Supplemental oxygen therapy in chronic obstructive pulmonary disease: is less is more? How much is too much?

PURPOSE OF REVIEW: Currently available evidence supporting the use of supplemental oxygen therapy (SOT) in chronic obstructive pulmonary disease (COPD) is complex, and data on the mortality reduction associated with SOT usage in patients with severe daytime resting hypoxemia have not been updated since the development of other treatments. RECENT FINDINGS: No reduction in mortality was found when SOT was used in patients with moderate resting daytime, isolated nocturnal, or exercise-induced hypoxemia. However, some of these patients obtain other significant benefits during SOT, including increased exercise endurance, and a mortality reduction is possible in these 'responders'. The adverse effects of long-term oxygen therapy also need to be considered, such as reduced mobility and social stigma. Furthermore, conservative SOT could improve outcomes in the setting of COPD exacerbations compared with higher concentration oxygen regimens. Compared with usual fixed-dose SOT, automated oxygen administration devices might reduce dyspnea during exercise and COPD exacerbations. SUMMARY: Current recommendations for SOT need to be revised to focus on patients who respond best and benefit most from this therapy. A conservative approach to SOT can reduce side effects compared with higher concentration oxygen regimens, and automated oxygen administration devices may help to optimize SOT.

Poor correlation between diaphragm ultrasound and invasive gold standard technique derived respiratory muscle strength assessment in patients after hospitalization for COVID-19.

INTRODUCTION: Individuals who survive acute coronavirus disease 2019 (COVID-19) might experience diaphragm muscle weakness. Diaphragm ultrasound may be an easy-to-obtain bedside tool for determining diaphragm function. However, twitch transdiaphragmatic pressure (twPdi) following magnetic stimulation (MS) of the phrenic nerves is the gold standard for non-volitional assessment of diaphragm strength. This study investigated whether diaphragm thickening ratio (DTR) measured on diaphragm ultrasound reflects diaphragm strength as measured by twPdi following MS of the phrenic nerves or other (volitional) invasively obtained pressure values and could therefore be used to accurately diagnose diaphragm weakness. METHODS: One year after discharge, 50 individuals (14 female, age 58±12 years) who had been hospitalised and treated for moderate-severe COVID-19 underwent standard spirometry and diaphragm ultrasound. TwPdi following cervical MS of the phrenic nerve and volitional inspiratory manoeuvres (Sniff and Mueller manoeuvre) were measured using oesophageal and gastric balloon catheters after transnasal placement. RESULTS: At follow-up, no clinically meaningful restrictive lung function impairment was evident on spirometry. On diaphragm ultrasound, diaphragm dysfunction, i. e. an impaired diaphragm thickening ratio was detected in 24% (12/50) of participants. An objective diagnosis of diaphragm dysfunction, defined as twPdi <16 cmH2O, was made in 60% (30/50) of participants. The measurement results of the two methods did not agree, given that there were many false negative, but also false positive results, so diaphragm ultrasound diagnosed in parts other patients with diaphragm dysfunction than TwPdi. Diaphragm ultrasound had a sensitivity of 26.67% and a specificity of 80.0% in the detection of diaphragm dysfunction (Positive predictive value 66.67%, negative predictive value 42.10%). CONCLUSION: Diagnosis of diaphragm weakness in individuals who have recovered from COVID-19 cannot be made accurately on diaphragm ultrasound (via DTR), but requires twPdi as the gold standard for assessment of diaphragm strength.

Diaphragm Muscle Weakness Might Explain Exertional Dyspnea 15 Months after Hospitalization for COVID-19.

