Sleep Duration and Cognitive Function: The Akershus Cardiac Examination 1950 Study.

INTRODUCTION: Sleep duration is proposed as a lifestyle-related risk factor for cognitive impairment. We investigated the association between sleep duration and cognitive function in a large population-based cohort aged 62-65 years. METHODS: Cross-sectional analyses from the Akershus Cardiac Examination 1950 Study. Linear and nonlinear models were conducted to explore the association between self-reported sleep duration and cognitive function, adjusted for established risk factors for cognitive impairment. RESULTS: We included 3,348 participants, mean age (SD) was 63.9 ± 0.6 years, 48.2% were women, and 47.9% had education >12 years. Mean sleep duration (SD) was 7.0 ± 1.0 h, and 10.2% had abnormal sleep duration (<6 or >8 h). Individuals reporting <6 h or >8 h of sleep scored significantly lower on MoCA test and delayed recall trial in adjusted analysis. CONCLUSIONS: Sleep duration showed an inverted U-shaped association with global cognitive function and memory, suggesting that both shortened and prolonged sleep are related to adverse brain health.

Trajectory of cardiac troponin T following moderate-to-severe COVID-19 and the association with cardiac abnormalities.

BACKGROUND: COVID-19 has been associated with cardiac troponin T (cTnT) elevations and changes in cardiac structure and function, but the link between cardiac dysfunction and high-sensitive cardiac troponin T (hs-cTnT) in the acute and convalescent phase is unclear. OBJECTIVE: To assess whether hs-cTnT concentrations are associated with cardiac dysfunction and structural abnormalities after hospitalization for COVID-19, and to evaluate the performance of hs-cTnT to rule out cardiac pathology. METHODS: Patients hospitalized with COVID-19 had hs-cTnT measured during the index hospitalization and after 3-and 12 months, when they also underwent an echocardiographic study. A subset also underwent cardiovascular magnetic resonance imaging (CMR) after 6 months. Cardiac abnormalities were defined as left ventricular hypertrophy or dysfunction, right ventricular dysfunction, or CMR late gadolinium. RESULTS: We included 189 patients with hs-cTnT concentrations measured during hospitalization for COVID-19, and after 3-and 12 months: Geometric mean (95%CI) 13 (11-15) ng/L, 7 (6-8) ng/L and 7 (6-8) ng/L, respectively. Cardiac abnormalities after 3 months were present in 45 (30%) and 3 (8%) of patients with hs-cTnT ≥ and < 5 ng/L at 3 months, respectively (negative predictive value 92.3% [95%CI 88.5-96.1%]). The performance was similar in patients with and without dyspnea. Hs-cTnT decreased from hospitalization to 3 months (more pronounced in intensive care unit-treated patients) and remained unchanged from 3 to 12 months, regardless of the presence of cardiac abnormalities. CONCLUSION: Higher hs-cTnT concentrations in the convalescent phase of COVID-19 are associated with the presence of cardiac pathology and low concentrations (< 5 ng/L) may support in ruling out cardiac pathology following the infection.

Changes in cardiopulmonary exercise capacity and limitations 3-12 months after COVID-19.

RATIONALE: To describe cardiopulmonary function during exercise 12 months after hospital discharge for coronavirus disease 2019 (COVID-19), assess the change from 3 to 12 months, and compare the results with matched controls without COVID-19. METHODS: In this prospective, longitudinal, multicentre cohort study, hospitalised COVID-19 patients were examined using a cardiopulmonary exercise test (CPET) 3 and 12 months after discharge. At 3 months, 180 performed a successful CPET, and 177 did so at 12 months (mean age 59.3 years, 85 females). The COVID-19 patients were compared with controls without COVID-19 matched for age, sex, body mass index and comorbidity. Main outcome was peak oxygen uptake (V'O2  peak). RESULTS: Exercise intolerance (V'O2  peak <80% predicted) was observed in 23% of patients at 12 months, related to circulatory (28%), ventilatory (17%) and other limitations including deconditioning and dysfunctional breathing (55%). Estimated mean difference between 3 and 12 months showed significant increases in V'O2  peak % pred (5.0 percentage points (pp), 95% CI 3.1-6.9 pp; p<0.001), V'O2  peak·kg-1 % pred (3.4 pp, 95% CI 1.6-5.1 pp; p<0.001) and oxygen pulse % pred (4.6 pp, 95% CI 2.5-6.8 pp; p<0.001). V'O2  peak was 2440 mL·min-1 in COVID-19 patients compared to 2972 mL·min-1 in matched controls. CONCLUSIONS: 1 year after hospital discharge for COVID-19, the majority (77%), had normal exercise capacity. Only every fourth had exercise intolerance and in these circulatory limiting factors were more common than ventilator factors. Deconditioning was common. V'O2  peak and oxygen pulse improved significantly from 3 months.

