Monitoring COPD patients: systemic and bronchial eosinophilic inflammation in a 2-year follow-up.

BACKGROUND: High blood eosinophils seem to predict exacerbations and response to inhaled corticosteroids (ICS) treatment in patients with chronic obstructive pulmonary disease (COPD). The aim of our study was to prospectively evaluate for 2 years, blood and sputum eosinophils in COPD patients treated with bronchodilators only at recruitment. METHODS: COPD patients in stable condition treated with bronchodilators only underwent monitoring of lung function, blood and sputum eosinophils, exacerbations and comorbidities every 6 months for 2 years. ICS was added during follow-up when symptoms worsened. RESULTS: 63 COPD patients were enrolled: 53 were followed for 1 year, 41 for 2 years, 10 dropped-out. After 2 years, ICS was added in 12/41 patients (29%) without any statistically significant difference at time points considered. Blood and sputum eosinophils did not change during follow-up. Only FEV1/FVC at T0 was predictive of ICS addition during the 2 year-follow-up (OR:0.91; 95% CI: 0.83-0.99, p = 0.03). ICS addition did not impact on delta (T24-T0) FEV1, blood and sputum eosinophils and exacerbations. After 2 years, patients who received ICS had higher blood eosinophils than those in bronchodilator therapy (p = 0.042). Patients with history of ischemic heart disease increased blood eosinophils after 2 years [p = 0.03 for both percentage and counts]. CONCLUSIONS: Blood and sputum eosinophils remained stable during the 2 year follow-up and were not associated with worsened symptoms or exacerbations. Almost 30% of mild/moderate COPD patients in bronchodilator therapy at enrollment, received ICS for worsened symptoms in a 2 year-follow-up and only FEV1/FVC at T0 seems to predict this addition. History of ischemic heart disease seems to be associated with a progressive increase of blood eosinophils.

Analysis of Patients with Asthma and Mixed Granulocytic Inflammatory Pattern in Sputum.

BACKGROUND: Patients with asthma usually present airway inflammation classified as eosinophilic, neutrophilic, mixed granulocytic, and paucigranulocytic pattern according to sputum inflammatory cells. OBJECTIVE: The aim of the study was to analyze clinical and biological characteristics of patients with asthma and mixed granulocytic pattern in comparison with the other groups. METHODS: Induced sputum was used to assess airway inflammation; lung function was evaluated as well as blood leukocytes and disease control. History of comorbidities was collected. RESULTS: We retrospectively analyzed 231 subjects with asthma; patients with mixed granulocytic pattern were more frequently male compared with paucigranulocytic subjects, older than eosinophilic and paucigranulocytic patients with increased number and vitality of sputum cells compared to eosinophilic and paucigranulocytic patients and higher cumulative illness rating score, related to increased age. Smoking history, age of disease onset, and ICS treatment were not associated with higher mixed granulocytic pattern occurrence. Subjects with neutrophilic inflammation (mixed granulocytic and neutrophilic patterns considered altogether) were more frequently obese. In subjects under 67 years of age (median of the enrolled subjects), arterial hypertension was the only comorbidity more frequent in mixed granulocytic than in the other groups. 137/231 subjects were re-valuated during follow-up. Lung function of patients with mixed granulocytic, neutrophilic, and paucigranulocytic patterns improved less than that of eosinophilic patients. CONCLUSION: Aging and presence of comorbidities, in particular obesity and hypertension, are characteristics of patients with asthma and mixed granulocytic pattern. They could respond less well to treatment than eosinophilic patients.

Global burden of new-onset hypertension associated with severe acute respiratory syndrome coronavirus 2 infection.

Several reports documented a specific effect of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) on blood pressure (BP), during and after the acute phase of infection. Clinical studies demonstrated that coronavirus disease 2019 (COVID-19) is associated with an increased risk of a persistent increase in BP requiring a new or intensified anti-hypertensive treatment during hospitalization. The picture is further complicated by the evidence from large databases showing an increased risk of new-onset hypertension in COVID-19 survivors on the long term. To further elucidate the epidemiological burden of this phenomenon, we performed a pooled analysis of 4 studies reporting crude incidence rates of new-onset hypertension among COVID-19 patients and contemporary controls. Overall, COVID-19 was associated with a 65% increased risk of new-onset hypertension when compared with controls (p<0.0001); furthermore, incidence of new-onset hypertension was 9% and 5% among COVID-19 patients and controls, respectively. In both the acute phase and recovery from infection, the interaction between spike proteins of SARS-CoV-2 and angiotensin converting enzyme 2 (ACE2) receptors remain the most plausible mechanism explaining the raise in BP (ranking new onset hypertension as one of the most prevalent cardiovascular sequelae of COVID-19). In this area of research, it is worth to mention that new variants of SARS-CoV-2 exhibit specific mutations in the spike protein that promotes entry into viral cells via ACE2. Thus, the enhanced spike affinity for ACE2 of new variants has the potential to increase the risk of new-onset hypertension when compared with the original Wuhan strain.

