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Biomedical subjects

D Levy

Publications and source records attributed to D Levy.

At least 181 records · Page 10Linked to original sources

Antecedent hypertension confers increased risk for adverse outcomes after initial myocardial infarction.

Several studies have examined the association of blood pressure (BP) after myocardial infarction (MI) with a risk for adverse outcome; however, few studies have investigated prognosis after MI as a function of BP before MI. Our goal was to examine the relation of antecedent hypertension to risk of adverse outcomes after initial MI. From 1967 to 1990, 404 subjects followed at the Framingham Heart Study developed an initial MI. These subjects were classified on the basis of preinfarction BP into normotensive (BP<140/90 mm Hg and not receiving antihypertensive treatment; n=118), stage I-untreated hypertension (BP 140 to 159/90 to 99 mm Hg; n=89), and stage II to IV or treated hypertension (BP > or =160/100 mm Hg or treated hypertension; n=197). Cox models were used to adjust for age, sex, smoking, glucose intolerance, total cholesterol, and prior cardiovascular disease. Antecedent hypertension was related to risk of adverse outcome after MI. Compared with normotensive individuals, stage II to IV hypertensives were at increased risk for reinfarction (hazard ratio [HR], 2.20; 95% confidence interval [CI], 1.20 to 4.04). A similar but nonsignificant association was seen in stage I hypertensives (HR, 1.91; 95% CI, 0.97 to 3.77). Stage II to IV hypertensives were at increased risk for all-cause mortality compared with normotensive persons (HR, 1.45; 95% CI, 1.07 to 1.98). Thus, even after MI, a history of antecedent hypertension remains predictive of adverse outcome. These findings are consistent with beneficial effects of BP control in primary and secondary prevention settings. Effective BP control may both reduce the risk for an initial MI and improve outcome in the event that an MI occurs.

Aged↗

Heritability of left ventricular mass: the Framingham Heart Study.

Left ventricular hypertrophy is associated with an increased risk for cardiovascular disease. The known determinants of left ventricular hypertrophy only partially explain its variability. The purpose of this study was to estimate heritability of left ventricular mass. The study sample included adults in the original Framingham Heart Study and the Framingham Offspring Study who were not receiving antihypertensive medications and who were free of coronary heart disease, congestive heart failure, diabetes mellitus, renal insufficiency, valvular heart disease, and severe left ventricular hypertrophy. Intraclass correlations for left ventricular mass among first-degree relatives, second-degree relatives, and unrelated spouse pairs were calculated to determine the contribution of heredity to the variability in left ventricular mass. After adjustments for age, height, weight, and systolic blood pressure, the intraclass correlations between first-degree relatives were .15 (parent-child, P<.001) to .16 (siblings, P<.001), between second-degree relatives the correlation was .06 (P=NS), and between spouses it was .05 (P=NS). The estimated heritability of adjusted left ventricular mass was between .24 and .32. The proportion of the variance in sex-specific left ventricular mass explained by age, height, weight, and systolic blood pressure was .26 in men and .34 in women. On the basis of intraclass correlations for left ventricular mass, incorporation of adjusted left ventricular mass of a parent or sibling would increase the explained variance by an additional .02 to .03. Heredity explains a small, but discernible proportion of the variance in left ventricular mass. Studies are currently under way to identify genetic markers that predict an individual's predisposition to left ventricular hypertrophy. This knowledge may lead to advances in the prevention of left ventricular hypertrophy, which is strongly associated with cardiovascular morbidity and mortality.

Adult↗

Dependence of middle ear gas composition on pulmonary ventilation.

