Robert Fagard
Catholic University of Leuven
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Featured researches published by Robert Fagard.
Hypertension | 2005
Véronique Cornelissen; Robert Fagard
Previous meta-analyses of randomized controlled trials on the effects of chronic dynamic aerobic endurance training on blood pressure reported on resting blood pressure only. Our aim was to perform a comprehensive meta-analysis including resting and ambulatory blood pressure, blood pressure–regulating mechanisms, and concomitant cardiovascular risk factors. Inclusion criteria of studies were: random allocation to intervention and control; endurance training as the sole intervention; inclusion of healthy sedentary normotensive or hypertensive adults; intervention duration of ≥4 weeks; availability of systolic or diastolic blood pressure; and publication in a peer-reviewed journal up to December 2003. The meta-analysis involved 72 trials, 105 study groups, and 3936 participants. After weighting for the number of trained participants and using a random-effects model, training induced significant net reductions of resting and daytime ambulatory blood pressure of, respectively, 3.0/2.4 mm Hg (P<0.001) and 3.3/3.5 mm Hg (P<0.01). The reduction of resting blood pressure was more pronounced in the 30 hypertensive study groups (−6.9/−4.9) than in the others (−1.9/−1.6; P<0.001 for all). Systemic vascular resistance decreased by 7.1% (P<0.05), plasma norepinephrine by 29% (P<0.001), and plasma renin activity by 20% (P<0.05). Body weight decreased by 1.2 kg (P<0.001), waist circumference by 2.8 cm (P<0.001), percent body fat by 1.4% (P<0.001), and the homeostasis model assessment index of insulin resistance by 0.31 U (P<0.01); HDL cholesterol increased by 0.032 mmol/L−1 (P<0.05). In conclusion, aerobic endurance training decreases blood pressure through a reduction of vascular resistance, in which the sympathetic nervous system and the renin-angiotensin system appear to be involved, and favorably affects concomitant cardiovascular risk factors.
The Lancet | 1999
Jan A. Staessen; Harry A. Roels; Dmitri Emelianov; T. Kuznetsova; Lutgarde Thijs; Jaco Vangronsveld; Robert Fagard
BACKGROUNDnChronic low-level exposure to cadmium may promote calcium loss via urinary excretion. We undertook a prospective population study to investigate whether environmental exposure to cadmium lowers bone density and increases risk of fractures.nnnMETHODSnWe measured urinary cadmium excretion, a biomarker of lifetime exposure, in people from ten districts of Belgium, of which six districts bordered on three zinc smelters. We also measured cadmium in soil and in vegetables from the districts, and collected data on incidence of fractures and height loss. Bone density was measured at the forearm just above the wrist by single photon absorptiometry, and calculated as the mean of six proximal and four distal scans.nnnFINDINGSnMean cadmium excretion at baseline was 8.7 nmol daily. Across the ten districts, mean cadmium concentration in soil ranged from 0.8 to 14.7 mg/kg, and from 0.1 to 4.0 mg/kg dry weight in vegetables. Median follow-up was 6.6 years. Mean forearm bone density in proximal and distal scans was 0.54 g/cm2 and 0.43 g/cm2 in men, and 0.44 g/cm2 and 0.34 g/cm2 in women. In postmenopausal women, a twofold increase in urinary cadmium correlated with 0.01 g/cm2 decrease in bone density (p<0.02). The relative risks associated with doubled urinary cadmium were 1.73 (95% CI 1.16-2.57; p=0.007) for fractures in women and 1.60 (0.94-2.72, p=0.08) for height loss in men. Cadmium excretion in districts near smelters was 22.8% higher (p=0.001) than in other districts, with fracture rates of 16.0 and 10.3 cases per 1000 person-years, respectively, and a population-attributable risk of 35.0%.nnnINTERPRETATIONnEven at a low degree of environmental exposure, cadmium may promote skeletal demineralisation, which may lead to increased bone fragility and raised risk of fractures.
