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All aspects of health care are under intense scrutiny, none more so than the competence of health care professionals to diagnose and manage disease. Correctly, patients expect those who minister to them to be competent and properly trained. Concepts of what constitutes a good and a bad doctor vary widely. Good may equate with sympathy, yet sympathy is no substitute for ability. The question of competence has received relatively scant attention but is now an important issue. Establishing competence requires setting standards and usually setting conditions for maintaining clinical acumen and ability. Such is laudable, particularly as it can bring about constructive retraining and can divert specific clinical problems to those best able to deal with them. Specific circumscribed procedures have been an obvious first target for criteria of competence. Such procedures are amenable to audit and are performed in sufficient numbers to establish average rates for success, failure, and efficiency. Standards of competence have been suggested for areas such as angioplasty and stenting.1 Cardiac electrophysiological procedures have also been examined and are similarly amenable to suggestions for levels of competence.2 3 Competence involves exposure to and performance of procedures but more importantly it should include an audit of complications and success. It is to be expected that those with the greatest exposure are likely to be those most competent although this relation is not necessarily so simple. Experience in dealing with complications or anticipating their occurrence plays a large part in the successful performance of many clinical procedures, cardiac electrophysiological ones included. Establishing and maintaining levels of competence in those performing procedures is very desirable. It identifies those who can be expected to offer safe modern care, and it helps to identify manpower needs for given disease situations. There are, however, problems with establishing strict guidelines for …

OBJECTIVE--To assess the possible benefits of intravenous isosorbide dinitrate in acute myocardial infarction and oral isosorbide mononitrate in subacute myocardial infarction. METHODS--316 patients presenting with acute myocardial infarction were entered into double blind placebo controlled clinical trials assessing infarct size by enzyme release, ventricular size and function by echocardiography, reperfusion by continuous 12 lead ST segment monitoring and late potentials by high resolution electrocardiography. RESULTS--301 patients, of whom 292 (97%) received thrombolytic treatment, were randomised on admission to intravenous isosorbide dinitrate or placebo. Overall, there was no significant effect of treatment on infarct size, ST segment resolution, ventricular remodelling, or late potentials at day 3. A trend was observed towards a reduction in infarct size in patients with non-Q wave infarction treated with isosorbide dinitrate. Heterogeneity of nitrate effect was observed in relation to the degree of ST segment elevation on presentation with a clear benefit of isosorbide dinitrate in patients with moderate ST segment elevation (472 U/l v 704 U/l, P = 0.003) and a trend towards a deleterious effect in patients with marked ST segment elevation (1152 U/l v 1058 U/l, P = 0.2). ST segment re-elevation was more common among patients receiving nitrate treatment than in those assigned to placebo (29 v 16, P < 0.05). Some 160 patients underwent a further randomisation to sustained release isosorbide mononitrate or placebo on day 3. Echocardiographic volumes after 6 weeks of treatment were similar in the two groups. CONCLUSIONS--No benefit was observed with administration of nitrates in the treatment groups as a whole for either acute or subacute infarction. There was, however, evidence of heterogeneity of effect in the different subgroups of acute infarction, and the possibility that nitrates may have differing actions in different groups of patients should be considered.

Epicardial activation and repolarisation sequences were investigated in patients with upright or inverted T waves in left ventricular leads of the surface electrocardiogram. Fifteen patients were studied: 10 were undergoing coronary artery bypass grafting (upright T waves) and five aortic valve replacement (four patients with T inversion). Monophasic action potentials were recorded intraoperatively from eight to 10 left ventricular sites in each patient. In patients with upright T waves there was an inverse relation between the duration of the monophasic action potential and the activation time (mean slope -1.44). As a consequence, activation and repolarisation proceeded in opposite directions. Dispersion of repolarisation time (14 ms) was less than dispersion of activation time (23 ms). In patients with T wave inversion caused by aortic stenosis there was no relation between the duration of action potential and activation time; the repolarisation sequence resembled the activation sequence, and the dispersion of repolarisation time was greater than the dispersion of activation time (31 and 26 ms respectively). These results show that there are epicardial repolarisation gradients in man and that these are related to the configuration of the T wave. In patients with upright T waves an inverse relation between the duration of the action potential and the activation time reduces the dispersion of the repolarisation time. When the T wave was inverted this relation was no longer found and the dispersion of repolarisation increased.