Do malpractice claim clinical case vignettes enhance diagnostic accuracy and acceptance in clinical reasoning education during GP training?

BACKGROUND: Using malpractice claims cases as vignettes is a promising approach for improving clinical reasoning education (CRE), as malpractice claims can provide a variety of content- and context-rich examples. However, the effect on learning of adding information about a malpractice claim, which may evoke a deeper emotional response, is not yet clear. This study examined whether knowing that a diagnostic error resulted in a malpractice claim affects diagnostic accuracy and self-reported confidence in the diagnosis of future cases. Moreover, suitability of using erroneous cases with and without a malpractice claim for CRE, as judged by participants, was evaluated. METHODS: In the first session of this two-phased, within-subjects experiment, 81 first-year residents of general practice (GP) were exposed to both erroneous cases with (M) and erroneous cases without (NM) malpractice claim information, derived from a malpractice claims database. Participants rated suitability of the cases for CRE on a five-point Likert scale. In the second session, one week later, participants solved four different cases with the same diagnoses. Diagnostic accuracy was measured with three questions, scored on a 0-1 scale: (1) What is your next step? (2) What is your differential diagnosis? (3) What is your most probable diagnosis and what is your level of certainty on this? Both subjective suitability and diagnostic accuracy scores were compared between the versions (M and NM) using repeated measures ANOVA. RESULTS: There were no differences in diagnostic accuracy parameters (M vs. NM next step: 0.79 vs. 0.77, p = 0.505; differential diagnosis 0.68 vs. 0.75, p = 0.072; most probable diagnosis 0.52 vs. 0.57, p = 0.216) and self-reported confidence (53.7% vs. 55.8% p = 0.390) of diagnoses previously seen with or without malpractice claim information. Subjective suitability- and complexity scores for the two versions were similar (suitability: 3.68 vs. 3.84, p = 0.568; complexity 3.71 vs. 3.88, p = 0.218) and significantly increased for higher education levels for both versions. CONCLUSION: The similar diagnostic accuracy rates between cases studied with or without malpractice claim information suggests both versions are equally effective for CRE in GP training. Residents judged both case versions to be similarly suitable for CRE; both were considered more suitable for advanced than for novice learners.

[Musculoskeletal injections during the GP residency; deliberations of GP residents on the administration of musculoskeletal injections]. / Musculoskeletale injecties in de huisartsopleiding.

OBJECTIVE: Musculoskeletal injections can alleviate pain in certain problems of the musculoskeletal system. A significant part of general practitioners (GPs) does not feel competent to administer these injections while it is also known that medical residents of several specialties lack confidence in surgical and other technical skills. However, it is not known whether GP residents feel competent in these skills at the end of their residency and which factors are associated with this self-assessed competence. METHOD: To find out how GP residents think about musculoskeletal injections, twenty Dutch GP residents were interviewed in their final year using semi-structured interview techniques. These interviews were analyzed using template analysis. RESULTS: GP residents often experience a certain reluctance in the administration of musculoskeletal injections even though they mostly find that these injections do belong in primary care. The most named barriers are a low self-assessed competence and fear of septic arthritis, while other factors relate to the resident (confidence, coping style, and views on the specialty), the supervisor (their attitude), the patient (their situation and preferences), the injection (feasibility and estimated effectiveness) and the practice organization (office hours). CONCLUSION: GP residents consider many factors in their decision to administer musculoskeletal injections, most importantly their own competence and a fear of complications. Medical departments can help their residents through education on the decision-making process and the risks of certain interventions and provide opportunities to improve specific technical skills.

Thirty-Minute Office Blood Pressure Monitoring in Primary Care.

