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Biomedical subjects

Anthony Barnett

Publications and source records attributed to Anthony Barnett.

6 recordsLinked to original sources
PubMed2006

Prevention of loss of renal function over time in patients with diabetic nephropathy.

Management of hypertension is the mainstay of prevention and treatment of diabetic renal disease; evidence suggests that tight blood pressure control slows renal disease progression in established diabetic nephropathy. Inhibition of the renin-angiotensin-aldosterone system (RAAS) has renoprotective effects over and above those achieved by lowering systemic blood pressure. To date, however, no long-term study using hard end points has directly compared current mechanisms for RAAS inhibition, angiotensin II receptor blockade (ARB) and angiotensin-converting enzyme (ACE) inhibition. This issue was addressed in the recently published Diabetics Exposed to Telmisartan and Enalapril (DETAIL) study, a head-to-head comparison of telmisartan and enalapril in 250 patients with hypertension and type 2 diabetes mellitus and early-stage nephropathy. After 5 years' treatment, change in glomerular filtration rate (GFR), the primary efficacy end point, was equivalent in the 2 treatment groups, as were all secondary end points. The expected steep decline in GFR in the first year was followed by a lesser decrease in the second year and then almost complete stabilization of renal function at > or =3 years. Over 5 years, no patient went into end-stage renal disease or required dialysis. There were also no increases in albumin excretion rate, nor was there an increase in creatinine beyond 200 mumol/L. Incidence of cardiovascular morbidity and mortality was extremely low in both treatment groups, a remarkable outcome given that almost 50% of patients had evidence of cardiovascular disease at randomization. Inhibition of the RAAS should play a major part in management of patients with type 2 diabetes with nephropathy, for which both telmisartan and enalapril provide long-term renoprotection.

Angiotensin II Type 1 Receptor Blockers↗
PubMed2006

Individual calibration for estimating free-living walking speed using the MTI monitor.

PURPOSE: This study was conducted to devise a new individual calibration method to enhance MTI accelerometer estimation of free-living level walking speed. METHOD: Five female and five male middle-aged adults walked 400 m at 3.5, 4.5, and 5.5 km x h(-1), and 800 m at 6.5 km x h(-1) on an outdoor track, following a continuous protocol. Lap speed was controlled by a global positioning system (GPS) monitor. MTI counts-to-speed calibration equations were derived for each trial, for each subject for four such trials with each of four MTI, for each subject for the average MTI, and for the pooled data. Standard errors of the estimate (SEE) with and without individual calibration were compared. To assess accuracy of prediction of free-living walking speed, subjects also completed a self-paced, "brisk" 3-km walk wearing one of the four MTI, and differences between actual and predicted walking speed with and without individual calibration were examined. RESULTS: Correlations between MTI counts and walking speed were 0.90 without individual calibration, 0.98 with individual calibration for the average MTI, and 0.99 with individual calibration for a specific MTI. The SEE (mean +/- SD) was 0.58 +/- 0.30 km x h(-1) without individual calibration, 0.19 +/- 0.09 km x h(-1) with individual calibration for the average MTI monitor, and 0.16 +/- 0.08 km x h(-1) with individual calibration for a specific MTI monitor. The difference between actual and predicted walking speed on the "brisk" 3-km walk was 0.06 +/- 0.25 km x h(-1) using individual calibration and 0.28 +/- 0.63 km x h(-1) without individual calibration (for specific accelerometers). CONCLUSION: MTI accuracy in predicting walking speed without individual calibration might be sufficient for population-based studies but not for intervention trials. This individual calibration method will substantially increase precision of walking speed predicted from MTI counts.

Acceleration↗
PubMed2006

Preventing renal complications in type 2 diabetes: results of the diabetics exposed to telmisartan and enalapril trial.

Patients with type 2 diabetes are prone to hypertension and persistent protein leakage from the kidney (microalbuminuria or macroalbuminuria). A progressive decline in renal function can lead to overt diabetic nephropathy and ESRD. The likelihood of cardiovascular disease also is increased. Control of hypertension is paramount to prevent these life-threatening complications. Agents that target the renin-angiotensin system--angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers--have been shown to be renoprotective. The groundbreaking Diabetics Exposed to Telmisartan And enalaprIL (DETAIL) trial was designed to address the absence of comparative data on the long-term effects of an angiotensin II receptor blocker versus an angiotensin-converting enzyme inhibitor on renoprotection and survival in 250 patients with hypertension and early type 2 diabetic nephropathy. The primary purpose of the 5-yr double-blind, double-dummy, randomized study was to establish whether 40 to 80 mg of telmisartan conferred similar (i.e., noninferior) renoprotection to 10 to 20 mg of enalapril as determined by the change from baseline in GFR, measured by the plasma clearance of iohexol. Secondary end points included the emergence of ESRD and all-cause mortality. Telmisartan was not inferior to enalapril in reducing the decline in GFR: Mean annual declines in GFR were 3.7 and 3.3 ml/min per 1.73 m(2) with telmisartan and enalapril, respectively. During the 5-yr study period, no patient developed a serum creatinine >200 micromol/L, and none required dialysis. There were only six deaths in each treatment group during the study, with half being due to cardiovascular events.

Angiotensin II Type 1 Receptor Blockers↗
PubMed2006

Using recovery modalities between training sessions in elite athletes: does it help?

Achieving an appropriate balance between training and competition stresses and recovery is important in maximising the performance of athletes. A wide range of recovery modalities are now used as integral parts of the training programmes of elite athletes to help attain this balance. This review examined the evidence available as to the efficacy of these recovery modalities in enhancing between-training session recovery in elite athletes. Recovery modalities have largely been investigated with regard to their ability to enhance the rate of blood lactate removal following high-intensity exercise or to reduce the severity and duration of exercise-induced muscle injury and delayed onset muscle soreness (DOMS). Neither of these reflects the circumstances of between-training session recovery in elite athletes. After high-intensity exercise, rest alone will return blood lactate to baseline levels well within the normal time period between the training sessions of athletes. The majority of studies examining exercise-induced muscle injury and DOMS have used untrained subjects undertaking large amounts of unfamiliar eccentric exercise. This model is unlikely to closely reflect the circumstances of elite athletes. Even without considering the above limitations, there is no substantial scientific evidence to support the use of the recovery modalities reviewed to enhance the between-training session recovery of elite athletes. Modalities reviewed were massage, active recovery, cryotherapy, contrast temperature water immersion therapy, hyperbaric oxygen therapy, nonsteroidal anti-inflammatory drugs, compression garments, stretching, electromyostimulation and combination modalities. Experimental models designed to reflect the circumstances of elite athletes are needed to further investigate the efficacy of various recovery modalities for elite athletes. Other potentially important factors associated with recovery, such as the rate of post-exercise glycogen synthesis and the role of inflammation in the recovery and adaptation process, also need to be considered in this future assessment.

Athletic Injuries↗