Background 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. Purpose 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. Methods A total of 104 COPD patients underwent echocardiography before cardio-pulmonary exercise testing (CPET) and 1–2 minutes after peak exercise. Patients were divided into two groups based on peak E/e': patients with stress induced left ventricular diastolic dysfunction (LVDD) - E/e' >15 (HFpEF) and patients LVDD (without 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. Results Stress induced LVDD occurred in 67/104 patients (64%). Those patients had lower work load, lower VO2 consumption, lower minute ventilation and higher VE/VCO2 slope in comparison to patients without. Except for prostglandine E2, none of the inflammatory, oxidative stress markers correlated to stress E/e'. The best independent predictors for HFpEF were RAVI, right ventricular parasternal diameter and RV E/A >0.75. Their combination predicted HFpEF with the accuracy of 91.2%. Conclusion There is a high prevalence of 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 HFpEF. FUNDunding Acknowledgement Type of funding sources: None.

Background Oxidative stress and inflammation have been implicated in the pathogenesis of diastolic dysfunction (DD) and are both present in chronic obstructive pulmonary disease (COPD). Purpose To evaluate the role of oxidative stress markers (8-isoprostane) and inflammation (prostaglandin E2, resistin) in the pathogenesis of stress induced left ventricular diastolic dysfunction (LVDD) in non-severe COPD. Materials and methods 104 patients with non-severe COPD (FEV1 > 50%) and preserved left ventricular ejection fraction >50% underwent incremental cardio-pulmonary exercise testing (CPET). Echocardiography was performed before CPET and 1-2 minutes after peak exercise. Peak E/e’ ratio >15 was a marker for stress LVDD. Urine concentration of 8-isoprostanes was assumed as surrogate marker for oxidative stress; urine concentration of prostaglandine-E2 and plasma resistin levels as inflammatory markers. Mass spectrometry was applied for 8-isoprostane and prostglandine E2 (Cayman. Chemical) measurement. Values were normalised to urine creatinine (µmol/l/cre). ELISA was applied for resistin measurement (Raybio_Human) (ng/ml). Results Patients were divided into two groups: subjects with stress LVDD (67) and subjects without stress LVDD (37). 8-isoprostane levels were higher in subjects with LVDD vs those without LVDD (32.9 vs 29.67µmol/l/cre; p< 0.05). The same is observed regarding resistin plasma levels (22.51 vs 15.68ng/ml). Urine concentrations of prostaglandin E2 did not differ between the two groups (50.76 vs 51.07 µmol/l/cre) Conclusions In non-severe COPD patients the levels of oxidative stress (8-isoprostanes) and inflammation (resistin) seem to be associated with stress induced left ventricular diastolic dysfunction.

The majority of the SARS-CoV-2 infected patients fully recover within a few weeks. However, a significant proportion of them, independently of their age, still have multi-organ damage, similar to that during the acute phase of infection, or symptoms for a longer term afte r recovery. “Postacute-COVID-19 (Long COVID-19 Syndrome)” is a term used for COVID-19 patients who are still symptomatic 4 and 12 weeks after the onset of acute symptoms and “Post-COVID-19-syndrome” ‒ for those with symptoms for longer than 12 weeks after the onset of acute symptoms. The severity of the initial infection does not correlate with the probability for and with the severity of long-term symptoms. This review comments on the multiorgan effects of Long COVID-19 Syndrome: respiratory, cardiovascular, hematological, renal, gastrointestinal, neurological, and metabolic ones. Recommendations for follow-up and rehabilitation for the recovery of Long COVID-19 Syndrome patients are discussed in detail.

The SARS-CoV-2 coronavirus (COVID-19) pandemic is due to lack of prior immunity and there is no certain management, regarding the complications of this viral illness. The target organ for COVID-19 infection are the lungs. Patients may develop acute lung injury that can be complicated by acute respiratory failure, as well as multiorgan failure. The pathophysiology of COVID-19 infection is characterized with inflammatory changes, associated with coagulopathy. Recent data suggests diffuse bilateral pulmonary inflammation observed in COVID-19 infection that is related to a novel pulmonary-specific vasculopathy, defined as pulmonary intravascular coagulopathy (PIC), distinct from disseminated intravascular coagulopathy (DIC). The coagulopathy associated with COVID-19 is distinguished by initial elevation of D-dimer and fibrin/fibrinogen degradation products. Abnormalities in prothrombin time (PT), partial thromboplastin time (APTT) and platelet counts are not common in the early stages of the infection. This suggests the early screening measurement of D-dimer and fibrinogen. The implications for COVID-19-associated-coagulopathy is the established thromboembolic prophylaxis and standard management for sepsis-induced coagulopathy or DIC. High levels of D-dimer are a marker of higher mortality risk. However, current studies do not show the common use of full therapeutical doses of anticoagulants, unless there are other clinical indications. Bleeding in COVID-19 infection is uncommon, even when a laboratory constellation for DIC is present. However, if it occurs, standard guidelines for DIC management should be followed.

Background Data regarding echocardiographic structural and functional abnormalities in right ventricular diastolic dysfunction (RVDD), cardio-pulmonary exercise testing (CPET) abnormalities and their association with exercise capacity among non-severe chronic obstructive pulmonary disease (COPD) patients without pulmonary arterial hypertension (PAH) at rest is limited. Purpose The aim of the study was to find echocardiographic parameters of the right ventricle that may be predictors for stress RVDD in non-severe COPD patients without PAH and to determine their correlation with the 6-minute walking test (6-MWT). Methods We applied a ramp protocol of CPET in 104 patients. Dynamic hyperinflation (ICdyn) was measured. Emphysema was evaluated by Goddard score. Echocardiography was performed before and 1–2 minutes after peak CPET. Stress RVDD was assumed if peak E/e'>6.0. Exercise capacity was evaluated by the 6-MWT. ROC analysis detected the best cut-off values of the RV echocardiographic predictors for stress RVDD. Multivariate analysis with covariates left ventricle (LV) (LV E/A at rest; LV E/e' at rest; stress LV E/A; stress LV E/e'), lung function (FEV1), ICdyn, Goddard score, age, sex, and BMI was performed. A p-value <0.05 was accepted of statistical significance. Results 78% of the patients had stress RVDD. RV wall thickness (RVWT), right atrial volume index (RAVI) and exercise systolic PAH were significantly higher in COPD patients with stress RVDD. After multivariable regression analysis RAVI and rest RV E/e' ratio >5.1 remained independent predictors for stress RVDD; RAVI and RVWT were independent predictors for diminished exercise capacity (6-MWT). Conclusion There is a high prevalence of stress induced RVDD in non-severe COPD patients without PAH at rest. RAVI and rest RV E/e'>5.1 are the best predictors for stress E/e' >6; RAVI and RVWT are associated with decrements in exercise capacity. Funding Acknowledgement Type of funding source: None