Aortic pulse wave velocity is a worldwide accepted index to evaluate aortic stiffness and can be assessed noninvasively by several methods. This study sought to determine if commonly used noninvasive devices can all accurately estimate aortic pulse wave velocity. Pulse wave velocity was estimated in 102 patients (aged 65±13 years) undergoing diagnostic coronary angiography with 7 noninvasive devices and compared with invasive aortic pulse wave velocity. Devices evaluating carotid-femoral pulse wave velocity (Complior Analyse, PulsePen ET, PulsePen ETT, and SphygmoCor) showed a strong agreement between each other ( r >0.83) and with invasive aortic pulse wave velocity. The mean difference ±SD with the invasive pulse wave velocity was −0.73±2.83 m/s ( r =0.64) for Complior-Analyse: 0.20±2.54 m/s ( r =0.71) for PulsePen-ETT: −0.04±2.33 m/s ( r =0.78) for PulsePen ET; and −0.61±2.57 m/s ( r =0.70) for SphygmoCor. The finger-toe pulse wave velocity, evaluated by pOpmètre, showed only a weak relationship with invasive aortic recording (mean difference ±SD =−0.44±4.44 m/s; r =0.41), and with noninvasive carotid-femoral pulse wave velocity measurements ( r <0.33). Pulse wave velocity estimated through a proprietary algorithm by BPLab (v.5.03 and v.6.02) and Mobil-O-Graph showed a weaker agreement with invasive pulse wave velocity compared with carotid-femoral pulse wave velocity (mean difference ±SD =−0.71±3.55 m/s, r =0.23; 1.04±2.27 m/s, r =0.77; and −1.01±2.54 m/s, r =0.71, respectively), revealing a negative proportional bias at Bland-Altman plot. Aortic pulse wave velocity values provided by BPLab and Mobil-O-Graph were entirely dependent on age-squared and peripheral systolic blood pressure (cumulative r 2 =0.98 and 0.99, respectively). Thus, among the methods evaluated, only those assessing carotid-femoral pulse wave velocity (Complior Analyse, PulsePen ETT, PulsePen ET, and SphygmoCor) appear to be reliable approaches for estimation of aortic stiffness.

A 16-year-old boy was admitted to our emergency department, in Lombardy, complaining of intense pain in his chest-radiating to his left arm-which had started 1 h earlier. The day before he had a fever of 38•3°C that decreased after 100 mg of nimesulide. He reported no other symptoms, no medical history, and no contact with anyone with confirmed COVID-19.We found his vital signs to be normal apart from his temperature which was raised at 38•5°C. On auscultation of the patient's chest, we heard normal heart sounds, no pericardial rub, and no abnormal respiratory signs. We found no lymphadenopathy, no rash, and no areas of localised tenderness on the chest wall. An electrocardiogram (ECG) showed inferolateral ST-segment elevation (figure) and a transthoracic echocardiography showed hypokinesia of the inferior and inferolateral segments of the left ventricle, with a preserved ejection fraction of 52%; no pericardial effusion was seen. Investigations showed raised high-sensitivity cardiac troponin I (9449 ng/L), creatine phosphokinase (671•0 U/L), C-reactive protein (32•5 mg/L), and lactate dehydrogenase (276•0 U/L) concentrations (appendix). The leucocyte count was 12•75 × 10⁹ per L, the neutrophil count was 10•04 × 10⁹ per L, and the lymphocyte count was 0•78 × 10⁹ per L.We gave the boy aspirin to relieve his pain and transferred him to the coronary care unit with a working diagnosis of acute myocarditis. The patient's pain gradually improved and after 2 h had completely resolved.However, during the first night, he reported further chest pain; the ECG was repeated but no significant changes were seen (appendix). We started him on intravenous ibuprofen 600 mg three times a day and both his symptoms and raised temperature resolved. Tests for autoantibodies and cardiotropic viruses were negative (appendix). On day 3, a nasopharyngeal swab test for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) was positive, so we started hydroxychloroquine and antiviral therapy. Serial measurements of the patient's troponin concentration showed a gradual reduction from a peak of 16 862 ng/L on day 1, to 39 ng/L on day 8. The inflammatory markers also returned to normal and the ST-segment elevation on ECG resolved (appendix).On day 11-after nasopharyngeal swabs taken on 2 consecutive days were negative-MRI T2-weighted short-tau inversion recovery sequences showed changes supporting the diagnosis of acute myocarditis (figure; appendix). On day 12, he was well, asymptomatic, and allowed home.Notably, throughout the entire time he was in hospital, our patient did not have any of the signs or symptomsapart from a fever-typically reported in COVID-19; his peripheral oxygen saturation levels remained within normal limits and two chest x-rays, on days 3 and 6, were clear (appendix). Paediatric patients reporting chest pain and other features suggestive of acute myocarditis-with or without respiratory symptoms-should, we believe, also be tested for SARS-CoV-2 (video). ContributorsWe were all involved in the care and management of ...