Exercise Dyspnea Research Articles

Nebulized fentanyl does not improve exercise capacity or dyspnoea in fibrosing interstitial lung disease.

Exercise intolerance and exertional dyspnoea are hallmarks of fibrosing interstitial lung disease (FILD) and are associated with worse prognosis and quality of life. Activation of pulmonary vagal afferents influences the ventilatory pattern and contributes to the sensation of dyspnoea. We tested the hypothesis that nebulized fentanyl, which might attenuate aberrant pulmonary afferent activity in FILD, reduces ventilation and dyspnoea while extending exercise endurance time (EET). In this randomized, single-blind, placebo-controlled study, eight FILD patients (two males, 71±6years of age) performed incremental cardiopulmonary cycle exercise tests following nebulization of either fentanyl citrate (100 µg) or 0.9% saline. Previous work indicated that this dose was unlikely to produce central effects. Comparisons between treatment conditions at rest were undertaken using Student's paired t-test, and exercise data were evaluated with two-way ANOVA with repeated measures. Dyspnoea was assessed using the Borg dyspnoea scale. Resting respiratory variables were not different following treatment with fentanyl and saline; however, resting heart rate was lower following fentanyl (P=0.002) and remained lower throughout exercise compared with placebo (P=0.008). Fentanyl did not increase EET (placebo 334±117s vs. fentanyl 348±126s, P=0.250) although overall minute ventilation was reduced slightly (mean difference: -0.97 L/min, P=0.022). There were no differences in ratings of dyspnoea intensity or unpleasantness between the conditions either at rest or at end-exercise. Nebulized fentanyl did not improve EET or exercise dyspnoea but did decrease minute ventilation during exercise, although the extent of this reduction appears clinically insignificant. These findings suggest that nebulized fentanyl is unlikely to offer significant benefits for enhancing exercise capacity in FILD.

Every Patent Foramen Ovale Should Be Closed.

At present, the patent foramen ovale (PFO) does not receive the deserved medical attention. The PFO poses a serious threat to health and even the life of mankind. The first respective case report in the medical literature dates back to the 19th century. It led to death. The fact that a PFO is present in roughly 25% of people underscores its overall potential to cause harm. Yet at the same time, the sheer number discourages the medical community from screening for it and from treating it. About 5% of the population have particularly dangerous forms of PFOs. Such PFOs portray a high enough risk for clinical events, the likes of death, stroke, myocardial infarction, or ocular, visceral, and peripheral embolism, to justify screening for them. Highly significant health incidents being at stake, it appears obvious that PFO closure should be used for primary prevention. This is supported by the fact that closing a PFO is the simplest intervention in cardiology, with presumably the highest clinical yield. Being mainly a preventive measure, PFO closure represents a mechanical vaccination. When closing PFOs for one of the rarer therapeutic indications (migraine, platypnea orthodeoxia, etc.), patients automatically profit from the collateral benefit of getting, at the same time, mechanically vaccinated for life against paradoxical embolism. Vice versa, closing a PFO for the prevention of paradoxical embolism betters or cures migraine or exercise dyspnea not infrequently, thereby improving quality of life as a collateral benefit.

Gestion de la péricardite constrictive : à travers l’étude de 43 cas opérés

Chronic constrictive pericarditis is a rare condition characterized by clinical signs of right heart failure, due to the symphysis of the two pericardial leaflets.Our study focused on a retrospective analysis of 43 CCP surgery observations collected over an 11-year period (2003–2013).The mean age of the patients was 32 years; 65% were male; exercise dyspnea (95%) was the most frequent sign. Two main etiologies were observed: tuberculosis 58% and idiopathic causes 42%. All of our patients received a subtotal pericardectomy per median sternotomy, of which 95% had no cardiopulmonary bypass.

