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Healthcare workers exposed to coronavirus (COVID-19) may not have adequate access to personal protective equipment (PPE), safety procedures, and diagnostic protocols. Our objective was to evaluate the reality and perceptions about personal safety among healthcare workers in Latin America. This is a cross-sectional, online survey-based study administered to 936 healthcare professionals in Latin America from 31 March 2020 to 4 April 2020. A 12-item structured questionnaire was developed. A total of 936 healthcare workers completed the online survey. Of them, 899 (95.1%) were physicians, 28 (2.9%) were nurses, and 18 (1.9%) were allied health professionals. Access to protective equipment was as follows: gel hand sanitizer (n = 889; 95%), disposable gloves (n = 853; 91.1%), disposable gowns (n = 630; 67.3%), disposable surgical masks (785; 83.9%), N95 masks (n = 516; 56.1%), and facial protective shields (n = 305; 32.6%). The vast majority (n = 707; 75.5%) had access to personal safety policies and procedures, and 699 (74.7%) participants had access to diagnostic algorithms. On a 1-to-10 Likert scale, the participants expressed limited human resources support (4.92 ± 0.2; mean ± SD), physical integrity protection in the workplace (5.5 ± 0.1; mean ± SD), and support from public health authorities (5.01 ± 0.12; mean ± SD). Healthcare workers in Latin America had limited access to essential PPE and support from healthcare authorities during the COVID-19 pandemic.

Cardiac amyloidosis is an under-recognized and potentially fatal cause of heart failure and other cardiovascular manifestations. It is caused by deposition of misfolded precursor proteins as fibrillary amyloid deposits in cardiac tissues. The two primary subtypes of systemic amyloidosis causing cardiac involvement are immunoglobulin light chain (AL), a plasma cell dyscrasia, and transthyretin (ATTR), itself subdivided into a hereditary subtype caused by a gene mutation of the ATTR protein, and an age-related wild type, which occurs in the absence of a gene mutation. Clinical recognition requires a high index of suspicion, inclusive of the extracardiac manifestations of both subtypes. Diagnostic workup includes screening for serum and/or R ESUM E L'amylose cardiaque est une cause sous-reconnue et potentiellement mortelle d'insuffisance cardiaque et d'autres manifestations cardiovasculaires. Elle est caus ee par le d epôt, dans les tissus cardiaques, de prot eines pr ecurseurs mal repli ees prenant la forme de fibrilles amyloïdes. On distingue deux grands sous-types d'amylose syst emique entraînant une atteinte cardiaque : l'amylose à chaînes l egères d'immunoglobulines (AL), une forme de dyscrasie plasmocytaire; et l'amylose à transthyr etine (ATTR), dont il existe un sous-type h er editaire, caus e par une mutation du gène codant pour la TTR, et un sous-type à TTR sauvage, li e au vieillissement et se produisant en l'absence de mutation g enique. La reconnaissance clinique n ecessite

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Background-Endothelin-1 (ET-1) plays an important role in the maintenance of vascular tone and pathological states such as ischemia/reperfusion (I/R) injury, coronary vasospasm, and cardiac allograft vasculopathy. We assessed the effects of elevated ET-1 levels as seen after I/R to determine if ET-1 modulates nitric oxide (NO) production via the translocation of specific protein kinase C (PKC) isoforms. Methods and Results-Human saphenous vein endothelial cells (HSVECs) (nϭ8) were incubated with ET-1 or phosphate-buffered saline (PBS) for 24 hours. NO production was determined in the supernatant by measuring nitrate/nitrite levels. Protein expression of endothelial nitric oxide synthase (eNOS), inducible NOS (iNOS), caveolin-1 and PKC were determined. Lastly, PKC translocation and activity were assessed after exposure to the drug of interest. HSVECs exposed to ET-1 displayed decreased NO production. PKC inhibition reduced NO production, whereas PKC activation increased production. NO production was maintained when HSVECs exposed to ET-1 were treated with the PKC agonist, PMA. eNOS protein expression was reduced after ET-1 treatment. PKC inhibition also downregulated eNOS protein expression, whereas PMA upregulated expression. ET-1 exposure led to a significant increase in PKC␦ and PKC translocation compared with control, whereas translocation of PKC was inhibited. ET-1 exposure significantly reduced overall PKC activity compared with control. Conclusions-Our study demonstrates that high levels of ET-1 impair endothelial NO production via an isoform-specific PKC-mediated inhibition of eNOS expression. ET-1 antagonism with bosentan stimulates translocation of PKC and leads to increased PKC activity and NO production. ET-1 antagonism may provide a novel therapeutic strategy to improve vascular homeostasis.

The disclosure information of the authors and reviewers is available from the CCS on their guidelines library at www.ccs.ca.This statement was developed following a thorough consideration of medical literature and the best available evidence and clinical experience. It represents the consensus of a Canadian panel comprised of multidisciplinary experts on this topic with a mandate to formulate disease-specific recommendations. These recommendations are aimed to provide a reasonable and practical approach to care for specialists and allied health professionals obliged with the duty of bestowing optimal care to patients and families, and can be subject to change as scientific knowledge and technology advance and as practice patterns evolve. The statement is not intended to be a substitute for physicians using their individual judgement in managing clinical care in consultation with the patient, with appropriate regard to all the individual circumstances of the patient, diagnostic and treatment options available and available resources. Adherence to these recommendations will not necessarily produce successful outcomes in every case.

Tyrosine kinase inhibitors (TKIs) have revolutionized the treatment and outcomes of chronic myeloid leukemia (CML). Despite their significant impact on the management of CML, there is growing evidence that TKIs may cause cardiovascular and/or metabolic complications. In this review, we present the current evidence regarding the cardiovascular safety profiles of BCR-ABL TKIs. Methodological challenges of studies that reported the cardiovascular safety of TKIs are discussed. We also propose management strategies for cardiovascular surveillance and risk factor modification during treatment with these agents.

The ADVENT-HF trial will help to determine whether treating SDB by ASV in patients with HFrEF improves morbidity and mortality.