Pulmonary function testing in COPD: looking beyond the curtain of FEV1.
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ABSTRACT:
SUBMITTER: Kakavas S
PROVIDER: S-EPMC8105397 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:BACKGROUND:The prognostic value of chronic obstructive pulmonary disease (COPD) as a comorbidity in heart failure has been well documented. However, the role of pulmonary function indices in patients with heart failure and preserved ejection fraction (HFpEF) remains to be elucidated. METHODS:Subjects with HFpEF received pulmonary function tests and echocardiogram. Total lung capacity (TLC), residual volume (RV), forced expiratory flow rate between 25% and 75% of vital capacity (FEF25-75), forced expiratory volume in the 1st second (FEV1), forced vital capacity (FVC), and vital capacity (VC) were measured. Echocardiographic indices, including pulmonary artery systolic pressure (PASP), the ratio of early ventricular filling flow velocity to the septal mitral annulus tissue velocity (E/e'), and left ventricular mass (LVM), were recorded. National Death Registry was linked for the identification of mortality. RESULTS:A total of 1194 patients (72.4±13.2 years, 59% men) were enrolled. PASP, E/e' and LVM were associated with either obstructive (RV/TLC, FEV1 and FEF25-75) or restrictive (VC and TLC) ventilatory indices. During a mean follow-up of 23.0±12.8 months, 182 patients died. Subjects with COPD had a lower survival rate than those without COPD. While VC, FVC, RV/TLC, and FEV1 were all independently associated with all-cause mortality in patients without COPD, only FEF25-75 was predictive of outcomes in those with COPD. CONCLUSIONS:The abnormalities of pulmonary function were related to the cardiac hemodynamics in patients with HFpEF. In addition, these ventilatory indices were independently associated with long-term mortality, especially in those without COPD.
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Project description:Abstract Infants with forms of pulmonary hypertension (PH) that persist or develop beyond the first week of life are an understudied group of patients with up to 40%-60% mortality. The clinical management of the progressive PH that develops in these infants is challenging because of the nonspecific signs and symptoms of clinical presentation, the limited diagnostic sensitivity of standard echocardiographic techniques, and the lack of proven therapies. The signaling mechanisms that underlie the structural and functional abnormalities in the pulmonary circulation of these infants are not yet clear. The ability to improve outcomes for these patients awaits technological advances to improve diagnostic capabilities and therapeutic discoveries made in basic science laboratories that can be tested in randomized clinical trials.
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Project description:The National Institute of Diabetes and Digestive and Kidney Diseases-supported Kidney Research National Dialogue asked the scientific community to formulate and prioritize research objectives aimed at improved understanding of kidney function and disease progression. Over the past 2 years, 1600 participants posted almost 300 ideas covering all areas of kidney disease. An overriding theme that evolved through these discussions is the need to move beyond pathology to take advantage of basic science and clinical research opportunities to improve diagnostic classification and therapeutic options for people with primary glomerular disease. High-priority research areas included focus on therapeutic targets in glomerular endothelium and podocytes, regenerating podocytes through developmental pathways, use of longitudinal phenotypically defined disease cohorts to improve classification schemes, identifying biomarkers, disease-specific therapeutics, autoantibody triggers, and changing the clinical research culture to promote participation in clinical trials. Together, these objectives provide a path forward for improving clinical outcomes of glomerular disease.
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Project description:RationaleClinical phenotyping, therapeutic investigations as well as genomic, airway secretion metabolomic and metagenomic investigations can benefit from robust, nonlinear modeling of FEV1 in individual subjects. We demonstrate the utility of measuring FEV1 dynamics in representative cystic fibrosis (CF) and chronic obstructive pulmonary disease (COPD) populations.MethodsIndividual FEV1 data from CF and COPD subjects were modeled by estimating median regression splines and their predicted first and second derivatives. Classes were created from variables that capture the dynamics of these curves in both cohorts.ResultsNine FEV1 dynamic variables were identified from the splines and their predicted derivatives in individuals with CF (n = 177) and COPD (n = 374). Three FEV1 dynamic classes (i.e. stable, intermediate and hypervariable) were generated and described using these variables from both cohorts. In the CF cohort, the FEV1 hypervariable class (HV) was associated with a clinically unstable, female-dominated phenotypes while stable FEV1 class (S) individuals were highly associated with the male-dominated milder clinical phenotype. In the COPD cohort, associations were found between the FEV1 dynamic classes, the COPD GOLD grades, with exacerbation frequency and symptoms.ConclusionNonlinear modeling of FEV1 with splines provides new insights and is useful in characterizing CF and COPD clinical phenotypes.