PURPOSE: Automated office blood pressure monitoring during 30 minutes (OBP30) may reduce overtreatment of patients with white-coat hypertension in primary health care. OBP30 results approximate those of ambulatory blood pressure monitoring, but OBP30 is much more convenient. In this study, we compared OBP30 with routine office blood pressure (OBP) readings for different indications in primary care and evaluated how OBP30 influenced the medication prescribing of family physicians. METHODS: All consecutive patients who underwent OBP30 for medical reasons over a 6-month period in a single primary health care center in the Netherlands were enrolled. We compared patients' OBP30 results with their last preceding routine OBP reading, and we asked their physicians why they ordered OBP30, how they treated their patients, and how they would have treated their patients without it. RESULTS: We enrolled 201 patients (mean age 68.6 years, 56.7% women). The mean systolic OBP30 was 22.8 mm Hg lower than the mean systolic OBP (95% CI, 19.8-26.1 mm Hg). The mean diastolic OBP30 was 11.6 mm Hg lower than the mean diastolic OBP (95% CI, 10.2-13.1 mm Hg). Considerable differences between OBP and OBP30 existed in patients with and without suspected white-coat hypertension, and differences were larger in individuals aged 70 years or older. Based on OBP alone, physicians said they would have started or intensified medication therapy in 79.1% of the studied cases (95% CI, 73.6%-84.6%). In fact, with the results of OBP30 available, physicians started or intensified medication therapy in 24.9% of cases (95% CI, 18.9%-30.9%). CONCLUSIONS: OBP30 yields considerably lower blood pressure readings than OBP in all studied patient groups. OBP30 is a promising technique to reduce overtreatment of white-coat hypertension in primary health care.

Anxiety and the Risk of Stroke: The Rotterdam Study.

BACKGROUND AND PURPOSE: It is unclear whether anxiety is a risk factor for stroke. We assessed the association between anxiety and the risk of incident stroke. METHODS: This population-based cohort study was based on 2 rounds of the Rotterdam Study. Each round was taken separately as baseline. In 1993 to 1995, anxiety symptoms were measured using the Hospital Anxiety and Depression Scale-Anxiety (HADS-A). In 2002 to 2004, anxiety disorders were assessed using the Munich version of the Composite International Diagnostic Interview. Participants were followed up for incident stroke until January 2012. RESULTS: In the sample undergoing HADS-A (N=2625; mean age at baseline, 68.4 years), 332 strokes occurred during 32 720 years of follow-up. HADS-A score was not associated with the risk of stroke during complete follow-up (adjusted hazard ratio, 1.02; 95% confidence interval, 0.74-1.43; for HADS-A≥8 compared with HADS-A <8), although we did find an increased risk after a shorter follow-up of 3 years (adjusted hazard ratio, 2.68; 95% confidence interval, 1.33-5.41). In the sample undergoing the Munich version of the Composite International Diagnostic Interview (N=8662; mean age at baseline, 66.1 years), 340 strokes occurred during 48 703 years of follow-up. Participants with any anxiety disorder had no higher risk of stroke than participants without anxiety disorder (adjusted hazard ratio, 0.95; 95% confidence interval, 0.64-1.43). We also did not observe an increased risk of stroke for the different subtypes of anxiety. CONCLUSIONS: Anxiety disorders were not associated with stroke in our general population study. Anxiety symptoms were only related to stroke in the short term, which needs further exploration.

Role of Prestroke Vascular Pathology in Long-Term Prognosis After Stroke: The Rotterdam Study.

BACKGROUND AND PURPOSE: Mortality after stroke remains high for years, mostly because of cardiovascular causes. Given that cardiovascular pathology plays an important role in causing the initial stroke, such prestroke pathology might also influence the prognosis after stroke. Within the population-based Rotterdam Study, we examined the proportion of deaths after stroke that are attributable to pre-existent cardiovascular risk factors before stroke (the population attributable risk). METHODS: We examined 1237 patients with first-ever stroke and 4928 stroke-free participants (between 1990 and 2012), matched on age, sex, examination round, and stroke date (index date). Cardiovascular risk factors measured on ≈4 years before index date were used as determinants. Participants were continuously followed up for mortality (≈6 years) after the index date. We calculated separate and combined population attributable risk of hypertension, total cholesterol, high-density lipoprotein-cholesterol, body mass index, diabetes mellitus, smoking, transient ischemic attack, and atrial fibrillation. RESULTS: Nine hundred and nineteen patients with stroke and 2654 stroke-free participants died. The combined population attributable risk in patients with stroke was 27% (95% confidence interval, 14%-45%) and in stroke-free participants was 19% (95% confidence interval, 12%-29%). Population attributable risks of diabetes mellitus, smoking, and atrial fibrillation were higher in patients with stroke than in the reference group because of a higher prevalence of risk factors. In addition, people with atrial fibrillation and stroke had a higher hazard ratio for death than those with only atrial fibrillation. CONCLUSIONS: One quarter of deaths after stroke could theoretically be prevented with rigorous cardiovascular prevention and treatment, but this should preferably start before stroke occurrence. In addition, research into factors explaining the remaining deaths needs to be encouraged.