Rationale: Dyspnea is often a persistent symptom after acute coronavirus disease (COVID-19), even if cardiac and pulmonary function are normal. Objectives: This study investigated diaphragm muscle strength in patients after COVID-19 and its relationship to unexplained dyspnea on exertion. Methods: Fifty patients previously hospitalized with COVID-19 (14 female, age 58 ± 12 yr, half of whom were treated with mechanical ventilation, and half of whom were treated outside the ICU) were evaluated using pulmonary function testing, 6-minute-walk test, echocardiography, twitch transdiaphragmatic pressure after cervical magnetic stimulation of the phrenic nerve roots, and diaphragm ultrasound. Diaphragm function data were compared with values from a healthy control group. Measurements and Main Results: Moderate or severe dyspnea on exertion was present at 15 months after hospital discharge in approximately two-thirds of patients. No significant pulmonary function or echocardiography abnormalities were detected. Twitch transdiaphragmatic pressure was significantly impaired in patients previously hospitalized with COVID-19 compared with control subjects, independent of initial disease severity (14 ± 8 vs. 21 ± 3 cm H2O in mechanically ventilated patients vs. control subjects [P = 0.02], and 15 ± 8 vs. 21 ± 3 cm H2O in nonventilated patients vs. control subjects [P = 0.04]). There was a significant association between twitch transdiaphragmatic pressure and the severity of dyspnea on exertion (P = 0.03). Conclusions: Diaphragm muscle weakness was present 15 months after hospitalization for COVID-19 even in patients who did not require mechanical ventilation, and this weakness was associated with dyspnea on exertion. The current study, therefore, identifies diaphragm muscle weakness as a correlate for persistent dyspnea in patients after COVID-19 in whom lung and cardiac function are normal. Clinical trial registered with www.clinicaltrials.gov (NCT04854863).

[Weaning from prolonged mechanical ventilation on a specialised weaning unit: a retrospective comparison of patients with and without SARS-CoV-2 infection]. / Entwöhnung von der Langzeitbeatmung nach ARDS auf einer spezialisierten Weaning-Einheit ­ ein retrospektiver Vergleich von Patienten mit und ohne SARS-CoV-2 Infektion.

BACKGROUND: Available data on patients requiring prolonged mechanical ventilation due to severe COVID-19 are sparse. Here we compare patients with ARDS related or not related to SARS-CoV-2 infection treated in a specialised weaning unit. METHODS: A retrospective analysis of all patients with prolonged mechanical ventilation associated with an ARDS admitted from the 21st November 2013 to the 23rd July 2021 to the weaning unit of the University Hospital RWTH Aachen was performed. ARDS patients with COVID-19 (cARDS) were compared to patients with ARDS not related to COVID-19 (ncARDS). RESULTS: In total, n=129 patients in prolonged need for mechanical ventilation after ARDS were treated in the weaning unit, of whom n=38 had been suffering from ARDS related to COVID-19. Both patients groups were similar in terms of demographic parameters, underlying chronic illnesses, severity of ARDS and the duration of mechanical ventilation before being admitted to the weaning unit. During ICU stay, prone positioning and therapy with systemic corticosteroids was used more frequently in cARDS patients. Furthermore, therapy with vasoconstrictors was needed more often (cARDS: 42.1% vs. ncARDS 12.1%; p=0.0003) and urinary output was lower (cARDS: 1980 ml vs. ncARDS: 2600 ml; p=0.0037) in this patient group. The clinical course of the weaning process was similar in patients with cARDS and ncARDS, there were no significant differences in the occurrence of complications and the duration of mechanical ventilation. There were n=5 deaths (13.2%) in the cARDS and n=15 deaths (16.5%) in the ncARDS group. After hospital discharge, n=4 patients required non-invasive ventilation whereas out-of-hospital invasive ventilation was only necessary in one patient (all in the ncARDS group). CONCLUSION: After having survived the acute phase, the disease prognosis of patients with severe COVID-19 is favourable and most patients can be successfully weaned from mechanical ventilation. In addition, there were only minor differences compared to patients with ARDS unrelated to COVID-19.

Diaphragm dysfunction as a potential determinant of dyspnea on exertion in patients 1 year after COVID-19-related ARDS.

Some COVID-19 patients experience dyspnea without objective impairment of pulmonary or cardiac function. This study determined diaphragm function and its central voluntary activation as a potential correlate with exertional dyspnea after COVID-19 acute respiratory distress syndrome (ARDS) in ten patients and matched controls. One year post discharge, both pulmonary function tests and echocardiography were normal. However, six patients with persisting dyspnea on exertion showed impaired volitional diaphragm function and control based on ultrasound, magnetic stimulation and balloon catheter-based recordings. Diaphragm dysfunction with impaired voluntary activation can be present 1 year after severe COVID-19 ARDS and may relate to exertional dyspnea.This prospective case-control study was registered under the trial registration number NCT04854863 April, 22 2021.

Safety and efficacy of transcatheter mitral valve repair in patients with COPD; results from real-world cohort.

