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Aims To assess the risk of death from coronary disease, and all causes associated with body mass index and weight gain from age 20 to middle age.Methods and Results In this study, 6874 men aged 47 to 55 years at baseline and free of a history of myocardial infarction were followed with respect to mortality from coronary disease and from all causes over an average follow-up of 19·7 years, and with respect to non-fatal myocardial infarction for 11·8 years. High body mass index predicted death from coronary disease, but only at levels above 27·5m.kg−2. Men with stable weight (defined as ±4% change from age 20) had the lowest death rate from coronary disease and the lowest risk of non-fatal myo-cardial infarction. Relative risk of coronary death increased with increasing weight gain, from 1·57 (1·14–2·15) (after adjustment for age, physical activity, and smoking) in the group who gained 4 to 10%, to 2·76 (1·97–3·85) in men with a weight gain of more than 35% (Pfor trend 0·0001), compared to men who remained stable. After further adjustment for serum cholesterol, systolic blood pressure, and diabetes, relative risks were reduced but still significantly elevated in all weight gain groups (Pfor trend 0·004). Data concerning non-fatal myocardial infarction were available for the first 11·8 years and showed a relative risk of 3·35 (2·05–5·47) after adjustment for age, physical activity, and smoking in men with a weight gain of more than 35%.Conclusion Weight gain from age 20, even a very moderate increase, is strongly associated with an increased risk of coronary death and non-fatal myocardial infarction. [ABSTRACT FROM PUBLISHER]

Objectives: Although many studies have described prognosis in patients with coronary heart disease (CHD), few have compared outcome in men with clinical evidence of CHD with healthy men from the general population over an extended follow-up. This study aimed to compare long-term prognosis in men with a history of myocardial infarction (MI) and in men with angina pectoris (AP) without MI, with men without clinical signs of CHD.Design: Longitudinal general population study.Setting: City of Göteborg, Sweden.Subjects: From a general population sample, 195 men who had survived an MI for 0-19 years (median 3 years) and 314 men with AP but no MI (uncomplicated AP) at baseline in 1974-77 were identified and compared with 6591 men without clinical coronary disease. All were aged 51-59 years. Incident non-fatal and fatal cases occurring until the beginning of 1983 were also followed (n = 317).Main Outcome Measures: Death from CHD, from other causes and from all causes during a follow-up of at least 16 years.Results: Overall survival was 72% amongst men without coronary disease, 53% amongst men with uncomplicated AP and 34% amongst men with past MI at baseline. In survivors of MI the risk-factor-adjusted relative risk (RR) of coronary death during follow-up was 6.67 (95% confidence interval (CI) 5.29-8.39), of dying from non-cardiovascular causes 1.35 (0.96-1.91), and of dying from any cause 3.20 (2.67-3.83). During the first 4 years after the baseline examination, the adjusted RR of CHD death was 15.96 (10. 29-24.74), and of dying from any cause 5.22 (3.68-7.41). During the last 4 years of follow-up, relative risk was still 5.87 (3.44-10.01) for CHD death and 2.93 (2.05-4.18) for death from any cause. In men with uncomplicated AP, the adjusted relative risk of CHD death during the first 4 years was 4.05 (2.27-7.22) and 3.23 (2.10-4.96) during the last 4-year period. After the first year, the incident MI cases had the same average annual mortality (about 5%) as the prevalent cases.Conclusions: In survivors of MI, mortality risk remained high even after an extended follow-up. Men with angina had a better prognosis, but still a compromised survival compared with the general population. [ABSTRACT FROM AUTHOR]

