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J Lodder

Publications and source records attributed to J Lodder.

At least 19 recordsLinked to original sources
PubMed1999

Primary prevention of arterial thromboembolism in non-rheumatic atrial fibrillation in primary care: randomised controlled trial comparing two intensities of coumarin with aspirin.

OBJECTIVE: To investigate the effectiveness of aspirin and coumarin in preventing thromboembolism in patients with non-rheumatic atrial fibrillation in general practice. DESIGN: Randomised controlled trial. PARTICIPANTS: 729 patients aged >/=60 years with atrial fibrillation, recruited in general practice, who had no established indication for coumarin. Mean age was 75 years and mean follow up 2. 7 years. SETTING: Primary care in the Netherlands. INTERVENTIONS: Patients eligible for standard intensity coumarin (international normalised ratio 2.5-3.5) were randomly assigned to standard anticoagulation, very low intensity coumarin (international normalised ratio 1.1-1.6), or aspirin (150 mg/day) (stratum 1). Patients ineligible for standard anticoagulation were randomly assigned to low anticoagulation or aspirin (stratum 2). MAIN OUTCOME MEASURES: Stroke, systemic embolism, major haemorrhage, and vascular death. RESULTS: 108 primary events occurred (annual event rate 5.5%), including 13 major haemorrhages (0.7% a year). The hazard ratio was 0.91 (0.61 to 1.36) for low anticoagulation versus aspirin and 0.78 (0.34 to 1.81) for standard anticoagulation versus aspirin. Non-vascular death was less common in the low anticoagulation group than in the aspirin group (0.41, 0.20 to 0.82). There was no significant difference between the treatment groups in bleeding incidence. High systolic and low diastolic blood pressure and age were independent prognostic factors. CONCLUSION: In a general practice population (without established indications for coumarin) neither low nor standard intensity anticoagulation is better than aspirin in preventing primary outcome events. Aspirin may therefore be the first choice in patients with atrial fibrillation in general practice.

Aged↗
PubMed1999

Interobserver agreement in the assessment of cerebral atrophy on CT using bicaudate and sylvian-fissure ratios.

To assess the interobserver variability of cerebral-atrophy measures on CT, three investigators measured the bicaudate ratio (BCR) and the sylvian-fissure ratio (SFR) on 20 CT studies of patients with ischaemic stroke. The intraclass correlation coefficient of BCR measurements was 0.82 [95% confidence interval (CI) 0.75-0.94], and that of SFR measurements 0.69 (95% CI 0.57-0.89). The range of pairwise-calculated Pearson correlation coefficients was smaller for measurement of the BCR (0.89-0.92) than for the SFR measurements (0.66-0.84).

Atrophy↗
PubMed1999

Primary prevention of arterial thromboembolism in nonrheumatic atrial fibrillation: the PATAF trial study design.

Patients with nonrheumatic atrial fibrillation (NRAF) have a higher risk of thromboembolism than patients in sinus rhythm. Several trials have been conducted to establish the best preventive regimen in patients with NRAF, but not in the primary-care setting. The Primary Prevention of Arterial Thromboembolism in Nonrheumatic Atrial Fibrillation (PATAF) study, a primary-care-based trial, was set up to compare the preventive efficacy of low-intensity anticoagulation (AC), target range International Normalized Ratio (INR) 1.1 < INR < 1.6 and regular-intensity AC (2.5 < INR < 3.5) therapies with that of aspirin 150 mg/d for the occurrence of thromboembolism in NRAF patients. Patients eligible for regular-intensity AC were randomly assigned to aspirin at 150 mg/d, low-intensity AC, or regular AC in group I. In cases of noneligibility for regular AC, the trial randomized patients between aspirin and low-intensity AC (assigned to group II). Primary outcome events were stroke (including intracranial hemorrhage), systemic embolism, major hemorrhage, or vascular death. Analysis of the data was based on Cox regression to compute the hazard ratio (HR) with a 95% confidence interval, using the likelihood ratio test. The trial randomized 729 patients. Patient enrollment and follow-up has been stopped, and the final analysis is now complete. We shall publish the main results as soon as possible.

Aged↗
PubMed1998

Gait disorder and parkinsonian signs in patients with stroke related to small deep infarcts and white matter lesions.