The middle ear (ME) steady state gas composition resembles that of mixed venous blood. We changed arterial and venous blood gases by artificially ventilating anesthetized guinea pigs and measured simultaneous ME gas changes during spontaneous breathing, hyperventilation, and hypoventilation. During hyperventilation, PaCO2 and PvCO2 (a = arterial, v = venous) decreased from 46.0 and 53.0 mm Hg to 17.9 and 37.5 mm Hg, respectively, while PaO2 and PvO2 (85.6 and 38.2 mm Hg) did not change. This was accompanied by an ME PCO2 decrease from 70.4 to 58.8 mm Hg and a PO2 decrease from 36.8 to 25.4 mm Hg. During hypoventilation, PaCO2 and PvCO2 increased to 56.8 and 66.4 mm Hg, while PvO2 decreased to 21.8 mm Hg. The ME PCO2 increased simultaneously to 88.8 mm Hg and the ME PO2 decreased to 25.4 mm Hg. The ME PO2 decrease during hyperventilation may be explained by a 33% decrease in ME mucosa perfusion, calculated from the ME ventilation-perfusion ratio. This study shows that ME gas composition follows fluctuations of blood gas levels and thus may affect total ME pressure.

Animals↗

Endovascular stents for carotid artery occlusive disease.

PURPOSE: To study the feasibility and safety of endovascular stenting of cervical carotid artery stenosis. METHODS: Between April 1994 and May 1997, 108 consecutive patients (58 men; mean age 70.1 years) with > or = 70% carotid stenosis were treated with percutaneous stent implantation under a protocol that featured independent neurological review. Forty-four percent were asymptomatic. Over half the lesions (59%) were in the internal carotid artery; the mean stenosis was 86%. Palmaz stents were implanted without cerebral protection following preliminary balloon dilation; two Wallstents were used in long lesions. RESULTS: Carotid stents were successfully placed in 108 of 114 (95%) lesions. Of the 6 technical failures, 5 were access related and 1 was due to seizures during balloon dilation. Two major (1.8%) and 2 minor (1.8%) strokes occurred (3.7% stroke rate for 108 patients; 3.5% in 114 procedures), all in symptomatic patients, one of whom died. There were 5 (4.4%) transient ischemic attacks and 2 (1.8%) brief seizure episodes during dilation. One patient died of a cardiac event on day 20. The all stroke or death rate was 5.3% based on 114 arteries at risk (5.6% in 108 patients). In the mean 6-month follow-up (range 1 to 36) of 97 eligible patients, 3 (3.1%) died from unrelated causes. There was 1 restenosis (1.0%) from a stent compression, which was successfully redilated. There were no neurological sequelae, cranial palsies, or cases of stent or vessel thrombosis in follow-up. CONCLUSIONS: The use of stents in the treatment of cervical carotid occlusive disease appears feasible, effective in the short term, and without excessive risk of periprocedural stroke.

Adult↗

Radiographic hand osteoarthritis: incidence, patterns, and influence of pre-existing disease in a population based sample.

OBJECTIVE: Osteoarthritis (OA) is the most common type of arthritis; involvement of joints in the hand is highly prevalent, especially in the elderly. Few data are available on the incidence of hand OA in men and women or on the association between OA in one hand joint with incidence in others. METHODS: We studied the cumulative incidence of radiographic hand OA in a population based group of men and women, and evaluated whether baseline OA in one joint affected OA rates in other joints in the hand. Study subjects were 751 members of the Framingham Study cohort, who had a baseline right hand radiograph taken in 1967-1969 (mean age 55+/-5.58) and followup radiographs 24 years later. RESULTS: In those without OA at baseline, women had more incident disease than men in almost all hand joints, but the joints most frequently affected were the same in both sexes: the distal interphalangeal (DIP), followed by the base of the thumb, proximal interphalangeal (PIP), and metacarpophalangeal (MCP) joints. The MCP joint group was the only one in which the incidence in men was comparable to incidence in women. Prevalent OA in one or more joints in a row (e.g., MCP) markedly increased the risk of incident OA in other joints in the same row. Also, prevalent OA in one joint in a finger (a ray) increased the risk of incident OA in other joints in that ray. Prevalent OA in either DIP or PIP joints at baseline substantially increased the risk of incident OA in all other hand joints. Thumb base OA at baseline increased risk in MCP joints, and to a lesser extent, DIP and PIP joints. CONCLUSION: Cumulative incidence was generally higher in women than men, baseline OA in one joint in a row markedly increased the risk of developing OA in other joints in the same row, and baseline OA in a joint in a ray similarly increased risk in that ray. Interphalangeal joint OA at baseline appeared to increase subsequent OA in all hand joints, baseline OA in the thumb was not as strong a predictor. This descriptive information on incidence of radiographic hand OA should generate new hypotheses about why OA affects hands in particular patterns.