Genetics of Hypertension: From Monogenic Analysis to GETomics.

Arterial hypertension is the most frequent cardiovascular risk factor all over the world, and it is one of the leading drivers of the risk of cardiovascular events and death. It is a complex trait influenced by heritable and environmental factors. To date, the World Health Organization estimates that 1.28 billion adults aged 30-79 years worldwide have arterial hypertension (defined by European guidelines as office systolic blood pressure ≥ 140 mmHg or office diastolic blood pressure ≥ 90 mmHg), and 7.1 million die from this disease. The molecular genetic basis of primary arterial hypertension is the subject of intense research and has recently yielded remarkable progress. In this review, we will discuss the genetics of arterial hypertension. Recent studies have identified over 900 independent loci associated with blood pressure regulation across the genome. Comprehending these mechanisms not only could shed light on the pathogenesis of the disease but also hold the potential for assessing the risk of developing arterial hypertension in the future. In addition, these findings may pave the way for novel drug development and personalized therapeutic strategies.

[Secondary hypertension: diagnosis and treatment]. / Ipertensione arteriosa secondaria: diagnosi e trattamento.

Hypertension does not recognize obvious pathogenic causes in the majority of patients (essential hypertension). However, a secondary underlying cause of hypertension can be recognized in 5-10% of unselected hypertensive patients, and this prevalence may increase to more than 20% in patients with hypertension that is difficult to control or frankly resistant to treatment. In children, secondary hypertension is most often due to aortic coarctation, distal thoracic or abdominal aortic stenosis, or specific gene mutations. In adults or elderly individuals, secondary hypertension is most often due to atherosclerotic renal artery stenosis, primary hyperaldosteronism, and Cushing's disease or syndrome. Parenchymal nephropathy and hyperparathyroidism can cause hypertension at all ages, while pheochromocytoma and paraganglioma tend to occur more often in adolescents or young adults. In general, secondary hypertension should be suspected in subjects with: (a) onset of hypertension under 30 years of age especially if in the absence of hypertensive family history or other risk factors for hypertension; (b) treatment-resistant hypertension; c) severe hypertension (>180/110 mmHg), malignancy, or hypertensive emergencies; d) rapid rise in blood pressure values in previously well controlled patients. Any clinical signs suspicious or suggestive of hypertension from endocrine causes, a "reverse dipping" or "non-dipping'" profile at 24 h ambulatory blood pressure monitoring not justified by other factors, signs of obvious organ damage may be helpful clues for diagnosis. Finally, patients snoring or with clear sleep apnea should also be considered for possible secondary hypertension.

Evaluation of physical activity before and after respiratory rehabilitation in normal weight individuals with asthma: a feasibility study.

Background: Individuals with asthma spend less time engaging in physical activity compared to the general population. Increasing physical activity has become a patient-centered goal for the treatment of treatable traits of individuals with asthma. There are data showing the possible effects of a pulmonary rehabilitation program on physical activity in obese individuals with asthma but not in normal-weight asthmatics. The objective of this feasibility study is to estimate the number of daily steps and time spent on activity in normal-weight individuals with asthma, measured before and after a pulmonary rehabilitation program. Methods: Normal-weight individuals with moderate to severe asthma were evaluated. The individuals measured their daily steps with an accelerometer for 5 days before and after a pulmonary rehabilitation program. The study was registered on ClinicalTrials.gov: NCT05486689. Results: In total, 17 participants were enrolled; one dropout and data on the time in activity of two individuals are missing due to a software error during the download. Data from 16 patients were analyzed. The median number of steps/day at baseline was 5,578 (25th, 75th percentiles = 4,874, 9,685) while the median activity time was 214 min (25th, 75th percentiles = 165, 239). After the rehabilitation program, the number of daily steps increased by a median value of 472 (p-value = 0.561) and the time in activity reduced by 17 min (p-value = 0.357). We also found a significant difference in quality of life, muscle strength, and exercise capacity. Conclusions: The results of this study make it possible to calculate the sample size of future studies whose main outcome is daily steps in normal-weight individuals with asthma. The difficulties encountered in downloading time in activity data do not allow the same for this outcome. Clinical Trial Registration: ClinicalTrials.gov, identifier NCT05486689.

