Trends of COPD in Spain: Changes Between Cross Sectional Surveys 1997, 2007 and 2017.

INTRODUCTION: We aim to describe the changes in prevalence and risk factors associated to chronic obstructive pulmonary disease (COPD) in Spain, comparing three population-based studies conducted in three timepoints. METHODS: We compared participants from IBERPOC conducted in 1997, EPISCAN conducted in 2007 and EPISCAN II in 2017. COPD was defined as a postbronchodilator FEV1/FVC (forced expiratory volume in 1s/forced vital capacity) ratio <0.70, according to GOLD criteria; subsequently, also as the FEV1/FVC below the lower limit of normal (LLN). RESULTS: COPD prevalence in the population between 40 and 69 years decreased from 21.6% (95% CI 20.7%-23.2%) in 1997 to 8.8% (95% CI 8.2%-9.5%) in 2017, a 59.2% decline (p<0.001). In 2007, the prevalence was 7.7% (95% CI 6.8%-8.7%) with an upward trend of 1.1 percentage points in 2017 (p=0.073). Overall COPD prevalence decreased in men and women, although a significant increase was observed in the last decade in females (p<0.05). Current smokers significantly increased in the last decades (25.4% in 1997, 29.1% in 2007 and 23.4% in 2017; p<0.001). Regrettably, COPD underdiagnosis was constantly high, 77.6% in 1997, 78.4% in 2007, and to 78.2% in 2017 (p=0.95), higher in younger ages (40-49 yrs and 50-59 yrs) and also higher in women than in men in all three studies (p<0.05). CONCLUSIONS: We report a significant reduction of 59.2% in the prevalence of COPD in Spain from 1997 to 2017 in subjects aged 40-69 years. Our study highlights the significant underdiagnosis of COPD, particularly sustained in women and younger populations.

Prevalence of Chronic Obstructive Pulmonary Disease in an Urban Area. Changes in COPD Ten Years on.

Purpose: The prevalence of Chronic obstructive pulmonary disease (COPD) in Spain has been evaluated in the last ten years by EPISCAN in 2007 and EPISCAN II in 2017. This study describes changes in the prevalence of COPD in an urban region of Spain in the last 10 years, its risk factors and underdiagnosis. Patients and Methods: Participants from the Autonomous Community of Madrid (Spain) were selected from both studies up to the age of 80 years. A descriptive analysis of their sociodemographic and clinical characteristics, as well as by gender, was conducted. COPD was defined by a post-bronchodilator ratio <0.70. Results: The prevalence of COPD in the Autonomous Community of Madrid increased non-significantly from 11.0% (95% CI: 8.9-13.5%) to 12.1% (95% CI: 9.6-15.1, p=0.612). However, the prevalence by gender showed an increase in women (5.6% to 14.7%, p<0.001) and a decrease in men (17.6% to 9.8%, p=0.08). Underdiagnosis was reduced from 81.0% to 67.9% (p=0.006), although with greater underdiagnosis in women (86.4% in EPISCAN and 100% in EPISCAN II). Smoking was higher in men than in women in EPISCAN (31.2% vs 23.0%, p<0.01) but with no differences by gender in EPISCAN II (25.5% men vs 26.0% women, p=0.146). Age, smoking, low BMI, and a sedentary lifestyle were consistently associated with COPD. Conclusion: In 10 years in Madrid, there have been no changes in the global prevalence of COPD, but there have been important changes in women, with an increase in its prevalence, smoking habit and underdiagnosis.

Predictors of Hearing-Aid Outcomes.

Over 360 million people worldwide suffer from disabling hearing loss. Most of them can be treated with hearing aids. Unfortunately, performance with hearing aids and the benefit obtained from using them vary widely across users. Here, we investigate the reasons for such variability. Sixty-eight hearing-aid users or candidates were fitted bilaterally with nonlinear hearing aids using standard procedures. Treatment outcome was assessed by measuring aided speech intelligibility in a time-reversed two-talker background and self-reported improvement in hearing ability. Statistical predictive models of these outcomes were obtained using linear combinations of 19 predictors, including demographic and audiological data, indicators of cochlear mechanical dysfunction and auditory temporal processing skills, hearing-aid settings, working memory capacity, and pretreatment self-perceived hearing ability. Aided intelligibility tended to be better for younger hearing-aid users with good unaided intelligibility in quiet and with good temporal processing abilities. Intelligibility tended to improve by increasing amplification for low-intensity sounds and by using more linear amplification for high-intensity sounds. Self-reported improvement in hearing ability was hard to predict but tended to be smaller for users with better working memory capacity. Indicators of cochlear mechanical dysfunction, alone or in combination with hearing settings, did not affect outcome predictions. The results may be useful for improving hearing aids and setting patients' expectations.

