Publications by authors named "Miguel Divo"

Rationale: Chronic lung diseases are associated with increased risk of mortality due to coronary heart disease (CHD). Nonetheless, the population attributable fraction (PAF) of lung function impairment relative to other established cardiovascular risk factors is unclear.

Objective: To evaluate the PAF of low lung function for CHD mortality Methods: We harmonized and pooled lung function and clinical data across 8 US general population cohorts.

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Individuals with chronic obstructive pulmonary disease (COPD) are often at risk for or have comorbid cardiovascular disease and are likely to die of cardiovascular-related causes. To prioritize a list of research topics related to the diagnosis and management of patients with COPD and comorbid cardiovascular diseases (heart failure, atherosclerotic vascular disease, and atrial fibrillation) by summarizing existing evidence and using consensus-based methods. A literature search was performed.

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Body mass index (BMI) is associated with chronic obstructive pulmonary disease (COPD) mortality, but the underlying mechanisms are unclear. The effect of genetic variants aggregated into a polygenic score may elucidate the causal mechanisms and predict risk. To examine the associations of genetically predicted BMI with all-cause and cause-specific mortality in COPD.

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The mean pulmonary arterial wedge pressure (mPAWP) is the critical hemodynamic factor differentiating group 1 pulmonary arterial hypertension (PAH) from group 2 pulmonary hypertension associated with left heart disease. Despite the discrepancy between the mPAWP upper physiologic normal and current PAH definitions, the implications of the initial mPAWP for PAH clinical trajectory are poorly understood. To model longitudinal mPAWP trajectories in PAH over 10 years and examine the clinical and hemodynamic factors associated with trajectory membership.

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Most patients with chronic obstructive pulmonary disease (COPD) have at least one additional, clinically relevant chronic disease. Those with the most severe airflow obstruction will die from respiratory failure, but most patients with COPD die from non-respiratory disorders, particularly cardiovascular diseases and cancer. As many chronic diseases have shared risk factors (eg, ageing, smoking, pollution, inactivity, and poverty), we argue that a shift from the current paradigm in which COPD is considered as a single disease with comorbidities, to one in which COPD is considered as part of a multimorbid state-with co-occurring diseases potentially sharing pathobiological mechanisms-is needed to advance disease prevention, diagnosis, and management.

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Background: The lifetime risk of developing clinical COPD among smokers ranges from 13% to 22%. Identifying at-risk individuals who will develop overt disease in a reasonable timeframe may allow for early intervention. We hypothesised that readily available clinical and physiological variables could help identify ever-smokers at higher risk of developing chronic airflow limitation (CAL).

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Objective: To improve problem list documentation and care quality.

Materials And Methods: We developed algorithms to infer clinical problems a patient has that are not recorded on the coded problem list using structured data in the electronic health record (EHR) for 12 clinically significant heart, lung, and blood diseases. We also developed a clinical decision support (CDS) intervention which suggests adding missing problems to the problem list.

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Rationale And Objective: Patients with chronic obstructive pulmonary disease (COPD), usually diagnosed after the 6th decade, frequently suffer from comorbidities. Whether COPD patients 50 years or younger (Young COPD) have similar comorbidities with the same frequency and mortality impact as aged-matched controls or older COPD patients is unknown.

Methods: We compared comorbidity number, prevalence and type in 3 groups of individuals with ≥ 10 pack-years of smoking: A Young (≤ 50 years) COPD group (n = 160), an age-balanced control group without airflow obstruction (n = 125), and Old (> 50 years) COPD group (n = 1860).

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Article Synopsis
  • COPD patients have lower psoas density (PsD) compared to matched controls, which relates to their exercise intolerance and higher mortality rates.
  • A study measured PsD in 220 COPD patients and 58 controls, finding that lower PsD was significantly linked to all-cause mortality during a follow-up period of about 76.5 months.
  • The findings suggest that assessing muscle quality through PsD on chest CT can help predict long-term outcomes in COPD patients and may aid clinicians in managing their care.
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  • The study explored the use of chest CT imaging to identify comorbidities in COPD patients, highlighting that many were underdiagnosed compared to clinical assessments.
  • Over 78 months, researchers found that certain comorbidities, like coronary artery calcification and bronchiectasis, were significantly linked to increased mortality risk.
  • The findings suggest that utilizing CT scans to systematically detect comorbidities may offer valuable insights for improving patient care in COPD management.
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Rationale: Poor muscle quality in COPD patients relates to exercise intolerance and mortality. Muscle quality can be estimated on computed tomography (CT) by estimating psoas density (PsD). We tested the hypothesis that PsD is lower in COPD patients than in controls and relates to all-cause mortality.

