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BackgroundIn animal models of pulmonary arterial hypertension (PAH), angiotensin converting enzyme type 2 (ACE2) and Angiotensin 1–7 [Ang-(1–7)] have been shown to have vasodilatory, anti-proliferative, anti-fibrotic and anti-hypertrophic properties. However, the status and role of the ACE2-Ang-(1–7) axis in human PAH is incompletely understood.MethodsWe studied 85 patients with a diagnosis of PAH of distinct etiologies. Fifty-five healthy blood donors paired for age and sex served as controls. Blood samples were obtained from the pulmonary artery in patients with PAH during right heart catheterisation. Peripheral blood was obtained for both groups. Ang-(1–7) and angiotensin II (AngII) were measured by zone capillary electrophoresis. Aldosterone, Angiotensin-(1–9), Angiotensin A, (Ang-A) and ACE2 were measured by ELISA, and ACE2 activity was determined enzymatically.ResultsOf the 85 patients, 47 had idiopathic PAH, 25 had PAH-associated with congenital heart disease, and 13 had PAH-associated with collagen vascular disease. Compared to controls, patients with PAH had a higher concentration of AngII [(1.03(IQR 0.72–1.88) versus 0.19(IQR 0.10–0.37)pmoles·mL−1;p<0.001)] and of aldosterone [(88.7(58.7–132) versus 12.9(9.55–19.9)ng·dL−1;p<0.001)]. Conversely, PAH patients had a lower concentration of Ang-(1–7) than controls [(0.69(0.474–0.91) versus 4.07(2.82–6.73)pmoles·mL−1;p<0.001)], and a lower concentration of Ang-(1–9), and Ang-A. Similarly, the ACE2 concentration was higher than in controls [(8.7(5.35–13.2) versus 4.53(1.47–14.3)ng·mL−1;p=0.011)], whereas the ACE2 activity was significantly reduced [(1.88(1.08–2.81) versus 5.97(3.1–17.8)nmoles·mL−1;p<0.001)]. No significant differences were found among the three different etiologic forms of PAH.ConclusionsThe AngII-ACE2-Ang- (1–7) axis appears to be altered in human PAH and we propose that this imbalance, in favour of AngII, plays a role in the pathogenesis of the severe PAH. Further mechanistic studies are warranted.

In the coronavirus disease 2019 (COVID-19) era, the presence of acute respiratory failure is generally associated with acute respiratory distress syndrome; however, it is essential to consider other differential diagnoses that require different, and urgent, therapeutic approaches. Herein we describe a COVID-19 case complicated with bilateral spontaneous pneumothorax. A previously healthy 45-year-old man was admitted to our emergency department with sudden-onset chest pain and progressive shortness of breath 17 days after diagnosis with uncomplicated COVID-19 infection. He was tachypneic and presented severe hypoxemia (75% percutaneous oxygen saturation). Breath sounds were diminished bilaterally on auscultation. A chest X-ray revealed the presence of a large bilateral pneumothorax. A thoracic computed tomography (CT) scan confirmed the large bilateral pneumothorax, with findings consistent with severe COVID-19 infection. Chest tubes were inserted, with immediate clinical improvement. Follow-up chest CT scan revealed resolution of bilateral pneumothorax, reduction of parenchymal consolidation, and formation of large bilateral pneumatoceles. The patient remained under observation and was then discharged home. Bilateral spontaneous pneumothorax is a very rare, potentially life-threatening complication in patients with COVID-19. This case highlights the importance of recognizing this complication early to prevent potentially fatal consequences.

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Objective To investigate whether a simplified inflammation-based risk scoring system comprising three readily available biomarkers (albumin, C-reactive protein, and leukocytes) may predict major adverse outcomes in patients with COVID-19. Methods Upon admission to the emergency room, the inflammation-based risk scoring system was applied and patients were classified as having mild, moderate, or severe inflammation. In-hospital occurrence of thrombosis, need for mechanical ventilation, and death were recorded. Results One-hundred patients (55 ± 13 years; 71% men) were included and classified as having mild (29%), moderate (12%), or severe (59%) inflammation. The need for mechanical ventilation differed among patients in each group (16%, 50%, and 71%, respectively; P < 0.0001), yielding a 4.1-fold increased risk of requiring mechanical ventilation in patients with moderate inflammation and 5.4 for those with severe inflammation. On the contrary, there were no differences for the occurrence of thrombosis (10%, 8%, and 22%, respectively; P = 0.142) or death (21%, 42%, and 39%, respectively; P = 0.106). In the multivariate analysis, only severe inflammation (hazard ratio [HR] = 4.1), D-dimer > 574 ng/mL (HR = 3.0), and troponin I ≥ 6.7 ng/mL (HR = 2.4) at hospital admission were independent predictors of the need for mechanical ventilation. Conclusion The inflammation-based risk scoring system predicts the need for mechanical ventilation in patients with severe COVID-19.