OBJECTIVE: To evaluate the safety and efficacy of transcatheter mitral valve repair (TMVR) in patients with chronic obstructive pulmonary disease (COPD). BACKGROUND: Heart failure and COPD share many clinical features and commonly coexist. Data about the safety and efficacy of TMVR in patients with COPD is not conclusive. METHODS: Three hundred and forty consecutive patients undergoing TMVR were retrospectively included. COPD diagnosis was based on pulmonary function tests (PFTs). Intra-hospital, 30-day- and 1-year outcomes were compared between both groups. RESULTS: Eighty-two patients had COPD (24%). There was no difference in intra-hospital mortality between patients with and without COPD (both 5%, p = 0.95). Among patients who had a successful procedure and survived to discharge there was a trend toward more rehospitalization due to decompensated heart failure at 30-day follow-up in patients with COPD (12.9% vs. 6.8%, p = 0.08) with no difference in mortality. At median follow-up of 1 year, New York heart association (NYHA) category was comparable among both groups and there was no significant difference in rehospitalization (COPD: 29.9% vs. non-COPD: 34%, p = 0.5). There was a trend toward increased 1-year mortality in COPD patients (31.2% vs. 20.6%, p = 0.06). However, a composite endpoint of rehospitalization or death at 1 year did not differ between both groups (48% vs. 42.5%, p = 0.4). Regression analysis showed no correlation between COPD severity and worse TMVR outcomes. CONCLUSIONS: COPD is highly prevalent among patients undergoing TMVR. However, TMVR seems to be safe and effective in COPD patients. COPD severity and PFT impairment alone should not be considered as a contraindication for TMVR.

Mathematical Arterialization of Capillary Blood for Blood Gas Analysis in Critically Ill Patients.

BACKGROUND: In clinical practice, capillary blood taken from hyperemized earlobes (CBGE) or fingertips (CBGF) is frequently used as substitute for arterial blood (ABG) for blood gas analysis. While there is a close agreement between ABG and CBGE/CBGF regarding pH and pCO2, pO2 is often underestimated by CBG. Recently, a software tool (v-TAC®; Roche Diagnostics, Risch-Rotkreuz, Switzerland) has been developed to calculate ABG values based on a peripheral venous blood gas analysis supplemented with peripheral oxygen saturation. OBJECTIVE: Here we investigate whether v-TAC can also be used to calculate ABG values from capillary blood samples. METHODS: Patients (n = 85) with an indwelling arterial line were included in the study. A reference ABG sample (ABG1) was obtained, followed by CBGE, CBGF, and finally a second ABG (ABG2). Results of CBGE/CBGF before and after mathematical arterialization by v-TAC (aCBGE/aCBGF) were compared to ABG1. RESULTS: After mathematical arterialization by v-TAC, the mean bias in pO2 between ABG1 and CBGE went down from 5.24 mm Hg (95% limit of agreement [95% LoA]: -14.19 to 24.67) to 0.18 mm Hg (95% LoA: -11.84 to 12.20) and was in a similar range as the mean bias between ABG1 and ABG2 (0.39 mm Hg [95% LoA: -13.46 to 14.24]). Differences in pH and pCO2 between arterial and capillary samples were small before and after mathematical arterialization. Very similar results were obtained when using fingertip instead of earlobe capillary blood. CONCLUSION: In summary, v-TAC can be used for mathematical arterialization of capillary blood samples for blood gas analysis resulting in increased diagnostic accuracy for pO2.

Broncho-alveolar lavage in patients with acute respiratory distress syndrome due to COVID-19.

As data about microbiological testing and the cellular composition of the broncho-alveolar lavage (BAL) fluid in patients ventilated due to coronavirus disease 2019 (COVID-19) are lacking, this was investigated in a retrospective analysis (n = 58). Co-infection with pathogens was detected in 31 patients, whereas the analysis of BAL cellularity showed an increased total cell count and an alveolitis dominated by neutrophils. None of the physicians performing bronchoscopies in COVID-19 patients had serological evidence of severe acute respiratory syndrome coronavirus 2 infection.

The bidirectional relationship between chronic obstructive pulmonary disease and coronary artery disease.