Asthma and hypertension: the role of airway inflammation.

Introduction: Asthma is a chronic inflammatory respiratory disease often associated with comorbidities. Among cardiovascular comorbidities, arterial hypertension seems to create an additional health burden in asthmatics. However, evidence on this relationship is lacking. Objective: Our study aims to evaluate the characteristics of hypertensive asthmatics, focusing on the role of inflammation as a possible link between these diseases. Methods: We conducted a monocentric retrospective analysis consecutively including asthmatics who underwent induced sputum (IS) at our asthma referral center. Patients were divided in two groups according to presence or absence of history of hypertension. Clinical, functional, and inflammatory (airway and systemic) data were collected. Results: Data on two hundred and sixty asthmatic patients were analyzed. Seventy-nine (30.4%) of them had a diagnosis of hypertension requiring a specific pharmacological treatment. Asthmatics with hypertension were more frequently male (p = 0.047), older (p < 0.001), and with higher body max index (BMI) (p < 0.001) when compared to normotensive patients. No difference concerning asthma control, severity and pharmacological treatment was observed between the two groups (all p > 0.05); distribution of comorbidities and lung function impairment (forced expiratory volume in the first second (FEV1) and forced vital capacity (FVC); all p < 0.05) were statistically different between groups. Mixed granulocytic airway inflammation was prevalent in the hypertensive asthmatics (p = 0.014). Interestingly, a multivariable analysis revealed that age ≥ 65 years and an increased percentage of sputum neutrophils (≥61%) were independent predictors of hypertensive status (p < 0.001). Conclusion: Our data suggest that neutrophilic airway inflammation (as evaluated by induced sputum) is strictly associated with hypertension. In clinical practice, phenotyping asthmatic patients with comorbidities like hypertension could be useful also from a therapeutic point of view. Additional studies are mandatory to further elucidate the role of neutrophilic airway inflammation in asthma with cardiovascular diseases.

Sex-related differences in non-ischemic myocardial injury in the emergency department: A real-world perspective.

BACKGROUND: Myocardial injury is associated with adverse outcomes. No data are reported about sex differences in incidence and factors associated with myocardial injury in an emergency department (ED) setting from a real-world perspective. We aimed to assess whether sex plays a major role in the diagnosis of myocardial injury in the ED. METHODS: In this subanalysis of a retrospective study, patients presenting at the ED with at least one high-sensitivity cardiac troponin T (hs-cTnT) value and without acute coronary syndromes diagnosis were compared. RESULTS: 31,383 patients were admitted to the ED, 4660 had one hs-cTnT value, and 3937 were enrolled: 1943 females (49.4%) and 1994 males (50.6%). The diagnosis of myocardial injury was higher among men (36.8% vs. 32.9%, p < 0.01). Male sex was independently associated with myocardial injury. An older age, an elevated NT-proB-type Natriuretic Peptide and a lower estimated glomerular filtrate rate were independently associated with myocardial injury in both sexes. CONCLUSIONS: In the ED, from a real-world perspective, myocardial injury occurred more frequently in males, and it was associated with older age and the presence of cardiac, lung, and kidney disease but not higher hs-cTnT values.

Unlocking the Long-Term Effectiveness of Benralizumab in Severe Eosinophilic Asthma: A Three-Year Real-Life Study.

Background: Benralizumab has been shown to restore good control of severe eosinophilic asthma (SEA). Robust data on benralizumab effectiveness over periods longer than 2 years are scarce. Methods: This retrospective multicentric study was conducted on 108 Italian SEA patients treated with benralizumab for up to 36 months. Partial and complete clinical remission (CR) were assessed. Data were analyzed with descriptive statistics or using linear, logistic, and negative binomial mixed-effect regression models. Results: At 36 months, benralizumab reduced the exacerbation rate by 89% and increased the forced expiratory volume in 1 second (FEV1) (+440 mL at 36 months, p < 0.0001). Benralizumab improved asthma control as well as sinonasal symptoms in patients with chronic rhinosinusitis with nasal polyposis (CRSwNP). Up to 93.33% of patients either reduced or discontinued OCS; benralizumab also decreased ICS use and other asthma medications. Overall, 84.31% of patients achieved partial or complete CR. Conclusions: Benralizumab improved asthma and sinonasal outcomes up to 36 months. These findings support the potential of benralizumab to induce CR, emphasizing its role as a disease-modifying anti-asthmatic drug for the management of SEA. Further research is warranted to expand these findings by minimizing data loss and assessing benralizumab's long-term safety.

