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BACKGROUND Takotsubo cardiomyopathy, also referred to as apical ballooning syndrome (ABS), stress cardiomyopathy, or broken heart syndrome, initially described in Japan, is characterized by transient wall motion abnormalities involving the apical segment. Several variants have been described, including reverse type, mid-ventricular type, and the focal type. In the reverse type, there is basal hypokinesis and apical hyperkinesis. Stress cardiomyopathy is most likely to occur in middle-aged women and the underlying etiology is believed to be related to catecholamine release due to intense stress. CASE REPORT We report an extremely rare case of reverse takotsubo cardiomyopathy (rTTC) in a young woman with COVID-19 who was treated with Casirivimab-Imdevimab therapy. Our report is the second to reveal rTTC in a patient with COVID-19 in which obstructive coronary artery disease was definitively ruled out by coronary CT angiography. CONCLUSIONS Cardiovascular involvement in COVID-19 has been linked to increased morbidity and mortality rates. Recent reports have suggested the occasional occurrence of TTC and the rare occurrence of reverse takotsubo cardiomyopathy (rTTC) in patients with COVID-19. In fact, to the best of our knowledge, this is only the fifth reported case of rTTC in a patient with COVID-19; importantly, 3 out of the 4 of the previous reported cases lacked definitive ischemic work-up to rule out obstructive coronary artery disease due to the critical condition of the patients.

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BACKGROUND The eustachian valve is rarely involved in bacterial endocarditis. Patients who present with bacteremia and evidence of organic septic emboli should raise the suspicion of endocarditis as a possible differential diagnosis. This case series describes 2 unique cases of eustachian valve endocarditis (EVE) in patients who had a history of intravenous drug use; although 63% of EVE is caused by Staphylococcus aureus, the causative agent in our first case was methicillin-resistant Staphylococcus epidermidis (MRSE), which is only the third reported case of EVE caused by Staphylococcus epidermidis. Of note, the previous 2 cases of MRSE EVE were also found to be associated with cardiovascular hardware. CASE REPORT The first case of the series describes EVE by MRSE with an endovascular graft acting as the nidus of infection. Second case of EVE was caused by methicillin-sensitive Staphylococcus epidermidis (MSSA), the source of bacteremia being a rectovesicular abscess. Although initial transthoracic echoes were negative in both cases, subsequent transesophageal echoes were able to detect vegetations on the eustachian valves. Treatment included 4-6 weeks of culture-directed antibiotic therapy for both of our cases. CONCLUSIONS EVE may be an under-diagnosed sequelae of staphylococcal bacteremia, especially in the intravenous drug abuse population, further reinforcing the importance of systemically visualizing all cardiac valves, including the eustachian valves, while performing echocardiography.

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Experimental studies implicate late systolic load as a determinant of impaired left-ventricular relaxation. We aimed to assess the relationship between the myocardial loading sequence and left-ventricular contraction and relaxation. Time-resolved central pressure and time-resolved left-ventricular geometry were measured with carotid tonometry and speckle-tracking echocardiography, respectively, for computation of time-resolved ejection-phase myocardial wall stress (EP-MWS) among 1214 middle-aged adults without manifest cardiovascular disease from the general population. Early diastolic annular velocity and systolic annular velocities were measured with tissue Doppler imaging, and segment-averaged longitudinal strain was measured with speckle-tracking echocardiography. After adjustment for age, sex, and potential confounders, late EP-MWS was negatively associated with early diastolic mitral annular velocity (standardized ß=-0.25; P<0.0001) and mitral inflow propagation velocity (standardized ß=-0.13; P=0.02). In contrast, early EP-MWS was positively associated with early diastolic mitral annular velocity (standardized ß=0.18; P<0.0001) and mitral inflow propagation velocity (standardized ß=0.22; P<0.0001). A higher late EP-MWS predicted a lower systolic mitral annular velocity (standardized ß=-0.31; P<0.0001) and lesser myocardial longitudinal strain (standardized ß=0.32; P<0.0001), whereas a higher early EP-MWS was associated with a higher systolic mitral annular velocity (standardized ß=0.16; P=0.002) and greater longitudinal strain (standardized ß=-0.24; P=0.002). The loading sequence remained independently associated with early diastolic mitral annular velocity after adjustment for systolic mitral annular velocity or systolic longitudinal strain. In the context of available experimental data, our findings support the role of the myocardial loading sequence as a determinant of left-ventricular systolic and diastolic function. A loading sequence characterized by prominent late systolic wall stress was associated with lower longitudinal systolic function and diastolic relaxation.

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The need for left ventricular mass (LVM) normalization to body size is well recognized. Currently used allometric exponents to normalize LVM may not account for the confounding effect of sex. Because sex is a strong determinant of body size and LVM, we hypothesized that these are subject to potential bias. We analyzed data from 7528 subjects enrolled in the Asklepios Study (n=2524) and the Multiethnic Study of Atherosclerosis (limited access data set; n=5,004) to assess metric relationships between LVM and body size, generate normative data for indexed LVM, and compare the ability of normalization methods to predict cardiovascular events. The allometric exponent that adequately described the LVM-body height relationship was 1.7 in both studies and significantly different from both the unity and 2.7, whereas the LVM-body surface area relationship was approximately linear. LVM/height(2.7) consistently demonstrated important residual relationships with body height and systematically misclassified subjects regarding the presence of LVH. LVH defined by LVM/height(1.7) was more sensitive than LVM/body surface area to identify obesity-related LVH and was most consistently associated with cardiovascular events and all-cause death. In contrast to current assumptions, LVM/height(2.7) is not an adequate method to normalize LVM for body size. We provide more appropriate normalization methods, normative data by 2D echocardiography and gradient-echo cardiac MRI, and cutoffs for defining LVH, along with prognostic validation data.

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