Heart | 2003
Robert Fagard
Cardiac enlargement in athletes was already recognised by the end of the 19th century through percussion of the chest in cross country skiers, and was later confirmed by use of radiography and evidence from necropsy. The advent of echocardiography allowed investigators to gain a better insight into the heart of athletes, and these findings were in general confirmed by other techniques such as magnetic resonance imaging. The present review will focus on the impact of different sports and training on cardiac structure and function, and on electrocardiographic alterations associated with athlete’s heart.nn### Left ventriclenn#### Cross sectional studiesnnPhysical exercise is associated with haemodynamic changes and alters the loading conditions of the heart. In dynamic exercise the emphasis is on movement with no or minimal development of force. The main haemodynamic features are increases in heart rate and stroke volume, the two components of cardiac output. Systemic vascular resistance drops but the net result is a slight to moderate rise in blood pressure. The load on the heart is predominantly that of volume. In static exercise force is developed with no or minimal movement. The haemodynamic consequences involve a slight elevation of cardiac output, caused by the increase of heart rate, and a more pronounced rise of blood pressure, resulting in a pressure load on the heart. From a theoretical point of view the haemodynamic alterations and the ventricular loading conditions during exercise could, in the long run, lead to left ventricular hypertrophy (LVH). Volume load would lead to enlargement of the left ventricular internal diameter and a proportional increase of wall thickness; this type of adaptation is termed eccentric LVH. The pressure load would induce thickening of the ventricular wall with unchanged internal dimension, or concentric LVH. It was suggested that these cardiac adaptations serve to normalise wall stress.nnIndividual studies showed that cardiac adaptations …
The Lancet | 2001
Jan A. Staessen; Tim S. Nawrot; Elly Den Hond; Lutgarde Thijs; Robert Fagard; Karel Hoppenbrouwers; Gudrun Koppen; Vera Nelen; Greet Schoeters; Dirk Vanderschueren; Etienne Van Hecke; Luc Verschaeve; Robert Vlietinck; Harry A. Roels
BACKGROUNDnHuman exposure to chemicals is normally monitored by measurement of environmental pollutants in external media. We investigated whether biomarkers in adolescents can show exposure to, and health effects of, common environmental pollutants.nnnMETHODSnWe recruited 200 17-year-old adolescents (120 girls) from a rural control area and from two suburbs polluted by a lead smelter and two waste incinerators. We measured biomarkers of exposure and of effect in blood and urine samples, and obtained questionnaire data. School doctors measured testicular volume and staged sexual maturation.nnnFINDINGSnInternal exposure was mostly within current standards. Concentrations of lead and cadmium in blood, PCBs (polychlorinated biphenyls) and dioxin-like compounds in serum samples, and metabolites of VOCs (volatile organic compounds) in urine were higher in one or both suburbs than in the control area. Children who lived near the waste incinerators matured sexually at an older age than others, and testicular volume was smaller in boys from the suburbs than in controls. Biomarkers of glomerular or tubular renal dysfunction in individuals were positively correlated with blood lead. Biomarkers of DNA damage were positively correlated with urinary metabolites of PAHs (polycyclic aromatic hydrocarbons) and VOCs. Interpretation Biomarkers can be used to detect environmental exposure to pollutants and measure their biological effects before overt disease develops. Our findings suggest that current environmental standards are insufficient to avoid measurable biological effects.
Hypertension | 1991
Robert Fagard; Jan A Staessen; Lutgarde Thijs; A Amery
The outcome of 143 male hypertensive patients, investigated in the period 1972-1982, was ascertained in 1989 to determine if brachial artery pressure measured during a progressive graded exercise test on the bicycle ergometer is a better predictor of mortality and cardiovascular events than pressure at rest During the total follow-up time of 1,573 patient years, 27 patients suffered at least one fatal or nonfatal cardiovascular event and 13 patients died. Using the Cox regression model, the age-adjusted relative hazard rates of systolic pressure at supine rest, at 50 W, at peak work load, and at 50% of peak exercise capacity were significant for total mortality (psO.Ol) and for cardiovascular events (p^0.03). Pressure during exercise, however, did not significantly (p=0.11-0.97) predict the outcome of the patients when age and pressure at rest were taken into account The results were similar for diastolic pressure. In conclusion, intra-arterial pressures at rest and during submaximal and peak exercise significantly predict mortality and the incidence of cardiovascular events in hypertensive men, independent of age. However, there is no additional prognostic precision of the exercise pressures when age and the rest pressure are taken into account
American Journal of Cardiology | 1989
Roger Van Hoof; Peter Hespel; Robert Fagard; Paul Lijnen; Jan A Staessen; A Amery
The effect of 4 months of physical training on resting, exercise and 24-hour blood pressure (BP) was studied using a randomized crossover design in 26 healthy, sedentary men, with an average age of 39 +/- 10 (standard deviation) years. Peak oxygen uptake increased by 14% (p less than 0.001) and the physical working capacity at a heart rate of 130 beats/min by 25% (p less than 0.001). The heart rate was reduced by 7 beats/min at night (p less than 0.01) and by 6 beats/min during the day (p less than 0.001). Training-induced changes of BP varied according to measuring conditions. A decrease in BP at rest while sitting in the morning in the laboratory was significant for diastolic (-5 mm Hg, p less than 0.01) but not for systolic BP. During exercise, systolic BP was significantly lower after training, when measured at the same submaximal workloads. However, when workload was expressed as a percentage of peak oxygen uptake, systolic BP was not different before and after training. When measured during 24 hours, the training-induced change in BP was not significant at night either for systolic or diastolic BP. During the day the decrease in diastolic BP was significant (-5 mm Hg, p less than 0.001), but the change in systolic BP was not.