Several ways to evaluate the sound transmission properties of middle ear implants are now established. Besides computer-based simulations using acoustic and electrical analog circuits or finite element analysis, measurements can be performed with temporal bone preparations. Experiments with these preparations consider various anatomical properties, but a large number of parameters influence the outcome of measurements. To facilitate standardized measurements, a mechanical middle ear model was developed that allows comparison of the transfer function of middle ear implants on defined conditions. The model approximates the impedances of the tympanic membrane and inner ear with the aid of thin, flexible membranes. The implants are fit between the membranes, and displacement at an artificial stapes footplate is measured with an optical probe. Fundamental influences on the sound transmission properties of nine different middle ear implants (total ossicular replacement prostheses) were examined. Although the material and shape were different, some of the prostheses revealed very similar transfer functions. The mass of the implant showed the largest influence on sound conduction. With a higher mass, the frequency area above approximately 1 kHz was found to be significantly deteriorated. The lightest implant used was 4 mg and showed the best overall results. These findings show that middle ear prostheses should be as light as possible for optimum high-frequency transmission. [ABSTRACT FROM AUTHOR]

Diabetic patients with acute myocardial infarction have a poor prognosis, which has been attributed to a higher incidence of congestive heart failure and fatal reinfarction. This study reports on the one-year morbidity and mortality in a randomized study with the aim of testing whether insulin–glucose infusion initiated as soon as possible after onset of myocardial infarction and followed by long-term subcutaneous insulin treatment may have a beneficial effect on outcome in diabetic patients. In all, 306 patients were recruited to the insulin-treated group, while 314 patients served as controls.The overall mortality after one year was l9% in the insulin group compared to 26% among controls (P<0.05). The treatment effect was most pronounced in patients with out prior insulin medication and at low cardiovascular risk. In this stratum the in-hospital mortality was reduced by 58% (P<0.05) and the one-year mortality by 52% (P<0.02).The most frequent cause of death in all patients was congestive heart failure (66%), but cardiovascular mortality (congestive heart failure, fatal reinfarction, sudden death and stroke) tended to be decreased in insulin-treated patients. However, this difference did not reach the level of statistical significance. The number of reinfarctions was 53 (28% fatal) in the insulm group compared to 55 (45% fatal) in the control group. The two groups did not differ as regards need for hospital care or coronary revascularization during the year of follow-up.In summary, left ventricular failure and fatal reinfarctions contribute to increased mortality in diabetic patients following acute myocardial infarction. Intensive insulin treatment lowered this mortality during one year of follow-up. [ABSTRACT FROM PUBLISHER]

An analysis of the cost-effectiveness of simvastatin was conducted, based on the Scandinavian Simvastatin Survival Study (4S). The total cost of hospitalization in the placebo group was 5·28 million Swedish kronor (SEK) (£5·l5 million), compared with SEK 36·0 million (£3·51 million) in the simvastatin group. This amounts to a 32% reduction, or a saving of SEK 16·8 million (£1·6 million) or SEK 7560 (£738) per patient.The net cost per patient for the duration of the study (5·4 years) was SEK 13 540 (£1324). Simvastatin treatment saved an estimated 0·377 undiscounted life years (0·240 life years discounted at 5% per annum). The cost of simvastatin therapy per discounted life-year saved was therefore SEK 56 400 (£5502) Sensitivity analysis, examining the effect of different life expectancies, costs of initiation and monitoring of simvastatin therapy, and discount rates, showed the results to be stable.Conclusion The cost per life-year saved of simvastatin in the treatment of post-myocardial infarction and angina patients, as determined from 4S data, is well within the range normally considered cost-effective. [ABSTRACT FROM PUBLISHER]

Audiological experience indicates, that results of tone and speech audiometric tests show only a loose correlation with the ability in social hearing. That is why the influence of presbyacusis upon social hearing was investigated using a psychological test, the so-called 'Social Hearing Handicap Index' (SHHI). The results indicate the influence of presbyacusis on social hearing. The SHHI gets worse with increasing presbyacusis, though in the oldest patient group some individuals with normal social hearing were found. There was only little influence of the hard of hearing component. The social hearing was mainly effected by the disturbance of the selective ability. This is valid for the social hearing handicap within and between the examined groups. Significant differences between female and male patients could not be revealed. [ABSTRACT FROM AUTHOR]

