting in chronic inflammation might explain these results.

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PubMed2006

TGF-beta 1 polymorphisms and risk of myocardial infarction and stroke: the Rotterdam Study.

BACKGROUND AND PURPOSE: Inflammation plays a pivotal role in the pathogenesis of atherosclerosis and of cardiovascular and cerebrovascular complications. Transforming growth factor-beta1 (TGF-beta1) is a pleiotropic cytokine with a central role in inflammation. Little is known of the relation of variations within the gene and risk of cardiovascular and cerebrovascular disease. We therefore investigated 5 polymorphisms in the TGF-beta1 gene (-800 G/A, -509 C/T, codon 10 Leu/Pro, codon 25 Arg/Pro, and codon 263 Thr/Ile) in relation to the risk of myocardial infarction and stroke in a population-based study. METHODS: Participants (N=6456) of the Rotterdam Study were included in the current study. Analyses of the relations of genotypes with the risk of myocardial infarction and stroke were performed according to Cox proportional-hazards methods. All analyses were adjusted for age, sex, conventional cardiovascular risk factors, and medical history. RESULTS: We found no association with the risk of myocardial infarction. A significantly increased risk of stroke was found, associated with the T allele of the -509 C/T polymorphism (relative risk, 1.26; (95% CI, 1.06 to 1.49) and the Pro variant of the codon 10 polymorphism (relative risk, 1.24; 95% CI, 1.04 to 1.48). CONCLUSIONS: No association between the TGF-beta1 polymorphisms and myocardial infarction was observed; however, the -509 C/T and codon 10 Leu/Pro polymorphisms were associated with the risk of stroke.

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PubMed2006

High serum C-reactive protein level is not an independent predictor for stroke: the Rotterdam Study.

BACKGROUND: Current guidelines recommend the assessment of C-reactive protein (CRP) levels with a high-sensitivity assay in cardiovascular risk prediction. Recent studies have put forward that although elevated CRP is a risk factor for cardiovascular disease, it is not helpful in the prediction of cardiovascular disease risk. We studied the importance of CRP as a risk factor and as a risk predictor of future stroke. METHODS AND RESULTS: The present study was based on 6430 participants of the Rotterdam Study who at baseline (1990-1993) were > or = 55 years of age, were stroke free, and had blood taken. Strokes were classified as hemorrhagic, ischemic, or unspecified. Ischemic strokes were further subclassified. Whether stroke risk varied with baseline CRP serum levels was assessed with Cox proportional hazards models. Whether CRP was helpful in the prediction of individual stroke risk was assessed with receiver operating characteristic curves and by comparing the distribution of strokes between predicted risk strata. During an average of 8.2 years of follow-up, 498 first-ever strokes occurred. High CRP levels were significantly associated with risk of any stroke (age- and sex-adjusted hazard ratio per SD, 1.14; 95% confidence interval, 1.04 to 1.24) and risk of ischemic stroke (age- and sex-adjusted hazard ratio per SD, 1.17; 95% confidence interval, 1.04 to 1.32). Taking CRP levels into account did not improve the individual stroke risk prediction, however, regardless of whether it was based on the Framingham stroke risk score or on age and sex only. CONCLUSIONS: Although CRP levels are associated with stroke risk, their use in the assessment of individual stroke risk seems limited.

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PubMed2006

Lipoprotein-associated phospholipase A2 activity and risk of heart failure: The Rotterdam study.

AIMS: Evidence is accumulating that inflammation plays a role in the pathophysiology of heart failure. Lipoprotein-associated phospholipase A2 (Lp-PLA2) has pro-inflammatory properties. We investigated whether Lp-PLA2 activity is associated with heart failure. METHODS AND RESULTS: Lp-PLA2 activity was determined in a random sample of 1820 subjects from the Rotterdam Study, a population-based cohort study among persons aged 55 years and over. During a mean follow-up of 6.7 years, 94 heart failure cases occurred. We excluded participants with heart failure or coronary heart disease at baseline and we accounted for incident coronary heart disease during follow-up. We used Cox proportional hazard models to compute hazard ratios adjusted for age, sex, non-HDL cholesterol, HDL cholesterol, body mass index, systolic blood pressure, diastolic blood pressure, hypertension, diabetes mellitus, smoking, and C-reactive protein. The hazard ratio per unit increase of Lp-PLA2 activity was 1.03 [95% confidence interval (95% CI 1.01-1.05]; P for trend was 0.011. Hazard ratios for the second, third, and fourth quartiles were 1.06 (95% CI 0.55-2.04), 1.43 (95% CI 0.73-2.81), and 2.33 (95% CI 1.21-4.49), respectively, using the lowest quartile of Lp-PLA2 activity as the reference category. CONCLUSION: This study suggests that Lp-PLA2 activity is independently associated with incident heart failure.