Rethinking the Role of the Renin-Angiotensin System in the Pandemic Era of SARS-CoV-2.

After assessing the levels of spread and severity of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, academic literature focused on the pathophysiology of coronavirus disease 2019 (COVID-19) [...].

Complications of SARS-CoV-2 Infection During Cardiac Rehabilitation: A Case Series.

INTRODUCTION: Vaccination strongly reduces the risk of hospitalization and death due to coronavirus disease 2019 (COVID-19). However, the severity of the acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection and the degree of protection exerted over time by vaccination remains to be fully elucidated among hospitalized comorbid and vulnerable patients with SARS-CoV-2 infection. METHODS: We report a case series of nine hospitalized vulnerable patients who developed a SARS-CoV-2 infection during a cardiac rehabilitation inpatient program. RESULTS: Age ranged from 50 to 81 years. All but one patient had received at least three doses of anti-COVID-19 vaccine more than 4 months before the cardiac event. Indications for cardiac rehabilitation included acute coronary syndromes, congestive heart failure, heart valve surgery, and coronary artery bypass graft. After the confirmed diagnosis of SARS-CoV-2 infection, all patients developed symptoms. Eight patients developed at least one SARS-CoV-2-related complication, including a significant increase in high-sensitivity troponin I levels, new-onset hypoxemia, persistent atrial fibrillation, non-sustained ventricular tachycardia and recurrent sinus arrest, pericardial effusion, and a persistent increase in blood pressure. CONCLUSION: Almost all patients developed complications which, however, did not evolve towards more severe expressions of the disease. These data suggest that even in this new phase of the pandemic, vaccination may exert a potential role to reduce the risk of progression towards more severe disease of SARS-CoV-2 infection in vulnerable patients with cardiovascular comorbidities.

mRNA Metabolism and Hypertension.

Hypertension is the most frequent cardiovascular risk factor all over the world. It remains a leading contributor to the risk of cardiovascular events and death. In the year 2015, about 1.5 billion of adult people worldwide had hypertension (as defined by office systolic blood pressure ≥ 140 mmHg or office diastolic blood pressure ≥ 90 mmHg). Moreover, the number of hypertensive patients with age ranging from 30 to 79 years doubled in the last 30 years (from 317 million men and 331 million women in the year 1990 to 652 million men and 626 million women in 2019) despite stable age-standardized prevalence worldwide. Despite such impressive growth, the proportion of controlled hypertension is very low. A better understanding of the pathogenesis of hypertension may contribute to the development of innovative therapeutic strategies. In this context, alterations of the messenger RNA metabolism have been recently evaluated as contributors to the pathogenesis of hypertension, and pharmacological modulation of RNA metabolism is under investigation as potential and novel therapeutic armamentarium in hypertension.

The spike effect of acute respiratory syndrome coronavirus 2 and coronavirus disease 2019 vaccines on blood pressure.

Among the various comorbidities potentially worsening the clinical outcome in patients hospitalized for the acute respiratory syndrome coronavirus-2 (SARS-CoV-2), hypertension is one of the most prevalent. However, the basic mechanisms underlying the development of severe forms of coronavirus disease 2019 (COVID-19) among hypertensive patients remain undefined and the direct association of hypertension with outcome in COVID-19 is still a field of debate. Experimental and clinical data suggest that SARS-CoV-2 infection promotes a rise in blood pressure (BP) during the acute phase of infection. Acute increase in BP and high in-hospital BP variability may be tied with acute organ damage and a worse outcome in patients hospitalized for COVID-19. In this context, the failure of the counter-regulatory renin-angiotensin-system (RAS) axis is a potentially relevant mechanism involved in the raise in BP. It is well recognized that the efficient binding of the Spike (S) protein to angiotensin converting enzyme 2 (ACE2) receptors mediates the virus entry into cells. Internalization of ACE2, downregulation and malfunction predominantly due to viral occupation, dysregulates the protective RAS axis with increased generation and activity of angiotensin (Ang) II and reduced formation of Ang1,7. Thus, the imbalance between Ang II and Ang1-7 can directly contribute to excessively rise BP in the acute phase of SARS-CoV-2 infection. A similar mechanism has been postulated to explain the raise in BP following COVID-19 vaccination ("Spike Effect" similar to that observed during the infection of SARS-CoV-2). S proteins produced upon vaccination have the native-like mimicry of SARS-CoV-2 S protein's receptor binding functionality and prefusion structure and free-floating S proteins released by the destroyed cells previously targeted by vaccines may interact with ACE2 of other cells, thereby promoting ACE2 internalization and degradation, and loss of ACE2 activities.

