The present study showed that impaired RV systolic function, hypertrophy, and dilation were present even at a slight increase of mPAP, which indicates an early impact on RV function and structure in patients with COPD. RV isovolumic acceleration, performance index, and strain could detect subclinical disease and separate controls from those with no PH.
The present study aimed to explore the prevalence of pre-capillary pulmonary hypertension (PH) and characterise haemodynamic vascular responses to physical exercise in chronic obstructive pulmonary disease (COPD) outpatients, where left ventricular dysfunction and comorbidities were excluded.98 patients with COPD underwent right heart catheterisation at rest and during supine exercise. Mean pulmonary artery pressure (Ppa), pulmonary capillary wedge pressure (Ppcw) and cardiac output (CO) were measured at rest and during exercise. Exercise-induced increase in mean Ppa was interpreted relative to increase in blood flow, mean Ppa/CO, workload (W) and mean Ppa/W. Pulmonary vascular resistance (PVR) and pulmonary artery compliance (PAC) were calculated. PH at rest was defined as mean Ppa at rest o25 mmHg and Ppcw at rest ,15 mmHg.Prevalence of PH was 5%, 27% and 53% in Global Initiative for Chronic Obstructive Lung Disease stages II, III and IV, respectively. The absolute exercise-induced rise in mean Ppa did not differ between subjects with and without PH. Patients without PH showed similar abnormal haemodynamic responses to exercise as the PH group, with increased PVR, reduced PAC and steeper slopes for mean Ppa/CO and mean Ppa/W.Exercise revealed abnormal physiological haemodynamic responses in the majority of the COPD patients. The future definition of PH on exercise in COPD should rely on the slope of mean Ppa related to cardiac output and workload rather than the absolute values of mean Ppa.
ObjectivePatients with chronic obstructive pulmonary disease (COPD) often have abnormal ECGs. Our aim was to separate the effects on ECG by airway obstruction, emphysema and right ventricular (RV) afterload in patients with COPD.MethodsA cross-sectional study was performed on 101 patients with COPD without left heart disease and 32 healthy age-matched controls. Body mass index (BMI) was measured, and pulmonary function tests, ECG, echocardiography and right heart catheterisation (only patients) were performed. Variables were grouped into (1) airway obstruction by FEV% (percentage of forced expiratory volume)_predicted, (2) emphysema by residual volume/total lung capacity and residual volume (percent of predicted) and (3) RV afterload by mean pulmonary pressure, artery compliance, vascular resistance and RV wall thickness.ResultsIn multivariate regression analysis, emphysema correlated negatively to R+S amplitudes in horizontal and frontal leads, RV/left ventricle (LV) end-diastolic volume ratio to horizontal amplitudes and BMI negatively to frontal amplitudes. Increased airway obstruction, RV afterload and BMI correlated with horizontal QRS-axis clockwise rotation. Airway obstruction, RV afterload, RV/LV end-diastolic volume ratio and BMI correlated to the Sokolow-Lyon Index for RV, and RV afterload negatively to Sokolow-LyonIndex for LV. Several classical ECG changes could, however, not be ascribed to specific mechanisms.ConclusionsIn COPD, the various pathophysiological mechanisms modify the ECG differently. Increased airway obstruction and RV afterload mainly increase the Sokolow-Lyon Index for RV mass and associate with clockwise rotation of the horizontal QRS-axis, whereas emphysema reduces the QRS amplitudes. BMI is an equally important determinant for the majority of the ECG changes.
In an outpatient COPD population where LV disease was thoroughly excluded, we observed that only PaO2 was a significant predictor of mPAP. PaO2 at rest and peak exercise below 9.5 kPa (71 mmHg) and 8.5 kPa (64 mmHg), respectively, indicates the need for further evaluation of coexisting PH.
BackgroundExercise tolerance decreases as COPD progresses. Pulmonary hypertension (PH) is common in COPD and may reduce performance further. COPD patients with and without PH could potentially be identified by cardiopulmonary exercise test (CPET). However, results from previous studies are diverging, and a unified conclusion is missing. We hypothesized that CPET combined with arterial blood gases is useful to discriminate between COPD outpatients with and without PH.MethodsIn total, 93 COPD patients were prospectively included. Pulmonary function tests, right heart catheterization, and CPET with blood gases were performed. The patients were divided, by mean pulmonary artery pressure, into COPD-noPH (<25 mmHg) and COPD-PH (≥25 mmHg) groups. Linear mixed models (LMMs) were fitted to estimate differences when repeated measurements during the course of exercise were considered and adjusted for gender, age, and airway obstruction.ResultsVentilatory and/or hypoxemic limitation was the dominant cause of exercise termination. In LMM analyses, significant differences between COPD-noPH and COPD-PH were observed for PaO2, SaO2, PaCO2, ventilation, respiratory frequency, and heart rate. PaO2 <61 mmHg (8.1 kPa) during unloaded pedaling, the only load level achieved by all the patients, predicted PH with a sensitivity of 86% and a specificity of 78%.ConclusionDuring CPET, low exercise performance and PaO2 strongly indicated PH in COPD patients.
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