Vascular parkinsonism is thought to be a distinct parkinsonian syndrome associated with small deep infarcts and white matter lesions (WMLs). We studied the prevalence of parkinsonian features (bradykinesia, rigidity, tremor, and gait disorder) in relation to small deep or territorial infarcts and WMLs on computed tomography (CT) in 62 lacunar and 41 territorial stroke patients, at 3.0 (median) years of follow up. One or more parkinsonian signs were found in 36% of these patients; 11% clinically had parkinsonism. Parkinsonian signs were found more frequently in lacunar than in territorial stroke patients: bradykinesia in 45% and 7%, rigidity in 13% and 7%, tremor in 6% and 7%, and gait disorder in 16% and 7%, respectively. Patients with WMLs at study entry (n = 16) were compared with those without WMLs (n = 87): 56% and 25% had bradykinesia, 25% and 8% rigidity, 25% and 3% tremor, and 38% and 8% gait disorder, respectively. Regression analysis with adjusted odds ratios ([a]OR) showed that WMLs at study entry were associated with bradykinesia ([a]OR 8.0, 95% confidence interval [CI] 1.6-41.6), gait disorder ([a]OR 7.1, 95% CI 1.5-33.7), and tremor ([a]OR 7.0, 95% CI 1.2-40.3). Bradykinesia was associated with lacunar stroke at study entry ([a]OR 11.5, 95% CI 2.4-54.9). Thus, one third of our stroke patients had one or more parkinsonian signs, and 10% clinically had a parkinsonian syndrome that differed from Lewy body parkinsonism: infrequent resting tremor, but frequent gait disorder. Parkinsonian signs were associated with WMLs and lacunar stroke. Therefore, this study favors a distinct vascular parkinsonian syndrome.

Adult↗
PubMed1997

Mitral annulus calcification is not an independent risk factor for stroke: a cohort study of 657 patients.

All studies but one in the past have shown a strong relative risk of mitral annulus calcification for stroke, but the contribution of associated cardiac and vascular risk factors, especially carotid atheroma has not been appreciated. We studied the risk of stroke in selected patients with mitral annular calcification, adjusting for clinical, echocardiographic and therapeutic factors influencing stroke risk. Of 8,160 consecutive patients with echocardiograms, 657 with and 562 without mitral annulus calcification were followed for a mean of 2.4 years (range 1-6.6) to determine stroke risk by means of proportional hazards models with clinical, echocardiographic, and therapeutic variables that influence the risk of stroke. We also determined the association of mitral annulus calcification with subtypes of ischaemic brain lesions generally considered to be specific for an underlying cardioembolic cause. We therefore distinguished between territorial, small deep, and asymptomatic (silent) brain infarcts. Fifty-one patients with mitral annulus calcification and 27 controls had a stroke in the follow-up period. Mitral annulus calcification was not significantly associated with stroke in proportional hazards models (hazard ratio 0.76, 95% confidence interval 0.42-1.36, P = 0.3), or with any of the stroke subtypes, or with the presence of silent brain infarcts after adjustments for risk factors for generalized vascular disease Hypertension and carotid atheroma, with or without stenosis, ipsilateral or contralateral to the side of the stroke, were significantly associated with stroke in our patients. This study does not support the view that mitral annulus calcification is a risk factor for stroke. As others have found strong associations between mitral annulus calcification and cardiac and vascular risk factors for stroke, the increased risk of stroke in patients with mitral annulus calcification reported may be explained by these confounding risk factors. Therefore, in our opinion, mitral annulus calcification requires treatment of cardiovascular risk factors, but generally no specific measures such as surgery or oral anticoagulants are required to lower the risk of stroke.

Aged↗
PubMed1997

Cardiac valve calcification: characteristics of patients with calcification of the mitral annulus or aortic valve.

