Background: The demonstration that severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2) enters the cell via the angiotensin-converting enzyme 2 receptor has raised concerns that, in hereditary angioedema (HAE), a disease characterized by bradykinin-mediated angioedema attacks, coronavirus disease 2019 (COVID-19) may trigger angioedema attacks, increase the frequency and/or severity of attacks, or cause more severe symptoms of COVID-19. Objective: The objective was to evaluate the severity of COVID-19 in patients with HAE, the course of HAE attacks, angioedema activity, and the quality-of-life scores during COVID-19 pandemic. Methods: Patients diagnosed with HAE for at least 6 months were included in the study. The 7-day Angioedema Activity Score and the Angioedema Quality of Life (AE-QoL) Questionnaire were first completed at the onset of the pandemic between March 12 and June 1, 2020, then during SARS-CoV-2 infection, and in the third month after recovering from COVID-19. Results: Ten of 67 patients with HAE (14.9%) were diagnosed with COVID-19. The median (interquartile range) age of the 10 patients diagnosed with COVID-19 was 35.5 years (28.0‐55.0 years). Six of the 10 patients (60%) were women. During COVID-19, five of the 10 patients (50%) had no angioedema attack. Two patients with severe HAE experienced a significant increase in angioedema activity during COVID-19 compared with their basal activity scores. The remaining three patients had a similar or lower attack frequency than their basal level. Four (40%) of the 10 patients had a relative increase in their attacks during the convalescence period. There was no statistically significant difference among pre-COVID-19, during COVID-19 and post-COVID-19 periods in function, mood, fear and/or shame, nutrition, and total scores of the AE-QoL Questionnaire although the fear dimension was relatively more affected (p = 0.06). Conclusion: Although the sample size was small, analysis of our data supported that the symptoms of COVID-19 were not more severe in HAE. Also, there was no significant difference in the AE-QoL Questionnaire scores, the frequency, and severity of angioedema attacks during the course of COVID-19 in the patients with HAE.

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This study has been presented as a oral presentation at the XXVI. National Allergy and Clinical Immunology Congress between 9-13 November 2019 and presented as a poster EAACI Digital Congress 06 -08 June 2020.

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Purpose Smoking is a well‐known risk factor for coronary artery diseases. It is also associated with nicotine‐induced myocardial dysfunction. The aim of this study was to evaluate the right and left atrial and ventricular functions in apparently healthy smokers. Methods We included consecutively 80 healthy smokers (56 males, mean age:35.5 ± 8.4 years) and 70 healthy nonsmokers (44 males, mean age:33.9 ± 9.5 years). None of the subjects had any additional cardiovascular risk factor other than smoking. The right and left atrial and ventricular functions were assessed by both conventional and speckle tracking echocardiography. Results Although there was no significant difference in left ventricular ejection fraction, the smokers had significantly lower ventricular global longitudinal strain than controls (−19.9 ± 2.0% vs −21.2 ± 1.9%, P < .001 and −18.4 ± 2.1% vs −21.8 ± 2.2%, P < .001, respectively, for the left and right ventricle). Smokers had also lower atrial reservoir and conduit strains: 35.9 ± 11.1% vs 40.2 ± 11.2%, P = .022 and 16.7 ± 6.8% vs 19.4 ± 6.8%, P = .016, respectively, for the left atrium, and 33.0 ± 10.6% vs 37.6 ± 11.2%, P = .011 and 15.2 ± 5.6% vs 18.0 ± 6.3%, P = .004, respectively, for the right atrium). Conclusion Even in apparently healthy people with no other cardiovascular risk factors, smoking is associated with impaired atrial and ventricular functions.