1-Alkyl-2-acetylglycerophosphocholine Esterase↗

PubMed2006

High-dose testosterone is associated with atherosclerosis in postmenopausal women.

OBJECTIVES: To study the long-term effects of androgen treatment on atherosclerosis in postmenopausal women. METHODS: In a population-based study in 513 naturally postmenopausal women aged 54-67 years, we studied the association between self-reported intramuscularly administered high-dose estrogen-testosterone therapy (estradiol- and testosterone esters) and aortic atherosclerosis. Aortic atherosclerosis was diagnosed by radiographic detection of calcified deposits in the abdominal aorta, which have been shown to reflect intima atherosclerosis. Hormone therapy users were compared with never users. RESULTS: Intramuscular hormone therapy use for 1 year or longer was reported by 25 women. In almost half of these women severe atherosclerosis of the aorta was present (n=11), while in women without hormone use severe atherosclerosis of the aorta was present in less than 20% (OR 3.1; 95% CI, 1.1-8.5, adjusted for age, years since menopause, smoking, and body mass index). The association remained after additional adjustment for diabetes, cholesterol level, systolic blood pressure, or alcohol use. No association was found for hormone use less than 1 year. CONCLUSION: Our results suggest that high-dose testosterone therapy may adversely affect atherosclerosis in postmenopausal women and indicate that androgen replacement in these women may not be harmless.

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PubMed2006

Association between calcification in the coronary arteries, aortic arch and carotid arteries: the Rotterdam study.

OBJECTIVE: The present study was performed to examine the prevalence of and associations between calcification in the coronary arteries, aortic arch and carotid arteries, assessed by multislice computed tomography (MSCT), in an elderly population. METHODS AND RESULTS: This study was part of the population-based Rotterdam study. From October 2003 until July 2004, subjects underwent a 16-slice MSCT scan. Calcification was quantified by calculating the Agatston, volume and mass score. Current analyses were performed in 600 subjects (mean age 74 years). The prevalences of calcification in the coronary and carotid arteries were higher in men compared to women. However, aortic arch calcification was more prevalent among women. In men, correlation coefficients based on the Agatston score ranged from 0.40 (between coronary and aortic arch calcification) to 0.54 (between aortic arch and carotid calcification) (p<0.001). Correlation coefficients for women ranged from 0.30 (between coronary and aortic arch calcification) to 0.40 (between coronary and carotid calcification) (p<0.001). CONCLUSIONS: While the prevalences of calcification in the coronary and the carotid arteries were higher in men compared to women, aortic arch calcification was more prevalent among women. Moderate to strong correlations between calcification in different vessel beds were found.

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PubMed2006

Is diabetes mellitus a risk factor for open-angle glaucoma? The Rotterdam Study.

PURPOSE: To investigate whether diabetes mellitus is a risk factor for open-angle glaucoma (OAG). DESIGN: Prospective population-based cohort study. PARTICIPANTS: Participants ages > or =55 years from the Rotterdam Study, The Netherlands. METHODS: Participants at risk for incident OAG (iOAG) underwent at baseline (1990-1993) and follow-up (1997-1999) the same ophthalmic examination including intraocular pressure (IOP) measurement, visual field testing, and simultaneous stereo optic disc photography. At baseline, diabetes mellitus was defined as the use of antidiabetic medication and/or a random or postload glucose value > or =11.1 mmol/l. The diagnosis of OAG was made with an algorithm based on optic disc measures and visual fields, independent of the IOP. MAIN OUTCOME MEASURE: Incident OAG. RESULTS: In total, 3837 participants without OAG at baseline were reexamined. After a mean follow-up time of 6.5 years, iOAG developed in 87 persons. The relative risk of iOAG associated with baseline diabetes was 0.82 (0.33-2.05). After adjustment for age, gender, follow-up time, IOP, IOP-lowering treatment, body mass index, and systemic hypertension, the relative risk of iOAG was 0.65 (0.25-1.64). CONCLUSIONS: In this prospective population-based study, diabetes mellitus was not a risk factor for OAG.