Journal of Hypertension | 2009
Véronique Cornelissen; Jozef Arnout; Paul Holvoet; Robert Fagard
Objective It is not well known which exercise intensity is needed to obtain blood pressure reductions in response to endurance training. We therefore compared the effect of training at lower and higher intensity on blood pressure, and, in addition on other cardiovascular risk factors, in at least 55-year-old sedentary men and women. Methods We used a randomized crossover design comprising three 10-week periods. In the first and third periods, participants exercised at, respectively, lower and higher intensity (33 and 66% of heart rate reserve) in random order, with a sedentary period in between. Training programmes were identical except for intensity and were performed three times, 1 h per week. Thirty-nine (18 men) out of 48 randomized participants completed the study; age averaged 59 years. Results The change of aerobic power from baseline to the end of each period was more pronounced (P < 0.05) with higher intensity (+3.70 ml/kg min; P < 0.001) than with lower intensity training (+2.31 ml/kg min; P < 0.001). Systolic blood pressures at rest and during submaximal exercise were reduced with both intensities (P < 0.01), whereas diastolic office blood pressure was significantly reduced after higher intensity only (P < 0.01). There were no significant differences in blood pressure reduction between intensities. Ambulatory blood pressure remained unchanged after training. Only higher intensity training reduced weight (−1.09 kg; P < 0.001), body fat (−0.85%; P < 0.001), plasma triglycerides (−0.17 mmol/l; P < 0.05) and oxidized low-density lipoprotein (−5.92 U/l; P < 0.01). Conclusion Higher and lower intensity training reduces systolic office and exercise blood pressure to a similar extent, but does not alter ambulatory blood pressure; only higher intensity training favourably affects anthropometric characteristics and blood lipids.
American Heart Journal | 1991
E Bielen; Robert Fagard; A Amery
Abstract The heritability of left ventricular structure and function was studied in 53 pairs of monozygotic and dizygotic twins, aged 18 to 31 years, by means of M-mode and Doppler echocardiography. A significant fraction of the phenotypic variances of left ventricular wall thickness was explained by genetic variance. For the left ventricular internal dimension, however, no genetic effect was found after correction for body weight. After appropriate adjustment a genetic component of 32% was found for aortic peak flow velocity, 55% for stroke distance, and 47% for minute distance. The early and late diastolic peak flow velocities at the mitral valve showed a genetic component estimated at 43% and 26%, repectively. The inheritance of the late/early diastolic peak flow velocity ratio was estimated at 53%. In conclusion, these data suggest a significant genetic component for left ventricular structural features but not for cavity dimension. A significant influence of heredity was detected for left ventricular inflow and outflow characteristics.
Occupational and Environmental Medicine | 1991
Jan A. Staessen; Antoon Amery; Alfred Bernard; P. Bruaux; Jean-Pierre Buchet; F Claeys; P De Plaen; G. Ducoffre; Robert Fagard; Robert Lauwerys
The objective was to investigate the hypothesis that environmental exposure to cadmium may affect calcium metabolism in the population at large. The 1987 participants (965 men and 1022 women), from 20 to 80 years old, constituted a random sample of the population of four Belgian districts. The urinary excretion of cadmium, a measure of lifetime exposure, averaged 9.3 nmol/24 h in men (range 0.4-324 nmol/24 h) and 7.1 nmol/24 h (range 0.1-71 nmol/24 h) in women. Serum alkaline phosphatase activity and the urinary excretion of calcium correlated significantly and positively with urinary cadmium excretion in both men and women, and serum total calcium concentration negatively with urinary cadmium excretion in men only. The regression coefficients obtained after adjustment for significant covariates indicated that when urinary cadmium excretion increased twofold, serum alkaline phosphatase activity and urinary calcium excretion rose by 3-4% and 0.25 mmol/24 h respectively, whereas in men serum total calcium concentration fell by 6 mumol/l. After adjustment for significant covariates the relation between serum total calcium concentration and urinary cadmium excretion was not significant in women. The findings suggest that even at environmental exposure levels calcium metabolism is gradually affected, as cadmium accumulates in the body. The morbidity associated with this phenomenon in industrialised countries remains presently unknown and requires further investigation.
American Journal of Cardiology | 1992
E Bielen; Robert Fagard; Paul Lijnen; Tikma B. Tjandra-Maga; René Verbessert; A Amery
The effects on cardiac structure and function of antihypertensive regimens with different effects on the renin-angiotensin system were compared. In a 1-year study, 32 patients with essential hypertension were randomized to treatment with either the converting enzyme inhibitor lisinopril or the calcium antagonist isradipine; hydrochlorothiazide could be added. Blood pressure (BP) decreased significantly (p less than 0.001) and similarly in the 2 treatment groups. Left ventricular (LV) mass was already significantly reduced after 16 weeks of treatment (p less than 0.001) and remained decreased thereafter, with no difference in the response to the 2 treatment regimens. The change in LV mass was related to the decrease in systolic BP for the total study group (p less than 0.001) and for each treatment group separately. During the 3-week run-out period on placebo, BP and LV mass increased again (p less than 0.01). Afterload decreased during active treatment (p less than 0.001), and fractional shortening of the LV internal diameter was significantly increased (p less than 0.01) to a similar extent in both groups. The ratio of peak mitral flow velocities during atrial contraction and early filling was reduced after 1 year of active treatment in the total study group (p less than 0.01); this change was similar in both groups. The data suggest that the regression of LV mass during antihypertensive therapy is mainly related to the decrease in systolic BP.