The Influence of Cochlear Mechanical Dysfunction, Temporal Processing Deficits, and Age on the Intelligibility of Audible Speech in Noise for Hearing-Impaired Listeners.

The aim of this study was to assess the relative importance of cochlear mechanical dysfunction, temporal processing deficits, and age on the ability of hearing-impaired listeners to understand speech in noisy backgrounds. Sixty-eight listeners took part in the study. They were provided with linear, frequency-specific amplification to compensate for their audiometric losses, and intelligibility was assessed for speech-shaped noise (SSN) and a time-reversed two-talker masker (R2TM). Behavioral estimates of cochlear gain loss and residual compression were available from a previous study and were used as indicators of cochlear mechanical dysfunction. Temporal processing abilities were assessed using frequency modulation detection thresholds. Age, audiometric thresholds, and the difference between audiometric threshold and cochlear gain loss were also included in the analyses. Stepwise multiple linear regression models were used to assess the relative importance of the various factors for intelligibility. Results showed that (a) cochlear gain loss was unrelated to intelligibility, (b) residual cochlear compression was related to intelligibility in SSN but not in a R2TM, (c) temporal processing was strongly related to intelligibility in a R2TM and much less so in SSN, and (d) age per se impaired intelligibility. In summary, all factors affected intelligibility, but their relative importance varied across maskers.

Forward-masking recovery and the assumptions of the temporal masking curve method of inferring cochlear compression.

The temporal masking curve (TMC) method is a behavioral technique for inferring human cochlear compression. The method relies on the assumptions that in the absence of compression, forward-masking recovery is independent of masker level and probe frequency. The present study aimed at testing the validity of these assumptions. Masking recovery was investigated for eight listeners with sensorineural hearing loss carefully selected to have absent or nearly absent distortion product otoacoustic emissions. It is assumed that for these listeners basilar membrane responses are linear, hence that masking recovery is independent of basilar membrane compression. TMCs for probe frequencies of 0.5, 1, 2, 4, and 6 kHz were available for these listeners from a previous study. The dataset included TMCs for masker frequencies equal to the probe frequencies plus reference TMCs measured using a high-frequency probe and a low, off-frequency masker. All of the TMCs were fitted using linear regression, and the resulting slope and intercept values were taken as indicative of masking recovery and masker level, respectively. Results for on-frequency TMCs suggest that forward-masking recovery is generally independent of probe frequency and of masker level and hence that it would be reasonable to use a reference TMC for a high-frequency probe to infer cochlear compression at lower frequencies. Results further show, however, that reference TMCs were sometimes shallower than corresponding on-frequency TMCs for identical probe frequencies, hence that compression could be overestimated in these cases. We discuss possible reasons for this result and the conditions when it might occur.

Across-frequency behavioral estimates of the contribution of inner and outer hair cell dysfunction to individualized audiometric loss.

Identifying the multiple contributors to the audiometric loss of a hearing impaired (HI) listener at a particular frequency is becoming gradually more useful as new treatments are developed. Here, we infer the contribution of inner (IHC) and outer hair cell (OHC) dysfunction to the total audiometric loss in a sample of 68 hearing aid candidates with mild-to-severe sensorineural hearing loss, and for test frequencies of 0.5, 1, 2, 4, and 6 kHz. It was assumed that the audiometric loss (HLTOTAL) at each test frequency was due to a combination of cochlear gain loss, or OHC dysfunction (HLOHC), and inefficient IHC processes (HLIHC), all of them in decibels. HLOHC and HLIHC were estimated from cochlear I/O curves inferred psychoacoustically using the temporal masking curve (TMC) method. 325 I/O curves were measured and 59% of them showed a compression threshold (CT). The analysis of these I/O curves suggests that (1) HLOHC and HLIHC account on average for 60-70 and 30-40% of HLTOTAL, respectively; (2) these percentages are roughly constant across frequencies; (3) across-listener variability is large; (4) residual cochlear gain is negatively correlated with hearing loss while residual compression is not correlated with hearing loss. Altogether, the present results support the conclusions from earlier studies and extend them to a wider range of test frequencies and hearing-loss ranges. Twenty-four percent of I/O curves were linear and suggested total cochlear gain loss. The number of linear I/O curves increased gradually with increasing frequency. The remaining 17% I/O curves suggested audiometric losses due mostly to IHC dysfunction and were more frequent at low (≤1 kHz) than at high frequencies. It is argued that in a majority of listeners, hearing loss is due to a common mechanism that concomitantly alters IHC and OHC function and that IHC processes may be more labile in the apex than in the base.