Left ventricular diastolic dysfunction in non-severe chronic obstructive pulmonary disease - a step forward in cardiovascular comorbidome.

Chronic obstructive pulmonary disease (COPD) augments the likelihood of having left ventricular diastolic dysfunction (LVDD)-precursor of heart failure with preserved ejection fraction (HFpEF). LVDD shares overlapping symptomatology (cough and dyspnea) with COPD. Stress induced LVDD is indicative of masked HFpEF. Our aim was to evaluate the predictive value of inflammatory, oxidative stress, cardio-pulmonary and echocardiographic parameters at rest for the diagnosis of stress LVDD in non-severe COPD patients, who complain of exertional dyspnea and are free of overt cardiovascular diseases. A total of 104 COPD patients (26 patients with mild and 78 with moderate COPD) underwent echocardiography before cardio-pulmonary exercise testing (CPET) and 1-2 minutes after peak exercise. Patients were divided into two groups based on peak average E/e': patients with stress induced left ventricular diastolic dysfunction (LVDD)-E/e' > 15 masked HFpEF and patients without LVDD-without masked HFpEF. CPET and echocardiographic parameters at rest were measured and their predictive value for stress E/e' was analysed. Markers for inflammation (resistin, prostaglandine E2) and oxidative stress (8-isoprostanes) were also determined. Stress induced LVDD occurred in 67/104 patients (64%). Those patients showed higher VE/VCO2 slope. None of the CPET parameters was an independent predictor for stress LVDD.Except for prostglandine E2, none of the inflammatory or oxidative stress markers correlated to stress E/e'. The best independent predictors for stress LVDD (masked HFpEF) were RAVI, right ventricular parasternal diameter and RV E/A >0.75. Their combination predicted stress LVDD with the accuracy of 91.2%. There is a high prevalence of masked HFpEF in non-severe COPD with exertional dyspnea, free of overt cardiovascular disease. RAVI, right ventricular parasternal diameter and RV E/A >0.75 were the only independent clinical predictors of masked HFpEF. 288.

The link between dynamic hyperinflation, autonomic dysfunction and exercise testing parameters with masked heart failure in patients with non-severe obstructive pulmonary disease.

OBJECTIVES: Autonomic dysfunction (AD) and dynamic hyperinflation (DH) have been implicated as pathophysiological mechanisms of heart failure with preserved ejection fraction (HFpEF) in chronic obstructive pulmonary disease (COPD) patients. Their association, however, remains elusive: The aims of the study were: (1) to determine the prevalence of AD and DH in non-severe COPD patients, with exertional dyspnea, without clinically overt cardio-vascular (CV) comorbidities; (2) to analyze the correlation and clinical significance between DH, AD, and maksed HFpEF. METHODS: We applied CPET in 68 subjects. Echocardiography was performed before CPET and 1-2 min after peak exercise. IC manoeuvres were applied. Patients were divided into two groups: patients with and without masked HFpEF. Wilkoff method calculated the meatabolic - chronotropic relationship (MCR). Chronotropic incompetence (CI) and abnormal HR recovery (HRR) were determined. RESULTS: The prevalence of CI was 77 vs. 52% in patients with/without masked HFpEF; of abnormal HRR - 98 vs. 62% respectively; of DH - 53 vs. 29%. ICdyn was associated with AD. Univariate regression showed association between masked HFpEF, ICdyn, HRR, oxygenuptake ('VO2), 'VO2 at anaerobic threshold, oxygen (O2) pulse and 'VE/'VCO2 slope. None of these parameters is an independent predictor for masked HFpEF. CONCLUSIONS: DH, AD, and masked HFpEF are prevalent in non-severe COPD patients, who complain of exertional dyspnea and are free of clinically overt CV comorbidities. DH is independently associated with AD. Neither AD, nor DH and CPET are independent predictors for masked HFpEF.

Stress echocardiography for left ventricular diastolic dysfunction detection in patients with non-severe chronic obstructive pulmonary disease: a cross-sectional study.