Right ventricular-arterial coupling and exercise-induced tricuspid regurgitation

Abstract Background Right Ventricular-pulmonary Artery (RV-PA) coupling is prognostic in a variety of cardiovascular disorders, including heart failure with preserved ejection fraction, pulmonary hypertension and severe aortic stenosis. The functional aspects of RV-PA coupling are less investigated than rest ones especially in what is their interaction with tricuspid regurgitation (TR). Purpose We sought to understand the association of RV-PA coupling with extent of exercise induced TR by combining gas exchange abnormalities through cardiopulmonary exercise test (CPET) imaging. Methods We prospectively studied patients with indication to perform a CPET imaging test due to dyspnoea and underlying heart disease of any left ventricular ejection fraction. Demographics, baseline characteristics, echo and CPET parameters [(e.g. VE/VCO2 slope and peak oxygen consumption (pVO2)] were evaluated across 3 sub-cohorts phenotyped according to TR severity pattern at rest and at peak exercise . Mitral and tricuspid regurgitation degree were adjudicated accordingly to ESC guidelines. RV-PA coupling function was assessed through the ratio between tricuspid annular plane systolic excursion (TAPSE), and non-invasive pulmonary artery systolic pressure (PASP) with echocardiography. Dynamic TR was defined as detection of at least moderate TR grade from rest to stress. Results A total of 73 patients (age 67±13 years, 52% men), with a mean LVEF of 50±14% were studied. Overall 50 (69%) patients had less than moderate TR which did not increase during stress (Controls), 11 (15%) patients exhibited a dynamic TR pattern (Group 1), and 12 (16%) already had significant TR at rest (Group 2). TAPSE/PASP at rest and peak exercise were significantly lower in Group 1 and 2 compared to Controls (Figure), while the mean PAP/cardiac output (CO) ratio at rest and at peak exercise were significantly higher (Table). As to gas exchange data, Group 1 and 2 exhibited a lower median peak VO2, while Group 2 patients had also a higher median VE/VCO2 slope compared to Controls (Table). 10 (14%) patients showed at least moderate mitral regurgitation (significant MR) at rest and the prevalence of significant MR at peak was higher in group 1 and 2 compared to Controls (Table). A weak negative correlation was found between TAPSE/PASP slope and E/e’ ratio at peak exercise (r =-0.435, p<0.01). Conclusion In presence of exercise dyspnoea, patients with dynamic TR during maximal exercise exhibit a worse degree of RV-PA coupling and gas exchange profile compared to the group without significant exercise-induced TR. Moreover, the exercise-induced TR profile behaves similarly to the one of those presenting with moderate to severe TR already detectable at rest. Phenotyping dynamic TR and RV-PA warrants further evidence on therapies and outcomes prediction in exertional dyspnoea patients.FigureTable

Abstract 14279: Improved Pressure-Flow Relationship With Sacubitril/Valsartan: A 6-min Walk Stress Echocardiographic Study

Background: In the clinical setting, there are various techniques for stress echocardiography, of which the 6-minute walk (6MW) test is a straightforward and utilized one. An abnormal hemodynamic response to exercise is indicated by a ΔmPAP/ΔCO slope of greater than 3 mmHg/L/min between rest and exercise. This response is associated with impaired prognosis in patients with exercise dyspnea and several cardiovascular diseases. Hypothesis: Our hypothesis was that pressure-flow relationship of the pulmonary circulation obtained by 6MW stress echocardiography would be enhanced with treatment. Aims: The aim of this study was to assess the effects of administration of Sacubitril/Valsartan on cardiac function in heart failure. Methods: We prospectively enrolled 39 patients with heart failure. The 6MW test was performed indoors in a flat, straight corridor. The peak tricuspid regurgitation jet, early diastolic transmitral flow velocity and early diastolic mitral motion were obtained by echocardiography post-6MW. We calculated the slope of ΔmPAP/ΔCO as a parameter of pulmonary hypertension. Follow-up echocardiographic studies were performed after 1 year. Results: Left ventricular diameter and volume were significantly reduced (LVDd; 59.3±7.7mm vs 56.0±8.6mm, P<0.001, LVEDV; 160.7±49.6ml vs 136.0±54.3ml, P<0.001), and LVEF was significantly improved (37.6±11.3% vs 44.9±11.5%, P<0.001). Among the 31 patients who underwent 6MW stress echocardiographic study at baseline and 1 year later, 6MW distance increased after treatment (380m vs 430m, P=0.003). The ΔmPAP/ΔCO by 6MW stress decreased with treatment (6.9mmHg/L/min vs 2.8mmHg/L/min, P=0.002). Conclusions: Initiation of Sacubitril/Valsartan was associated with improvement of left ventricular size and LVEF. Additionally, the 6MW distance increased and the ΔmPAP/ΔCO was improved to within normal range with treatment. Sacubitril/Valsartan distinctly improved cardiac reactivity to exercise.