Age Distribution↗

Relationships between myoelectric activity, strength, and MRI of lumbar extensor muscles in back pain patients and normal subjects.

Eight normal individuals and eight patients with chronic back pain were evaluated. They undertook a treatment program lasting 8 weeks, with two exercise sessions each week. Myoelectric activity, lumbar extensor strength, and cross-sectional magnetic resonance imaging appearance of the lumbar paraspinal extensor muscles was assessed at the beginning and end of the program. Initial baseline and final extensor strength measurements were done isometrically at seven points through full range. Surface myoelectric activity was monitored during both flexion and extension exercise. Subsequently, electromyographic (EMG) signals were analyzed for mean frequency (MPF) and amplitude (RMS). An average functional improvement of 65% and reduction of pain complaint of 41% occurred in the eight patients with chronic low back pain. Extensor strength improved an average of 48% contrasted to 6% for the normal subjects. Four patients who showed severe fatty infiltration in the extensors had a decrease in the degree of infiltration and no change in muscle mass. Changes in fatty infiltration did not correlate with strength changes. The dynamic EMG changes documented a decrease in amplitude (RMS) and a smaller decrease in frequency (MPF) for the same resistance when used at the beginning and end of the program. Structural changes in the muscles are not always needed to achieve strength gains or symptomatic improvement.

Back Pain↗

Neuroendovascular management of intracranial aneurysms.

Intracranial aneurysms are a common disease constituting a significant health problem worldwide. Aneurysmal subarachnoid hemorrhage, cerebral aneurysms, classification of aneurysms, and management of aneurysms are discussed.

Cerebrovascular Circulation↗

Impact of reduced heart rate variability on risk for cardiac events. The Framingham Heart Study.

BACKGROUND: Although heart rate variability (HRV) is altered in a variety of pathological conditions, the association of reduced HRV with risk for new cardiac events has not been studied in a large community-based population. METHODS AND RESULTS: The first 2 hours of ambulatory ECG recordings obtained on subjects of the Framingham Heart Study who were free of clinically apparent coronary heart disease or congestive heart failure were reprocessed to assess HRV. Five frequency-domain measures and three time-domain measures were obtained. The associations between HRV measures and the incidence of new cardiac events (angina pectroris, myocardial infarction, coronary heart disease death, or congestive heart failure) were assessed with proportional hazards regression analyses. There were 2501 eligible subjects with a mean age of 53 years. During a mean follow-up of 3.5 years, cardiac events occurred in 58 subjects. After adjustment for age, sex, cigarette smoking, diabetes, left ventricular hypertrophy, and other relevant risk factors, all HRV measures except the ratio of low-frequency to high-frequency power were significantly associated with risk for a cardiac event (P = .0016 to .0496). A one-standard deviation decrement in the standard deviation of total normal RR intervals (natural log transformed) was associated with a hazard ratio of 1.47 for new cardiac events (95% confidence interval of 1.16 to 1.86). CONCLUSIONS: The estimation of HRV by ambulatory monitoring offers prognostic information beyond that provided by the evaluation of traditional cardiovascular disease risk factors.

Adult↗

Determinants of heart rate variability.