Minor Myocardial Scars in Association with Cardiopulmonary Function after COVID-19.

BACKGROUND: Myocardial scars detected by cardiovascular magnetic resonance (CMR) imaging after COVID-19 have caused concerns regarding potential long-term cardiovascular consequences. OBJECTIVE: The objective of this study was to investigate cardiopulmonary functioning in patients with versus without COVID-19-related myocardial scars. METHODS: In this prospective cohort study, CMR was performed approximately 6 months after moderate-to-severe COVID-19. Before (∼3 months post-COVID-19) and after (∼12 months post-COVID-19) the CMR, patients underwent extensive cardiopulmonary testing with cardiopulmonary exercise tests, 24-h ECG, and echocardiography. We excluded participants with overt heart failure. RESULTS: Post-COVID-19 CMR was available in 49 patients with cardiopulmonary tests at 3 and 12 months after the index hospitalization. Nine (18%) patients had small late gadolinium enhancement-detected myocardial scars. Patients with myocardial scars were older (63.2 ± 13.2 vs. 56.2 ± 13.2 years) and more frequently men (89% vs. 55%) compared to those without scars. Cardiorespiratory fitness was similar in patients with and without scars, i.e., peak oxygen uptake: 82.1 ± 11.5% versus 76.3 ± 22.5% of predicted, respectively (p = 0.46). The prevalence of ventricular premature contractions and arrhythmias was low and not different by the presence of myocardial scar. Cardiac structure and function assessed by echocardiography were similar between the groups, except for a tendency of greater left ventricular mass in those with scars (75 ± 20 vs. 62 ± 14, p = 0.02 and p = 0.08 after adjusting for age and sex). There were no significant associations between myocardial scar and longitudinal changes in cardiopulmonary function from 3 to 12 months. CONCLUSION: Our findings imply that the presence of minor myocardial scars has limited clinical significance with respect to cardiopulmonary function after COVID-19.

Novel oxygen desaturation parameters are associated with cardiac troponin I: Data from the Akershus Sleep Apnea Project.

Novel diagnostic markers for obstructive sleep apnea beyond the apnea-hypopnea index (AHI) have been introduced. There are no studies on their association with markers of subclinical myocardial injury. We assessed the association between novel desaturation parameters and elevated cardiac troponin I and T. Participants with polysomnography (498) from the Akershus Sleep Apnea study were divided into normal and elevated biomarker groups based on sex-specific concentration thresholds (cardiac troponin I: ≥4 ng/L for women, ≥6 ng/L for men; and cardiac troponin T: ≥7 ng/L for women, ≥8 ng/L for men). Severity of obstructive sleep apnea was evaluated with the AHI, oxygen desaturation index, total sleep time with oxygen saturation below 90% (T90), lowest oxygen saturation (Min SpO2 %), and novel oxygen desaturation parameters: desaturation duration and desaturation severity. How the AHI and novel desaturation parameters predicted elevated cardiac troponin I and cardiac troponin T levels was assessed by the area under the curve (AUC). Based on multivariable-adjusted linear regression, the AHI (ß = 0.004, p = 0.012), desaturation duration (ß = 0.007, p = 0.004), and desaturation severity (ß = 0.147, p = 0.002) were associated with cardiac troponin I levels but not cardiac troponin T. T90 was associated with cardiac troponin I (ß = 0.006, p = 0.009) and cardiac troponin T (ß = 0.005, p = 0.007). The AUC for the AHI 0.592 (standard error 0.043) was not significantly different from the AUC of T90 (SD 0.640, p = 0.08), desaturation duration 0.609 (SD 0.044, p = 0.42) or desaturation severity 0.616 (SD 0.043, p = 0.26) in predicting myocardial injury as assessed by cardiac troponin I. Oxygen desaturation parameters and the AHI were associated with cardiac troponin I levels but not cardiac troponin T levels. Novel oxygen desaturation parameters did not improve the prediction of subclinical myocardial injury compared to the AHI.