Interpretation of Ambulatory Blood Pressure Monitoring for Risk Stratification in Hypertensive Patients: The 'Ambulatory Does Prediction Valid (ADPV)' Approach.

Several outcome-based prospective investigations have provided solid data which support the prognostic value of 24 h ambulatory blood pressure over and beyond cardiovascular traditional risk factors. Average 24 h, daytime, and nighttime blood pressures are the principal components of the ambulatory blood pressure profile that have improved cardiovascular risk stratification beyond traditional risk factors. Furthermore, several additional ambulatory blood pressure measures have been investigated. The correct interpretation in clinical practice of ambulatory blood pressure monitoring needs a standardization of methods. Several algorithms for its clinical use have been proposed. Implementation of the results of ambulatory blood pressure monitoring in the management of individual subjects with the aim of improving risk stratification is challenging. We suggest that clinicians should focus attention on ambulatory blood pressure components which have been proven to act as the main independent predictors of outcome (average 24 h, daytime, and nighttime blood pressure, pulse pressure, dipping status, BP variability).

COVID-19, vaccines and deficiency of ACE2 and other angiotensinases. Closing the loop on the "Spike effect".

The role of a dysregulated renin-angiotensin system (RAS) in the pathogenesis of COVID-19 is well recognized. The imbalance between angiotensin II (Ang II) and Angiotensin1-7 (Ang1,7) caused by the interaction between SARS-CoV-2 and the angiotensin converting enzyme 2 (ACE2) receptors exerts a pivotal role on the clinical picture and outcome of COVID-19. ACE2 receptors are not the exclusive angiotensinases in nature. Other angiotensinases (PRCP, and POP) have the potential to limit the detrimental effects of the interactions between ACE2 and the Spike proteins. In the cardiovascular disease continuum, ACE2 activity tends to decrease, and POP/PRCP activity to increase, from the health status to advanced deterioration of the cardiovascular system. The failure of the counter-regulatory RAS axis during the acute phase of COVID-19 is characterized by a decrease of ACE2 expression coupled to unchanged activity of other angiotensinases, therefore failing to limit the accumulation of Ang II. COVID-19 vaccines increase the endogenous synthesis of SARS-CoV-2 spike proteins. Once synthetized, the free-floating spike proteins circulate in the blood, interact with ACE2 receptors and resemble the pathological features of SARS-CoV-2 ("Spike effect" of COVID-19 vaccines). It has been noted that an increased catalytic activity of POP/PRCP is typical in elderly individuals with comorbidities or previous cardiovascular events, but not in younger people. Thus, the adverse reactions to COVID-19 vaccination associated with Ang II accumulation are generally more common in younger and healthy subjects. Understanding the relationships between different mechanisms of Ang II cleavage and accumulation offers the opportunity to close the pathophysiological loop between the risk of progression to severe forms of COVID-19 and the potential adverse events of vaccination.

Blood Pressure Increase following COVID-19 Vaccination: A Systematic Overview and Meta-Analysis.

Coronavirus disease 2019 (COVID-19) vaccines proved a strong clinical efficacy against symptomatic or moderate/severe COVID-19 and are considered the most promising approach for curbing the pandemic. However, some questions regarding the safety of COVID-19 vaccines have been recently raised. Among adverse events to vaccines and despite a lack of signal during phase III clinical trials, an increase in blood pressure (BP) after COVID-19 vaccination has been reported as a potential adverse reaction. We systematically analyze this topic and undertook a meta-analysis of available data to estimate the proportion of patients with abnormal BP or raise in BP after vaccination. Six studies entered the final analysis. Overall, studies accrued 357,387 subjects with 13,444 events of abnormal or increased BP. After exclusion of outlier studies, the pooled estimated proportion of abnormal/increased BP after vaccination was 3.20% (95% CI: 1.62-6.21). Proportions of cases of stage III hypertension or hypertensive urgencies and emergencies was 0.6% (95% CI: 0.1% to 5.1%). In conclusion, abnormal BP is not rare after COVID-19 vaccination, but the basic mechanisms of this phenomenon are still unclear and require further research.