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PubMed2006

Complement factor H polymorphism, complement activators, and risk of age-related macular degeneration.

CONTEXT: The evidence that inflammation is an important pathway in age-related macular degeneration (AMD) is growing. Recent case-control studies demonstrated an association between the complement factor H (CFH) gene, a regulator of complement, and AMD. OBJECTIVES: To assess the associations between the CFH gene and AMD in the general population and to investigate the modifying effect of smoking, serum inflammatory markers, and genetic variation of C-reactive protein (CRP). DESIGN, SETTING, AND PARTICIPANTS: Population-based, prospective cohort study of individuals aged 55 years or older (enrollment between March 20, 1990, and July 31, 1993, and 3 follow-up examinations that were performed between September 1, 1993, and December 31, 2004) in Rotterdam, the Netherlands. The CFH Y402H polymorphism was determined in a total of 5681 individuals. Information on smoking, erythrocyte sedimentation rate, CRP serum levels, and haplotypes of the CRP gene were assessed at baseline. MAIN OUTCOME MEASURES: All severity stages of prevalent and incident AMD, graded according to the international classification and grading system for AMD. RESULTS: The frequency of CFH Y402H was 36.2% (4116/11,362 alleles). At baseline, there were 2062 persons (36.3%) with any type of AMD (prevalent cases), including 78 (1.4%) with late AMD (stage 4). During follow-up (mean, 8 years; median, 10 years), 1649 (35.5%) of 4642 participants progressed to a higher stage of AMD (incident cases), including 93 (5.6%) who developed late AMD. The odds ratio (OR) of AMD increased in an allele-dose manner with 2.00 (95% confidence interval [CI], 1.56-2.55) for stage 2 AMD, 4.58 (95% CI, 2.82-7.44) for stage 3 AMD, and 11.02 (95% CI, 6.82-11.81) for stage 4 (late, vision threatening) AMD for homozygous persons. Cumulative risks calculated by Kaplan-Meier analysis of late AMD by age 95 years were 48.3% for homozygotes, 42.6% for heterozygotes, and 21.9% for noncarriers. The population-attributable risk for CFH Y402H was 54.0%. Elevated erythrocyte sedimentation rates further increased the OR to 20.2 (95% CI, 9.5-43.0), elevated serum CRP levels to 27.7 (95% CI, 10.7-72.0), and smoking to 34.0 (95% CI, 13.0-88.6) for homozygotes compared with noncarriers without these determinants. The CRP haplotypes conferring high levels of CRP significantly increased the effect of CFH Y402H (P<.01). CONCLUSIONS: The CFH Y402H polymorphism may account for a substantial proportion of AMD in individuals similar to those in the Rotterdam Study and may confer particular risk in the presence of environmental and genetic stimulators of the complement cascade.

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PubMed2006

The Generation R Study: Design and cohort profile.

The Generation R Study is a population-based prospective cohort study from fetal life until young adulthood. The study is designed to identify early environmental and genetic causes of normal and abnormal growth, development and health from fetal life until young adulthood. The study focuses on four primary areas of research: (1) growth and physical development; (2) behavioral and cognitive development; (3) diseases in childhood; and (4) health and healthcare for pregnant women and children. In total, 9778 mothers with a delivery date from April 2002 until January 2006 were enrolled in the study. Of all eligible children at birth, 61% participate in the study. Data collection in the prenatal phase included physical examinations, questionnaires, fetal ultrasound examinations and biological samples. In addition, more detailed assessments are conducted in a subgroup of 1232 pregnant women and their children. The children form a prenatally recruited birth-cohort that will be followed until young adulthood. Eventually, results forthcoming from the Generation R Study have to contribute to the development of strategies for optimizing health and healthcare for pregnant women and children.

Adolescent↗

PubMed2006

The influence of the alpha-adducin G460W polymorphism and angiotensinogen M235T polymorphism on antihypertensive medication and blood pressure.