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Project description:AimThe role of the right ventricle (RV) in pulseless electrical activity (PEA) is poorly defined outside of pulmonary embolism. We aimed to (1) describe the continuous electrocardiographic (ECG) manifestations of RV strain (RVS) preceding PEA/Asystole in-hospital cardiac arrest (IHCA), and (2) determine the prevalence and clinical causes of RVS in PEA/Asystole IHCA.MethodsIn this retrospective cross-sectional study, we evaluated 140 patients with continuous ECG data preceding PEA/Asystole IHCA. We iteratively defined the RVS continuous ECG pattern using the development cohort (93 patients). Clinical cause determination was blinded from ECG analysis in the validation cohort (47 patients).ResultsThe overall cohort had mean age 62.1 ± 17.1 years, 70% return of spontaneous circulation and 30% survival to discharge. RVS continuous ECG pattern was defined as progressive RV depolarization delay in lead V1 with at least one supporting finding of RV ischaemia or right axis deviation. Using this criterion, 66/140 (47%) cases showed preceding RVS. In patients with RVS, no pulmonary embolism was found in 9/13 (69%) autopsies and 8/10 (80%) CT chest angiograms. The positive and negative predictive value of RVS pattern for diagnosing a respiratory cause of PEA/Asystole in the validation cohort was 81% [95% CI 64-98%] and 58% [95% CI 36-81%], respectively.ConclusionRVS continuous ECG pattern preceded 47% of PEA/Asystole IHCA and is predictive of a respiratory cause of cardiac arrest, not just pulmonary embolism. These suggest that rapid elevations in pulmonary pressures and resultant RV failure may cause PEA in respiratory failure.
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Project description:The extracellular matrix (ECM) is a diverse microenvironment that maintains bidirectional communication with surrounding cells to regulate cell and tissue homeostasis. The classical definition of the ECM has more recently been extended to include non-fibrillar proteins that either interact or are structurally affiliated with the ECM, termed the 'matrisome.' In addition to providing the structure and architectural support for cells and tissue, the matrisome serves as a reservoir for growth factors and cytokines, as well as a signaling hub via which cells can communicate with their environment and vice-versa. The matrisome is a master regulator of tissue homeostasis and organ function, which can dynamically and appropriately respond to any stress or injury. Failure to properly regulate these responses can lead to changes in the matrisome that are maladaptive. Hepatic fibrosis is a canonical example of ECM dyshomeostasis, leading to accumulation of predominantly collagenous ECM; indeed, hepatic fibrosis is considered almost synonymous with collagen accumulation. However, the qualitative and quantitative alterations of the hepatic matrisome during fibrosis are much more diverse than simple accumulation of collagens and occur long before fibrosis is histologically detected. A deeper understanding of the hepatic matrisome and its response to injury could yield new mechanistic insights into disease progression and regression, as well as potentially identify new biomarkers for both. In this review, we discuss the role of the ECM in liver diseases and look at new "omic" approaches to study this compartment.
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Project description:This study's objective was to examine the characteristics of patients with chronic obstructive pulmonary disease (COPD) presenting with various exercise tolerance levels. A total of 235 patients with stable COPD were classified into 4 groups: (1) LoFlo + HiEx-patients with a six-minute walking distance (6MWD) ≥350 m and percentage of predicted forced expiratory volume in 1 s (%FEV1.0) <50%; (2) HiFlo + HiEx-patients with a 6MWD ≥350 m and a %FEV1.0 ≥50%; (3) LoFlo + LoEx-patients with a 6MWD < 350 m and %FEV1.0 < 50%; and (4) HiFlo + LoEx-patients with a 6MWD <350 m and %FEV1.0 ≥ 50%. Aspects of physical ability in the HiFlo + LoEx group were significantly lower than those in the HiFlo + HiEx group. The HiFlo + LoEx group was characterized by a history of hospitalization for respiratory illness within the past year, treatment with at-home oxygen therapy, and lacking daily exercise habits. Following three months of pulmonary rehabilitation, the LoFlo + HiEx group significantly improved in the modified Medical Research Council dyspnea score, maximum gait speed, and 6MWD, while the HiFlo + LoEx group significantly improved in the percentage of maximal expiratory pressure, maximum gait speed, 6MWD, incremental shuttle walking distance, and St. George's Respiratory Questionnaire score. The HiFlo + LoEx group had the greatest effect of three-month pulmonary rehabilitation compared to other groups.