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A reversible conductive hearing loss produced during the first 4 weeks post partum caused marked alterations in the development of click-evoked auditory brainstem (ABR) and middle latency (MLR) responses in guinea pigs. The early component PI in the ABR in controls showed adult-like latencies at the time of birth, while the later ABR components P and P and all components investigated in the MLR showed postnatal development characterized by a shortened latency that persisted for the whole period of investigation. The course of the ABR latencies showed the sharpest decrease during the first 2-3 weeks of life, while that for the MLR took place during the first 5 weeks. In addition to the increased ABR thresholds and lengthened ABR latencies due to the conductive hearing loss, development of the ABR inter-peak latencies (IPL) and MLR latencies was retarded. The IPL reached control values 1 week after the end of the deprivation phase, while the delay in MLR started later (4th week) and lasted longer than did that in the ABR. These findings showed that a long-lasting postnatal conductive hearing loss does not generate sustained impairment at the level of the brainstem but can evoke longer-lasting deficiencies at higher stations of the auditory pathway. [ABSTRACT FROM AUTHOR]

Reversible conductive hearing loss created during the first 4 weeks post partum caused marked alterations in the maturation of binaural interaction components in the auditory brainstem responses of guinea pigs. In untreated control animals all three components investigated demonstrated postnatal development in terms of latency shortening that was completed during the first 3 weeks of life. Plugging of both external ear canals caused a significant delay in the maturation of the late component DN, where latency values of the controls were reached only 2 weeks after the end of the treatment, i.e. after 6 weeks of life. Monaural deprivation likewise led to a retarded development of peak latencies during the phase of imbalanced sensory imput. After the end of the one-sided conductive hearing loss the maturation process was markedly enhanced, even resulting in latency values for DN and DP that were significantly shorter than those of the controls. This phenomenon persisted until the end of the study period and was the case for both plugged and untreated ears in this group of animals. The time course of latencies in two other groups of experimental animals which were deprived in the same way as adults suggests that the effects observed are due to a sensitive period in the maturation process of the auditory pathway. [ABSTRACT FROM AUTHOR]

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Noise-induced alterations of the click-evoked compound potential (CAP) were studied by means of electrodes chronically implanted near the round window in 15 pigmented guinea pigs aged 3-6 months. The potentials were recorded before, during and after exposure to continuous pink noise maintained at an intensity of 80, 90 or 100 dB SPL for 120 h. During the exposure phase the CAP thresholds of all the animals tested increased exponentially, nearly leveling out by approximately 48 h to form an asymptotic threshold shift. Recovery after the end of exposure also occurred exponentially, with a return to the original threshold for neural excitation after at most 72 h. There was no detectable change in amplitude, latency or inter-peak interval of the CAP when correlated with the change in threshold. [ABSTRACT FROM AUTHOR]

Copyright of Archives of Oto-rhino-laryngology is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Archives of Oto-rhino-laryngology is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Archives of Oto-rhino-laryngology is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Archives of Oto-rhino-laryngology is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Auditory brain stem responses of the guinea pig were recorded at five electrode positions located on a line from the ipsilateral to the contralateral mastoid. With monaural stimuli the amplitudes of the first two potentials had their maxima at ipsilateral recording locations, the third potential showed no significant changes at the five electrode positions, while the fourth and fifth potential had their maxima at contralateral recording sites. With binaural stimuli the amplitudes of all potentials showed a symmetric distribution with respect to the vertex. Moreover, binaural interactions could be inferred by comparing the sum of the monaural with the binaural responses. Clinical aspects are discussed in the light of these results. [ABSTRACT FROM AUTHOR]

Copyright of Archives of Oto-rhino-laryngology is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

