COPD is the third leading cause of death in the United States and is associated with signifi cant morbidity and health-care-related expenditures mostly due to acute exacerbations. 1,2 Patients with COPD may develop subclinical or overt pulmonary vascular disease, and the presence of pulmonary hypertension (PH) is an important predictor of both COPD and exacerbation-related morbidity and mortality, particularly in patients with severe disease. [3][4][5][6][7][8] Although PH can occur in patients with mild to moderate COPD because of pulmonary infl ammation and endothelial or cardiac dysfunction, it more commonly occurs and becomes clinically apparent when airfl ow limitation is severe and is believed to be primarily due to hypoxic vasoconstriction of small pulmonary arteries that result in intimal hyperplasia as well as smooth muscle hypertrophy and hyperplasia. [9][10][11] Right-sided heart catheterization (RHC) remains the gold standard for diagnosis of pulmonary vascular disease. 12 Although noninvasive strategies, such as Doppler echocardiography, allow the measurement of pulmonary artery systolic pressure (PASP), this modality is often problematic in patients with COPD because of lung hyperinfl ation and diffi culty in obtaining clear

Background COPD causes significant morbidity and concomitant pulmonary vascular disease and cardiac dysfunction are associated with poor prognosis. CT-detected relative pulmonary artery enlargement defined as a pulmonary artery to ascending aorta diameter ratio greater than one (PA:A>1) is a marker for pulmonary hypertension and predicts COPD exacerbations. However, little is known about the relationship between the PA:A ratio, pulmonary blood volume, and cardiac function. Methods and Results A single-center prospective cohort study of COPD patients was conducted. Clinical characteristics and CT metrics, including the PA:A and pulmonary blood vessel volume were measured. Ventricular functions, volumes, and dimensions were measured by cine cardiac magnetic resonance imaging (cMRI) with 3D analysis. Linear regression examined the relationships between clinical characteristics, CT and cMRI metrics, and 6-minute walk distance (6MWD). Twenty four patients were evaluated and those with PA:A>1 had higher right ventricular (RV) end-diastolic and end-systolic volume indices accompanied by lower RV ejection fraction (EF) (52±7% vs 60±9%, p=0.04). The PA:A correlated inversely with total intraparenchymal pulmonary blood vessel volume and the volume of distal vessels with a cross sectional area of <5 mm2. Lower forced expiratory volume, PA:A>1, and hyperinflation correlated with reduced RVEF. Both PA diameter and reduced RVEF were independently associated with reduced 6MWD. Conclusions The loss of blood volume in distal pulmonary vessels is associated with PA enlargement on CT. CMRI detects early RV dysfunction and remodeling in non-severe COPD patients with a PA:A>1. Both RV dysfunction and PA enlargement are independently associated with reduced walk distance.

A new portable digital recorder (SNORESAT) that uses the sound of snoring and arterial oxygen saturation (SaO2) to monitor breathing abnormalities during sleep was constructed and compared in the laboratory with standard overnight polysomnography (PSG). The device digitally records sound from a transducer applied to the chest and SaO2 from a commercially available ear oximeter. A snore is identified when the moving time average of the sound exceeds a threshold voltage level longer than 0.26 s. The stored data are transferred to a personal computer for poststudy analysis. An analysis algorithm identifies a respiratory disturbance event when a quiet period of 10 to 120 s separates two snores and is associated with a fall in SaO2 exceeding 3%. The respiratory disturbance index (RDI), mean apnea duration, mean lowest SaO2, and number of desaturations > 3% are computed. A total of 129 referrals to the sleep apnea outpatient clinic underwent simultaneous all-night recording of PSG and SNORESAT. Using the computed RDI recorded by the SNORESAT, the sensitivity and specificity of the monitor in detecting sleep apnea syndrome (SAS) ranged between 84 and 90% and 95 and 98%, respectively, depending on the PSG value of RDI used to define SAS (range, > or = 7 to > or = 20 events/h). Using a PSG value of RDI > or = 10, or > or = 20 RD/h as the definition for SAS, the prevalence of SAS in the referral population was 45 and 31%, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Rationale: Hospitalization for acute exacerbation of chronic obstructive pulmonary disease (COPD) is associated with significant morbidity and health care costs, and hospitals in the United States are now penalized by the Centers for Medicare and Medicaid Services for excessive readmissions. Identifying patients at risk of readmission is important, but modifiable risk factors have not been clearly established, and the potential contributing role of psychological disease has not been examined adequately. We hypothesized that depression and anxiety would increase the risk of both short-and long-term readmissions for acute exacerbation of COPD.Objectives: To characterize the associations between depression and anxiety and COPD readmission risk. Methods:We examined the medical records for all patients with a primary diagnosis of acute exacerbation of COPD by International Classification of Diseases, Ninth Revision codes admitted to the University of Alabama at Birmingham Hospital between November 2010 and October 2012. Those who did not meet the standardized study criteria for acute exacerbation of COPD and those with other respiratory illnesses as the primary diagnosis were excluded. Comorbidities were recorded on the basis of physician documentation of the diagnosis and/or the use of medications in the electronic medical record. Multivariable regression analyses identified factors associated with readmission for acute exacerbation of COPD at 1 year and within 30 and 90 days.Measurements and Main Results: Four hundred twenty-two patients were included, with 132 readmitted in 1 year. Mean age was 64.8 6 11.7 years, and mean percent predicted FEV 1 was 48.1 6 18.7%. On univariate analysis, readmitted patients had lower percent predicted FEV 1 (44.9 6 17.3% vs. 50.2 6 19.4%; P = 0.05) and a higher frequency of depression (47.7% vs. 23.4%; P , 0.001). On multivariable analysis, 1-year readmission was independently associated with depression (adjusted odds ratio [OR], 2.67; 95% confidence interval [CI], 1.59-4.47) and in-hospital tobacco cessation counseling (adjusted OR, 0.34; 95% CI, 0.18-0.66). Depression also predicted readmission at 30 days (adjusted OR, 3.83; 95% CI, 1.84-7.96) and 90 days (adjusted OR, 2.47; 95% CI, 1.34-4.55).Conclusions: Depression is an independent risk factor for both short-and long-term readmissions for acute exacerbation of COPD and may represent a modifiable risk factor. In-hospital tobacco cessation counseling was also associated with reduced 1-year readmission.

Background-Hypertension is a risk factor for incident heart failure (HF). However, the effect of uncontrolled blood pressure (BP) on incident HF in older adults with hypertension has not been prospectively examined in propensity-matched studies.

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Scientific Knowledge on the Subject: COPD progresses over decades so little is known about longitudinal changes in individual patients, and whether there are different patterns of disease progression in different patient subgroups.What this Study Adds to the Field: Computational modelling of CT biomarkers suggests there are two patterns of disease progression in COPD. These disease progression patterns or 'subtypes' can be used to stratify individuals into two groups with distinct clinical characteristics, and to stage individuals along their disease time-course. Early stages of both subtypes are identifiable in a proportion of 'healthy smokers' providing a biomarker of early COPD.

A Medicare BPCI intervention did not reduce 30-day all-cause readmission rates or overall costs after hospitalization for acute exacerbation of COPD. Although additional studies enrolling larger numbers of patients at multiple centers may demonstrate the efficacy of our BPCI initiative for COPD readmissions, this is unlikely to be cost effective at any single center.