It is unlikely that oxygen supplementation in COPD patients with chronic respiratory failure reduce cardiac troponin level.

BACKGROUND: Cardiac troponin T (cTnT) is a biomarker of myocardial injury frequently elevated in COPD patients, potentially because of hypoxemia. This non-randomised observational study investigates whether long-term oxygen treatment (LTOT) reduces the cTnT level. METHODS: We compared cTnT between COPD patients who were candidates for LTOT (n = 20) with two reference groups. Patients from both reference groups were matched with the index group using propensity score.Reference groups consists of institutional pulmonary rehabilitation patients (short-term group) (n = 105 after matching n = 11) and outpatients at a pulmonary rehabilitation clinic (long-term group)(n = 62 after matching n = 10). Comparison was done within 24 h after LTOT initiation in first reference group and within 6 months after inclusion in the second group. RESULTS: The geometric mean of (standard deviation in parentheses) cTnT decreased from 17.8 (2.3) ng/L (between 8 and 9 a.m.) to 15.4 (2.5) ng/L between 1 and 2 p.m. in the LTOT group, and from 18.4 (4.8) ng/L to15.4 (2.5) ng/L in group (1) The corresponding long-term results were 17.0 (2.9) ng/L at inclusion (between 10 and 12 a.m.) to 18.4 (2.4) ng/L after 3 months in the LTOT-group, and from 14.0 (2.4) ng/L to 15.4 (2.5) ng/L after 6 months in group (2) None of the differences in cTnT during the follow-up between the LTOT-group and their matched references were significant. CONCLUSION: Initiation of LTOT was not associated with an early or sustained reduction in cTnT after treatment with oxygen supplementation.

Incidence of thrombotic complications in hospitalised and non-hospitalised patients after COVID-19 diagnosis.

Infection with coronavirus disease-2019 (COVID-19) may predispose for venous thromboembolism (VTE). There is wide variation in reported incidence rates of VTE in COVID-19, ranging from 3% to 85%. Therefore, the true incidence of thrombotic complications in COVID-19 is uncertain. Here we present data on the incidence of VTE in both hospitalised and non-hospitalised patients from two ongoing prospective cohort studies. The incidence of VTE after diagnosis of COVID-19 was 3·9% [95% confidence interval (CI): 2·1-7·2] during hospitalisation, 0·9% (95% CI: 0·2-3·1) in the three months after discharge and 0·2% (95% CI: 0·00-1·25) in non-hospitalised patients, suggesting an incidence rate at the lower end of that in previous reports.

Persistent symptoms 1.5-6 months after COVID-19 in non-hospitalised subjects: a population-based cohort study.

This study assessed symptoms and their determinants 1.5-6 months after symptom onset in non-hospitalised subjects with confirmed COVID-19 until 1 June 2020, in a geographically defined area. We invited 938 subjects; 451 (48%) responded. They reported less symptoms after 1.5-6 months than during COVID-19; median (IQR) 0 (0-2) versus 8 (6-11), respectively (p<0.001); 53% of women and 67% of men were symptom free, while 16% reported dyspnoea, 12% loss/disturbance of smell, and 10% loss/disturbance of taste. In multivariable analysis, having persistent symptoms was associated with the number of comorbidities and number of symptoms during the acute COVID-19 phase.

Cardiopulmonary exercise capacity and limitations 3†months after COVID-19 hospitalisation.