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Project description:Few studies have investigated the significance of decreased FEV(1) in non-COPD, nonasthmatic healthy subjects. We hypothesized that a lower FEV(1) in these subjects is a potential marker of an increased susceptibility to obstructive lung disease such as asthma and COPD. This was a cross-sectional analysis of 1505 Japanese adults. We divided the population of healthy adults with no respiratory diseases whose FEV(1)/FVC ratio was ? 70% (n = 1369) into 2 groups according to their prebronchodilator FEV(1) (% predicted) measurements: < 80% (n = 217) and ? 80% (n = 1152). We compared clinical data - including gender, age, smoking habits, total IgE levels, and annual decline of FEV(1) - between these 2 groups. In addition, as our group recently found that TSLP variants are associated with asthma and reduced lung function, we assessed whether TSLP single nucleotide polymorphisms (SNPs) were associated with baseline lung function in non-COPD, nonasthmatic healthy subjects (n = 1368). Although about half of the subjects with lower FEV(1) had never smoked, smoking was the main risk factor for the decreased FEV(1) in non-COPD, nonasthmatic subjects. However, the subjects with lower FEV(1) had a significantly higher annual decline in FEV(1) independent of smoking status. Airflow obstruction was associated with increased levels of total serum IgE (P = 0.029) and with 2 functional TSLP SNPs (corrected P = 0.027-0.058 for FEV(1)% predicted, corrected P = 0.015-0.033 for FEV(1)/FVC). This study highlights the importance of early recognition of a decreased FEV(1) in healthy subjects without evident pulmonary diseases because it predicts a rapid decline in FEV(1) irrespective of smoking status. Our series of studies identified TSLP variants as a potential susceptibility locus to asthma and to lower lung function in non-COPD, nonasthmatic healthy subjects, which may support the contention that genetic determinants of lung function influence susceptibility to asthma.
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Project description:Key pointsPeak oxygen uptake, a primary determinant of prognosis, mortality and quality of life, is diminished in patients with chronic obstructive pulmonary disease (COPD), with mounting evidence supporting an important role for peripheral dysfunction, particularly within skeletal muscle. In patients with severe COPD and activity-matched controls, muscle oxygen transport and utilization were assessed at peak effort during single-leg knee-extensor exercise (KE), where ventilation is assumed to be submaximal. This strategy removes ventilation as the major constraint to exercise capacity in COPD, allowing maximal muscle function to be attained and evaluated. During maximal KE, both convective arterial oxygen delivery to the skeletal muscle microvasculature and subsequent diffusive oxygen delivery to the mitochondria were diminished in patients with COPD compared to control subjects. These findings emphasize the importance of factors, beyond the lungs, that influence exercise capacity in this patient population and may, ultimately, influence the prognosis, mortality and quality of life for patients with COPD.AbstractPeak oxygen uptake ( V?O2peak ), a primary determinant of prognosis, mortality and quality of life, is diminished in patients with chronic obstructive pulmonary disease (COPD). Mounting evidence supports an important role of the periphery, particularly skeletal muscle, in the diminished V?O2peak with COPD. However, the peripheral determinants of V?O2peak have not been comprehensively assessed in this cohort. Thus, the hypothesis was tested that both muscle convective and diffusive oxygen (O2 ) transport, and therefore skeletal muscle peak O2 uptake ( V?MO2peak ), are diminished in patients with COPD compared to matched healthy controls, even when ventilatory limitations (i.e. attainment of maximal ventilation) are minimized by using small muscle mass exercise. Muscle O2 transport and utilization were assessed at peak exercise from femoral arterial and venous blood samples and leg blood flow (by thermodilution) in eight patients with severe COPD (forced expiratory volume in 1s (FEV1 ) ± SEM = 0.9 ± 0.1 l, 30% of predicted) and eight controls during single-leg knee-extensor exercise. Both muscle convective O2 delivery (0.44 ± 0.06 vs. 0.69 ± 0.07 l min-1 , P < 0.05) and muscle diffusive O2 conductance (6.6 ± 0.8 vs. 10.4 ± 0.9 ml min-1 mmHg-1 , P < 0.05) were ?1/3 lower in patients with COPD than controls, resulting in an attenuated V?MO2peak in the patients (0.27 ± 0.04 vs. 0.42 ± 0.05 l min-1 , P < 0.05). When cardiopulmonary limitations to exercise are minimized, the convective and diffusive determinants of V?MO2peak , at the level of the skeletal muscle, are greatly attenuated in patients with COPD. These findings emphasize the importance of factors, beyond the lungs, that may ultimately influence this population's prognosis, mortality and quality of life.
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Project description: Not available
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