Myocardial Perfusion is Compromised in Patients with COPD and Associated with Reduced Functional Capacity

Introduction: Chronic Obstructive Pulmonary Disease (COPD) is the 3rd leading cause of death worldwide and carries with it significant cardiovascular mortality. Arterial stiffness is a known risk factor for cardiovascular disease that contributes to worsening myocardial blood flow and limits functional capacity, a marker of disease prognosis and quality of life in COPD. Myocardial perfusion is decided by a careful balance between myocardial blood flow and workload and has been strongly associated with cardiovascular mortality. Despite the convincing relationship between COPD and cardiovascular disease, to date, studies investigating myocardial perfusion and its relationship to functional capacity in COPD remains unexplored. Purpose: This study sought to test the hypothesis that myocardial perfusion is reduced in COPD and associated to functional capacity. Methods: Ten patients with COPD (GOLD Stage II-IV) with no overt signs of cardiovascular disease or diagnosis and 10 demographically matched, apparently healthy controls participated in this study completing a comprehensive analysis of vascular function and functional capacity. Carotid femoral applanation tonometry was used to assess myocardial perfusion (subendocardial viability ratio (SEVR)) and arterial stiffness (Pulse Wave Velocity (PWV)). Functional Capacity was measured via six-minute walk test distance (6MWT) with dyspnea being measured on a 0-10 scale. Results: Patients with COPD exhibited significantly ( p=0.041) reduced myocardial perfusion (SEVR: ΔCOPD=131±19% vs. ΔControl=153±28%) and increased arterial stiffness (PWV: ΔCOPD=8±1 m/s vs. ΔControl=6±1 m/s, p=0.013) when compared to matched controls. Functional Capacity was significantly ( p<0.001) reduced in patients with COPD (6MWT Distance: ΔCOPD=274±87 m vs. ΔControl=476±99 m) while exhibiting significantly ( p=0.02) increased post exercise dyspnea (ΔCOPD=3.1±2.4 vs. ΔControl=0.8±1.2 a.u.). Myocardial perfusion was strongly associated to 6MWT distance ( p=0.038; r=0.693) and arterial stiffness was negatively associated with dyspnea ( p=0.015; r=-0.850). Conclusion: Our data supports that patient with COPD exhibit poor myocardial perfusion that is associated to worse functional capacity, key component of quality of life and mortality in this population. This preliminary data highlights the importance of cardiovascular screening in COPD as it emphasizes how myocardial perfusion impairments may predict prognosis in this population even when no diagnosis of cardiovascular disease is present. Future studies are warranted to investigate if impaired myocardial perfusion plays a causational role in decreasing functional capacity and its potential as a therapeutic target. Supported by American Heart Association (18CDA34110323 PRM & PRE905812 KC/PRM). This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

253 EXCERCISE-INDUCED PULMONARY HYPERTENSION AND CORONARY ARTERY ANOMALY: AN UNUSUAL ASSOCIATION

Abstract A healthy 55-year-old competitive sportsman, with familial history of early sudden cardiac death, came to our attention following the finding of asymptomatic exercise-induced myocardial ischemia (ST depression in V3- V6). Computed tomography (CT) coronary angiogram excluded atherosclerotic disease but showed a dominant right coronary artery (RCA) originating from left Valsalva sinus and with an interarterial course between the ascending aorta and the pulmonary artery. Both the trunk of the pulmonary artery and the right ventricle were reported as mildly dilated Transthoracic echocardiography showed a normal left ventricle (LV), while confirmed right ventricle (RV) dilatation, moderate tricuspid regurgitation (TR) and interatrial septal aneurysm. Stress echocardiography excluded inducible ischemia, but highlighted exercise-induced pulmonary hypertension (PH) (PAPs 25 → 70 mmHg), while a transesophageal echo confirmed a left-to-right shunt due to a 8-mm Patent Foramen Ovale (PFO). Rheumatological, thromboembolic and parenchymal lung diseases were excluded as possible causes of exercise-induced PH; a rest right heart catheterization (RHC) showed a Qp/Qs ratio at the upper limits of normal range without PH. Nuclear stress testing identified trivial asymptomatic septal ischemia. The patients started medium dose of beta-blockers and early follow-up was planned. This clinical case raises some questions: why is RV dilated? What role does PFO play? What is the cause of the inducible ischemia? What is the pathogenesis of exercise-induced PH? Pulmonary Arterial Hypertension, in early stages, often manifests only under exertion, but it is usually characterized by exercise dyspnea and low oxygen saturation. Moreover, intracardiac shunts may be involved in developing PH. In this specific case, pulmonary trunk may be expanded by pressure overload, causing the compression of aberrant RCA and consequent ischemic abnormalities. RV dilatation might be explained by exercise-induced PH itself, but it was not severe and has to be demonstrated by exercise right heart catheterization. The main questions are: which is the primary etiology of right chamber enlargement and myocardial ischemia? Which is the most appropriate therapeutic approach (i.e. conservative vs interventional)?