OBJECTIVES: This study sought to examine clinical determinants of heart rate variability and to report normative reference values for eight heart rate variability measures. BACKGROUND: Although the clinical implications of heart rate variability have been described, clinical determinants and normative values of heart rate variability measures have not been studied systematically in a large community-based population. METHODS: The first 2 h of ambulatory electrocardiographic recordings obtained in Framingham Heart Study subjects attending a routine examination were reprocessed for heart rate variability. Recordings with transient or persistent nonsinus rhythm, premature beats > 10% of total beats, < 1-h recording time or processed time < 50% of recorded time were excluded; subjects receiving antiarrhythmic medications also were excluded. Among five frequency domain and three time domain measures that were obtained, low frequency power (0.04 to 0.15 Hz), high frequency power (0.15 to 0.40 Hz) and the standard deviation of total normal RR intervals based on 2-h recordings were selected for the principal analyses. Variables with potential physiologic effects or possible technical influences on heart rate variability measures were chosen for multiple linear regression analysis. Normative values, derived from a subset of healthy subjects, were adjusted for age and heart rate. RESULTS: There were 2,722 eligible subjects with a mean age (+/-SD) of 55 +/- 14 years. Three separate multiple linear regression analyses revealed that higher heart rate, older age, beta-adrenergic blocking agent use, history of myocardial infarction or congestive heart failure, diuretic use, diastolic blood pressure > or = 90 mm Hg, diabetes mellitus, consumption of three or more cups of coffee per day and smoking were associated with lower values of one or more heart rate variability measures, whereas longer processed time, start time in the morning, frequent supraventricular and ventricular premature beats, female gender and systolic blood pressure > or = 160 mm Hg were associated with higher values. Age and heart rate were the major determinants of all three selected heart rate variability measures (partial R2 values 0.125 to 0.389). Normative reference values for all eight heart rate variability measures are presented. CONCLUSIONS: Age and heart rate must be taken into account when assessing heart rate variability.

Adult↗

The role of hypertension in the pathogenesis of heart failure. A clinical mechanistic overview.

Hypertension plays a key role in the evolution of the syndrome of heart failure. Hypertension has been identified as the chief precursor of left ventricular hypertrophy. Hypertensive left ventricular hypertrophy can lead to ventricular diastolic dysfunction; it is also a risk factor for myocardial infarction, which is a principal cause of left ventricular systolic dysfunction. Asymptomatic left ventricular dysfunction, whether systolic or diastolic, culminates in clinically overt heart failure when a threshold is exceeded or when other precipitating factors are superimposed. The onset of overt heart failure heralds a bleak outcome. These structural and functional changes associated with hypertension evolve over decades and are preventable with effective antihypertensive treatment. These observations emphasize the importance of early diagnosis and effective treatment of hypertension to prevent cardiac complications.

Heart Failure↗

The functional expression of sodium-dependent bile acid transport in Madin-Darby canine kidney cells transfected with the cDNA for microsomal epoxide hydrolase.

Previous studies have suggested that the enzyme microsomal epoxide hydrolase (mEH) is able to mediate sodium-dependent transport of bile acids such as taurocholate into hepatocytes (von Dippe, P., Amoui, M., Alves, C., and Levy, D.(1993) Am. J. Physiol. 264, G528-G534). In order to characterize directly the putative transport properties of the enzyme, a pCB6 vector containing the cDNA for this protein (pCB6-mEH) was transfected into Madin-Darby canine kidney (MDCK) cells, and stable transformants were isolated that could express mEH at levels comparable with the levels expressed in hepatocytes. Sodium-dependent transport of taurocholate was shown to be dependent on the expression of mEH and to be inhibited by the bile acid transport inhibitor 4,4'-diisothiocyanostilbene-2,2'disulfonic acid (DIDS), as well as by other bile acids. Kinetic analysis of this system indicated a Km of 26.3 microM and a Vmax of 117 pmol/mg protein/min. The Km value is essentially the same as that observed in intact hepatocytes. The transfected MDCK cells also exhibited sodium-dependent transport of cholate at levels 150% of taurocholate in contrast to hepatocytes where cholate transport is only 30% of taurocholate levels, suggesting that total hepatocyte bile acid transport is a function of multiple transport systems with different substrate specificities, where mEH preferentially transports cholate. This hypothesis is further supported by the observation that a monoclonal antibody that partially protects (26%) taurocholate transport from inhibition by DIDS in hepatocytes provides almost complete protection (88%) from DIDS inhibition of hepatocyte cholate transport, suggesting that taurocholate is also taken up by an alternative system not recognized by this antibody. Additional support for this concept is provided by the observation that the taurocholate transport system is almost completely protected (92%) from DIDS inhibition by this antibody in MDCK cells that express mEH as the only bile acid transporter. These results demonstrate that mEH is expressed on the surface of hepatocytes as well as on transfected MDCK cells and is able to mediate sodium-dependent transport of taurocholate and cholate.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗

Comparison of enalapril versus nifedipine to decrease left ventricular hypertrophy in systemic hypertension (the PRESERVE trial).