BACKGROUND: This study aimed to describe cardiopulmonary function during exercise 3 months after hospital discharge for COVID-19 and compare groups according to dyspnoea and intensive care unit (ICU) stay. METHODS: Participants with COVID-19 discharged from five large Norwegian hospitals were consecutively invited to a multicentre, prospective cohort study. In total, 156 participants (mean age 56.2 years, 60 females) were examined with a cardiopulmonary exercise test (CPET) 3 months after discharge and compared with a reference population. Dyspnoea was assessed using the modified Medical Research Council (mMRC) dyspnoea scale. RESULTS: Peak oxygen uptake (V'O2  peak) <80% predicted was observed in 31% (n=49). Ventilatory efficiency was reduced in 15% (n=24), while breathing reserve <15% was observed in 16% (n=25). Oxygen pulse <80% predicted was found in 18% (n=28). Dyspnoea (mMRC ≥1) was reported by 47% (n=59). These participants had similar V'O2  peak (p=0.10) but lower mean±sd V'O2  peak·kg-1 % predicted compared with participants without dyspnoea (mMRC 0) (76±16% versus 89±18%; p=0.009) due to higher body mass index (p=0.03). For ICU- versus non-ICU-treated participants, mean±sd V'O2  peak % predicted was 82±15% and 90±17% (p=0.004), respectively. Ventilation, breathing reserve and ventilatory efficiency were similar between the ICU and non-ICU groups. CONCLUSIONS: One-third of participants experienced V'O2  peak <80% predicted 3 months after hospital discharge for COVID-19. Dyspnoeic participants were characterised by lower exercise capacity due to obesity and lower ventilatory efficiency. Ventilation and ventilatory efficiency were similar between ICU- and non-ICU-treated participants.

Dyspnoea, lung function and CT findings 3†months after hospital admission for COVID-19.

The long-term pulmonary outcomes of coronavirus disease 2019 (COVID-19) are unknown. We aimed to describe self-reported dyspnoea, quality of life, pulmonary function and chest computed tomography (CT) findings 3 months following hospital admission for COVID-19. We hypothesised outcomes to be inferior for patients admitted to intensive care units (ICUs), compared with non-ICU patients.Discharged COVID-19 patients from six Norwegian hospitals were enrolled consecutively in a prospective cohort study. The current report describes the first 103 participants, including 15 ICU patients. The modified Medical Research Council (mMRC) dyspnoea scale, the EuroQol Group's questionnaire, spirometry, diffusing capacity of the lung for carbon monoxide (D LCO), 6-min walk test, pulse oximetry and low-dose CT scan were performed 3 months after discharge.mMRC score was >0 in 54% and >1 in 19% of the participants. The median (25th-75th percentile) forced vital capacity and forced expiratory volume in 1 s were 94% (76-121%) and 92% (84-106%) of predicted, respectively. D LCO was below the lower limit of normal in 24% of participants. Ground-glass opacities (GGO) with >10% distribution in at least one of four pulmonary zones were present in 25% of participants, while 19% had parenchymal bands on chest CT. ICU survivors had similar dyspnoea scores and pulmonary function as non-ICU patients, but higher prevalence of GGO (adjusted OR 4.2, 95% CI 1.1-15.6) and lower performance in usual activities.3 months after admission for COVID-19, one-fourth of the participants had chest CT opacities and reduced diffusing capacity. Admission to ICU was associated with pathological CT findings. This was not reflected in increased dyspnoea or impaired lung function.

Cardiac pathology 6 months after hospitalization for COVID-19 and association with the acute disease severity.