The potential for prevention of dementia across two decades: the prospective, population-based Rotterdam Study.

BACKGROUND: Cardiovascular factors and low education are important risk factors of dementia. We provide contemporary estimates of the proportion of dementia cases that could be prevented if modifiable risk factors were eliminated, i.e., population attributable risk (PAR). Furthermore, we studied whether the PAR has changed across the last two decades. METHODS: We included 7,003 participants of the original cohort (starting in 1990) and 2,953 participants of the extended cohort (starting in 2000) of the Rotterdam Study. Both cohorts were followed for dementia until ten years after baseline. We calculated the PAR of overweight, hypertension, diabetes mellitus, cholesterol, smoking, and education. Additionally, we assessed the PAR of stroke, coronary heart disease, heart failure, and atrial fibrillation. We calculated the PAR for each risk factor separately and the combined PAR taking into account the interaction of risk factors. RESULTS: During 57,996 person-years, 624 participants of the original cohort developed dementia, and during 26,177 person-years, 145 participants of the extended cohort developed dementia. The combined PAR in the original cohort was 0.23 (95 % CI, 0.05-0.62). The PAR in the extended cohort was slightly higher at 0.30 (95 % CI, 0.06-0.76). The combined PAR including cardiovascular diseases was 0.25 (95 % CI, 0.07-0.62) in the original cohort and 0.33 (95 % CI, 0.07-0.77) in the extended cohort. CONCLUSIONS: A substantial part of dementia cases could be prevented if modifiable risk factors would be eliminated. Although prevention and treatment options of cardiovascular risk factors and diseases have improved, the preventive potential for dementia has not declined over the last two decades.

Subclinical cardiac dysfunction increases the risk of stroke and dementia: the Rotterdam Study.

OBJECTIVE: To investigate the association between cardiac function and the risk of stroke and dementia in elderly free of clinical cardiac disease. Additionally, we investigated the relation between cardiac function and MRI markers of subclinical cerebrovascular disease. METHODS: This study was conducted within the population-based Rotterdam Study. A total of 3,291 participants (60.8% female, age-range 58-98 years) free of coronary heart disease, heart failure, atrial fibrillation, stroke, and dementia underwent echocardiography in 2002-2005 to measure cardiac function. Follow-up finished in 2012. In 2005-2006, a random subset of 577 stroke-free people without dementia underwent brain MRI on which infarcts and white matter lesion volume were assessed. RESULTS: During 21,785 person-years of follow-up, 164 people had a stroke and during 19,462 person-years of follow-up, 208 people developed dementia. Measures of better diastolic function, such as higher E/A ratio, were associated with a lower risk of stroke (hazard ratio [HR] 0.82; 95% confidence interval [CI] 0.69; 0.98) and dementia (HR 0.82; 95% CI 0.70; 0.96). Better systolic function, measured as higher fractional shortening, was only associated with a lower risk of stroke (HR 0.84; 95% CI 0.72; 0.98). Better diastolic function was related to a lower prevalence of silent infarcts on MRI, especially lacunar infarcts. CONCLUSIONS: In elderly free of clinical cardiac disease, worse diastolic function is associated with clinical stroke, dementia, and silent infarcts on MRI, whereas worse systolic function is related only to clinical stroke. These findings can form the basis for future research on the utility of cardiac function as potential intervention target for prevention of neurologic diseases.

Subjective memory complaints and the risk of stroke.