Feasibility of a nasal breathing training during pulmonary rehabilitation. A pilot randomized controlled study

Hyperventilation syndrome (HVS) is a common source of dyspnea and disability. While pulmonary rehabilitation (PR) including breathing exercises is indicated, randomized controlled trial are warranted to recommend one type of breathing exercise than another. We aimed to compare during PR, the effect of 5 sessions of nasal ventilation exercise (NV+PR) versus voluntary hypoventilation (vHV+PR) on exercise dyspnea (primary outcome) and capacity and health-related quality of life in patients.In this open label randomized controlled trial, 19 HVS patients (age=48.3 ± 15.2 y.o, female/male=18/1, Nijmegen score=33 ± 7.7) were randomized in a NV+PR (n = 9) or vHV+PR (n = 10) group. Modified Medical Research Council (mMRC) dyspnea, 6-minute walking distance (6MWD) with nasal/oral ventilation were assessed before and after 3 months of PR, and questionnaires (Nijmegen, VQ-11).There was a significant effect of PR of but no significant difference between groups in the improvements of dyspnea@max exercise (time effect (T): p < 0.01; group (G): p = 0.63; group*time interaction (G*T): p = 0.49), mMRC dyspnea (T: p < 0.01; G: p = 0.45; G*T: p = 0.62), 6MWD (T: p < 0.05; G: p = 0.36; G*T: p = 0.31), VQ-11 (T: p < 0.001; G: p = 0.16; G*T: p = 0.09) and plasma HCO3- (T: p < 0.05; G: p = 0.93; G*T; p = 0.36), Yet, Nijmegen score (T: p < 0.01; G: p = 0.32; G*T: p < 0.05) improvement was larger in NV+PR group. The exercise oronasal breathing shift during the 6MWT was significantly delayed in all patients (T: p < 0.05; G: p = 0.30; G*T: p = 0.32) and positively correlated with plasma HCO3-(r = 0.42; p < 0.05).Nasal exercise was not superior versus voluntary hypoventilation during PR in HVS patients. Yet, nasal exercise appeared feasible, leading to acquisition of a nasal breathing pattern during walking, improvement of PR outcomes and ventilatory alkalosis. The link between nasal breathing and hyperventilation is discussed in the light of the nasal ventilation rhythm in the limbic system and its role on the limbic emotional and ventilatory functions.

Factors affecting the success of pulmonary rehabilitation in asthma

Objective The majority of patients with asthma limit their physical activity due to the fear of exercise dyspnea. Regular exercise, on the other hand, is currently suggested as one of the non-pharmaceutical treatment alternatives for patients with asthma since it improves their quality of life and symptom control. This study aimed to investigate the indicators of success in patients with asthma receiving pulmonary rehabilitation (PR). Methods A total of 131 patients with the diagnosis of asthma were included in the study. All patients attended an 8-week comprehensive, multidisciplinary, outpatient and individualized PR program. Results The factors related to the gains in dyspnea perception, exercise capacity, peripheral muscle strength, respiratory muscle strength and quality of life were evaluated. In the multivariate linear regression analysis, the gain in dyspnea perception is related to baseline dyspnea. The gain in exercise capacity is related to baseline exercise capacity and the amount of smoking. The gain in peripheral muscle strength is related to gender. The gain in respiratory muscle strength is related to age, and finally the gain in quality of life is related to baseline dyspnea and anxiety levels. Conclusions Especially men, young people, heavy smokers, and those with low initial exercise capacity, high perception of dyspnea, and high anxiety are more likely to benefit from PR.

EFFECTS OF DIFFERENT EXERCISE THERAPIES ON OBSTRUCTION, DYSPNEA, AND QUALITY OF LIFE IN COPD PATIENTS: A SYSTEMATIC REVIEW

Abstract&#x0D; Objective: Chronic obstructive pulmonary disease (COPD) is the third leading cause of death and it causes pulmonary and extrapulmonary symptoms, also impacts the quality of life. Rigorous evidence on manual and mechanical chest physiotherapy is still scarce. Therefore, this review aims to evaluate the effects of different exercise therapies on obstruction, dyspnea and quality of life in obstructive patients.&#x0D; Materials and Methods: Databases such as Medline, BioMed Central, CINHAL and Cochrane were reviewed. We performed a systematic review of randomized controlled trials published from 2011 to 2020, to evaluate the effects of exercise therapies on obstruction, dyspnea and quality of life in obstructive patients. Methodological quality and risk of bias were assessed using the Cochrane tool.&#x0D; Results: Most of the trials supported the effectiveness of mechanical chest physiotherapy in improving obstruction, dyspnea and quality of life.&#x0D; Conclusion: High-to-moderate evidence shows that mechanical chest physiotherapy is useful in the improvement of obstruction, dyspnea and quality of life in obstructive patients.&#x0D; &#x0D; Keywords: Borg dyspnea scale, COPD, High-frequency chest wall oscillation, mMRC dyspnea scale, St. George Respiratory Questionnaire, Spirometry&#x0D;

