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Graphical abstract, Highlights • Multiple cardiac myxomas are rare, most commonly seen in the left atrium. • Myxomas are most commonly attached on the left atrial side of the interatrial septum. • Echocardiography is key in acute CVA to identify cardioembolic sources. • TEE can provide definitive diagnosis and location of multiple cardiac myxomas.

A 35-year-old male with history of recurrent arrhythmias presented for pulmonary vein isolation. He underwent pre-procedural screening for thromboembolism risk with transesophageal echocardiogram. He had an incidental finding of a rare fenestrated membrane overlying his left atrial appendage. Additional work-up throughout his clinical course revealed genetic mutations in the LMNA and SNTA1 genes. There have been no previous reported genetic mutations reported in cases with LAA membranes.

Edwardsiella tardais a freshwater marine member of the family Enterobacteriaceae which often colonizes fish, lizards, snakes, and turtles but is an infrequent human pathogen. Indium-111- (111In-) labeled white blood cell (WBC) scintigraphy is an imaging modality which has a wide range of reported sensitivity and specificity (from 60 to 100% and from 68 to 92%, resp.) for diagnosing acute and chronic infection. We describe a case of suspectedE. tardaprosthetic aortic valve and mitral valve endocarditis with probable vegetations and new mitral regurgitation on transthoracic and transesophageal echocardiograms which was supported with the use of111In-labeled WBC scintigraphy.

Background Echocardiography can be a useful tool in diagnosis and guiding therapy in cardiovascular diseases. However, repeating studies without change in clinical status is inappropriate and not cost effective. This is frequently seen in heart failure patients on readmission. The goal of this study was to identify repeat studies which did not meet appropriateness criteria and identify ways to reduce the institutional burden of such studies. Methods A cross sectional review was performed on 915 inpatient transthoracic echocardiograms between the dates of August 1, 2017 through August 31, 2017. All studies performed at our institution during these dates were reviewed. Studies were placed into one of three categories based on the date of their most recent previous echocardiogram: one week, 8-30 days, and 31-90 days. Indications were identified for each repeat study and deemed appropriate based on clinical situation. Appropriate complete repeat studies included: cardiac arrest, cardiac surgery, and significant arrhythmia (ventricular tachycardia or fibrillation). Results Of the 915 inpatient transthoracic echocardiograms performed at our institution during a one month period, 18.3% (167/915) had a complete transthoracic echocardiogram done within the last three months. 26.3% (44/167) of the repeat studies were in the previous 31 to 90 days. 73.7% (123/167) had studies within the last 30 days, and 37.7% (63/167) were in the last 7 days. 33.5% (56/167) were limited studies. 13.8% (23/167) had appropriate indications for complete repeat study. 46.7% (78/167) of complete repeat exams could have been considered for a limited exam instead of complete exam or avoided. 8.5% (78/915) total studies could have been considered for a limited exam instead of complete exam or avoided. 24.0% (40/167) of repeated studies with had an indication listed as “congestive heart failure” or “cardiomyopathy”, with the majority of these studies being repeated within one month. Conclusions Limited echocardiography is more cost effective than repeating complete studies on inpatients who have had a recent complete echocardiogram and should be considered as an alternative. Evaluating change in left ventricular ejection fraction is an excellent use of limited echocardiography. We propose a new tool in the electronic medical record to prompt providers to consider this when ordering ultrasound exams on their patients.

When cortical neurons are exposed to hemoglobin, they undergo oxidative stress that ultimately results in iron-dependent cell death. Heme oxygenase (HO)-2 is constitutively expressed in neurons and catalyzes heme breakdown. Its role in the cellular response to hemoglobin is unclear. We tested the hypothesis that HO-2 attenuates hemoglobin neurotoxicity by comparing reactive oxygen species (ROS) formation and cell death in wild-type and HO-2 knockout cortical cultures. Consistent with prior observations, hemoglobin increased ROS generation, detected by fluorescence intensity after dihydrorhodamine 123 or dichlorofluorescin-diacetate loading, in wild-type neurons. This fluorescence was significantly attenuated in cultures prepared from HO-2 knockout mice, and cell death as determined by propidium iodide staining was decreased. In other experiments, hemoglobin exposure was continued for 19 h; cell death as quantified by LDH release was decreased in knockout cultures, and was further diminished by treatment with the HO inhibitor tin protoporphyrin IX. In contrast, HO-2 knockout neurons were more vulnerable than wild-type neurons to inorganic iron. HO-1, ferritin, and superoxide dismutase expression in HO-2 -/- cultures did not differ significantly from that observed in HO-2 +/+ cultures; cellular glutathione levels were slightly higher in knockout cultures. These results suggest that heme breakdown by heme oxygenase accelerates the oxidative neurotoxicity of hemoglobin, and may contribute to neuronal injury after CNS hemorrhage.

Hemoglobin is an oxidative neurotoxin that may contribute to cell injury after CNS trauma and hemorrhagic stroke. Prior studies have demonstrated that concomitant treatment with iron-chelating antioxidants prevents its neurotoxicity. However, the efficacy of these agents when applied hours after hemoglobin has not been determined, and is the subject of the present investigation. Consistent with prior observations, an increase in reactive oxygen species generation, detected by 2',7'-dichlorofluorescin oxidation, was observed when mixed neuronal/astrocyte cultures prepared from mouse cortex were exposed to hemoglobin alone. However, this oxidative stress developed slowly. A significant increase in the dichlorofluorescein signal compared with control, untreated cultures was not observed until four hours after addition of hemoglobin, and was followed by loss of membrane integrity and propidium iodide staining. Treating cultures with the 21-aminosteroid U74500A or the ferric iron chelator deferoxamine four hours after initiating hemoglobin treatment markedly attenuated reactive oxygen species production within 2 h. Continuous exposure to 5 micro M hemoglobin for 24 h resulted in death of about three-quarters of neurons, without injuring astrocytes. Most neuronal loss was prevented by concomitant treatment with U74500A; its effect was not significantly attenuated if treatment was delayed for 2-4 h, and it still prevented over half of neuronal death if treatment was delayed for 8 h. Similar neuroprotection was produced by delayed treatment with deferoxamine or the lipid-soluble iron chelator phenanthroline. None of these agents had any effect on neuronal death when added to cultures 12 h after hemoglobin. These results suggest that hemoglobin is a potent but slowly-acting neurotoxin. The delayed onset of hemoglobin neurotoxicity may make it an attractive target for therapeutic intervention.

This case report describes a rare case of ventricular septal defect due to non-penetrating trauma in a 43 year old male involved in a motor vehicle collision. The diagnosis was made by echocardiogram and the patient was taken immediately to the operating room for emergent surgical repair of the ventricular septal defect and survived.