High-Sensitivity Cardiac Troponin T and the Diagnosis of Cardiovascular Disease in the Emergency Room: The Importance of Combining Cardiovascular Biomarkers with Clinical Data.

Background. Nowadays, it is still not possible to clinically distinguish whether an increase in high-sensitivity cardiac troponin (hs-cTn) values is due to myocardial injury or an acute coronary syndrome (ACS). Moreover, predictive data regarding hs-cTnT in an emergency room (ER) setting are scarce. This monocentric retrospective study aimed to improve the knowledge and interpretation of this cardiac biomarker in daily clinical practice. Methods. Consecutive adult patients presenting at the ER and hospitalized with a first abnormal hs-cTnT value (≥14 ng/L) were enrolled for 6 months. The baseline hs-cTnT value and the ensuing changes and variations were correlated with the clinical presentation and the type of diagnosis. Subsequently, multivariable models were built to assess which clinical/laboratory variables most influenced hospital admissions in the investigated population analyzed according to the final reason for hospitalization: (1) cardiovascular vs. non-cardiovascular diagnosis, and (2) ACS vs. non-ACS one. Results. A total of 4660 patients were considered, and, after a first screening, 4149 patients were enrolled. Out of 4129 patients, 1555 (37.5%) had a first hs-cTnT ≥14 ng/L, and 1007 (65%) were hospitalized with the following types of diagnosis: ACS (182; 18%), non-ACS cardiovascular disease (337; 34%) and non-cardiovascular disease (487; 48%). Higher hs-cTnT values and significant hs-cTnT variations were found in the ACS group (p < 0.01). The mean percentage of variation was higher in patients with ACS, intermediate in those with non-ACS cardiovascular disease, and low in those with non-cardiovascular disease (407.5%, 270.6% and 12.4%, respectively). Only syncope and CRP (OR: 0.08, 95% CI: 0.02−0.39, p < 0.01 and OR: 0.9988, 95% CI: 0.9979−0.9998, p = 0.02, respectively) or CRP (OR: 0.9948, 95% CI: 0.9908−0.9989, p = 0.01) and NT-proBNP (OR: 1.0002, 95% CI: 1.0000−1.0004, p = 0.02) were independent predictors of a cardiovascular disease diagnosis. On the other hand, only chest pain (OR: 22.91, 95% CI: 3.97−132.32, p < 0.01) and eGFR (OR: 1.04, 95% CI: 1.004−1.083, p = 0.03) were associated with the ACS diagnosis. Conclusions. Differently from the investigated biomarkers, in this study, only clinical variables predicted hospitalizations in different patients' subgroups.

Combined Use of Electrocardiography and Ultrasound to Detect Cardiac and Pulmonary Involvement after Recovery from COVID-19 Pneumonia: A Case Series.

BACKGROUND: Although severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) may cause an acute multiorgan syndrome (coronavirus disease 2019 (COVID-19)), data are emerging on mid- and long-term sequelae of COVID-19 pneumonia. Since no study has hitherto investigated the role of both cardiac and pulmonary ultrasound techniques in detecting such sequelae, this study aimed at evaluating these simple diagnostic tools to appraise the cardiopulmonary involvement after COVID-19 pneumonia. METHODS: Twenty-nine patients fully recovered from COVID-19 pneumonia were considered at our centre. On admission, all patients underwent 12-lead electrocardiogram (ECG) and transthoracic echocardiography (TTE) evaluation. Compression ultrasound (CUS) and lung ultrasound (LUS) were also performed. Finally, in each patient, pathological findings detected on LUS were correlated with the pulmonary involvement occurring after COVID-19 pneumonia, as assessed on thoracic computed tomography (CT). RESULTS: Out of 29 patients (mean age 70 ± 10 years; males 69%), prior cardiovascular and pulmonary comorbidities were recorded in 22 (76%). Twenty-seven patients (93%) were in sinus rhythm and two (7%) in atrial fibrillation. Persistence of ECG abnormalities from the acute phase was common, and nonspecific repolarisation abnormalities (93%) reflected the high prevalence of pericardial involvement on TTE (86%). Likewise, pleural abnormalities were frequently observed (66%). TTE signs of left and right ventricular dysfunction were reported in two patients, and values of systolic pulmonary artery pressure were abnormal in 16 (55%, despite the absence of prior comorbidities in 44% of them). Regarding LUS evaluation, most patients displayed abnormal values of diaphragmatic thickness and excursion (93%), which correlated well with the high prevalence (76%) of pathological findings on CT scan. CUS ruled out deep vein thrombosis in all patients. CONCLUSIONS: Data on cardiopulmonary involvement after COVID-19 pneumonia are scarce. In our study, simple diagnostic tools (TTE and LUS) proved clinically useful for the detection of cardiopulmonary complications after COVID-19 pneumonia.

