Left ventricular diastolic dysfunction and exertional ventilatory inefficiency in COPD

Abstract

Background: Left ventricular diastolic dysfunction (LVDD) is highly prevalent in COPD and conflicting results have emerged regarding the consequences on exercise capacity in the 6MWT. We sought to examine the ventilatory efficiency and variability metrics as the primary endpoint and aerobic capacity (V'O 2) as the secondary endpoint. Methods: Forty subjects were included and submitted to comprehensive lung function tests, detailed pulsed-Doppler echocardiography, and cardiopulmonary exercise testing. Four subjects were excluded due to concomitant cardiac disease and two owing to COPD exacerbation. Results: Seventeen COPD/LVDD+ and seventeen COPD/LVDD-individuals were closely matched for baseline characteristics. Throughout the exercise, there was no difference between-groups for primary (V' E /V'CO 2 slope and V' E /V'CO 2 nadir, p > 0.05 for both) or secondary endpoints (V'O 2peak %pred, p > 0.05). Ventilatory variability remained unchanged. However, after very well age-and sex-matched subgroup analysis, five-moderate and three-mild COPD/LVDD + subjects with elevated left ventricular filling pressure (E/e' > 13, n = 8), presented a downward-shifted V' E /V'CO 2 slope (25.7 ± 5.1 vs 33.4 ± 7.1, p = 0.031) and V' E /V'CO 2 nadir reduction (29.7 ± 3.9 vs 36.3 ± 7.2, p = 0.042) besides significantly better V'O 2peak %pred (92.1 ± 21.6% vs 75.8 ± 13.1%, p = 0.045) compared to 8 COPD/LVDD-controls. Ventilatory variability remained once again unchanged. Conclusions: COPD/LVDD overlap is not associated with worse exercise tolerance and/or wasted ventilation in excess compared to controls, even when suspected for elevated left ventricular filling pressure. Further studies are warranted to study specifically if augmented pulmonary blood transit time can allow better gas-exchange, thus preserving exercise capacity under specific conditions in COPD patients without heart failure.

Cardiopulmonary and Muscular Interactions: Potential Implications for Exercise (In)tolerance in Symptomatic Smokers Without Chronic Obstructive Pulmonary Disease

“…However, there was only a weak relationship between left ventricular dysfunction and tolerance to stress exercise testing in smokers without COPD (Grewal et al, 2009). Of note, we could not confirm these findings in patients with COPD (Muller et al, 2018). Downregulation of β-adrenoceptors (Laustiola et al, 1988) and blunted heart rate during exercise are described maladaptations to chronic smoking (Lauer et al, 1997).…”

Ventilatory inefficiency during graded exercise in COPD: A pragmatic approach

“…This calculation would take the form ηV ′ E = (CO 2 ‐ ACR /CO 2 ‐ MCR ) * 100 (For details, see Figure 2). The V′ E ‐V ´CO 2 slope, nadir, and intercept were previously described in detail by our research group (Muller et al., 2018), and broad literature is available (Neder et al., 2015; Ramos et al., 2013).…”

“…However, according to this author, “ The increase in both ventilation and carbon dioxide production should not persuade us that carbon dioxide production is the only determinant of ventilation during exercise in chronic heart failure or that the slope of a ‘best fit’ linear regression line between ventilation and carbon dioxide production ratio is an adequate description of that relation .” (Clark et al., 1992). The model proposed by Clark et al, and widely adopted in exercise physiology, was described as unfitting for patients with obstructive pulmonary diseases for the first time by Ferrazza et al (2009), and later by several authors (Caviedes et al., 2012; Muller et al., 2018; Neder et al., 2015; Rocha et al., 2017). The main criticism is that obstructive diseases might impose the downshifting of the V ′ E ‐ V ′CO 2 slope owing to severe ventilatory constraints and true deterioration in ηV ′ E , making this concept obsolete.…”

Pulmonary Arterial Pressure Changes Under Dobutamine Stress Echocardiography in Non-Anemic Iron Deficient COPD Subjects

“…In addition, LV diastolic function was performed by tissue and pulsed-Doppler echocardiography. Detailed methods for assessment of LV diastolic function have been previously published, 15 and included: (i) peak velocity of early diastole (E), peak atrial contraction velocity (A), and the E/A ratio, obtained by pulsed-wave Doppler on the mitral valve; (ii) Tissue pulsed-wave Doppler of the septal and lateral portions of the mitral annulus in diastole (E´) and the E/E´ ratio. The baseline and peak tricuspid reflux velocity (TRV) were obtained through continuous-wave Doppler at the right ventricle (RV) inlet, and the sPAP was measured by the peak gradient between the RV and the right atrium from the peak TRV, after right atrium pressure (RAP) acquisition and using the Bernoulli equation (sPAP = (TRV) 2 + RAP).…”