Pericardial effusion and systemic capillary leak syndrome late post-SARS-CoV-2 vaccination.

We report an interesting case of pericardial effusion associated with idiopathic systemic capillary leak syndrome (ISCLS) following administration of SARS-CoV-2 vaccine. This patient initially presented with dyspnoea and chest pain, with non-pitting oedema and clear lung fields. The diagnosis of ISCLS was made based on the clinical syndrome and laboratory evidence of polycythaemia and hypoalbuminaemia. An enlarging pericardial effusion was diagnosed on transthoracic echocardiogram. Daily point-of-care ultrasound (POCUS)-guided volume management and serial transthoracic echocardiograms contributed to avoidance of refractory shock, cardiac tamponade and critical care admission.

The Need for Telemedicine Integration Into Adult Cardiology Training Curricula in Canada.

COVID-19 brought telemedicine to the forefront of clinical cardiology. We aimed to examine the extent of trainees' involvement in and comfort with telemedicine practices in Canada with the use of a web-based self-administered survey. Eighty-six trainees from 12 training programs completed the survey (65% response rate). Results showed that before COVID-19, 39 trainees (45%) had telemedicine exposure, compared with 67 (78%) after COVID-19 (P < 0.001). However, only 44 trainees (51%) reported being comfortable or very comfortable with the use of telemedicine. Of the 67 trainees who were involved in telemedicine, 4 (6%) had full supervision during virtual visits, 13 (19%) had partial supervision, and 50 (75%) had minimal or no supervision. Importantly, 67 trainees (78%) expressed the need for telemedicine-specific training and 64 (74%) were willing to have their virtual visits recorded for the purpose of evaluation and feedback. Furthermore, 47 (55%) felt strongly or very strongly positive about incorporating telemedicine into their future practice. The main perceived barriers to telemedicine use were concerns about patients' engagement, fear of weakening the patient-physician relationship, and unfamiliarity with telemedicine technology. These barriers, together with training in virtual physical examination skills and medicolegal aspects of telemedicine, are addressed in several established internal medicine telemedicine curricula that could be adapted by cardiology programs. In conclusion, while the degree of telemedicine involvement since COVID-19 was high, the trainees' comfort level with telemedicine practice remains suboptimal likely due to lack of training and inadequate staff supervision. Therefore, a cardiology telemedicine curriculum is needed to ensure that trainees are equipped to embrace telemedicine in cardiovascular clinical care.

p38 mitogen-activated protein kinase (MAPK) is activated by noradrenaline and serves a cardioprotective role, whereas adrenaline induces p38 MAPK dephosphorylation.

1. The aim of the present study was to investigate the role of p38 mitogen-activated protein kinases (MAPK) in mediating the effect of noradrenaline (NA) on cardiomyocyte cell viability. 2. Cardiomyocytes from embryonic chick heart were treated with various concentrations of NA, phenylephrine or isoproterenol and p38 MAPK activation was determined by western blotting. Total cell death was assessed by the 3-(4,5-dimethyl-2 thiazoyl)-2,5-diphenyl-2H-tetrazolium bromide assay. Apoptosis was determined by specific DNA fragmentation. 3. At 100 micromol/L, NA produced a significant increase in cell death that was associated with microscopic changes and DNA fragmentation indicative of apoptosis. The p38 MAPK inhibitor SB202190 (at 1 micromol/L beginning 1 h before NA), reduced NA-induced p38 MAPK activation and significantly accentuated NA-induced cell death. In contrast, the mitogen-activated protein kinase kinase ERK1/2 inhibitor PD98059 (at 1 micromol/L beginning 1 h before NA) did not significantly alter NA-induced cell death. These effects of NA were mediated, in part, through alpha-adrenoceptor because phenylephrine (100 micromol/L), like NA, also induced p38 MAPK activation. However, 100 micromol/L isoproterenol produced a sustained dephosphorylation of p38 MAPK. 4. These data show that NA-induced p38 MAPK activation, through alpha-adrenoceptor, has a protective role in cardiomyocytes to antagonize NA-induced cell death. In contrast, beta-adrenoceptor stimulation produces dephosphorylation of p38 MAPK.