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The mortality pattern occurring 3 to 6 years after recovery from myocardial infarction is described in a group of 349 patients. Mortality in this group had been previously related to prognostic factors recorded prospectively at the time of adnission to hospitals, and separate coronary prognostic indicesfor hospital and three-year survival had been formulated. The present follow-up shows that mortality between 3 and 6 years can still be related to factors dependent on the degree of myocardial damage sustained, and can be predicted by the coronary prognostic indexfor 3-year survival. Hypertension also had an adverse effect on survival, but the effect which emerges over the 3-to 6-year follow-up is apparent only in patients with an otherwise good prognosis.We have previously reported on clinical factors, present on admission to hospital, which were associated with mortality in a group of 757 patients with myocardial infarction admitted to three hospitals in Auckland during one year (I966-67) (Norris et al., i969, 1970). We incorporated numerical weightings for these factors into coronary prognostic indices for survival in hospital (Norris et al., i969), and for 3 years after discharge from hospital (Norris et al., I970). The present paper reports progress of the 3-year survivors of this same group of patients at a median period of 6 years after discharge. It shows that the chances of survival between 3 and 6 years after recovery were, as in our shorter term surveys, associated with age and factors dependent on the severity of myocardial damage. These factors were radiological evidence of pulmonary venous congestion, pulmonary oedema, and cardiac enlargement at the time of the infarct. vival was correlated with risk factors (hypertension, diabetes, and obesity), recorded at the time of infarction, and with the coronary prognostic index for 3-year survival. The diagnosis of hypertension was based either on a positive history from the patient or his referring practitioner, or the finding of high blood pressure requiring treatment during hospital admission.Of 530 patients followed after discharge from hospital (Norris et al., I970), 357 were known to be alive at 3 years. Of these, 349 (98%) were traced at 6 years, comprising 66 per cent of those who were originally discharged from the hospitals in I966-67.Results Seventy-eight patients had died between the 3-and 6-year follow-ups, this number being 22 per cent of the 357 three-year survivors, and I5 per cent of the original group of 530. Mortality at 3 years had been 33 per cent, so that the total 6-year mortality rate was 48 per cent of hospital survivors.Mortality rates were related to the presence of the previously described clinical prognostic factors which had been present at the time of infarction 6 years before.

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Plasma noradrenaline concentration increases with age. This study was designed to investigate whether an increased rate of noradrenaline release into the circulation or a decrease in clearance is primarily responsible for this age related change in concentration. Sixteen healthy male subjects were studied, eight young (21-36 years) and eight old (65-78 years). Clearance was calculated from steady state noradrenaline concentrations during constant rate infusions of unlabelled noradrenaline. Clearance did not differ between the two groups: young 4.8 l/min (range 2.7-6.1), old 4.1 (range 2.6-8.2). The old subjects had significantly greater rates of release. Supine: young 10.3 nmol/min (range 5.3-17.6), old 19.7 (range 10.1-30), P less than 0.05. Standing: young 17.2 (range 11-36.4), old 29.2 (range 21.8-47.9), P less than 0.01. No significant relationship was found in either supine or standing position between rate of noradrenaline release and either systolic or diastolic blood pressure. These results indicate that plasma noradrenaline concentration rises with age because of an increased rate of release, but that this increased release is not responsible for the higher blood pressure seen in the elderly.

The authors conclude that repair of tympanic membrane perforations with hyaluronic acid ester films is not to be recommended.

A method to non-invasively and quantitatively measure muscle oxygen saturation (SmO(2)) using broadband continuous-wave diffuse reflectance near infrared (NIR) spectroscopy is presented. The method obtained SmO(2) by first correcting NIR spectra for absorption and scattering of skin pigment and fat, then fitting to a Taylor expansion attenuation model. A non-linear least squares optimization algorithm with set boundary constraints on the fitting parameters was used to fit the model to the acquired spectra. A data preprocessing/optimization scheme for accurately determining the initial values needed for the optimization was also employed. The method was evaluated on simulated muscle spectra with 4 different scattering properties, as well as on in vivo forearm spectra from 5 healthy volunteer subjects during arterial occlusion. Measurement repeatability was assessed on 24 healthy volunteers with 5 repeated measurements, each separated by at least 48 hours.