In a double blind study of metoprolol in the treatment of suspected acute myocardial infarction 698 patients (study group) received metoprolol and 697 a placebo (control group). Metoprolol was given in an intravenous dose of 15 mg as soon as possible after admission to hospital followed by 50 g by mouth four times a day for two days and thereafter 100 mg twice a day for three months. A placebo was similarly given. Congestive heart failure occurred in a similar percentage of patients in both the study (27%) and the control groups (30%). Its severity was estimated by calculating the total dose of frusemide given during the first four days in hospital. Less frusemide was given to patients treated with metoprolol compared with those given a placebo in the total series. An appreciably lower total dose of frusemide was given to patients included in the trial less than or equal to 12 hours after the onset of pain and treated with metoprolol compared with a placebo, while no difference was seen among patients treated later. The initial heart rate, systolic blood pressure, and infarct site affected the results. [ABSTRACT FROM PUBLISHER]

A total of 1395 patients aged 40 to 74 years were included in a double blind trial with the beta 1 selective blocker metoprolol in suspected acute myocardial infarction. Metoprolol was given intravenously (15 mg) as soon as possible after admission to hospital followed by 200 mg daily for three months. A placebo was given in the same manner. The severity of chest pain in the acute phase was calculated by recording the number of injections of analgesics given and the time from the start of blind treatment to the time when the last analgesic was given (duration of pain). The patients receiving metoprolol were given a lower mean number of injections of analgesics during the first four days and after randomisation than those receiving a placebo. The estimated duration of pain was shorter in the metoprolol group than in the placebo group. These effects were related to the initial heart rate, the initial systolic blood pressure, and the final site of the infarct as determined electrocardiographically. Thus metoprolol given in the acute phase of suspected or definite myocardial infarction appears to reduce the severity of chest pain. [ABSTRACT FROM PUBLISHER]

All patients under 60 years of age who were discharged from hospital after a first myocardial infarction between 1968 and 1977 in Göteborg were followed for a minimum of 24 months. The patients were unselected, and treatment was standardised. The patients were divided into five two yearly cohorts, and the prognostic comparability and mortality of these cohorts were assessed. There was a reduction in the two year mortality rate after discharge during the 10 year period. Small baseline differences between the cohorts were controlled by multivariate methods, and a subsequent analysis showed that there was a declining trend in mortality between 1968 and 1977. A higher tendency among smokers to give up smoking and a lower prevalence of angina pectoris could explain only part of the reduction in mortality. A small number of patients underwent a coronary bypass operation; the slight increase in the number of operations during the period cannot, however, account for the reduced mortality. Most of the patients in the later cohorts were treated with beta blockers, and this is the most likely explanation for the majority of the decline in mortality. [ABSTRACT FROM PUBLISHER]

Ten annual cohorts of men suffering from their first myocardial infarction have been followed up to a maximum period of 10.5 years. One thousand and twenty-three male patients of 1306 were smokers. Three months after the infarction 55% had stopped smoking and 45% continued smoking. These two groups were then compared and followed with regard to non-fatal reinfarctions and deaths. Preinfarction characteristics were shown to be similar for the two groups. The prognostic comparability of the two groups was tested using two multiple logistic models. Those who stopped smoking had a slightly higher predicted two year mortality after the infarction. In different age groups it is shown with life table technique that those who stopped smoking had a considerably higher survival rate and lower cumulative frequency of reinfarction. The present study shows a reversion of the expected prognosis after myocardial infarction caused by changing the smoking habit. [ABSTRACT FROM PUBLISHER]

Studies were made in Göteborg over a period of 6 years of all cases of acute myocardial infarction diagnosed among men below the age of 40. Thirty-six cases were registered and 8 of these died outside hospital. Three patients died early during the hospital stay. The remaining 25 patients were compared with a random sample from the general population in Göteborg with respect to conventional risk factors. Smoking, and high plasma cholesterol values were dominating findings among the patients, whereas there was no significant differences in blood pressure levels. Coronary angiography was performed in 18 patients of whom 2 showed normal coronary arteries and left ventricular angiograms. These 2 patients were the only ones free from risk factors. Of the remaining 16 patients, 10 had only one vessel affected. [ABSTRACT FROM PUBLISHER]