Despite the availability of a variety of effective antihypertensive drugs, inadequate control of blood pressure is common in hypertensive patients. The aim of this study was investigate whether the alpha-adducin G460W polymorphism or angiotensinogen M235T polymorphism has an effect on the mean difference in blood pressure in subjects using antihypertensive drugs. Data from the Rotterdam Study, a population-based prospective cohort study in the Netherlands, was used. This study started in 1990 and included 7983 subjects of 55 years and older. Data from three examination rounds were used. Subjects were included when their blood pressure was elevated at 1 or more examinations and/or a diuretic, beta-blocker, calcium antagonist, or ACE inhibitor was used. A marginal generalized linear model was used to assess the drug-gene interaction. In total, 3025 hypertensives were included. No drug-gene interaction on blood pressure levels was found. The mean difference in systolic blood pressure (SBP) between subjects with the W-allele and GG genotype of the alpha-adducin gene was for diuretic users 1.25 mmHg (95% CI:-2.86 to 5.35), for beta-blockers 0.02 mmHg (95% CI:-3.39 to 3.42), for calcium antagonists -0.70 mmHg (95% CI:-5.61 to 4.21), and for ACE inhibitors -3.50 mmHg (95% CI:-9.02 to 2.02). The mean difference in SBP between subjects with the TT and MM genotype was for diuretic users -2.33 mmHg (95% CI:-8.32 to 3.66), for beta-blocker -0.06 mmHg (95% CI:-4.91 to 4.79), for calcium antagonist 0.59 mmHg (95% CI:-5.95 to 7.13), and for ACE inhibitor -2.33 mmHg (95% CI:-9.66 to 5.01). The G460W polymorphism and the M235T polymorphism did not modify the difference in blood pressure levels among subjects who used diuretics, beta-blockers, calcium antagonists, or ACE inhibitors.

Adrenergic beta-Antagonists↗

PubMed2006

Corticosteroids and the risk of atrial fibrillation.

BACKGROUND: High-dose (pulse) corticosteroid therapy has been associated with the development of atrial fibrillation. This association, however, is mainly based on case reports. METHODS: To test the hypothesis that high-dose corticosteroid exposure increases the risk of new-onset atrial fibrillation, we performed a nested case-control study within the Rotterdam Study, a population-based cohort study among 7983 older adults. Cases were defined as persons with incident atrial fibrillation between July 1, 1991, and January 1, 2000. Their date of diagnosis was defined as the index date. All noncases within the Rotterdam Study who were alive and eligible on this index date were used as controls. Subsequently, we compared the proportion of cases and controls that received a corticosteroid prescription within 1 month preceding the index date. Corticosteroid exposure was categorized into high-dose exposure (oral or parenteral steroid at a daily dose > or =7.5 mg of prednisone equivalents) and low-intermediate-dose exposure (<7.5 mg of prednisone equivalents or inhaled corticosteroids). RESULTS: There were 385 eligible cases of new-onset atrial fibrillation during the study period. The risk of new-onset atrial fibrillation was significantly higher for persons who received a corticosteroid prescription within 1 month before the index date than for those without (odds ratio [OR], 3.75; 95% confidence interval [CI], 2.38-5.87). However, only high-dose corticosteroid use was associated with an increased risk (OR, 6.07; 95% CI, 3.90-9.42), whereas low-intermediate-dose use was not (OR, 1.42; 95% CI, 0.72-2.82). The association of atrial fibrillation with high-dose corticosteroid use was largely independent of the indication for corticosteroid therapy, since the risk of new-onset atrial fibrillation was not only increased in patients with asthma or chronic obstructive pulmonary disease (OR, 4.02; 95% CI, 2.07-7.81) but also in patients with rheumatic, allergic, or malignant hematologic diseases (OR, 7.90; 95% CI, 4.47-13.98). CONCLUSION: Our findings strongly suggest that patients receiving high-dose corticosteroid therapy are at increased risk of developing atrial fibrillation.

Adrenal Cortex Hormones↗

PubMed2006

Lipoprotein-associated phospholipase A2 and coronary calcification. The Rotterdam Coronary Calcification Study.

OBJECTIVES: Although several studies have recently suggested that lipoprotein-associated phospholipase A2 (Lp-PLA2) is an independent predictor of coronary events, only one study has examined the association between Lp-PLA2 and coronary calcification, using young adults. We investigated the association between Lp-PLA2 activity and coronary calcification assessed by electron-beam computed tomography (EBT) in a population of older participants. METHODS AND RESULTS: The Rotterdam Coronary Calcification Study is a population-based study in men and women aged >/=55 years. Coronary calcification assessed by EBT was quantified in a calcium score according to Agatston's method. Lp-PLA2 activity measured in samples collected 7 years before scanning (n=520) was associated with coronary calcification in men after adjustment for age. The odds ratio per standard deviation of Lp-PLA2 activity of having a total calcium score >1000 was 1.6 (95% confidence interval: 1.1-2.4), as compared to a total calcium score </=100. After adjustment for non-HDL and HDL-cholesterol, this association disappeared. In women, the association was less consistent. For Lp-PLA2 measured concurrently to scanning (n=703), no association was found with coronary calcification. CONCLUSIONS: Lp-PLA2 activity is moderately associated with coronary calcification after adjustment for age. The effect of Lp-PLA2 on coronary calcification may be exerted through its effect on LDL-cholesterol.

