Left atrial appendage strain predicts subclinical atrial fibrillation in embolic strokes of undetermined source.

Aims: Left atrial (LA) strain is promising in prediction of clinical atrial fibrillation (AF) in stroke patients. However, prediction of subclinical AF is critical in patients with embolic strokes of undetermined source (ESUS). The aim of this prospective study was to investigate novel LA and left atrial appendage (LAA) strain markers in prediction of subclinical AF in ESUS patients. Methods and results: A total of 185 patients with ESUS, mean age 68 ± 13years, 33% female, without diagnosed AF, were included. LAA and LA function by conventional echocardiographic parameters and reservoir strain (Sr), conduit strain (Scd), contraction strain (Sct), and mechanical dispersion (MD) of Sr were assessed with transoesophageal and transthoracic echocardiography. Subclinical AF was detected by insertable cardiac monitors during follow-up. LAA strain was impaired in 60 (32%) patients with subclinical AF compared to those with sinus rhythm: LAA-Sr, 19.2 ± 4.5% vs. 25.6 ± 6.5% (P < 0.001); LAA-Scd, -11.0 ± 3.1% vs. -14.4 ± 4.5% (P < 0.001); and LAA-Sct, -7.9 ± 4.0% vs. -11.2 ± 4% (P < 0.001), respectively, while LAA-MD was increased, 34 ± 24 ms vs. 26 ± 20 ms (P = 0.02). However, there was no significant difference in phasic LA strain or LA-MD. By ROC analyses, LAA-Sr was highly significant in prediction of subclinical AF and showed the best AUC of 0.80 (95% CI 0.73-0.87) with a sensitivity of 80% and a specificity of 73% (P < 0.001). LAA-Sr and LAA-MD were both independent and incremental markers of subclinical AF in ESUS patients. Conclusion: LAA function by strain and mechanical dispersion predicted subclinical AF in ESUS patients. These novel echocardiographic markers may improve risk stratification in ESUS patients.

Exercise capacity in COPD patients with exercise-induced pulmonary hypertension.

BACKGROUND: Pulmonary hypertension (PH) in patients with COPD is associated with reduced exercise capacity. A subgroup of COPD patients has normal mean pulmonary artery pressure (mPAP) at rest, but develops high mPAP relative to cardiac output (CO) during exercise, a condition we refer to as exercise-induced pulmonary hypertension (EIPH). We hypothesized that COPD patients with EIPH could be identified by cardiopulmonary exercise test (CPET) and that these patients have lower exercise capacity and more abnormal CPET parameters compared to COPD patients with normal hemodynamic exercise response. METHODS: Ninety-three stable outpatients with COPD underwent right heart catheterization with the measurement of mPAP, CO, and capillary wedge pressure at rest and during supine exercise. Resting mPAP <25 mmHg with ΔmPAP/ΔCO slope above or below 3 mmHg/L/min were defined as COPD-EIPH and COPD-normal, respectively. Pulmonary function tests and CPET with arterial blood gases were performed. Linear mixed models were fitted to estimate differences between the groups with adjustment for gender, age, and airflow obstruction. RESULTS: EIPH was observed in 45% of the study population. Maximal workload was lower in COPD-EIPH compared to COPD-normal, whereas other CPET measurements at peak exercise in % predicted values were similar between the two groups. After adjustment for gender, age, and airflow obstruction, patients with COPD-EIPH showed significantly greater increase in oxygen uptake, ventilation, respiratory frequency, heart rate, and lactate with increasing work load, as well as more reduction in pH compared to those with normal hemodynamic responses. CONCLUSION: COPD-EIPH could not be discriminated from COPD-normal by CPET. However, COPD-EIPH experienced a higher cost of exercise in terms of higher oxygen uptake, ventilation, respiratory frequency, heart rate, and lactate for a given increase in workload compared to COPD-normal.

Cardiopulmonary exercise test and PaO2 in evaluation of pulmonary hypertension in COPD.

Background: Exercise 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. Methods: In 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. Results: Ventilatory 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%. Conclusion: During CPET, low exercise performance and PaO2 strongly indicated PH in COPD patients.

Mechanisms of ECG signs in chronic obstructive pulmonary disease.

OBJECTIVE: Patients 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. METHODS: A 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. RESULTS: In 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. CONCLUSIONS: In 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.

Assessment of Right Ventricular Afterload in COPD.