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  • The study investigates how the lung's diffusing capacity for carbon monoxide (Dlco) changes over time in patients with Chronic Obstructive Pulmonary Disease (COPD) and identifies factors that might affect this change, particularly focusing on sex differences.
  • Results showed that COPD patients experience a more significant decline in Dlco compared to those without COPD, with an average yearly drop of 1.34% in COPD patients versus only 0.04% in controls.
  • Women with COPD exhibited lower initial Dlco values and a steeper annual decline compared to men, indicating that sex may play a crucial role in how lung function deteriorates in these patients.
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Background: Pulmonary artery enlargement (PAE) detected using chest computed tomography (CT) is associated with poor outcomes in chronic obstructive pulmonary disease (COPD). It is unknown whether nocturnal hypoxemia occurring in smokers, with or without COPD, obstructive sleep apnoea (OSA) or their overlap, may be associated with PAE assessed by chest CT.

Methods: We analysed data from two prospective cohort studies that enrolled 284 smokers in lung cancer screening programs and completing baseline home sleep studies and chest CT scans.

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  • Chronic obstructive pulmonary disease (COPD) has various phenotypes characterized by airflow limitation, and this study explores how body shape changes (somatotype) from early adulthood can indicate different disease trajectories.
  • Using a pictorial tool, 356 COPD patients reported their body shapes at various ages, revealing five distinct somatotype trajectories, indicating that most participants experienced increasing adiposity over time, except for a small group that remained lean.
  • Those maintaining a lean body shape throughout life showed more severe COPD symptoms, emphasizing the need to monitor smokers with this lean phenotype as they may face greater health risks.
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Chronic obstructive pulmonary disease (COPD) is a complex disease manifested primarily as airflow limitation that is partially reversible as confirmed by spirometry. COPD patients frequently develop systemic manifestations, such as skeletal muscle wasting and cachexia. COPD patients often develop other comorbid diseases, such as ischemic heart disease, heart failure, osteoporosis, anemia, lung cancer, and depression.

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The COVID-19 pandemic has profoundly affected health care delivery worldwide. A small yet significant number of patients with respiratory failure will require prolonged mechanical ventilation while recovering from the viral-induced injury. The majority of reports thus far have focused on the epidemiology, clinical factors, and acute care of these patients, with less attention given to the recovery phase and care of those patients requiring extended time on mechanical ventilation.

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Background: A disintegrin and metalloproteinase domain-15 (ADAM15) is expressed by activated leukocytes, and fibroblasts in vitro. Whether ADAM15 expression is increased in the lungs of COPD patients is not known.

Methods: ADAM15 gene expression and/or protein levels were measured in whole lung and bronchoalveolar lavage (BAL) macrophage samples obtained from COPD patients, smokers, and non-smokers.

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Background: Studies suggest that acute decreases in lung hyperinflation at rest improves cardiac function and increases lung vascular perfusion from decompression of a compromised heart. In those studies, changes in resting oxygen uptake induced by medications, an alternative explanation for compensatory increased cardiac function, were not explored.

Methods: This double-blind, multicenter, double-crossover study enrolled adults with chronic obstructive pulmonary disease, resting hyperinflation, and > 10% improvement in inspiratory capacity after 2 inhalations of budesonide/formoterol 160/4.

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Article Synopsis
  • The study aimed to analyze the comorbidities associated with heart failure (HF) in both men and women, focusing on their patterns and how these affect hospitalisation and mortality risks.
  • Conducted in Aragón, Spain, the research utilized electronic health records from over 14,000 HF patients to identify prevalent chronic diseases and their clustering into six specific multimorbidity patterns.
  • Findings showed that nearly all HF patients had multiple chronic conditions, with distinct patterns linked to varying levels of hospitalisation and mortality risk, highlighting the importance of understanding these patterns for better patient management.
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Background: Plasma metabolomics profile (PMP) in COPD has been associated with clinical characteristics, but PMP's relationship to survival has not been reported. We determined PMP differences between patients with COPD who died an average of 2 years after enrollment (Non-survivors, NS) compared to those who survived (S) and also with age matched controls (C).

Methods: We studied prospectively 90 patients with severe COPD and 30 controls.

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