AIMS: To determine whether mitral annular calcification and aortic valve calcification, with or without stenosis, are expressions of atherosclerotic disease. METHODS: The incidence of atherosclerotic risk factors was analysed in patients with mitral annular calcification and aortic valve calcification and in control patients from a prospective echocardiographic database of 8160 consecutive patients; 657 patients (8%) were identified with mitral annular calcification and 815 (9%) with a calcified aortic valve, of whom 515 (6.3%) had stenosis with a minimal aortic valve gradient of 16 mm Hg. In these patients, cardiac and vascular risk factors were compared with 568 control patients using multiple logistic regression analysis. RESULTS: Age (odds ratio (OR) varying from 5.78 to 104, depending on age class), female sex (OR 1.75), hypertension (OR 2.38), diabetes mellitus (OR 2.85), and hypercholesterolaemia (OR 2.95) were strongly and significantly associated with aortic valve calcification without stenosis, as were age (OR varying from 8.82 to 67, depending on age class), female sex (OR 2.22), hypertension (OR 2.72), diabetes mellitus (OR 2.49), and hypercholesterolaemia (OR 2.86) with mitral annular calcification. Age (OR varying from 1.11 to 7.7), hypertension (OR 1.91), and hypercholesterolaemia (OR 2.55) were strongly and significantly associated with stenotic aortic valve calcification. CONCLUSIONS: Mitral annular calcification and stenotic or non-stenotic aortic valve calcification have a high incidence of atherosclerotic risk factors, suggesting they should be considered as manifestations of generalised atherosclerosis.

Adult↗
PubMed1996

Significant progression of white matter lesions and small deep (lacunar) infarcts in patients with stroke.

OBJECTIVE: To investigate whether the extent of white matter lesions (WMLs) and the number of small deep infarcts and territorial infarcts progress over time in patients with stroke and to test the hypothesis that WMLs are associated with small deep infarcts. DESIGN: Computed tomographic follow-up study in a cohort of 107 patients with ischemic stroke (median follow-up, 3.0 years). SETTING: Primary and referral care center. PATIENTS: Sixty-three of 144 registered patients with a first-ever symptomatic lacunar stroke and 44 of 155 with a territorial stroke entered this study. Forty-seven (33%) of the nonparticipating patients with a lacunar stroke and 54 (35%) of those with a territorial stroke died, and 34 (24%) and 57 (37), respectively, refused computed tomographic follow-up. MAIN OUTCOME MEASURES: The extent of the WMLs and the number of small deep and territorial infarcts on computed tomographic scans at study entry and at follow-up. RESULTS: Progression of WMLs occurred in 26 patients (26%), and multivariate regression analysis showed that it was associated with symptomatic lacunar stroke at study entry (adjusted odds ratio [aOR], 5.0; 95% confidence interval [CI], 1.2-20.3), silent small deep infarcts at study entry (aOR, 6.0, 95% CI, 1.0-34.6), old age (aOR, 5.5; 95% CI, 1.3-23.1), and longer follow-up (aOR, 12.7; 95% CI, 1.8-89.0). We found progression of small deep infarcts in 41 patients (38%). The progression was associated with symptomatic lacunar stroke at study entry (aOR, 27.7; 95% CI, 6.3-120.9) and longer follow-up (aOR, 7.7; 95% CI, 1.4-41.3). Progression of both WMLs and small deep infarcts, which occurred in 16 patients (16%), was associated with symptomatic lacunar stroke at study entry (aOR, 34.1; 95% CI, 2.5-471.7), silent small deep infarcts at study entry (aOR, 12.5; 95% CI, 1.4-112.0), and longer follow-up (aOR, 29.7; 95% CI, 1.8-501.0). The number of territorial infarcts increased in 14 patients (13%). The increase was associated with symptomatic territorial stroke at study entry (aOR, 7.9; 95% CI, 1.5-40.8) and a history of ischemic heart disease (aOR, 6.6; 95% CI, 1.3-34.8). CONCLUSIONS: The marked progression of WMLs and small deep infarcts that occurred mainly in patients with lacunar stroke suggests that both WMLs and small deep (lacunar) infarcts are caused by a similar vasculopathy that affects small vessels, which is progressive despite standard stroke treatment.

Adult↗
PubMed1996

The size of territorial brain infarction on CT relates to the degree of internal carotid artery obstruction.

We studied the relationship between infarct size and degree of internal carotid artery stenosis in 227 stroke patients without a source of embolism in the heart, who had a CT-verified territorial brain infarct. We used logistic regression analysis adjusting for differences between groups in co-associated variables such as age, sex, hypertension, diabetes mellitus, and a history of ischaemic heart disease. Ipsilateral carotid stenosis greater than 50% was more strongly associated with large than small infarcts; adjusted odds ration [(a)OR]: 4.56; 95% confidence interval (CI): 1.21-17.2; P = 0.02. For ipsilateral carotid occlusion the association was even stronger--(a)OR: 36.80; 95% CI: 2.54-533; P = 0.007. When large infarcts were compared with infarcts of small and moderate size together the ORs were 2.29, 95% CI 1.14-4.58 and 2.57, 95% CI 1.17-5.67 for carotid stenosis or occlusion, respectively. Our data show a relationship between greater than 50% carotid stenosis or occlusion and large brain infarcts. We suggest that haemodynamic impairment may contribute to infarct size in territorial infarcts of non-cardiac origin.