1-Alkyl-2-acetylglycerophosphocholine Esterase↗

PubMed2006

Uric acid is a risk factor for myocardial infarction and stroke: the Rotterdam study.

BACKGROUND AND PURPOSE: The role of uric acid as a risk factor for myocardial infarction is controversial, and little is known about its role as a risk factor for stroke. Recent evidence suggests that uric acid may be an important causal agent in cardiovascular disease, for example, by inducing renal disease and hence hypertension. We investigated the association between serum uric acid and coronary heart disease and stroke in a large prospective population-based study. METHODS: The study was based on 4385 participants of the Rotterdam Study who, at baseline (1990 to 1993), were > or =55 years of age, free from stroke and coronary heart disease, and had blood taken. Follow-up for incident stroke and myocardial infarction was complete until January 1, 2002. Data were analyzed with Cox proportional hazards models with adjustment for relevant confounders. RESULTS: Average follow-up was 8.4 years. High serum uric acid levels were associated with risk of myocardial infarction and stroke; age- and sex-adjusted hazard ratios (95% CIs) for highest versus lowest quintile of uric acid were 1.68 (1.24 to 2.27) for cardiovascular disease (515 cases), 1.87 (1.12 to 3.13) for myocardial infarction (194 cases), 1.57 (1.11 to 2.22) for stroke (381 cases), 1.77 (1.10 to 2.83) for ischemic stroke (205 cases), and 1.68 (0.68 to 4.15) for hemorrhagic stroke (46 cases). Adjustment for other vascular risk factors only slightly attenuated these associations. Associations were stronger in persons without hypertension than in those with hypertension. CONCLUSIONS: Uric acid is a strong risk factor for myocardial infarction and stroke.

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PubMed2006

C-reactive protein gene haplotypes and risk of coronary heart disease: the Rotterdam Study.

AIMS: C-reactive protein is associated with risk of cardiovascular disease. However, whether C-reactive protein is a marker of severity of cardiovascular disease or actually is involved in its pathogenesis remains unknown. We investigated the relation between C-reactive protein haplotypes, representing the comprehensive variation of the C-reactive protein gene, and coronary heart disease. METHODS AND RESULTS: The Rotterdam Study is a prospective population-based study among men and women aged 55 years and older. C-reactive protein was associated with risk of coronary heart disease, with a multivariable adjusted hazard ratio of 1.9 (95% CI 1.5-2.4) for the highest vs. the lowest quartile. Four C-reactive protein haplotypes were present with overall frequencies of 32.8, 31.7, 29.5, and 5.9%. C-reactive protein serum levels were significantly different according to C-reactive protein haplotypes. C-reactive protein haplotypes were not associated with coronary heart disease. CONCLUSION: Steady-state C-reactive protein serum level is influenced by C-reactive protein gene haplotypes. Although elevated C-reactive protein level has lately been found to be a consistent and relatively strong risk factor for cardiovascular disease, our study does not support that the common variation in the C-reactive protein gene has a large effect on the occurrence of coronary heart disease.

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PubMed2006

A common polymorphism in the complement factor H gene is associated with increased risk of myocardial infarction: the Rotterdam Study.

OBJECTIVES: This study was designed to investigate the association between a common polymorphism (Tyr402His, rs1061170) in the complement factor H (CFH) gene and risk of coronary heart disease. BACKGROUND: The evidence that inflammation is an important mechanism in atherogenesis is growing. C-reactive protein (CRP), complement factors, and complement regulatory factors have all been linked to coronary heart disease. The CFH gene is an important regulator of the alternative complement cascade. We investigated its association with coronary heart disease. METHODS: The study was embedded in the Rotterdam Study, a prospective population-based study among men and women aged 55 years and over. A total of 5,520 participants without history of coronary heart disease was genotyped for the Tyr402His polymorphism of the CFH gene. Cox proportional hazards analysis was used to determine risk of myocardial infarction for Tyr402His genotypes. RESULTS: Mean age among participants was 69.5 years (SD 9.1 years). The overall frequency of the His allele was 36%; genotype frequencies were 41%, 45%, and 14% for TyrTyr, TyrHis, and HisHis, respectively. During a mean follow-up period of 8.4 years, 226 myocardial infarctions occurred. After adjustment for age, gender, established cardiovascular risk factors, and CRP level, HisHis homozygotes had a hazard ratio of 1.77 (95% confidence interval 1.23 to 2.55) for myocardial infarction. Total cholesterol level, diabetes mellitus, and smoking modified the effect. The Tyr402His polymorphism was not associated with established cardiovascular risk factors or CRP level. CONCLUSIONS: Our data suggest that the CFH gene determines susceptibility to myocardial infarction. This finding underscores the importance of the alternative complement system in cardiovascular disease.