Chronic obstructive pulmonary disease (COPD) and coronary artery disease (CAD) not only have smoking as a common risk factor, they also share epidemiological relationships and important mutual effects. There is good evidence to suggest that COPD is highly prevalent but underdiagnosed among CAD patients and vice versa. The symptoms of the two diseases can overlap, making differential diagnosis challenging. This highlights the importance of pulmonary function tests (PFTs) in patients with CAD but also a cardiological assessment in patients with COPD. Chronic obstructive pulmonary disease is a risk factor for the development of CAD independent of other cardiovascular risk factors, and the presence of COPD worsens prognosis in patients with CAD. Mechanisms underlying the associations between COPD and CAD have been less well studied, but inflammation is increasingly being recognized as an important factor linking the two diseases. Other potential contributors include increased oxidative stress, platelet activation, and arterial stiffness. The influence of medications used to treat one condition on the other one needs to be understood and taken into account in patient management. Physicians need to be aware of the important links between COPD and CAD, both of which are commonly encountered in clinical practice. This should help to optimize the management of both conditions to improve patient outcomes.

Whole-Body Plethysmography and Blood Gas Analysis in Patients with Acute Myocardial Infarction Undergoing Percutaneous Coronary Intervention.

BACKGROUND: Chronic obstructive pulmonary disease (COPD) and coronary heart disease (CHD) often occur together. However, COPD is underdiagnosed among CHD patients. OBJECTIVES: This study investigated the prevalence of COPD and relevant pulmonary function test (PFT) impairments in patients with acute myocardial infarction (AMI). METHODS: Patients undergoing coronary angiography for AMI were prospectively included. Body plethysmography, lung diffusing capacity, blood gas analysis, and echocardiography were performed. The following patient subgroups were compared: with versus without COPD, ST elevation myocardial infarction (STEMI) versus non-STEMI (NSTEMI). The prevalence of PFT impairments was also recorded. RESULTS: A total of 100 patients (51 with NSTEMI, 49 with STEMI) were included. Twenty patients had diagnosed COPD, of whom 15 were diagnosed for the first time; 80% of all COPD patients were not receiving COPD therapy. Patients with COPD had higher maximum creatine kinase (p = 0.008) and troponin T (p = 0.054) levels than those without COPD. Hypoxaemia was more common in COPD patients (lower oxygen saturation [p = 0.008] and partial pressure of oxygen [PaO2] [p = 0.005]). PaO2 was significantly lower in STEMI compared with NSTEMI (p = 0.017). Independent of a COPD diagnosis, 65 patients had relevant PFT impairments. CONCLUSIONS: The high prevalence of undiagnosed COPD and relevant pulmonary function impairments in this cohort of patients with AMI, and the fact that pulmonary disease was untreated in the majority of COPD patients, highlight the importance of a general pulmonary workup of patients with AMI. Furthermore, patients with CHD should undergo screening for COPD, given the fact that COPD patients had larger infarction size.

Characterization and Triggers of Dyspnea in Patients with Chronic Obstructive Pulmonary Disease or Chronic Heart Failure: Effects of Weather and Environment.

BACKGROUND AND OBJECTIVES: Dyspnea is one of the most disturbing symptoms for patients with chronic obstructive pulmonary disease (COPD) or heart failure (HF). This study investigated dyspnea triggers and factors associated with worsening dyspnea in patients with COPD or HF. METHODS: COPD support group members and HF patients with reduced ejection fraction (HFrEF) and no airway obstruction answered a questionnaire describing different weather conditions (rising/falling air pressure, sunny, foggy, rainy, windy, snowy, hazy, high ozone levels, and airborne pollen) and environmental circumstances (cooking, grilling, perfumes, cigarette smoke, gasoline odor, and flower scents) and were asked to estimate the occurrence and severity of dyspnea under these conditions using predefined scales. RESULTS: 230 patients with COPD and 90 with HFrEF (left ventricular ejection fraction 34 ± 10%, Tiffeneau index > 70%) were analyzed. COPD patients reported dyspnea more often than HF patients in almost all weather and environmental conditions (p = 0.004 to p < 0.001), with the exception of outdoor floral scents and cigarette smoke. Severe to very severe dyspnea was reported more in COPD versus HF in all weather and environmental conditions except sunny weather (p = 0.01 to p < 0.001). COPD was associated with more severe dyspnea than HF in all conditions (all p < 0.001). CONCLUSIONS: Dyspnea was triggered by a variety of weather and other environmental triggers in patients with COPD and occurred more often than in HF patients under the same conditions. Foggy weather and exposure to perfumes were associated with severe dyspnea in the majority of COPD patients, but only a minority of HF patients.