The PRESERVE (Prospective Randomized Enalapril Study Evaluating Regression of Ventricular Enlargement) study is designed to provide a definitive test of the ability of enalapril to achieve greater left ventricular (LV) mass reduction than nifedipine GITs (gastrointestinal treatment system) by a degree that would be prognostically meaningful on a population basis (10 g/m2). To achieve this goal, an ethnically diverse population of 480 men and women with essential hypertension and increased LV mass of screening echocardiography will be enrolled at clinical centers on 4 continents and studied by echocardiography at baseline and after 6 and 12 months' randomized therapy. Blinded readings of echocardiograms at a central laboratory will provide systematic information about treatment effects on LV structure, wall motion, and Doppler blood flow. The study power is at least 90% to test the primary hypotheses that enalapril will induce greater normalization of LV mass and diastolic filling than nifedipine. After the 1-year echocardiographic trial, the study population will be followed 3 more years to test the hypothesis that a reduction in LV mass, independent of blood pressure lowering, is associated with a reduction in the risk of morbid and fatal cardiovascular events.

Antihypertensive Agents↗

Absence of association or genetic linkage between the angiotensin-converting-enzyme gene and left ventricular mass.

BACKGROUND: Homozygous carries of the D allele of the angiotensin-converting-enzyme (ACE) gene have been reported to be at increased risk for various cardiovascular disorders, including left ventricular hypertrophy. We investigated the potential role of the ACE gene in influencing left ventricular mass. METHODS: Quantitative echocardiographic data and DNA samples were available for 2439 subjects from the Framingham Heart Study. ACE genotypes were determined by an assay based on the polymerase chain reaction. (The D allele of the ACE gene contains a deletion, whereas the I [insertion] allele does not.) Left ventricular mass and the prevalence of left ventricular hypertrophy, adjusted for clinical covariates, were analyzed according to genotype. Genetic linkage between the ACE locus and left ventricular mass was evaluated by quantitative analysis of pairs of siblings. RESULTS: The ACE genotype was associated neither with left ventricular mass nor with the prevalence of left ventricular hypertrophy. Mean (+/-SE) left ventricular mass (adjusted for sex) among subjects carrying the DD, DI, and II genotypes was 165+/-1.6, 165+/-1.3, and 166+/-2.0 g, respectively (P=0.90). The prevalence of left ventricular hypertrophy among the three genotype groups was 15.6 percent, 13.6 percent, and 15.6 percent, respectively (P=0.36), and the adjusted relative risk of left ventricular hypertrophy associated with the DD genotype was 1.10 (95 percent confidence interval, 0.86 to 1.19). Linkage analysis in 759 pairs of siblings using both the ACE D/I marker and a microsatellite polymorphism at the neighboring locus for the human growth hormone gene failed to support any role of ACE in influencing left ventricular mass. CONCLUSIONS: The ACE genotype showed no association with echocardiographically determined left ventricular mass, nor did it confer an increased risk of left ventricular hypertrophy. We found no appreciable role of the ACE gene in influencing left ventricular mass.

Adult↗

Impaired heart rate response to graded exercise. Prognostic implications of chronotropic incompetence in the Framingham Heart Study.