Abstract 14039: Myocardial Work Efficiency is Reduced in Nonobstructive Hypertrophic Cardiomyopathy Patients With Exercise-Induced Symptoms

Introduction: Despite normal ejection fraction, nonobstructive hypertrophic cardiomyopathy (nHCM; rest and provoked gradients &lt;30 mmHg) is associated with high rates of angina, arrhythmias and heart failure symptoms, as well as abnormalities of echo-based myocardial strain. Using Myocardial Work (MW) analysis, we investigated the potential mechanisms contributing to exercise-induced symptoms in nHCM. Methods and Results: Using validated methods (EchoPAC), longitudinal strain and non-invasive blood pressure were integrated to generate normalized left ventricular pressure curves and pressure-strain loops to derive global and segmental MW data in 14 nHCM patients with normal ejection fraction (&gt;55%) who underwent treadmill stress testing. Global myocardial work efficiency was expressed as the ratio of global constructive work over the sum of global constructive and wasted work. A total of 9 of 14 patients reported symptoms during exercise (chest pain, dyspnea, and palpitations) and this group had reduced global myocardial work efficiency compared to those without exercise-induced symptoms (85% vs 90%, respectively, p = 0.04, Figure 1). No statistical differences were noted in age, % men, maximal wall thickness, ejection fraction, E/e’ ratio, resting blood pressure, resting global strain and exercise performance between symptomatic and asymptomatic patients. Conclusions: Despite similar ventricular morphology, resting mechanics and exercise performance, nHCM patients with symptoms during exercise have worse myocardial work efficiency. Our data suggest that mechanisms potentially impacting global strain may be distinct from those affecting myocardial work efficiency. Understanding these differences may offer insights into management of exercise-induced symptoms.

Abstract 9711: Unexplained Dyspnea on Exertion: The Difference the Right Test Can Make

A 66-year-old male with past history of coronary atherosclerosis by angiography was referred for chronic dyspnea. He is a pastor and had noted dyspnea with prolonged standing or walking that resolved with sitting. Serial orthostatic vitals and natriuretic peptides were normal. Subsequent diagnostics included normal pulmonary function and ventilation-perfusion tests, and echocardiography with normal biventricular function, sizes, and estimated pressures. Given ongoing dyspnea, he underwent supine invasive cardiopulmonary exercise testing (iCPET). Resting invasive pressures and cardiac output were normal. At peak exercise, exertional dyspnea was absent but pressures increased to mean PAP 40 and PCWP 28 with preserved cardiac output and 77% predicted maximal aerobic capacity (pVO2). He was diagnosed with exercise induced heart failure with preserved ejection fraction and started on furosemide and spironolactone. On follow-up, he reported worsened dyspnea on therapy, most notably when upright. Stress cardiac MRI showed no scar. Given the positional nature of his symptoms, an iCPET was repeated in the upright position. His diuretics were stopped. Resting supine measurements were similar to the prior iCPET. Upright resting to peak exercise pressures changed minimally ( Figure ). His profound dyspnea recurred at peak exertion as MAP dropped unexpectedly with paradoxical bradycardia (Bezold-Jarisch reflex) and 62% pVO2. His diagnosis was reclassified as cardiac preload failure. He was advised to increase fluid and salt intake alongside use of leg stockings which remarkably improved his upright and exercise dyspnea symptoms at follow-up. This case highlights an advantage of upright iCPET over supine diagnostics in the comprehensive evaluation of unexplained dyspnea. Cardiac preload failure is the failure to augment preload with exercise and is a common but under-recognized cause of dyspnea often undiagnosed during supine resting and exercise testing.

Trajectories of COPD patients’ response to repeated pulmonary rehabilitation programs

Background and objectivePulmonary rehabilitation (PR) is essential in the management of chronic obstructive pulmonary disease (COPD), but the long-term effects and the outcomes of repeated programs especially in non-responders remain to be clarified. The aim of this study is to evaluate the long-term effect of PR 12 months after and the effect of repeated PR depending on the patient's response to the first PR. MethodsThis is a single center retrospective analysis of COPD patients admitted to two or three PR programs between January 2012 and December 2017, using the 6-min walking distance (6MWD) to determine the functional response to PR. ResultsOne hundred ninety patients completed PR twice and 62 completed PR three times with 10–14 months delay between programs. The effect of the first PR program (PR1) on 6MWD was mostly lost after one year. The 6MWD change after the second PR program (PR2) was smaller than after PR1 (+65 ± 30 m post-PR1, +44 ± 20 m post-PR2; p = 0.001). Out of the 149 responders post-PR1, 44 (30%) became non-responders post-PR2. Out of the 41 non-responders post-PR1, 23 (56%) became responders post-PR2. Patients with long term oxygen therapy and severe exercise dyspnea were most likely to remain non-responders to repeated PR. ConclusionThis study showed that most of the 6MWD improvement following PR disappears over 12 months and emphasized the clinical relevance of repeating PR including for non-responders to initial PR. However, some patients did not respond systematically to PR and may require specific PR modalities to improve their functional status.