BACKGROUND: Coronavirus disease 2019 (COVID-19) may cause myocardial injury and myocarditis, and reports of persistent cardiac pathology after COVID-19 have raised concerns of long-term cardiac consequences. We aimed to assess the presence of abnormal cardiovascular resonance imaging (CMR) findings in patients recovered from moderate-to-severe COVID-19, and its association with markers of disease severity in the acute phase. METHODS: Fifty-eight (49%) survivors from the prospective COVID MECH study, underwent CMR median 175 [IQR 105-217] days after COVID-19 hospitalization. Abnormal CMR was defined as left ventricular ejection fraction (LVEF) <50% or myocardial scar by late gadolinium enhancement. CMR indices were compared to healthy controls (n = 32), and to circulating biomarkers measured during the index hospitalization. RESULTS: Abnormal CMR was present in 12 (21%) patients, of whom 3 were classified with major pathology (scar and LVEF <50% or LVEF <40%). There was no difference in the need of mechanical ventilation, length of hospital stay, and vital signs between patients with vs without abnormal CMR after 6 months. Severe acute respiratory syndrome coronavirus 2 viremia and concentrations of inflammatory biomarkers during the index hospitalization were not associated with persistent CMR pathology. Cardiac troponin T and N-terminal pro-B-type natriuretic peptide concentrations on admission, were higher in patients with CMR pathology, but these associations were not significant after adjusting for demographics and established cardiovascular disease. CONCLUSIONS: CMR pathology 6 months after moderate-to-severe COVID-19 was present in 21% of patients and did not correlate with severity of the disease. Cardiovascular biomarkers during COVID-19 were higher in patients with CMR pathology, but with no significant association after adjusting for confounders. TRIAL REGISTRATION: COVID MECH Study ClinicalTrials.gov Identifier: NCT04314232.

Annual decline in forced expiratory volume and airway inflammatory cells and mediators in a general population-based sample.

BACKGROUND: Few studies have examined the relationships between sputum inflammatory markers and subsequent annual decline in forced expiratory volume in 1 s (dFEV1). This study investigated whether indices of airway inflammation are predictors of dFEV1 in a general population-based sample. METHODS: The study, conducted from 2003 to 2005, included 120 healthy Norwegian subjects aged 40 to 70 years old. At baseline, the participants completed a self-administered respiratory questionnaire and underwent a clinical examination that included spirometry, venous blood sampling, and induced sputum examination. From 2015 to 2016, 62 (52%) participants agreed to a follow-up examination that did not include induced sputum examination. Those with a FEV1/forced vital capacity (FVC) ratio <  0.70 underwent a bronchial reversibility test. The levels of cytokines, pro-inflammatory M1 macrophage phenotypes were measured in induced sputum using bead-based multiplex analysis. The associations between cytokine levels and dFEV1 were then analysed. RESULTS: The mean dFEV1 was 32.9 ml/year (standard deviation 26.3). We found no associations between dFEV1 and the baseline indices of sputum inflammation. Seven participants had irreversible airflow limitation at follow-up. They had lower FEV1 and gas diffusion at baseline compared with the remaining subjects. Moreover, two of these individuals had a positive reversibility test and sputum eosinophilia at baseline. CONCLUSIONS: In this cohort of presumably healthy subjects, we found no associations between sputum inflammatory cells or mediators and dFEV1 during 10 years of follow-up.

The association between circulating adiponectin levels, lung function and adiposity in subjects from the general population; data from the Akershus Sleep Apnea Project.

BACKGROUND: Circulating adiponectin (ADPN) levels are inversely associated with disease severity in patients with chronic obstructive pulmonary disease (COPD), while studies assessing the relationship between ADPN and lung function in subjects from the general population have shown diverging results. Accordingly, we hypothesized that ADPN would be associated with lung function in a population-based sample and tested how abdominal adiposity, metabolic syndrome, and systemic inflammation influenced this association. METHODS: We measured total ADPN in serum, forced vital capacity (FVC) and forced expiratory volume during the 1st second (FEV1) in 529 participants (median 50 years, 54.6% males) recruited from the general population. We assessed the association between ADPN and lung function by multivariate linear regression analyses and adjusted for age, gender, height, smoking habits, weight, body mass index, waist-hip ratio, metabolic syndrome, obstructive sleep apnoea (OSA) and C-reactive protein. RESULTS: The median (interquartile range) level of serum ADPN was 7.6 (5.4-10.4) mg/L. ADPN levels were positively associated with FVC % of predicted (beta 3.4 per SD adiponectin, p < 0.001)) in univariate linear regression analysis, but the association was attenuated in multivariate analysis (standardized beta 0.03, p = 0.573)). Among co-variates only WHR significantly attenuated the relationship. ADPN levels were also associated with FEV1% of predicted in bivariate analysis that adjusted for smoking (beta 1.4, p = 0.042)), but this association was attenuated and no longer significant in multivariate analysis (standardized beta -0.06, p = 0.254)). CONCLUSION: In this population-based sample no association between ADPN and lung function was evident after adjustment for covariates related to adiposity.