BACKGROUND AND PURPOSE: Persons with cognitive impairment, as assessed by cognitive tests, are at a higher risk of stroke. Subjective memory complaints might be an earlier marker for stroke, especially in persons with higher education. Their cognitive reserve might mask their cognitive impairment during cognitive testing. In a population-based setting, we investigated the association between subjective memory complaints and stroke. We simultaneously investigated the association between Mini-Mental State Examination and stroke. We also assessed whether these associations varied with educational level. METHODS: 9152 participants from the Rotterdam Study (baseline 1990-1993 or 2000-2001) completed the subjective memory complaints questionnaire and underwent Mini-Mental State Examination assessment. Subsequently, the entire cohort was followed for incident stroke until 2012. We used Cox proportional hazard models to estimate the associations between subjective memory complaints and Mini-Mental State Examination, with stroke. RESULTS: During a follow-up of 111 593 person years, 1134 strokes were identified, of which 663 were ischemic and 99 hemorrhagic. In the fully adjusted model, presence of subjective memory complaints was independently associated with a higher risk of stroke (hazard ratio, 1.20; 95% confidence interval, 1.04-1.39), but a higher Mini-Mental State Examination was not (hazard ratio per point increase, 0.99; 95% confidence interval, 0.95-1.02). The association between subjective memory complaints and risk of stroke was modified by educational level, with a higher risk of stroke in persons with a higher level of education (hazard ratio, 1.39; 95% confidence interval, 1.07-1.81). CONCLUSIONS: Subjective memory complaints might be an early indicator of stroke risk, especially in highly educated individuals.

Modifiable etiological factors and the burden of stroke from the Rotterdam study: a population-based cohort study.

BACKGROUND: Stroke prevention requires effective treatment of its causes. Many etiological factors for stroke have been identified, but the potential gain of effective intervention on these factors in terms of numbers of actually prevented strokes remains unclear because of the lack of data from cohort studies. We assessed the impact of currently known potentially modifiable etiological factors on the occurrence of stroke. METHODS AND FINDINGS: This population-based cohort study was based on 6,844 participants of the Rotterdam Study who were aged ≥55 y and free from stroke at baseline (1990-1993). We computed population attributable risks (PARs) for individual risk factors and for risk factors in combination to estimate the proportion of strokes that could theoretically be prevented by the elimination of etiological factors from the population. The mean age at baseline was 69.4 y (standard deviation 6.3 y). During follow-up (mean follow-up 12.9 y, standard deviation 6.3 y), 1,020 strokes occurred. The age- and sex-adjusted combined PAR of prehypertension/hypertension, smoking, diabetes mellitus, atrial fibrillation, coronary disease, and overweight/obesity was 0.51 (95% CI 0.41-0.62) for any stroke; hypertension and smoking were the most important etiological factors. C-reactive protein, fruit and vegetable consumption, and carotid intima-media thickness in combination raised the total PAR by 0.06. The PAR was 0.55 (95% CI 0.41-0.68) for ischemic stroke and 0.70 (95% CI 0.45-0.87) for hemorrhagic stroke. The main limitations of our study are that our study population comprises almost exclusively Caucasians who live in a middle and high income area, and that risk factor awareness is higher in a study cohort than in the general population. CONCLUSIONS: About half of all strokes are attributable to established causal and modifiable factors. This finding encourages not only intervention on established etiological factors, but also further study of less well established factors. Please see later in the article for the Editors' Summary.

Intracranial carotid artery atherosclerosis and the risk of stroke in whites: the Rotterdam Study.

IMPORTANCE: Intracranial atherosclerosis represents a relatively unexplored, but potentially important, cause of stroke in a white population. OBJECTIVE: To investigate the relationship between intracranial carotid artery calcification (ICAC) as a marker of intracranial atherosclerosis and the risk of stroke in whites. DESIGN, SETTING, AND PARTICIPANTS: A population-based cohort study in the general community with 6 years of follow-up was conducted (the Rotterdam Study). Between 2003 and 2006, a random sample of 2323 stroke-free persons (mean age, 69.5 years) underwent computed tomography scanning to quantify ICAC volume. All participants were continuously monitored for the occurrence of stroke until January 1, 2012. EXPOSURE: Atherosclerotic calcification in the intracranial internal carotid arteries. MAIN OUTCOME AND MEASURE: Incident stroke. RESULTS: During 14,055 person-years of follow-up, 91 participants had a stroke, of which 74 were ischemic. Larger ICAC volume was related to a higher risk of stroke, independent of cardiovascular risk factors, ultrasound carotid plaque score, and calcification in other vessels (fully adjusted hazard ratio per an increase of 1 SD in ICAC volume, 1.43 [95% CI, 1.04-1.96]). Intracranial carotid artery calcification contributed to 75% of all strokes; for aortic arch and extracranial carotid artery calcification this incidence was only 45% and 25%, respectively. CONCLUSIONS AND RELEVANCE: Our findings establish intracranial atherosclerosis as a major risk factor for stroke in the general white population and suggest that its contribution to the proportion of all strokes may be greater than that of large-artery atherosclerosis in more proximally located vessel beds.