Are there any long-term cardio-pulmonary limitations of hospitalized Covid-19 patients?

Abstract Background The Covid-19 pandemic has affected our lives for over a year and almost 500.000 people in Austria have been infected. Although many of them only had low or mild symptoms some had to be treated in the hospital. Even months after their infection some patients complain about fatigue, exercise intolerance and dyspnoea. The aim of this study was to perform a follow-up cardiopulmonary exercise test (CPET) on those patients, at 6 months after their hospitalization to find out if there are long-term cardio-pulmonary limitations (CPL) of Covid-19. We also wanted to check if there is any difference in outcome and CPL between patients who received oxygen therapy vs. without oxygen therapy. Methods 40 patients were included into this study (16 women = 40%; 24 men = 60%). All patients were hospitalized during their infection with Covid-19 (5 patients at ICU) and underwent CPET 6±2 month after discharge. 20 patients (50%) received oxygen therapy or ventilation during their hospitalization. CPET data were assessed at rest, during exercise and at recovery. Blood parameters including NT-pro BNP were collected and an interview and examination were performed. CPL was defined as VO2% of Predicted ≤84%, VE/CO2 Slope ≥34 and RER at peak of exercise ≥1.1. Results Median age of all patients was 46 years [interquartile range (IQR): 35.3–55.8], median BMI was 26.0 m2/kg [IQR: 23.0–29.0] and the median NTproBNP was 53.1 pg/mL [IQR: 24.0–95.6]. When comparing the two groups, we found higher percentage of CPL in patients who received oxygen therapy during their hospitalization (10% with oxygen vs. 5% without oxygen). Notably, the number of patients with a BMI ≥25 m2/kg was higher in the oxygen therapy group than in those without oxygen (80% vs. 45%). The median BMI without oxygen therapy was 24.0 [IQR: 20.3–26.8] vs. 29.0 [IQR: 25.0–31.0] with oxygen therapy (p=0.004). There were no significant differences in NT-proBNP levels (p=0.545). The median VO2% of predicted was 88.0% [72.5–98.0] without oxygen therapy vs. 84.5% [IQR: 70.8–91.8] with oxygen therapy (p=0.289), the median HR percentage of predicted was 92.5% [IQR: 85.5–97.8] without oxygen therapy vs. 94.5% [IQR: 88.3–103.5] with oxygen therapy (p=0.478), the median physical performance in watt in patients without oxygen therapy was 130.0 [IQR: 108.5–197.5] vs. 135.0 [IQR: 97.0–188.3] with oxygen therapy (p=0.820). Conclusion The findings of our study did not show any statistically significant difference in long-term CPL between patients who received oxygen therapy vs. those who didn't. Therefore, other causes of the exercise intolerance and dyspnoea have to be discussed multidisciplinary. Subclinical CPL in the absence of significant clinical symptoms represent a concern after a Covid-19 infection. Overall, 7.5% of our patients showed CPL although those patients didn't have any clinical symptoms. Therefore, CPET is a good method to discover asymptomatic patients with CPL. Funding Acknowledgement Type of funding sources: None.

Prostacyclin receptor agonist selexipag in a patient with high-risk idiopathic pulmonary arterial hypertension: a case report

We present a 48-year-old patient with World Health Organization class III idiopathic pulmonary arterial hypertension (IPAH), taking specific therapy with macitentan 10 mg a day, who was readmitted to the National Medical Research Center of Cardiology due to increase in exercise dyspnea and decrease in effort tolerance. According to a comprehensive examination, single factors of high risk and unfavorable prognosis were identified. Due to systemic hypotension when using inhaled iloprost, selexipag was added to therapy. According to control hospitalization, 8-month selexipag therapy improved the patient's condition, as well as high risk factors were not revealed. Selexipag is a selective oral prostacyclin receptor agonist recommended for longterm IPAH therapy in adult patients.