Premature Ventricular Complex is More Prevalent During Acute Exacerbated than Stable States of Chronic Obstructive Pulmonary Disease, and Is Related to Cardiac Troponin T.

During acute exacerbation of chronic obstructive pulmonary disease (AECOPD), myocardial stress may be aggravated. Sparse data exist concerning the prevalence and correlates of cardiac arrhythmias in the stable and exacerbated states of COPD. We hypothesized that AECOPD is associated with increased prevalence of cardiac arrhythmias independent of COPD-severity and co-morbidity, and explored possible mechanisms. A 24-hour Holter recording was obtained in 74 patients with stable COPD and 45 patients with AECOPD (mean age 54 years, 56% women). Any incidence of supraventricular tachycardia (SVT), frequent premature ventricular complex (PVC, >30/hour) and complex ventricular ectopy (bigeminy, trigeminy or non-sustained ventricular tachycardia) was recorded and compared between the two groups. Adjustments were made for by stable disease-related co-variates (demography, co-morbidity, COPD-severity) and by acute disease-related co-variates (heart rate, cardiac troponin T (cTnT), PO2, PCO2 and C-reactive protein (CRP)) in explorative analyses. The prevalence of SVT, frequent PVCs or complex ventricular ectopy was 40%, 27% and 33% in AECOPD, and 31%, 31% and 12% in stable COPD, respectively. Frequent PVC, but not SVT or complex ventricular ectopy, was significantly increased in AECOPD compared to stable COPD, odds ratio 3.03 (1.03-10.5, p = 0.039) when adjusted for stable disease-related co-variates. Higher heart rate, cTnT and CRP attenuated the association between AECOPD and frequent PVC to non-significant, while heart rate remained associated with frequent PVC. In conclusion, frequent PVC is more prevalent in exacerbated than in the stable states of COPD. Attenuation effects of cTnT, tachycardia and CRP suggest that cardiac stress or inflammation may be involved in mechanisms causing frequent PVC i AECOPD.

Biomarkers of cardiovascular injury and stress are associated with increased frequency of ventricular ectopy: a population-based study.

BACKGROUND: Asymptomatic ventricular arrhythmias are common and associated with increased risk of cardiovascular mortality. Cardiac troponins, natriuretic peptides and C-reactive protein (CRP) are also predictive of adverse cardiovascular events in the general population, but limited information is available on the relationship between these biomarkers and ventricular ectopy in a community-based population. The objectives were to evaluate the associations between ventricular ectopic activity and N-terminal pro-B-type natriuretic peptide (NT-proBNP), high sensitivity-troponin I (hs-TnI) and hs-CRP in a community-based setting. METHODS: We performed a 24 h Holter-recording and blood sampling in 498 subjects. Premature ventricular complexes (PVC) were classified as frequent at >5/h and the presence of any bigeminy, trigeminy or non-sustained ventricular tachycardia were classified as complex ventricular ectopy. The associations between biomarkers and ventricular arrhythmias were investigated by univariate and multivariate logistic regression analyses. RESULTS: Frequent PVC's and complex ventricular ectopy were detected in 46 (9%) and 47 (9%) participants respectively, and were associated with significantly (p < 0.001) higher concentrations of NT-proBNP and hs-TnI. The association between NT-proBNP and both frequent PVC's (p = 0.020) and complex ventricular ectopy (p = 0.001) remained significant after adjusting for conventional risk markers in multivariate analyses. CONCLUSION: Increased level of NT-proBNP was independently associated with ventricular ectopy, whereas no independent association was observed between hs-TnI and hs-CRP levels and ventricular ectopy in this community-based sample.

