Background: Currently, physicians face an unprecedented crisis with the novel coronavirus disease 2019 (COVID-19) pandemic. The impact of the pandemic on dual-physician households remains unknown. In this survey study, we examined the impact of the COVID-19 pandemic on dual-physician families and described gendered differences related to the impact of the pandemic. Methods: This was a cross-sectional survey distributed via e-mail and social media, with results collected from April 30, 2020 until May 26, 2020. Respondents were members of a dual-physician couple. Respondents provided information on demographic characteristics and the impact of the pandemic on their professional lives, personal lives, and well-being. Categorical variables were compared using chi-squared or Fisher's exact test. Ordinal variables were compared between genders using Cochran-Armitage trend test. Feeling emotionally and physically drained compared to pre-pandemic was analyzed as a binary outcome in a multivariable logistic model. Results: Of the 1799 physicians who completed the survey, 52% were between 30 and 39 years old, 81% selfidentified as women, and 62% were white. Women were more likely to report increased worry about their job security, finances, personal health, partner's health, and children's health ( p = 0.02, p = 0.01, p < 0.001, p < 0.001, and p < 0.001, respectively). Seventy-eight percent of respondents reported feeling more drained during the pandemic. Multivariable analysis revealed that female gender (odds ratio [OR] 2.4, 95% confidence interval [CI] 1.7-3.3, p < 0.001), and having children younger than 5 years of age (OR 1.43, 95% CI 1.05-1.95, p = 0.02) were associated with an increased risk of feeling more drained. Conclusions: Women were more likely to report increased worry about job security, finances, and health and had an increased risk of feeling more drained during the pandemic. While the COVID-19 pandemic is a significant stress for all physicians, women in dual-physician families were disproportionately affected, demonstrating the need for increased support from hospital administrations.

Thoracic aortic aneurysm and aortic dissection have a potent genetic underpinning with 20% of individuals having an affected relative. Heritable thoracic aortic diseases (HTAD) may be classified as syndromic (including Marfan syndrome, Loeys-Dietz syndrome, vascular Ehlers-Danlos syndrome and others) or non-syndromic (without recognisable phenotypes) and relate to pathogenic variants in multiple genes affecting extracellular matrix proteins, transforming growth factor-beta (TGF-β) signalling and smooth muscle contractile function. Clinical and imaging characteristics may heighten likelihood of an underlying HTAD. HTAD should be investigated in individuals with thoracic aortic aneurysm or aortic dissection, especially when occurring in younger individuals, in those with phenotypic features and in those with a family history of aneurysm disease. Screening family members for aneurysm disease is important. Consultation with a medical geneticist and genetic testing of individuals at increased risk for HTAD is recommended. Medical management and prophylactic aortic surgical thresholds are informed by an accurate clinical and molecular diagnosis.

A case of congenital cardiac rhabdomyoma presenting as left ventricular outflow tract obstruction is reported. Congenital cardiac tumours are rare. Rhabdomyomas are the most common. Fifty-one to 86% of them are associated with tuberous sclerosis. They have a tendency for spontaneous regression. The indications for surgery include haemodynamic compromise and intractable arrhythmias.

Objective Our goal was to determine the mechanism by which mitochondrial oxidative stress impairs collateral growth in the heart. Approach and Results Rats were treated with rotenone (mitochondrial complex I inhibitor that increases reactive oxygen species production) or sham-treated with vehicle and subjected to repetitive ischemia protocol for 10 days to induce coronary collateral growth. In control rats, repetitive ischemia increased flow to the collateral-dependent zone; however, rotenone treatment prevented this increase suggesting that mitochondrial oxidative stress compromises coronary collateral growth. In addition, rotenone also attenuated mitochondrial complex I activity and led to excessive mitochondrial aggregation. To further understand the mechanistic pathway(s) involved, human coronary artery endothelial cells were treated with 50 ng/ mL vascular endothelial growth factor, 1 µmol/L rotenone, and rotenone/vascular endothelial growth factor for 48 hours. Vascular endothelial growth factor induced robust tube formation; however, rotenone completely inhibited this effect (P<0.05 rotenone versus vascular endothelial growth factor treatment). Inhibition of tube formation by rotenone was also associated with significant increase in mitochondrial superoxide generation. Immunoblot analyses of human coronary artery endothelial cells with rotenone treatment showed significant activation of adenosine monophosphate activated kinase (AMPK)-α and inhibition of mammalian target of rapamycin and p70 ribosomal S6 kinase. Activation of AMPK-α suggested impairments in energy production, which was reflected by decrease in O2 consumption and bioenergetic reserve capacity of cultured cells. Knockdown of AMPK-α (siRNA) also preserved tube formation during rotenone, suggesting the negative effects were mediated by the activation of AMPK-α. Conversely, expression of a constitutively active AMPK-α blocked tube formation. Conclusions We conclude that activation of AMPK-α during mitochondrial oxidative stress inhibits mammalian target of rapamycin signaling, which impairs phenotypic switching necessary for the growth of blood vessels.