Genomewide association studies of stroke.

BACKGROUND: The genes underlying the risk of stroke in the general population remain undetermined. METHODS: We carried out an analysis of genomewide association data generated from four large cohorts composing the Cohorts for Heart and Aging Research in Genomic Epidemiology consortium, including 19,602 white persons (mean [+/-SD] age, 63+/-8 years) in whom 1544 incident strokes (1164 ischemic strokes) developed over an average follow-up of 11 years. We tested the markers most strongly associated with stroke in a replication cohort of 2430 black persons with 215 incident strokes (191 ischemic strokes), another cohort of 574 black persons with 85 incident strokes (68 ischemic strokes), and 652 Dutch persons with ischemic stroke and 3613 unaffected persons. RESULTS: Two intergenic single-nucleotide polymorphisms on chromosome 12p13 and within 11 kb of the gene NINJ2 were associated with stroke (P<5x10(-8)). NINJ2 encodes an adhesion molecule expressed in glia and shows increased expression after nerve injury. Direct genotyping showed that rs12425791 was associated with an increased risk of total (i.e., all types) and ischemic stroke, with hazard ratios of 1.30 (95% confidence interval [CI], 1.19 to 1.42) and 1.33 (95% CI, 1.21 to 1.47), respectively, yielding population attributable risks of 11% and 12% in the discovery cohorts. Corresponding hazard ratios were 1.35 (95% CI, 1.01 to 1.79; P=0.04) and 1.42 (95% CI, 1.06 to 1.91; P=0.02) in the large cohort of black persons and 1.17 (95% CI, 1.01 to 1.37; P=0.03) and 1.19 (95% CI, 1.01 to 1.41; P=0.04) in the Dutch sample; the results of an underpowered analysis of the smaller black cohort were nonsignificant. CONCLUSIONS: A genetic locus on chromosome 12p13 is associated with an increased risk of stroke.

Variation in fibrinogen FGG and FGA genes and risk of stroke: the Rotterdam Study.

Haplotypes of the fibrinogen gamma and alpha (FGG and FGA) genes are associated with the structure of the fibrin network and may therefore influence the risk of stroke. We investigated the relationship between common variation in these genes with ischemic and haemorrhagic stroke. The study was based on 6,275 participants of the prospective population-based Rotterdam Study who at baseline (1990-1993) were aged 55 years or over, free from stroke, and had successful assessment of at least one FGG or FGA single nucleotide polymorphisms (SNP). Common haplotypes were estimated using seven tagging SNPs across a 30 kb region containing the FGG and FGA genes. Follow-up for incident stroke was complete until January 1, 2005. Associations between constructed haplotypes and risk of stroke were estimated with an age- and sex-adjusted logistic regression model. We observed 668 strokes, of which 393 were ischemic and 62 haemorrhagic, during a median follow-up time of 10.1 years. FGG + FGA haplotype 3 (H3) was associated with an increased risk of ischemic stroke (odds ratio [OR] 1.36, 95% confidence interval [CI] 1.09-1.69) and the risk estimate for hemorrhagic stroke was 0.71 (95% CI 0.46-1.09) compared to the most frequent H1. The FGG and FGA genes were not associated with stroke or its subtypes when analyzed separately. In conclusion, risk of ischemic stroke was higher in FGG + FGA H3 than in H1. The results suggested that an opposite association may exist for haemorrhagic stroke.

Cyclooxygenase selectivity of nonsteroidal anti-inflammatory drugs and risk of stroke.