The 5-Repetition Sit-to-Stand Test as an Outcome Measure for Pulmonary Rehabilitation in Subjects With Asthma.

BACKGROUND: The 5-repetition sit-to-stand test (5STS) is valid and responsive in subjects with COPD, but there is a lack of information in subjects with asthma. We aimed to evaluate the usefulness of the 5STS as an outcome measure of pulmonary rehabilitation in subjects with asthma as compared to subjects with COPD. METHODS: We conducted a retrospective evaluation of subjects with asthma or COPD who underwent pulmonary rehabilitation. Both before and after in-patient pulmonary rehabilitation, subjects underwent the 5STS and the 6-min walk test; dyspnea was assessed with the Medical Research Council scale and the Barthel Index for dyspnea, and the burden of symptoms was assessed with the COPD Assessment Test. RESULTS: Of 475 patients admitted during the study period, 103 subjects with asthma and 108 with COPD were included. After pulmonary rehabilitation, the 5STS improved significantly in both populations (by a median value of -1.7 s [interquartile range -4.2 to -0.5] and -1.1 s [interquartile range -3.4 to 0.0] in subjects with asthma and COPD, respectively; P < .001 for both, P = .17 between groups) independent of body mass index, as did other outcome measures. The baseline 5STS correlated slightly but significantly with age, the 6-min walk test, and the Barthel Index for dyspnea in both populations, whereas it correlated significantly with the Medical Research Council scale only in subjects with asthma and correlated with COPD Assessment Test only in subjects with COPD. No significant correlations between changes in the 5STS and in other assessed outcome measures before and after pulmonary rehabilitation were observed in subjects with asthma, whereas changes in the 5STS correlated slightly but significantly only with changes in 6-min walk test in subjects with COPD. CONCLUSIONS: The 5STS was a reliable outcome measure of pulmonary rehabilitation in subjects with asthma. It must be specifically assessed and may be included in the tools for assessment of effects of pulmonary rehabilitation also in these patients.

Time course of exercise capacity in patients recovering from COVID-19-associated pneumonia.

OBJECTIVE: High prevalences of muscle weakness and impaired physical performance in hospitalized patients recovering from COVID-19-associated pneumonia have been reported. Our objective was to determine whether the level of exercise capacity after discharge would affect long-term functional outcomes in these patients. METHODS: From three to five weeks after discharge from acute care hospitals (T0), patients underwent a six-minute walk test (6MWT) and were divided into two groups according to the distance walked in percentage of predicted values: <75% group and ≥75% group. At T0 and three months later (T1), patients completed the Short Physical Performance Battery and the Euro Quality of Life Visual Analogue Scale, and pulmonary function and respiratory muscle function were assessed. In addition, a repeat 6MWT was also performed at T1. RESULTS: At T0, 6MWD values and Short Physical Performance Battery scores were lower in the <75% group than in the ≥75% group. No differences were found in the Euro Quality of Life Visual Analogue Scale scores, pulmonary function variables, respiratory muscle function variables, length of hospital stay, or previous treatment. At T1, both groups improved their exercise capacity, but only the subjects in the <75% group showed significant improvements in dyspnea and lower extremity function. Exercise capacity and functional status values returned to predicted values in all of the patients in both groups. CONCLUSIONS: Four weeks after discharge, COVID-19 survivors with exercise limitation showed no significant differences in physiological or clinical characteristics or in perceived health status when compared with patients without exercise limitation. Three months later, those patients recovered their exercise capacity.