AIM: To assess whether the simultaneous performance of exercise stress echocardiography and cardio-pulmonary testing (ESE-CPET) may facilitate the timely diagnosis of subclinical left ventricular diastolic dysfunction (LVDD) in patients with non-severe chronic obstructive pulmonary disease (COPD), preserved left ventricular systolic function, and exertional dyspnea or exercise intolerance. METHODS: This cross-sectional study, conducted between May 2017 and April 2018, involved 104 non-severe COPD patients with exertional dyspnea and preserved ejection fraction who underwent echocardiography before CPET and 1-2 minutes after peak exercise. Based on the peak E/e' ratio, patients were divided into the group with stress-induced LVDD - E/e'>15 and the group without stress-induced LVDD. We assessed the association between LVDD and the following CPET variables: minute ventilation, peak oxygen uptake (VO2), ventilatory efficiency, heart rate reserve, and blood pressure. RESULTS: During ESE-CPET, stress-induced LVDD occurred in 67/104 patients (64%). These patients had lower work load, peak VO2, O2 pulse, and minute ventilation (VE), and higher VE/VCO2 slope than patients without stress-induced LVDD (35.18±10.4 vs 37.01±11.11, P<0.05). None of the CPET variables correlated with E/e'. CONCLUSION: Combined ESE-CPET may distinguish masked LVDD in patients with non-severe COPD with exertional dyspnea and preserved left ventricular systolic function. None of the CPET variables was a predictor for subclinical LVDD.

8-isoprostanes and resistin as markers of vascular damage in non-hypersomnolent obstructive sleep apnoea patients.

BACKGROUND: Oxidative stress and inflammation are assumed as the main pathological triggers for vascular damage in hypersomnolent obstructive sleep apnoea (OSA) patients, whereas their exact role in less symptomatic population is currently unknown. AIM: To determine whether oxidative stress (urinary 8-isoprostane concentration) and inflammation (plasma resistin levels) are associated with vascular damage in non-hypersomnolent (Epworth Sleep Score <11) OSA patients. METHODS: A total of 325 consecutive patients have undergone standard polysomnography, and 256 of them were diagnosed with OSA. Excessive daytime sleepiness was assessed by the Epworth Sleepiness Scale (ESS). Only 86 patients with ESS <11 participated in the study. The control group was presented by 45 subjects without OSA. Endothelial function was assessed by ultrasonographic measurement of flow-mediated dilatation (FMD). Intima-media thickness (IMT) and ankle-brachial index (ABI) were determined by ultrasonography. Urinary 8-isoprostanes (Cayman Chemical, USA) were measured, applying mass spectrometry. Resistin (RayBio_ Human ResistinCat#:ELH-Resistin-001) plasma levels were detected by ELISA. RESULTS: In patients with OSA, flow-mediated dilatation was significantly lower than in control subjects (4·62% ±1·9) and (7·1% ±2·8), respectively (P: 0·013). The prevalence of plaques in a.carotis communis was higher in OSA (16% versus 4%). The same is observed regarding a.tibialis posterior (81% vs. 29%). The average IMT and ABI in OSA and in the control group were, respectively, (IMT - 800 µm versus. 666 µm); (ABI -1·06 versus 1·20). Urinary isoprostanes were higher in OSA patients (0·091 versus 0·078) and correlated negatively to FMD (r: -0·825, P: 0·00), IMT (r: -0·324, P: 0·003) and ABI (r: -0·226, P: 0·043). No association between resistin and the degree of vascular injury was found. CONCLUSIONS: In comparison with the control group, increased prevalence of endothelial dysfunction and vascular damage was established in OSA patients without excessive daytime sleepiness. Urinary 8-isoprostanes (oxidative stress markers) are closely associated with FMD (endothelial dysfunction), IMT and ABI (vascular damage). Resistin plasma levels correlated neither to FMD, nor to IMT or ABI.