BACKGROUND: In clinical trials, cyclooxygenase (COX)-2-selective nonsteroidal anti-inflammatory drugs (NSAIDs) were associated with an increased risk of thromboembolic events. We studied the association between NSAID use and risk of stroke in the prospective, population-based Rotterdam Study. METHODS: We followed 7636 persons free of stroke at baseline (1991-1993) for incident stroke until September 2004. Data on all filled prescriptions came from pharmacy records. With Cox regression models, we calculated crude and adjusted hazard ratios (HRs) of stroke for time-dependent current use, compared with never use, of NSAIDs grouped according to COX selectivity (COX-1 selective, nonselective, and COX-2 selective) and individual NSAIDs. RESULTS: At baseline, the mean age of the study sample was 70.2 years, and 61.3% were female. During 70 063 person-years of follow-up (mean, 9.2 years), 807 persons developed a stroke (460 ischemic, 74 hemorrhagic, and 273 unspecified). Current users of nonselective (HR, 1.72; 95% confidence interval [CI], 1.22-2.44) and COX-2-selective (HR, 2.75; 95% CI, 1.28-5.95) NSAIDs had a greater risk of stroke, but not users of COX-1-selective NSAIDs (HR, 1.10; 95% CI, 0.41-2.97). Hazard ratios (95% CIs) for ischemic stroke were 1.68 (1.05-2.69) for nonselective and 4.54 (2.06-9.98) for COX-2-selective NSAIDs. For individual NSAIDs, current use of the nonselective naproxen (HR, 2.63; 95% CI, 1.47-4.72) and the COX-2-selective rofecoxib (HR, 3.38; 95% CI, 1.48-7.74) was associated with a greater risk of stroke. Hazard ratios (95% CIs) for diclofenac (1.60 [1.00-2.57]), ibuprofen (1.47 [0.73-3.00]), and celecoxib (3.79 [0.52-27.6]) were greater than 1.00 but were not statistically significant. CONCLUSIONS: In the general population, we found a greater risk of stroke with current use of nonselective and COX-2-selective NSAIDs. The risk of stroke was not limited to the use of COX-2-selective NSAIDs.

Variation in the estrogen receptor alpha gene and risk of stroke: the Rotterdam Study.

BACKGROUND AND PURPOSE: Variations in the -397T>C (rs2234693) and -351A>G (rs9340799) single nucleotide polymorphisms of the estrogen alpha receptor (ESR1) gene were found to be strongly associated with risk of ischemic heart disease, although not all studies could replicate this finding. One study also reported an association with stroke. We assessed whether variations in the ESR1 gene are associated with the risk of stroke in the general population. METHODS: This prospective population-based study was based on 6229 Rotterdam Study participants who at baseline (1990-1993) were aged 55 years or older, free from stroke, and had assessment of the ESR1 rs2234693 and rs9340799 single nucleotide polymorphisms. Follow-up for incident stroke was complete until January 1, 2005. Data were analyzed with Cox proportional hazards models for men and women separately with adjustment for age. RESULTS: During an average follow-up time of 10.1 years, 659 strokes occurred, of which 386 were ischemic. Three common haplotypes were identified: -397T/-351A (carried by 78% of all participants), -397C/-351G (carried by 57%), and -397C/-351A (carried by 22%). Although we had at least 89% power to detect a relative risk of 1.5 (alpha=0.05) in all subgroups, we did not find any association between ESR1 haplotype carriership and risk of stroke and ischemic stroke. CONCLUSIONS: We have not been able to replicate the previously reported association between variations in the ESR1 gene and risk of stroke.

Prestroke cognitive performance, incident stroke, and risk of dementia: the Rotterdam Study.

BACKGROUND AND PURPOSE: Several studies indicate that stroke increases the risk of dementia. Most of these studies lacked the ability to take accurately assessed prestroke cognitive function into account. Whether the effects of stroke merely unravel an ongoing underlying dementing process or in fact cause the dementia has implications for the prevention of dementia in persons with cerebrovascular disease. We explored in a prospective cohort study whether stroke occurrence was related to a higher risk of subsequent dementia and whether this association was dependent on prestroke slope of cognitive function. METHODS: Cox proportional hazard models were used to relate incident stroke as a time-varying exposure with the risk of dementia in 6724 participants of the Rotterdam Study without dementia or stroke at baseline (49,361 person years of follow-up). Subsequently Cox proportional hazard models were performed to assess whether this association was dependent on slope of prestroke cognitive performance and other risk factors for cognitive decline. RESULTS: Independent of both level and the rate of change of prestroke cognitive performance and other risk factors for cognitive decline, incident stroke was associated with a more than doubled risk of subsequent dementia (hazard ratio, 2.1; 95% CI, 1.55 to 2.81). CONCLUSIONS: Prestroke cognitive function is not a major determinant of the effect of stroke on the risk of poststroke dementia.