Adult↗
PubMed1996

Late seizures following a first symptomatic brain infarct are related to large infarcts involving the posterior area around the lateral sulcus.

Controversies exist concerning factors that contribute to the occurrence of epileptic seizures after stroke. Therefore, we studied prospectively the occurrence of seizures in 322 patients with a first-ever CT-confirmed symptomatic territorial brain infarct involving the cortex. We also studied potential risk factors for seizures, and gave special attention to cortical infarct location. Fifty-four patients developed post-stroke seizures. We distinguished between early- and late-onset seizures, occurring within two weeks following stroke-onset, or later than two weeks, respectively. We found that patients of 65 years or older with a cardioembolic brain infarct involving the middle temporal or post-central gyrus, had an almost eight times increased risk of early-onset seizures, whereas patients with a large brain infarct involving the supramarginal or superior temporal gyrus, had a five times increased risk of late-onset seizures. We conclude that risk factors and epileptogenic cortical areas for post brain infarct seizures can be identified, which however, differ between early- and late-onset seizures. These two seizure types may also differ in terms of seizure mechanism. Our findings may influence the decision on prophylactic treatment with antiepileptic drugs in stroke patients.

Adult↗
PubMed1996

Comparison of seven sets of criteria used for the diagnosis of vascular dementia.

At least seven different sets of criteria are commonly used for the diagnosis of vascular dementia (VaD). These are the ischemic scales (IS) of Hachinski, Rosen and Loeb, the criteria from the DSM-III-R, those outlined by Erkinjuntti et al., the State of California Alzheimer's Disease Diagnostic and Treatment Centers (ADDTC) and the international workgroup of the American National Institute of Neurological Disorders and Stroke (NINDS) and the European "Association Internationale pour la Recherche et l'Enseignement en Neurosciences'. To investigate the differences and similarities of these criteria, we applied them to a sample of 124 demented patients from the Maastricht Memory Clinic. Only 8 patients were diagnosed as having VaD by all criteria. Depending on which criteria were used, the frequencies of VaD and Alzheimer's disease (AD) ranged from 6 to 32%, and from 48 to 56%, respectively. The IS of Hachinski and Rosen resulted in the highest frequencies of VaD, whereas the criteria of Erkinjuntti and those from the ADDTC and the NINDS workgroup yielded the lowest. The number of patients with VaD was reduced substantially when neuroradiological data and the temporal relationship between stroke and dementia were taken into consideration. We conclude that the seven sets of criteria cannot be regarded as interchangeable. Differences in the criteria for VaD and AD may be an overlooked source of interstudy variance

Aged↗
PubMed1996

Risk of stroke in a cohort of 815 patients with calcification of the aortic valve with or without stenosis.

BACKGROUND AND PURPOSE: We sought to establish the possible role of calcification of the aortic valve with or without stenosis as a risk factor for stroke. METHODS: Occurrences of stroke, stroke subtypes, and concomitant cardiovascular risk factors were prospectively analyzed in 300 patients with echocardiographic evidence of aortic valve calcification, 515 patients with calcified aortic valve stenosis, and 562 control subjects. RESULTS: Twenty-four patients with aortic valve calcification, 24 patients with calcified aortic valve stenosis, and 27 control subjects had a stroke during follow-up. Using Cox proportional hazards models, we found that strokes were not significantly associated with aortic valve calcification with or without stenosis, but hypertension and any carotid stenosis were associated. On multiple logistic regression analysis, we did not find any association between one of the two valve lesions and indirect possible indications of cardiogenic embolism such as territorial as opposed to small deep brain infarcts or the presence of silent brain infarcts. CONCLUSIONS: Aortic valve calcification with or without stenosis is not a risk factor for stroke.

Age Factors↗
PubMed1996

Stroke recovery.

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Benzodiazepines↗