The prognostic value of measurement of high-sensitive cardiac troponin T for mortality in a cohort of stable chronic obstructive pulmonary disease patients.

BACKGROUND: Cardiovascular disease (CVD) is a common comorbidity in chronic obstructive pulmonary disease (COPD). Cardiac troponin (cTn) elevation, indicating myocardial injury, is frequent during acute COPD exacerbations and associated with increased mortality. The prognostic value of circulating cTnT among COPD patients in the stable state of the disease is still unknown. The purpose of the present study was to assess the association between circulating cTnT measured by a high sensitive assay (hs-cTnT) and all-cause mortality among patients with stable COPD without overt CVD. METHODS: In a prospective cohort study we included 275 patients from the Akershus University Hospital's outpatient clinic and from Glittre, a pulmonary rehabilitation clinic. COPD-severity and cardiovascular risk factors were assessed, and time to all-cause death was recorded during a mean follow-up time of 2.8 years. RESULTS: One hundred-eighty patients (65%) had hs-cTnT concentrations ≥ the level of detection (5.0 ng/L) and 66 patients (24%) had hs-cTnT above the normal range (≥14.0 ng/L). In total, 47 patients (17%) died. hs-cTnT concentrations in the ranges <5.0, 5.0-13.9 and ≥14 ng/L were associated with crude mortality rates of 2.8, 4.4 and 11.0 per 100 patient-years, respectively. In adjusted analyses the hazard ratios (95% confidence intervals) for death were 1.7 (0.8-3.9) and 2.9 (1.2-7.2) among patients with hs-cTnT concentrations 5.0-13.9 and ≥14 ng/L, respectively, compared to patients with hs-cTnT <5.0 ng/L. CONCLUSIONS: hs-cTnT elevation is frequently present in patients with stable COPD without overt CVD, and associated with increased mortality, independently of COPD-severity and other cardiovascular risk factors.

Annual decline in forced expiratory volume is steeper in aluminum potroom workers than in workers without exposure to potroom fumes.

BACKGROUND: Aluminum potroom exposure is associated with increased mortality of COPD but the association between potroom exposure and annual decline in lung function is unknown. We have measured lung volumes annually using spirometry from 1986 to 1996. The objective was to compare annual decline in forced expiratory volume in 1 s (dFEV1) and forced vital capacity (dFVC). METHODS: The number of aluminum potroom workers was 4,546 (81% males) and the number of workers in the reference group was 651 (76% males). The number of spirometries in the index group and the references were 24,060 and 2,243, respectively. RESULTS: After adjustment for confounders, the difference in dFEV1 and dFVC between the index and reference groups were 13.5 (P < 0.001) and -8.0 (P = 0.060) ml/year. CONCLUSION: Aluminum potroom operators have increased annual decline in FEV1 relative to a comparable group with non-exposure to potroom fumes and gases.

Determinants of high sensitivity cardiac troponin T elevation in acute ischemic stroke.

BACKGROUND: A proportion of patients with acute ischemic stroke have elevated cardiac troponin levels and ECG changes suggestive of cardiac injury, but the etiology is unclear. The aims of this study were to assess the frequency of high sensitivity cardiac troponin T (hs-cTnT) elevation, to identify determinants and ECG changes associated with hs-cTnT elevation, to identify patients with myocardial ischemia and to assess the impact of hs-cTnT elevation on in-hospital mortality. METHODS: Patients discharged with a diagnosis of acute ischemic stroke during a 1-year period, were included. Patients diagnosed with acute myocardial infarction (MI) within the last 7 days before admission or during hospitalization were excluded. RESULTS: In all, 156 (54.4%) of 287 patients had elevated hs-cTnT. The factors independently associated with hs-cTnT elevation were age ≥ 76 years (OR 3.71 [95% CI 2.04-6.75]), previous coronary heart disease (CHD) (OR 2.61 [1.23-5.53]), congestive heart failure (OR 4.26 [1.15-15.82]), diabetes mellitus (OR 4.02 [1.50-10.76]) and lower eGFR (OR 0.97 [0.95-0.98]). Of the 182 patients who had two hs-cTnT measurements, 12 (6.6%) had both a rise or fall of hs-cTnT with at least one elevated value, and ECG manifestations of myocardial ischemia, e.g. meeting the criteria of acute MI. Both dynamic relative change (p = 0.026) and absolute change (p = 0.032) in hs-cTnT were significantly associated with higher in-hospital mortality. CONCLUSIONS: Established CHD and cardiovascular risk factors are associated with hs-cTnT elevation. Acute MI is likely underdiagnosed in acute ischemic stroke patients. Dynamic changes in troponin levels seem to be related to poor short-term prognosis.