Incidence and prognosis of transient neurological attacks.

CONTEXT: Transient neurological attacks (TNAs) are attacks with temporary (<24 hours) neurological symptoms. These symptoms can be focal, nonfocal, or a mixture of both. The prognostic significance of TNAs with focal symptoms (better known as transient ischemic attacks [TIAs]) is well understood. Conversely, hardly anything is known about the prognostic significance of TNAs with nonfocal or mixed symptoms. OBJECTIVE: To study the incidence and prognosis of focal TNAs (or TIAs), nonfocal TNAs, and mixed TNAs. DESIGN, SETTING, AND PARTICIPANTS: The study population comprised 6062 community-dwelling Rotterdam Study participants who were aged 55 years or older and free from stroke, myocardial infarction, and dementia at baseline (1990-1993). They were followed up for events until January 1, 2005. We analyzed the associations between incident TNAs and subsequent adverse events with age- and sex-adjusted Cox regression models. MAIN OUTCOME MEASURES: Stroke, ischemic heart disease, or dementia. RESULTS: During 60 535 person-years, 548 participants developed TNA (282 focal, 228 nonfocal, and 38 mixed). The incidence rate per 1000 person-years was 4.7 (95% confidence interval [CI], 4.1-5.2) for focal TNA, 3.8 (95% CI, 3.3-4.3) for nonfocal TNA, and 0.6 (95% CI, 0.4-0.9) for mixed TNA. Participants with focal TNA were at higher risk of subsequent stroke than participants without TNA (n = 46 vs 540; hazard ratio [HR], 2.14; 95% confidence interval [CI]; 1.57-2.91) but had an equal risk of ischemic heart disease and dementia. Nonfocal TNA patients were at higher risk of stroke (27 vs 540; HR, 1.56; 95% CI, 1.08-2.28) and dementia (30 vs 552; HR, 1.59; 95% CI, 1.11-2.26) than participants without TNA. Mixed TNA patients were at higher risk of stroke (6 vs 540; HR, 2.48; 95% CI, 1.11-5.56), ischemic heart disease (8 vs 779; HR, 2.26; 95% CI, 1.07-4.78), vascular death (8 vs 594; HR, 2.54; 95% CI, 1.31-4.91), and dementia (7 vs 552; HR, 3.46; 95% CI, 1.72-6.98) than participants without TNA. CONCLUSION: Patients who experience nonfocal TNAs, and especially those with mixed TNAs, have a higher risk of major vascular diseases and dementia than persons without TNA.

Decreased glomerular filtration rate is a risk factor for hemorrhagic but not for ischemic stroke: the Rotterdam Study.

BACKGROUND AND PURPOSE: Persons with early stages of chronic kidney disease, defined by a decreased glomerular filtration rate (GFR), have an increased risk of cardiovascular disease. It is unclear whether decreased GFR is a risk factor for stroke. We assessed the association between GFR and stroke in a prospective population-based cohort study. METHODS: The study was based on 4937 participants of the Rotterdam Study who at baseline (1990 to 1993) were aged 55 years or over, free from stroke, and had serum creatinine assessment. GFR was estimated with the Cockcroft-Gault equation. Follow-up for incident cerebrovascular disease was complete until January 1, 2005. Data were analyzed with Cox proportional hazards models with adjustment for relevant confounders and results were expressed as hazard ratios with 95% CIs. RESULTS: During an average follow-up of 10.2 years, 586 strokes (338 ischemic, 44 hemorrhagic, and 204 unspecified strokes) occurred. We found no association between GFR and risk of overall stroke or risk of ischemic stroke. In contrast, with decreasing GFR, the risk of hemorrhagic stroke strongly increased; the age- and sex-adjusted hazard ratio for hemorrhagic stroke was 4.10 (95% CI, 1.25 to 13.42) for lowest versus highest quartile of GFR, and there was a clear and highly significant dose-effect relationship. Adjustment for other vascular risk factors only slightly attenuated this association. CONCLUSIONS: Decreased GFR is a strong risk factor for hemorrhagic, but not ischemic stroke.