Serum phosphate and phosphate-regulatory hormones in COPD patients.

BACKGROUND: Fibroblast growth factor 23 (FGF23) regulates phosphate metabolism by increasing renal phosphate excretion and decreasing 1.25-dihydroxyvitamin D synthesis. Reports about hypophosphatemia in patients with chronic obstructive pulmonary disease (COPD) suggest altered phosphate metabolism. Therefore, we hypothesized that disturbances in phosphate-regulatory hormones such as FGF23 and parathyroid hormone (PTH) are present in COPD patients. METHODS: We investigated 40 COPD patients (63.5 ± 9.9 years, 27 male), each matched with two age- and sex-matched controls without any primary lung disease. COPD patients underwent lung function testing in advance. All patients had a glomerular filtration rate (GFR) > 60 mL/min/1.73m2. We measured concentrations of intact FGF23 (iFGF23) and c-terminal FGF23 (c-term FGF23), phosphate, parathyroid hormone (PTH) and C-reactive protein (CRP) levels in COPD patients and controls. RESULTS: Phosphate (1.0 ± 02 vs. 1.1 ± 0.2 mmol/L; p = 0.027), PTH (54.2 ± 29.4 vs. 68.7 ± 31.8 pg/mL; p = 0.002) and iFGF23 (46.3 ± 29.0 vs. 57.5 ± 33.5 pg/mL; p = 0.026 ) levels were significantly lower in COPD patients compared with controls. There was a significant negative correlation between c-term FGF23 and total lung capacity (r = - 0.4; p = 0.01), and between c-term FGF23 and CRP in COPD patients (r = 0.48; p = 0.002). iFGF23 and c-term FGF23 were positively correlated with phosphate and PTH in the control group. CONCLUSION: We confirmed lower average serum phosphate levels in COPD patients compared with controls. However, our data do not suggest a causative role for FGF23 or PTH in COPD because levels of both phosphate-lowering hormones appear to be adaptively decreased as well. Therefore, further investigations are needed to identify the pathogenesis of low phosphate levels in patients with COPD and the relationship between phosphate-regulatory hormones and disease progression.

[The pulmonary nodule: from incidental finding to pathological confirmation]. / Der Lungenrundherd: Vom Zufallsbefund zur histologischen Diagnosesicherung.

As the number of CT examinations of the lungs increases, so does the prevalence of incidentally discovered pulmonary nodules. While most lung nodules are benign, the risk of malignancy significantly rises with the presence of risk factors and specific imaging features. Upon encountering an incidental nodule, efforts should focus on achieving an accurate pathological diagnosis, particularly to ascertain malignancy while minimizing the risks associated with unnecessary diagnostic procedures. A comprehensive understanding of the typical characteristics and behavior of malignant lung nodules, along with a detailed patient history and standardized clinical and imaging risk assessment, is crucial for determining the optimal diagnostic approach. Additionally, the decision regarding histologic confirmation should consider the patient's comorbidities, preferences, and the examiner's expertise. Emerging sampling technologies provide methods for addressing peripheral lung nodules with minimal risk of complications.

Persistence of Diffusion Capacity Impairment and Its Relationship with Dyspnea 12 Months after Hospitalization for COVID-19.

Background: Dyspnea is a common persistent symptom after acute coronavirus disease 2019 illness (COVID-19). One potential explanation for post-COVID-19 dyspnea is a reduction in diffusion capacity. This longitudinal study investigated diffusion capacity and its relationship with dyspnea on exertion in individuals previously hospitalized with COVID-19. Methods: Eligible participants had been hospitalized for the treatment of acute COVID-19 and were assessed at 6 weeks, 6 months, and 12 months after discharge. Pulmonary function testing, diffusion capacity of carbon monoxide (DLCO), blood gas analysis and the level of dyspnea (Borg scale; before and after a 6 min walk test [6 MWT]) were performed. Participants were divided into subgroups based on the presence or absence of dyspnea during the 6 MWT at 12 months after hospitalization. Results: Seventy-two participants (twenty-two female, mean age 59.8 ± 13.5 years) were included. At 12 months after discharge, 41/72 participants (57%) had DLCO below the lower limit of normal and 56/72 (78%) had DLCO < 80% of the predicted value. Individuals with exertional dyspnea had significantly lower DLCO than those without exertional dyspnea (p = 0.001). In participants with DLCO data being available at three timepoints over 12 months (baseline, 6 months, and 12 months) after discharge (n = 25), DLCO improved between 6 weeks and 6 months after hospital discharge, but not thereafter (p = 0.017). Conclusions: About 2/3 of the post-COVID individuals in this study had impaired diffusion capacity at 12 months after hospital discharge. There was an association between persisting dyspnea on exertion and significantly reduced DLCO. Impaired diffusion capacity improved over the first 6 months after hospitalization but not thereafter.