BACKGROUND: Previous reports have suggested that an attenuated exercise heart rate response may be associated with coronary heart disease risk and with mortality. These observations may parallel the association between reduced heart rate variability during normal activities and adverse outcome. This investigation was designed to look at the prognostic implications of exercise heart rate response in a population-based sample. METHODS AND RESULTS: In this prospective cohort investigation, 1575 male participants (mean age, 43 years) in the Framingham Offspring Study who were free of coronary heart disease, who were not taking beta-blockers, and who underwent submaximal treadmill exercise testing (Bruce protocol) were studied. Heart rate response was assessed in three ways: (1) failure to achieve 85% of the age-predicted maximum heart rate, which has been the traditional definition of chronotropic incompetence; (2) the actual increase in heart rate from rest to peak exercise; and (3) the ratio of heart rate to metabolic reserve used by stage 2 of exercise ("chronotropic response index"). Proportional hazards analyses were used to evaluate the associations of heart rate responses with all-cause mortality and with coronary heart disease incidence during 7.7 years of follow-up. Failure to achieve target heart rate occurred in 327 (21%) subjects. During follow-up there were 55 deaths (14 caused by coronary heart disease) and 95 cases of incident coronary heart disease. Failure to achieve target heart rate, a smaller increase in heart rate with exercise, and the chronotropic response index were predictive of total mortality and incident coronary heart disease (P <.01). Failure to achieve target heart rate remained predictive of incident coronary heart disease even after adjusting for age, ST-segment response, physical activity, and traditional coronary disease risk factors (adjusted hazard ratio, 1.75; 95% confidence interval, 1.11 to 2.74; P=.02). After adjusting for the same factors, the increase in exercise heart rate remained inversely predictive of total mortality (P=.04) and coronary heart disease incidence (P=.0003). The chronotropic response index also was predictive of total mortality (P=.05) and incident coronary heart disease (P=.001) after adjusting for age and other risk factors. CONCLUSIONS: An attenuated heart rate response to exercise, a manifestation of chronotropic incompetence, is predictive of increased mortality and coronary heart disease incidence.

Adult↗

Factors associated with survival to 75 years of age in middle-aged men and women. The Framingham Study.

BACKGROUND: Whereas a variety of epidemiological studies have examined factors associated with overall and cause-specific morbidity and mortality, limited data exist about factors associated with longevity, particularly in middle-aged men and women. The present study examined factors associated with survival to 75 years of age in middle-aged men and women from the community-based Framingham Study. METHODS: After excluding persons with cancer, cardio-vascular disease, or diabetes, 747 men and 973 women from the Framingham Study, who were 50 years of age at the time of a routine clinical examination and who could potentially reach 75 years of age during follow-up, were studied. Logistic regression modeling was used to examine factors associated with survival to 75 years of age. RESULTS: Fewer cigarettes smoked per day, lower systolic blood pressure, and higher forced vital capacity were associated with longevity in both sexes. Lower heart rate in men and parental survival to 75 years of age in women were additionally associated with survival to 75 years of age. CONCLUSIONS: The results of this long-term prospective study suggest a number of lifestyle characteristics and one familial factor associated with increased life expectancy. These data lend further support to the positive impact on life expectancy of health promotional efforts directed at smoking cessation and control of hypertension in middle-aged men and women.

Age Factors↗

Congestive heart failure with normal left ventricular systolic function. Clinical approaches to the diagnosis and treatment of diastolic heart failure.

The syndrome of congestive heart failure with preserved left ventricular systolic function is common in clinical practice. The signs and symptoms of the disorder are similar to those of congestive heart failure with left ventricular systolic dysfunction, underscoring a need for routine evaluation of left and right ventricular systolic function in patients with congestive heart failure. The syndrome may be related to anatomic abnormalities that increase the resistance to ventricular filling, or to physiologic abnormalities of myocardial relaxation or compliance. Advancing age, often in association with hypertension, coronary artery disease, tachycardia, and atrial fibrillation, is commonly associated with the disorder. Randomized controlled clinical trials are needed to evaluate the efficacy of various therapeutic agents in reducing the risks associated with diastolic heart failure.

Algorithms↗

Do antioxidant micronutrients protect against the development and progression of knee osteoarthritis?

