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Biomedical subjects

H Harden

Publications and source records attributed to H Harden.

4 recordsLinked to original sources

What are appropriate rates of invasive procedures following acute myocardial infarction? A systematic review.

OBJECTIVE: To assess the evidence that higher rates of coronary angiography (CA) and revascularisation (RV) in the subacute phase of acute myocardial infarction (AMI) improve patient outcomes. DATA SOURCES: MEDLINE 1990 - December 1999, Current Contents 1990-1999, Cochrane Library (Issue 4, 1999), HealthSTAR 1990-1999, selected websites and bibliographies of retrieved articles. STUDY SELECTION AND DATA EXTRACTION: Studies selected were (1) randomised trials comparing outcomes of "invasive" versus "conservative" use of CA and RV following AMI; (2) observational studies with formal methods comparing outcomes of high versus low rates of use of these procedures; and (3) clinical practice guidelines (CPGs), expert panel statements and decision analyses which met critical appraisal criteria, and which specified procedural indications. Outcome measures were rates of mortality, re-infarction and limiting or unstable angina. DATA SYNTHESIS: 56 articles were identified; 24 met inclusion criteria. Pooled data from nine RCTs of "invasive" (CA rate 96%; RV rate 66%) versus "conservative" (CA rate 28%; RV rate 19%) strategies showed no significant differences in mortality or re-infarction rates. Pooled results from 12 observational studies showed no mortality differences, but an excess reinfarction rate (8.0% vs 6.4%; P<0.001) in high- versus low-rate populations. Evidence of survival benefit from procedural intervention was strongest for patients with recurrent ischaemia combined with left ventricular dysfunction. CONCLUSIONS: In the subacute phase of AMI, rates of CA and RV in excess of 30% and 20%, respectively, may not confer additional benefit in preventing death or re-infarction. However, variability between studies in design, patient selection, and extent of cross-over from medical to procedural groups, as well as limited data on symptom status, limits generalisability of results.

Angioplasty, Balloon, Coronary↗

A device for functional residual capacity controlled biofeedback of respiratory resistance.

A computer-aided procedure is presented providing subjects with analogous visual feedback of respiratory resistance, which is continuously measured using the forced oscillation method. Simultaneous pneumotachographical control of the breathing volume curve makes it possible to prevent reinforcement for decreases of respiratory resistance which are due to increases of functional residual capacity (FRC). Lung hyperinflation is an unsuitable way to reduce respiratory resistance; if it occurs, feedback is interrupted until the subject decreases his FRC to its initial level. Analysis of the data of 15 adult asthmatic subjects which underwent a 12-sessions feedback training showed that no substantial changes of FRC appeared within feedback trials. Advantages of this new biofeedback technique compared to other procedures are discussed with regard to volume control and feedback signal.

Airway Resistance↗

Dopaminergic neuronal responses to a non-amphetamine CNS stimulant.

The present study compares the effects of d-amphetamine (d-AMP) and the potent non-amphetamine CNS stimulant, amfonelic acid (AFA), on the firing rate of single midbrain dopaminergic (DA) neurons and on neostriatal DA metabolism (dihydroxyphenylacetic acid--DOPAC). The results indicate that AFA, like d-AMP, reduces the firing rate of DA neurons, although unlike d-AMP, AFA does not cause a decrease in neostriatal DOPAC content and, in fact, enhances that produced by haloperidol (HALO). The AFA-induced decrease in firing rate, like d-AMP, is reversed by the DA receptor blocker HALO, but again unlike d-AMP, the decrease in firing rate is not prevented by catecholamine synthesis inhibition with alpha-methyl-para-tyrosine. Thus, both amphetamine and amfonelic acid have identical electrophysiological effects on DA neurons but act by different mechanisms.

3,4-Dihydroxyphenylacetic Acid↗