[Pathophysiology, diagnosis, prognosis and treatment of pulmonary hypertension associated with chronic lung disease]. / Pulmonale Hypertonie bei Lungenerkrankungen und/oder Hypoxie.

The pathophysiology of pulmonary hypertension associated with chronic lung disease (PH-CLD) is complex, multifactorial, and not consistent among pulmonary diseases. However, pulmonary vasculopathy triggered by various factors, such as chronic alveolar hypoxia or cigarette smoking, seems to play a central role in the pathogenesis of PH-CLD. While the initial workup of PH-CLD is usually complicated by an overlap of symptoms of PH and the underlying lung disease, PH-CLD should be considered when there is a discrepancy between symptoms (especially exertional dyspnea) and pulmonary function tests. Clinical suspicion of PH-CLD can be strengthened by noninvasive diagnostic tools such as transthoracic echocardiography (TTE) or N-terminal pro-B-type natriuretic peptide (NT-pro-BNP). However, a right heart catheterization should only be performed in specialized centers to establish the diagnosis if therapeutic consequences for the patient were expected.The basic treatment of PH-CLD is optimal management of the underlying lung disease. Among the existing interventional and registry-based studies, only a small number of data suggests favorable outcomes when treating PH-CLD patients with PAH-specific medications. Some publications even suggest negative effects. Nevertheless, recent data on inhaled vasoactive therapy in PH-CLD showed positive results for inhaled Treprostinil, although long-term data for this therapeutic approach are still lacking. Treatment of PH-CLD patients with PAH-specific drugs should only be performed in specialized centers and preferably in the context of clinical trials.

Significance of Hypocapnia in the Risk Assessment of Patients with Pulmonary Hypertension.

Blood gas analysis is part of the diagnostic work-up for pulmonary hypertension (PH). Although some studies have found that the partial pressure of carbon dioxide (PaCO2) is an independent marker of mortality in individuals with pulmonary arterial hypertension (PH Group 1), there is a lack of data regarding the significance of PaCO2 in individuals with different types of PH based on the new 2022 definitions. Therefore, this study analyzed data from 157 individuals who were undergoing PH work-up, including right heart catheterization, using PH definitions from the 2022 European Society of Cardiology/European Respiratory Society guidelines. At diagnosis, N-terminal pro-B-type natriuretic peptide (NT-pro-BNP) levels were significantly higher, but the time-course of NT-pro-BNP levels during treatment was significantly more favorable in individuals with pulmonary arterial hypertension (PH Group 1) who did versus did not have hypocapnia (p = 0.026 and p = 0.017, respectively). These differences based on the presence of hypocapnia were not seen in individuals with PH Groups 2, 3, or 4. In conclusion, using the new definition of PH, hypocapnia may correlate with worse risk stratification at diagnosis in individuals with pulmonary arterial hypertension. However, hypocapnic individuals with pulmonary arterial hypertension may benefit more from disease-specific therapy than those without hypocapnia.

Eight Patients With Pilonidal Carcinoma in One Decade-Is the Incidence Rising?

INTRODUCTION: Carcinoma secondary to pilonidal disease is very rare with fewer than 130 reported cases so far. It is presumed that underreporting and underpublishing contribute to the low reported incidence. METHODS: A post was published on a closed Facebook group with about 30,000 Syrian doctors asking if anyone had ever seen a patient with pilonidal carcinoma before. The patients' data were collected retrospectively from the treating physicians. RESULTS: Between 2010 and 2019, we identified eight patients with pilonidal carcinoma. All patients were males with a mean age of 55.5 years. The mean interval between diagnosis of pilonidal disease and diagnosis of carcinoma was 6.9 years. A growing ulcer on the background of a pilonidal sinus disease was the presenting complaint in 50% of cases. Three patients were lost from follow-up after the diagnosis due to referral. All other five patients underwent surgical resection and three of them received postoperative chemoradiation. Four patients were followed for six months or longer: two died of metastases, one survived after recurrence and re-excision, and one survived with no recurrence. CONCLUSION: This paper presents the largest cohort of pilonidal carcinoma so far and the first that describes the disease in the Syrian population. Due to underreporting, the real incidence of pilonidal carcinoma exceeds what is reported so far in the literature.