BACKGROUND: We aimed to study whether pulmonary hypertension (PH) and elevated pulmonary vascular resistance (PVR) could be predicted by conventional echo Doppler and novel tissue Doppler imaging (TDI) in a population of chronic obstructive pulmonary disease (COPD) free of LV disease and co-morbidities. METHODS: Echocardiography and right heart catheterization was performed in 100 outpatients with COPD. By echocardiography the time-integral of the TDI index, right ventricular systolic velocity (RVSmVTI) and pulmonary acceleration-time (PAAcT) were measured and adjusted for heart rate. The COPD patients were randomly divided in a derivation (n = 50) and a validation cohort (n = 50). RESULTS: PH (mean pulmonary artery pressure (mPAP) ≥ 25mmHg) and elevated PVR ≥ 2Wood unit (WU) were predicted by satisfactory area under the curve for RVSmVTI of 0.93 and 0.93 and for PAAcT of 0.96 and 0.96, respectively. Both echo indices were 100% feasible, contrasting 84% feasibility for parameters relying on contrast enhanced tricuspid-regurgitation. RVSmVTI and PAAcT showed best correlations to invasive measured mPAP, but less so to PVR. PAAcT was accurate in 90- and 78% and RVSmVTI in 90- and 84% in the calculation of mPAP and PVR, respectively. CONCLUSIONS: Heart rate adjusted-PAAcT and RVSmVTI are simple and reproducible methods that correlate well with pulmonary artery pressure and PVR and showed high accuracy in detecting PH and increased PVR in patients with COPD. Taken into account the high feasibility of these two echo indices, they should be considered in the echocardiographic assessment of COPD patients.

Right ventricular dysfunction and remodeling in chronic obstructive pulmonary disease without pulmonary hypertension.

OBJECTIVES: The aim of the present study was to elucidate right ventricular (RV) function and structure in patients with chronic obstructive pulmonary disease (COPD) without pulmonary hypertension (PH). BACKGROUND: There is little knowledge of RV function and remodeling in COPD without PH. METHODS: Thirty-four controls and 98 patients with COPD were included. The study patients were divided into 2 groups by right heart catheterization: no PH (mean pulmonary artery pressure [mPAP] <25 mm Hg) and PH (mPAP ≥25 mm Hg). The echocardiographic tissue Doppler imaging variables of RV isovolumic acceleration, peak systolic strain, and RV myocardial performance index were measured at the basal free wall, and RV wall thickness and RV internal dimension were measured in the RV outflow tract. RESULTS: The increases in RV wall thickness and RV dimension were more evident when comparing controls with the no PH group (3.5 ± 0.5 mm to 5.5 ± 1.0 mm [p < 0.01] and 1.5 cm ± 0.2 to 2.0 ± 0.5 cm [p < 0.01]) than comparing the no PH group with the PH group (5.5 ± 1.0 mm to 6.6 ± 1.1 mm [p < 0.01] and 2.0 cm ± 0.5 to 2.1 ± 0.3 cm [p = NS]), respectively. Similarly, RV isovolumic acceleration, performance index, and strain deteriorated significantly when comparing controls with the no PH group and comparing the no PH group with the PH group (p < 0.01). Significant correlations were observed between mPAP and RV isovolumic acceleration, performance index, strain, and RV wall thickness (p < 0.01). RV impairment and increased RV wall thickness and RV dimensions were present even at slight elevations of mPAP (18 ± 3 mm Hg) in the no PH group. CONCLUSIONS: 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.

Pulmonary artery pressure and PaO2 in chronic obstructive pulmonary disease.

INTRODUCTION: Chronic obstructive pulmonary disease (COPD) is a common cause of pre-capillary pulmonary hypertension (PH). This complication may be overlooked in patients with COPD, as symptoms frequently are attributed to ventilatory limitation. Predictors of PH may identify patients with increased risk of morbidity and mortality. OBJECTIVE: The aims of this COPD study were to (i) evaluate the relationship between mean pulmonary artery pressure (mPAP) and PaO2, (ii) identify significant predictors of mPAP and PaO2 and (iii) use PaO2 as a marker of PH. METHODS: Altogether 95 COPD patients with mild to very severe airway obstruction and without left ventricular (LV) dysfunction were included. Pulmonary function tests, right heart catheterizations and exercise tests with blood gases were performed. RESULTS: Multivariate regression analyses showed that only PaO2 was a significant predictor of mPAP. FEV1 and mPAP were significant predictors of PaO2 both at rest and at peak exercise. PaO2 at peak exercise was better to identify pulmonary hypertension than PaO2 at rest. By combining PaO2 at rest and peak exercise, it was possible to predict PH with a detection rate of 76% and a false-positive rate of 24%. CONCLUSION: 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.

Haemodynamic responses to exercise in patients with COPD.

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 ≥25 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.