Prognostic value of high-sensitivity cardiac troponin T in acute ischemic stroke.

BACKGROUND: Cardiac troponins have been investigated as prognostic markers in the setting of ischemic stroke with diverging results. A new generation of highly sensitive troponin assays have recently been developed that allow for the detection of concentrations 5 to 10 times lower than those measureable with conventional assays. The aim of this study was to determine the association between high-sensitivity cardiac troponin T (hs-cTnT) elevation on admission and mortality after acute ischemic stroke. METHODS: Serum concentrations of hs-cTnT were measured at the time of admission in 347 patients with acute ischemic stroke. Clinical data and background information were obtained. Total follow-up time was 1.5 ± 0.7 years, and all-cause mortality was used as the outcome measure. RESULTS: Median hs-cTnT on admission in the whole group was 15.2 ng/L (interquartile range [IQR] 7.5-27.8), and was higher in nonsurvivors than survivors (28.2 ng/L [IQR 15.6-39.5] vs 11.4 ng/L [IQR 6.0-21.2]; P < .001). In multivariate analysis, high hs-cTnT (the fourth quartile) was independently associated with all-cause mortality during the follow-up period, with a hazard ratio of 1.65 (95% confidence interval [CI] 1.04-2.63; P = .035). The addition of hs-cTnT as a continuous variable to the multivariate model resulted in both incremental discrimination and reclassification of patients (C-index increase from 0.819 to 0.834 [P = .007]; integrated discrimination index 0.011 [95% CI 0.001-0.021; P = .028]). CONCLUSIONS: Circulating hs-cTnT levels are closely associated with the risk of death in patients with acute ischemic stroke, and even levels below the upper reference limit appear to have prognostic value.

COPD: Iron Deficiency and Clinical Characteristics in Patients With and Without Chronic Respiratory Failure.

Background: The prevalence of iron deficiency in patients with chronic obstructive pulmonary disease (COPD) varies in previous studies. We aimed to assess its prevalence according to 3 well-known criteria for iron deficiency, its associations with clinical characteristics of COPD, and mortality. Methods: In a cohort study consisting of 84 COPD patients, of which 21 had chronic respiratory failure, and 59 were non-COPD controls, ferritin, transferrin saturation (TSat), and mortality across 6.5 years were assessed. Associations between clinical characteristics and iron deficiency were examined by logistic regression, while associations with mortality were assessed in mixed effects Cox regression analyses. Results: The prevalence of iron deficiency in the study population was 10%-43% according to diagnostic criteria, and was consistently higher in individuals with COPD, peaking at 71% in participants with chronic respiratory failure. Ferritin < cutoff was significantly associated with forced expiratory volume in 1 second (FEV1) (odds ratio [OR] 0.33 per liter increase), smoking (OR 3.2), and cardiovascular disease (OR 4.7). TSat < 20% was associated with body mass index (BMI) (OR 1.1 per kg/m2 increase) and hemoglobin (OR 0.65 per g/dL increase). The combined criterion of low ferritin and TSat was only associated with FEV1 (OR 0.39 per liter increase). Mortality was not significantly associated with iron deficiency (hazard ratio [HR] 1.2-1.8). Conclusion: The prevalence of iron deficiency in the study population increased with increasing severity of COPD. Iron deficiency, defined by ferritin < cutoff, was associated with bronchial obstruction, current smoking, and cardiovascular disease, while TSat < 20% was associated with reduced levels of hemoglobin and increased BMI. Iron deficiency was not associated with increased mortality.