Effects of COPD on Left Ventricular and Left Atrial Deformation in Patients with Acute Myocardial Infarction: Strain Analysis Using Speckle-Tracking Echocardiography.

Myocardial strain analysis, which describes myocardial deformation (shortening or lengthening), provides more detailed information about left ventricular (LV) and atrial (LA) functions than conventional echocardiography and delivers prognostic information. To analyze the effects of COPD on left heart function upon acute myocardial infarction (AMI), consecutive AMI patients were retrospectively screened, and patients were included if a post-AMI echocardiography and results of recent pulmonary function tests (PFTs) were available. Strain analysis was performed by a cardiologist who was blinded to clinical information. Overall, 109 AMI patients were included (STEMI: 38%, non-STEMI: 62%). COPD patients (41%) had significantly more impaired LV "global-longitudinal-strain" (LV-GLS) compared to non-COPD patients (−15 ± 4% vs. −18 ± 4%; p < 0.001, respectively), even after adjusting for LV-ejection-fraction (LVEF) and age (mean estimated difference: 1.7%, p = 0.009). Furthermore, COPD patients had more impaired LA strain (LAS) than non-COPD patients in all cardiac cycle phases (estimated mean differences after adjusting for LVEF and age: during reservoir phase: −7.5% (p < 0.001); conduit phase: 5.5% (p < 0.001); contraction phase: 1.9% (p = 0.034)). There were no correlations between PFT variables and strain values. In conclusion, the presence of COPD was associated with more impaired LV and LA functions after AMI, as detected by strain analysis, which was independent of age, LVEF, and PFT variables.

Cardiopulmonary work up of patients with and without fatigue 6 months after COVID-19.

The pathogenesis of long-Covid symptoms remains incompletely understood. Therefore, we aimed to determine cardiopulmonary limitations 6 months after surviving COVID-19 using pulmonary function tests, echocardiographic studies to the point of analysis of global-longitudinal-strain (GLS), which describes the cycling myocardium deformation and provides better data on left ventricular (LV) dysfunction than LV ejection fraction (LVEF), and validated questionnaires. Overall, 60 consecutive hospitalized patients were included (61 ± 2 years, 40% treated in the ICU). At follow-up (194 ± 3 days after discharge), fatigue was the most prevalent symptom (28%). Patients with fatigue were more symptomatic overall and characterized by worse quality of life (QoL) scores compared to patients without fatigue (all p < 0.05), mainly due to limited mobility and high symptom burden. While PFT variables and LVEF were normal in the vast majority of patients (LVEF = 52% (45-52%)), GLS was significantly reduced (- 15% (- 18 to - 14%)). However, GLS values were not different between patients with and without fatigue. In conclusion, fatigue was the most prevalent long-Covid symptom in our cohort, which was associated with worse QoL mainly due to limited mobility and the high burden of concomitant symptoms. Patients showed a subtle myocardial dysfunction 6 months after surviving COVID-19, but this did not relate to the presence of fatigue.

Successful treatment of prolonged COVID-19 with Bamlanivimab in a patient with severe B-Cell aplasia due to treatment with an anti-CD20 monoclonal antibody: A case report.

A 71-year-old female patient with B-cell depletion due to treatment with an anti-CD20 monoclonal antibody was admitted for worsening COVID-19. Overall, she had persistent viral shedding, worsening respiratory failure, and progressive pneumonia that did not improve despite dexamethasone and antibiotic therapy. After administration of bamlanivimab, a monoclonal antibody with high affinity for the receptor-binding domain of the SARS-CoV-2 spike protein, inflammatory markers rapidly decreased, SARS-CoV2 RT-PCR became negative, and the patient improved clinically and radiologically. In conclusion, we demonstrated successful treatment of prolonged COVID-19 in a patient with severe B-cell aplasia with a virus-neutralizing monoclonal antibody.