Aims Little is known regarding acute heart failure (AHF) clinical characteristics and its hospital outcome in Latin America. This study sought to assess the prevalence of, and identify differences among, in‐hospital outcomes in patients hospitalized for AHF who were stratified by clinical phenotype at a hospital in Latin America. Methods and results This is a retrospective cohort study of patients with AHF who were hospitalized in the coronary care unit of a Latin American teaching hospital from January 2006 to December 2018. Cox regression analysis was used to identify predictors of mortality. Of 21 042 patients admitted, 7759 (36.6%) had AHF. Their median age was 62 years, and 35% were women. De novo heart failure was seen in 39.4% of patients. Most common was AHF‐associated acute coronary syndromes (ACS‐HF) in 43.0%, decompensated heart failure (DHF) in 33.7%, hypertensive heart failure (HT‐HF) in 11.8%, and cardiogenic shock (CS) in 5.2%. Pulmonary oedema (PO) (3.3%) and right heart failure (RHF) (3.0%) were least frequent. Coronary artery disease was the most frequent aetiology in 56.5% of patients, valvular heart disease in 22.4%, and cardiomyopathies in 12.3%. Other less frequent aetiology included adult congenital heart disease (2.5%), lung diseases (2.1%), acute aortic syndromes (1.4%), pericardial diseases (0.8%), and intracardiac tumours (0.3%). Aetiology could not be established in 1.6% of patients. Before admission, patients with worsening chronic heart failure and reduced ejection fraction were treated with renin–angiotensin system blockers (60.4%), beta‐blockers (42.5%), or spironolactone (34.4%). The percentages of patients given in‐hospital management with intravenous diuretics, vasodilators, inotropes, and vasopressors were 81.2%, 33.4%, 18.9%, and 20.4%, respectively. The overall in‐hospital mortality was 17.9% (71.3%, 43.9%, 23.8%, 14.9%, 13.6%, and 10.1% for CS, PO, RHF, DHF, ACS‐HF, and HT‐HF, respectively; P < 0.0001). Multivariate analysis revealed that PO (hazard ratio [HR] 2.68, 95% confidence interval [CI] 1.73–4.14, P < 0.0001) and CS (HR 3.37, 95% CI 2.12–5.35, P < 0.0001) were independent predictors of in‐hospital mortality. Use of intravenous diuretics was linked to reduction of in‐hospital mortality (HR 0.70, 95% CI 0.59–0.59, P < 0.0001). By contrast, increased in‐hospital mortality was associated with the use of intravenous inotrope or vasopressor (HR 1.49, 95% CI 1.27–1.76 and HR 2.91, 95% CI 2.41–3.51, P < 0.0001, respectively). Conclusions Real‐world evidence from a university hospital in Latin America shows that the high mortality among patients with AHF may depend, among other factors, on patients' AHF clinical phenotypes. The clinical characteristics and aetiologies of AHF appear to differ between these data from Mexico and those from European and US registries.

The first patient infected by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in Panama was reported on March 9, 2020. Here, we describe the first case of recovery from coronavirus disease 2019 (COVID-19) in the country. The patient was a 49-year-old male high school teacher, who did not show any primary symptoms of COVID-19 described by health authorities as the signs for medical attention. Nonetheless, he became severely ill over the course of 2 weeks and almost lost the battle against COVID-19. The identification of the first cluster of SARS-CoV-2 community transmission in the secondary school where the patient of this case report taught, led to the closure of the school and, a day after, the shutdown of the national education system, which may have prevented the spread and slowed the transmission rate of COVID-19 during the early stages of invasion. This case report highlights the need to increase awareness among healthcare professionals in Latin America to consider symptoms such as anosmia and dysgeusia as the sentinel signs of COVID-19 infection in order to prevent deaths, especially in high-risk patients.

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