A cardiovascular magnetic resonance imaging-based pilot study to assess coronary microvascular disease in COVID-19 patients

Coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) and is primarily characterised by a respiratory disease. However, SARS-CoV-2 can directly infect vascular endothelium and subsequently cause vascular inflammation, atherosclerotic plaque instability and thereby result in both endothelial dysfunction and myocardial inflammation/infarction. Interestingly, up to 50% of patients suffer from persistent exercise dyspnoea and a post-viral fatigue syndrome (PVFS) after having overcome an acute COVID-19 infection. In the present study, we assessed the presence of coronary microvascular disease (CMD) by cardiovascular magnetic resonance (CMR) in post-COVID-19 patients still suffering from exercise dyspnoea and PVFS. N = 22 patients who recently recovered from COVID-19, N = 16 patients with classic hypertrophic cardiomyopathy (HCM) and N = 17 healthy control patients without relevant cardiac disease underwent dedicated vasodilator-stress CMR studies on a 1.5-T MR scanner. The CMR protocol comprised cine and late-gadolinium-enhancement (LGE) imaging as well as velocity-encoded (VENC) phase-contrast imaging of the coronary sinus flow (CSF) at rest and during pharmacological stress (maximal vasodilation induced by 400 µg IV regadenoson). Using CSF measurements at rest and during stress, global myocardial perfusion reserve (MPR) was calculated. There was no difference in left ventricular ejection-fraction (LV-EF) between COVID-19 patients and controls (60% [57–63%] vs. 63% [60–66%], p = NS). There were only N = 4 COVID-19 patients (18%) showing a non-ischemic pattern of LGE. VENC-based flow measurements showed that CSF at rest was higher in COVID-19 patients compared to controls (1.78 ml/min [1.19–2.23 ml/min] vs. 1.14 ml/min [0.91–1.32 ml/min], p = 0.048). In contrast, CSF during stress was lower in COVID-19 patients compared to controls (3.33 ml/min [2.76–4.20 ml/min] vs. 5.32 ml/min [3.66–5.52 ml/min], p = 0.05). A significantly reduced MPR was calculated in COVID-19 patients compared to healthy controls (2.73 [2.10–4.15–11] vs. 4.82 [3.70–6.68], p = 0.005). No significant differences regarding MPR were detected between COVID-19 patients and HCM patients. In post-COVID-19 patients with persistent exertional dyspnoea and PVFS, a significantly reduced MPR suggestive of CMD—similar to HCM patients—was observed in the present study. A reduction in MPR can be caused by preceding SARS-CoV-2-associated direct as well as secondary triggered mechanisms leading to diffuse CMD, and may explain ongoing symptoms of exercise dyspnoea and PVFS in some patients after COVID-19 infection.

Cardiac performance in patients hospitalized with COVID-19: A 6-month follow-up study

IntroductionMyocardial injury is frequently observed in patients hospitalized with Coronavirus disease 2019 (COVID-19) pneumonia. Different cardiac abnormalities have been reported during the acute COVID-19 phase but there is limited information on late cardiac sequelae in patients who have recovered from acute COVID-19 illness.ObjectiveTo document the presence and quantify the extent of myocardial functional alterations in patients hospitalized 6 months earlier for COVID-19 infection.Methods and resultsWe conducted a prospective echocardiographic evaluation of 48 patients (58 ± 13 years, 69% male) hospitalized 6 ± 1 month earlier for a laboratory-confirmed and symptomatic COVID-19. Thirty-two (66.6%) had pre-existing cardiovascular risks factors (hypertension, T2DM or dyslipidemia) and three patients (6.2%) had a known prior myocardial infarction. Sixteen patients (33.3%) experienced myocardial injury during the index COVID-19 hospitalization as identified by a rise in cardiac troponin levels. Six months later, 60.4% of patients still reported clinical symptoms including exercise dyspnea for 56%. Echocardiographic measurements under resting conditions were not different between patients with vs. without myocardial injury during the acute COVID-19 phase. In contrast, low-level exercise (25 W for 3 minutes) induced a significant increase in the average E/e’ ratio (10.1 ± 4.3 vs. 7.3 ± 11.5, P = 0.01) and the systolic pulmonary artery pressure (33.4 ± 7.8 vs. 25.6 ± 5.3 mmHg, P = 0.02) in patients with myocardial injury during the acute COVID-19 phase. Sensitivity analyses showed that these alterations of left ventricular diastolic markers were observed regardless of cardiovascular disorders indicating SARS-CoV-2 infection as a primary cause.ConclusionsSix months after the acute COVID-19 phase, significant cardiac diastolic abnormalities are observed in patients who experienced myocardial injury but not in patients without cardiac involvement.

