Surgical management of extensive aortic root endocarditis with ventricular septal rupture: A case report

A 79-year-old man was referred for severe cardiac decompensation. Chest radiography showed severe pulmonary edema, and transesophageal echocardiography revealed a large quantity of vegetation on all aortic valve leaflets with severe aortic valve regurgitation, heterogeneous cavities adjacent to the aortic annulus, and ventricular septal rupture. We performed thorough and extensive debridement of the aortic root; including the infected ventricular septum, reconstructed the ventricular septum and aortic root using autologous and bovine pericardial patches; and placed a bioprosthetic stented valve. The patient was discharged without any complications, and without recurrence of the endocarditis in the four years post-surgery.

Detection of SARS-CoV-2 in a cat owned by a COVID-19−affected patient in Spain

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the etiological agent of COVID-19, is considered a zoonotic pathogen mainly transmitted human to human. Few reports indicate that pets may be exposed to the virus. The present report describes a cat suffering from severe respiratory distress and thrombocytopenia living with a family with several members affected by COVID-19. Clinical signs of the cat prompted humanitarian euthanasia and a detailed postmortem investigation to assess whether a COVID-19−like disease was causing the condition. Necropsy results showed the animal suffered from feline hypertrophic cardiomyopathy and severe pulmonary edema and thrombosis. SARS-CoV-2 RNA was only detected in nasal swab, nasal turbinates, and mesenteric lymph node, but no evidence of histopathological lesions compatible with a viral infection were detected. The cat seroconverted against SARS-CoV-2, further evidencing a productive infection in this animal. We conclude that the animal had a subclinical SARS-CoV-2 infection concomitant to an unrelated cardiomyopathy that led to euthanasia.

Norepinephrine Leads to More Cardiopulmonary Toxicities than Epinephrine by Catecholamine Overdose in Rats

While catecholamines like epinephrine (E) and norepinephrine (NE) are commonly used in emergency medicine, limited studies have discussed the harm of exogenously induced catecholamine overdose. We investigated the possible toxic effects of excessive catecholamine administration on cardiopulmonary function and structure via continuous 6 h intravenous injection of E and/or NE in rats. Heart rate, echocardiography, and ventricular pressure were measured throughout administration. Cardiopulmonary structure was also assessed by examining heart and lung tissue. Consecutive catecholamine injections induced severe tachycardia. Echocardiography results showed NE caused worse dysfunction than E. Simultaneously, both E and NE led to higher expression of Troponin T and connexin43 in the whole ventricles, which increased further with E+NE administration. The NE and E+NE groups showed severe pulmonary edema while all catecholamine-administering groups demonstrated reduced expression of receptor for advanced glycation end products and increased connexin43 levels in lung tissue. The right ventricle was more vulnerable to catecholamine overdose than the left. Rats injected with NE had a lower survival rate than those injected with E within 6 h. Catecholamine overdose induces acute lung injuries and ventricular cardiomyopathy, and E+NE is associated with a more severe outcome. The similarities of the results between the NE and E+NE groups may indicate a predominant role of NE in determining the overall cardiopulmonary damage. The results provide important clinical insights into the pathogenesis of catecholamine storm.

Rituximab Induced Pulmonary Edema Managed with Extracorporeal Life Support

Though rare, rituximab has been reported to induce severe pulmonary edema. We describe the first report of ECLS utilization for this indication. A 31-year-old female with severe thrombotic thrombocytopenic purpura developed florid pulmonary edema after rituximab infusion. Despite advanced ventilatory settings, she developed severe respiratory acidosis and remained hypoxemic with a significant vasopressor requirement. Since her pulmonary insult was likely transient, ECLS was considered. Due to combined cardiorespiratory failure, she received support with peripheral venoarterial ECLS. During her ECLS course, she received daily plasmapheresis and high dose steroids. Her pulmonary function recovered and she was decannulated after 8 days. She was discharged after 23 days without residual sequelae.

Heart MRI Identifies Patients At Higher Risk For Severe Pulmonary Edema After Bortezomib Plus Dexamethasone Treatment In Subclinical Heart Amyloidosis

Introduction Primary immunoglobulin amyloidosis (AL) is caused by deposition of insoluble amyloidoigenic fibrils of monoclonal light chains, which is often associated with an underlying plasma cell dyscrasia. The heterogeneous clinical manifestations commonly include nephrotic syndrome, hepatic failure, autonomic and sensory neuropathy. Cardiac involvement is most common in immunoglobulin variants of amyloidosis and is associated with significant mortality with survival of 17% by 2 years. Cardiac Magnetic Resonance (CMR) is a non-invasive technique that allows identification of heart involvement in 80% of biopsy proven patients (pts). In systemic amyloidosis with heart involvement, diuretics, despite representing backbone treatment of Congestive Heart Failure (CHF), exacerbation of hypotension and deterioration of cardiac performance are common features.(Dubrey.2012.QJM) Here, we describe a case of a 71 year-old man with subclinical AL amyloidosis who developed severe pulmonary edema during proteosomal inhibition (PI) plus dexamethasone induction. Methods Our pt presented with mediastinal mass (Fig. 1A) detected by the time of pre-operative evaluation for benign prostate hypertrophy surgery. He has a long-term-history of diabetes type 2 metabolically controlled and normal hemoglobin A1C. Further characterization of his mediastinal mass by chest tomography showed a 48 x 26 x 39 mm mass arising from posterior right lateral tracheal wall. Results Biopsy sections correlating with kappa light chain AL deposition by mass spectrometry (Fig. 2). Biochemical evidence of elevated kappa free light chain (FLC) and biclonal m-protein revealing IgG and IgA kappa protein by serum protein electrophoresis (SPEP) were observed. His bone marrow aspirate and biopsy was consistent with kappa MGUS (5% clonally restricted plasma cells). Despite no clinical or echocardiographic signs of cardiac dysfunction, left ventricle non-CAD scarring suggesting subclinical amyloid deposition was detected by CMR (Fig. 3). In an attempt to induce hematological response, Bortezomib (B) intravenously (IV) at 1.3 mg/m2 plus weekly oral dexamethasone were initiated. Severe pulmonary edema associated with hemoptysis developed during cycle (C) 1 day (d) 5 of treatment. His repeated chest angiography showed no evidence of pulmonary embolism. A bronchoscopy failed to revealed tracheal perforation. Progressive resolution of symptoms was achieved after administration of furosemide IV. After recovery, pt completed 4 cycles of B plus dexamethasone and proceeded with autologous stem cell transplantation without recurrent pulmonary edema episodes. Conclusions Our case suggests potential clinical phenotype associated with subclinical heart amyloid deposition, and propensity for acute pulmonary edema associated with PI recognized by CMR. Although pulmonary edema is uncommonly seen associated with PI in the treatment of plasma cell clonal disorders, clinically manifested acute pulmonary edema could result in high mortality (Hishao et al. Ann Pharmacother.2010). Our pt clinical manifestations could represent phenotypic expression of transiently impaired cardiac function as results of brisk elevation of unfolded serum FLC during PI (Obeng.Blood.2006). Lack of further similar episodes after PI re-exposure suggests low apoptotic threshold of secretory clone. Disclosures: No relevant conflicts of interest to declare.