Background. Whereas dependency of left ventricular outflow tract diameter (LVOTD) from body surface area (BSA) has been established and a BSA-based LVOTD formula has been derived, the relationship between LVOTD and aortic root and LV dimensions has never been explored. This may have implications for evaluation of LV output in heart failure (HF) and aortic stenosis (AS) severity. Methods. A cohort of 540 HF patients who underwent transthoracic echocardiography was divided in a derivation and validation subgroup. In the derivation subgroup (N=340) independent determinants of LVOTD were analyzed to derive a regression equation, which was used for predicting LVOTD in the validation subgroup (N=200) and compared with the BSA-derived formula. Results. LVOTD determinants in the derivation subgroup were sinuses of Valsalva diameter (SVD, beta=0.392, P<0.001), BSA (beta=0.229, P<0.001), LV end-diastolic diameter (LVEDD, beta=0.145, P=0.001), and height (beta=0.125, P=0.037). The regression equation for predicting LVOTD with the aforementioned variables (LVOTD=6.209+[0.201xSVD]+[1.802xBSA]+[0.03xLVEDD]+[0.025xHeight]) did not differ from (P=0.937) and was highly correlated with measured LVOTD (R=0.739, P<0.001) in the validation group. Repeated analysis with LV end-diastolic volume instead of LVEDD and/or accounting for gender showed similar results, whereas BSA-derived LVOTD values were different from measured LVOTD (P<0.001). Conclusion. Aortic root and LV dimensions affect LVOTD independently from anthropometric data and are included in a new comprehensive equation for predicting LVOTD. This should improve evaluation of LV output in HF and severity of AS, avoiding use of LVOT velocity-time integral alone, which can be misleading, especially when LV cavity and aortic root dimensions are abnormal.

There is increasing evidence that COVID-19 infection predisposes to thromboembolism. A 71 years-old male patient was admitted to ICU for COVID-19 related pneumonia. He developed a high troponin rise up to 6715 ng/L. By transthoracic echocardiography, we found akinesia of the full right ventricular apex with a mobile hyperechogenic mass, highly suggestive of thrombus. Unfractionated Heparin was started immediately. A subsequent echocardiogram showed no mass. To our knowledge, this is the first case showing a thrombus formation in the context of right ventricular apical akinesia in COVID-19 patients. There is upcoming evidence that the clinical relevance of thromboembolic complications may be a serious issue in COVID-19 patients even in the absence of any obvious risk factor. Our case clearly demonstrate that, in patients with COVID-19 infection and troponin rise, echocardiography should be performed to rule out possible thrombotic complications