OBJECTIVE: Cumulative damage to tissues, mediated by reactive oxygen species, has been implicated as a pathway that leads to many of the degenerative changes associated with aging. We hypothesized that increased intake of antioxidant micronutrients might be associated with decreased rates of osteoarthritis (OA) in the knees, a common age-related disorder. METHODS: Participants in the Framingham Osteoarthritis Cohort Study underwent knee evaluations by radiography at examinations 18 (1983-1985) and 22 (1992-1993). Usual dietary intake was assessed using the Food Frequency Questionnaire, administered at examination 20 (1988-1989). Knees without OA at baseline (Kellgren and Lawrence [K&L] grade < or = 1) were classified as having incident OA if they had a K&L grade > or = 2 at followup. Knees with OA at baseline were classified as having progressive OA if their score increased by > or = 1 at followup. Knees were also classified as having cartilage loss or osteophyte growth if their maximal joint space narrowing or osteophyte growth score increased by > or = 1 (range 0-3). The association of vitamin C, beta carotene, and vitamin E intake, ranked in sex-specific tertiles, with incidence and progression of OA was compared with that of a panel of nonantioxidant vitamins, Bl, B6, niacin, and folate, using logistic regression and generalized estimation equations to adjust for correlation between fellow knees. The lowest tertile for each dietary exposure was used as the referent category. Odds ratios (OR) were adjusted for age, sex, body mass index, weight change, knee injury, physical activity, energy intake, and health status. RESULTS: Six hundred forty participants received complete assessments. Incident and progressive OA occurred in 81 and 68 knees, respectively. We found no significant association of incident OA with any nutrient. A 3-fold reduction in risk of OA progression was found for both the middle tertile (adjusted OR = 0.3, 95% confidence interval [95% CI] 0.1-0.8) and highest tertile (adjusted OR = 0.3, 95% CI 0.1-0.6) of vitamin C intake. This related predominantly to a reduced risk of cartilage loss (adjusted OR = 0.3, 95% CI 0.1-0.8). Those with high vitamin C intake also had a reduced risk of developing knee pain (adjusted OR = 0.3, 95% CI 0.1-0.8). A reduction in risk of OA progression was seen for beta carotene (adjusted OR = 0.4, 95% CI 0.2-0.9) and vitamin E intake (adjusted OR = 0.7, 95% CI 0.3-1.6), but was less consistent. No significant associations were observed for the nonantioxidant nutrients. CONCLUSION: High intake of antioxidant micronutrients, especially vitamin C, may reduce the risk of cartilage loss and disease progression in people with OA. We found no effect of antioxidant nutrients on incident OA. These preliminary findings warrant confirmation.

Aged↗

Evolution of different therapeutic strategies in the treatment of cranial dural arteriovenous fistulas--report of 30 cases.

30 cases of cranial dural arteriovenous fistuals, treated between 1983 and 1992, are reported. Twelve presented with an aggressive clinical course including intracranial haemorrhage, progredient neurological deficit, medically intractable seizures, and cerebellar symptoms. The other 18 patients had a more benign clinical presentation with audible bruit, exophthalmus, chemosis, and cranial nerve dysfunction. One of the latter had symptoms of pseudotumour cerebri due to sinus occlusion with contralateral sinus stenosis. The most common location was at the transverse sinus, followed by the cavemous sinus, the tentorial ring, and the orbita. Four vessel angiography verified the diagnosis and demonstrated all fistulas, mainly supplied by branches of the external carotid artery. 16 of 18 benign lesions were treated by endovascular therapy alone. Two recent patients received adjuvant stereotactic radiosurgery. Among these 18 patients 2 remained untreated, one because of spontaneous fistula thrombosis prior to therapy and one because of poor medical condition. 12 of 16 treated benign dural fistulas were partially occluded. In 6 of them spontaneous fistula thrombosis occurred during the following months. Total endovascular obliteration was achieved in the remaining 4 patients. 7 of 12 aggressive fistulas were embolized only, one of them having additional radiosurgery. Two of them were totally obliterated and five partially. Surgery was performed in the remaining 5 aggressive fistulas. Complete microsurgical excision was achieved in 2 and partial in further two, who presented initially with a life-threatening intracerebral clot. In one early case ligation of the external carotid artery was done, which is now obsolete. Over all 20 of 28 treated patients became asymptomatic or improved clinically. 3 of the remaining 8 patients were unchanged, two deteriorated despite therapy, and 3 worsened after therapy. All of the latter complications occurred early in our series due to thromboembolic events during the procedure. One surgical patient suffered from a new facial nerve palsy postoperatively. Follow up time in all treated patients was between 1 and 139 months with a mean of 48,3 months.

Adolescent↗