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PubMed2006

An insulin-like growth factor-I promoter polymorphism is associated with increased mortality in subjects with myocardial infarction in an elderly Caucasian population.

We investigated whether an insulin-like growth factor I (IGF-I) promoter polymorphism is associated with excess mortality in elderly subjects with myocardial infarction (MI). This association was assessed in 7,983 subjects of the Rotterdam Study during 14 years of follow-up. Among 345 subjects who developed a MI, the risk of mortality was 1.49 times higher in the variant carriers of the IGF-I promoter polymorphism than in the nonvariant carriers (95% confidence interval 1.10 to 2.10, p = 0.02). The risk of death increased with the number of variant alleles. Our study suggests that genetically determined low IGF-I activity is an important determinant of mortality in subjects with MI.

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PubMed2006

Prevalence, incidence and lifetime risk of atrial fibrillation: the Rotterdam study.

AIMS: We aimed to investigate the prevalence and incidence of atrial fibrillation (AF) in a large European population-based study. METHODS AND RESULTS: The study is part of the Rotterdam study, a population-based prospective cohort study among subjects aged 55 years and above. The prevalence at baseline was assessed in 6808 participants. Incidence of AF was investigated during a mean follow-up period of 6.9 years in 6432 persons. We identified 376 prevalent and 437 incident cases. Overall prevalence was 5.5%, rising from 0.7% in the age group 55-59 years to 17.8% in those aged 85 years and above. The overall incidence rate was 9.9/1000 person-years. The incidence rate in the age group 55-59 years was 1.1/1000 person-years, rose to 20.7/1000 person-years in the age group 80-84 years and stabilized in those aged 85 years and above. Prevalence and incidence were higher in men than in women. The lifetime risk to develop AF at the age of 55 years was 23.8% in men and 22.2% in women. CONCLUSION: In this prospective study in a European population, the prevalence and incidence of AF increased with age and were higher in men than in women. The high lifetime risk to develop AF was similar to North American epidemiological data.

Age Distribution↗

PubMed2006

Incidence of recognized and unrecognized myocardial infarction in men and women aged 55 and older: the Rotterdam Study.

AIMS: Contemporary data on the incidence of unrecognized myocardial infarction (MI) among subjects aged 55 and older are limited. METHODS AND RESULTS: We studied the incidence of recognized and unrecognized MI in the Rotterdam Study, a population-based cohort of men and women aged 55 and older. The baseline examination was performed during 1990-93, with follow-up examinations during 1994-95, and 1997-2000. Baseline and follow-up 12-lead ECGs were analysed by the Modular ECG Analysis System. The 5148 participants who had no evidence of prevalent infarction were the subjects for analysis. Incident recognized infarction was defined as the occurrence of a fatal or non-fatal event coded as I21 according to the International Classification of Diseases, 10th edition. A repeat ECG was available in 4187 subjects. An unrecognized infarction was considered to have occurred if there was electrocardiographic evidence in the absence of a clinically recognized event. During a median follow-up of 6.4 years, 141 incident recognized infarctions occurred and the incidence rate of this event was 5.0 per 1000 person years. The incidence was higher in men (8.4) than in women (3.1). The incidence rate of unrecognized infarction was 3.8 per 1000 person years. Men (4.2) and women (3.6) had approximately similar incidence. Hence, the proportion of unrecognized infarction was lower in men (33%) than in women (54%). This difference in proportion of unrecognized infarctions was independent of age. CONCLUSION: A high proportion of incident MIs remains clinically unrecognized. As a history of MI is associated with an increased risk of repeat cardiovascular complications, our data suggest a need for periodical electrocardiographic screening to recognize (prevalent) infarctions and to install effective preventive treatment in those aged 55 and older.

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