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Table 3 Timeline sequence of patient’s critical clinical events

From: SLE strikes the heart! A rare presentation of SLE myocarditis presenting as cardiogenic shock

September 2019

Patient was diagnosed with SLE based on EULAR/ACR criteria and started on hydroxychloroquine after presenting with arthritis, alopecia, rash, and serologic evaluation. Findings of skin biopsy were suggestive of cutaneous SLE

3.7.20. HD#1

Patient presented to the emergency department of an outside facility with pleuritic chest pain, fatigue, dyspnea, fevers, and worsening rash. Laboratory workup was suggestive of SLE flare and sepsis likely secondary to MSSA bacteremia with a skin source. Broad-spectrum antibiotics and pulse dose corticosteroids (solumedrol 1 mg/kg for three days) initiated. Initial transthoracic echocardiogram demonstrated normal LVEF > 55% with no valvular pathology

3.9.20. HD #3

Patient was transferred to our facility per his insurance eligibility in a hemodynamically stable condition. Intravenous cefazolin was continued for MSSA bacteremia. Repeat blood and surveillance blood cultures were negative. TEE showed LVEF of > 45% but no evidence of valvular pathology

3.12.21. HD #6

With recurrence of dyspnea and pleuritic chest pain and hemodynamic instability, the patient was transferred to the ICU. A CT chest with pulmonary embolism protocol demonstrated possible pulmonary embolism, bilateral pleural effusions, dense consolidations with pulmonary nodules, and pericardial effusions. Serial TTE on the same day showed interval decline in LVEF of 45% down to 25% and worsening pericardial effusions. Treatment with heparin drip for possible pulmonary emboli, broad-spectrum IV antibiotics for possible septic emboli, solumedrol 500 mg IV q12h for severe SLE co-activity was started, hydroxychloroquine 400 mg daily was continued, and vasopressors for cardiogenic shock were initiated

3.13.20. HD #7

Guideline directed medical therapy for heart failure was escalated. A cardiac MRI demonstrated a reduced LVEF 25% and moderate global hypokinesis with worsening pericardial effusions; however, this limited study did not reveal an etiology explain his decompensation. The patient was transferred to an institution with capabilities to treat advanced heart failure

3.14.20. HD #8

A repeat TTE showed markedly decreased LVEF 10% with severe global hypokinesis. Intravenous steroids and guideline-directed heart failure therapy was continued

3.17.20. HD #11

In efforts to further explain cause of decompensation and unrevealing CMR, endomyocardial biopsy was performed along with a concurrent Left and right heart catheterization. Coronary angiogram showed normal cardiac output, cardiac index, left and right-sided filling pressures, and non-obstructive coronary arteries

3.18.20. HD #12

With improving hemodynamics on SLE and heart failure- targeted therapy, the patient was weaned off vasopressors, and repeat TTE showed mildly dilated left ventricle with improved LVEF 45% from previously 10%. The patient was discharged on oral medical therapy of heart failure, hydroxychloroquine, and prednisone for SLE, and IV antibiotics for MSSA bacteremia in a stable condition

Late March–April 2020

The patient was transitioned to four cycles of steroid-sparing therapy with Cyclophosphamide and later transitioned to mycophenolate mofetil due to favorable side effect risk profile. Hydroxychloroquine, and heart failure therapy were continued

September–November 2020

A repeat Cardiac MRI and TTE to assess interval SLE activity showed normal left ventricular systolic function and no evidence of myocardial scarring or pericardial effusions. Patient returned to normal baseline functional status