Diagnosis of Myxomatous Mitral Valve Disease (MMVD) in Aged Dogs

Background: Aging is a biological process, which affects many body systems and increases susceptibility to disease that is associated with a reduction in immune response, a decline in cognitive function and a diminished functional reserve of the cardiovascular, pulmonary and renal systems. Diseases of heart or cardiovascular system represents a major component of geriatric medicine among which, myxomatous mitral valve disease is more common among geriatric dogs. The present study is keeping on record about the diagnosis of myxomatous mitral valve disease in geriatric dogs in and around Hyderabad, Telangana state.Methods: A total of1695 geriatric dogs presented to various clinics including university veterinary clinical complex of Hyderabad, Telangana state during 2015 to 2020 were considered for this study. After confirming that they were free from any other systemic disease, medium to large size breed dogs above 8 years with the history of exercise intolerance, dyspnoea and cough were selected. Diagnostic protocol included, auscultation, chest x-ray and 2d-echocardiography to confirm mitral valve degeneration. Result: Myxomatous mitral valve disease was diagnosed in 427/695 geriatric dogs (61.43%) and were showing hyperechoeic thick mitral valve leaflets with kinking and prolapse. Further, echocardiography also revealed dilated left atrium and ventricle, hyperkinesis of interventricular septum, mitral valve degeneration and rupture of chordae tendineae with valuvular regurgitation.

Cardiac performance in patients hospitalized with COVID-19: a 6month follow-up study.

AimsMyocardial injury is frequently observed in patients hospitalized with coronavirus disease 2019 (COVID‐19) pneumonia. Different cardiac abnormalities have been reported during the acute COVID‐19 phase, ranging from infra‐clinic elevations of myocardial necrosis biomarkers to acute cardiac dysfunction and myocarditis. There is limited information on late cardiac sequelae in patients who have recovered from acute COVID‐19 illness. We aimed to document the presence and quantify the extent of myocardial functional alterations in patients hospitalized 6 months earlier for COVID‐19 infection.Methods and resultsWe conducted a prospective echocardiographic evaluation of 48 patients (mean age 58 ± 13 years, 69% male) hospitalized 6 ± 1 month earlier for a laboratory‐confirmed and symptomatic COVID‐19. Thirty‐two (66.6%) had pre‐existing cardiovascular risks factors (systemic hypertension, diabetes, or dyslipidaemia), and three patients (6.2%) had a known prior myocardial infarction. Sixteen patients (33.3%) experienced myocardial injury during the index COVID‐19 hospitalization as identified by a rise in cardiac troponin levels. Six months later, 60.4% of patients still reported clinical symptoms including exercise dyspnoea for 56%. Echocardiographic measurements under resting conditions were not different between patients with versus without myocardial injury during the acute COVID‐19 phase. In contrast, low‐level exercise (25W for 3 min) induced a significant increase in the average E/e′ ratio (10.1 ± 4.3 vs. 7.3 ± 11.5, P = 0.01) and the systolic pulmonary artery pressure (33.4 ± 7.8 vs. 25.6 ± 5.3 mmHg, P = 0.02) in patients with myocardial injury during the acute COVID‐19 phase. Sensitivity analyses showed that these alterations of left ventricular diastolic markers were observed regardless of whether of cardiovascular risk factors or established cardiac diseases indicating SARS‐CoV‐2 infection as a primary cause.ConclusionsSix months after the acute COVID‐19 phase, significant cardiac diastolic abnormalities are observed in patients who experienced myocardial injury but not in patients without cardiac involvement.

Health status can predict diaphragmatic muscle thickness in COPD: pilot study

Abstract Introduction: Among the systemic implications of chronic obstructive pulmonary disease (COPD) there are changes in the diaphragm and impact on health status. However, there are few studies on the possible relationship between these variables, and whether health status could predict diaphragmatic muscle thickness (DMT). Objective: To investigate whether there is a relationship between DMT and the prognostic mortality index Body Mass-Index, Airway Obstruction, Dyspnea and Exercise Capacity (BODE), dyspnea and health status, and to investigate whether health status can predict DMT in patients with COPD entering a pulmonary rehabilitation program. Methods: This is a pilot study with a cross-sectional design. Diaphragmatic muscle thickness was evaluated using ultrasound; health status through the COPD Assessment Test (CAT); the sensation of dyspnea by the modified Medical Research Council scale; and mortality, using the BODE index. Results: The sample consisted of 13 patients (68.69 ± 9.3 years) classified as having moderate to severe COPD. There was a strong and inverse correlation between diaphragmatic muscle thickness and health status (r = -0.735; p = 0.004). Simple regression analysis demonstrated that health status influenced diaphragmatic muscle thickness (β = -0.002; IC 95% - 0.004 to -0.001; p = 0.004), explaining 49% of the variance. However, no correlations were observed between diaphragmatic muscle thickness with dyspnea (r = 0.005; p = 0.985) or with the BODE mortality index (r = -0.219; p = 0.472). Conclusion: This pilot study demonstrated a strong inverse correlation between health status and DMT. In addition, health status was able to predict DMT in patients with COPD.