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Madgula et al. This is an open access article distributed under the terms of the Creative Commons Attribution License CC-BY 4.0., which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Background Rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) are autoimmune diseases with chronically elevated inflammatory activity. Treatments typically have been aimed at decreasing inflammation. While RA and SLE are known to have a high incidence of congestive heart failure (HF), the mechanism behind this remains elusive. We sought to assess the outcomes of HF patients with either RA or SLE as opposed to HF patients without RA or SLE. Methods We conducted a retrospective analysis of the Healthcare Utilization Project-National Inpatient Sample Database from 2010 to 2015 (third quarter). Patients with a primary admitting diagnosis of HF were queried, and those with or without a diagnosis of either SLE or RA were separated into two groups. In-hospital mortality, total charges (TOTCHG), and length of stay (LOS) were analyzed with a multivariate regression model adjusted for demographical and comorbidity variables, using generalized linear models with family binomial, gamma, and negative-binomial, respectively. A p-value smaller than 0.05 was deemed statistically significant. All the statistical analyses were performed in R 3.5.5

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A 56-year-old female patient was brought to our hospital after she suffered a witnessed cardiac arrest while flying on an airplane. She underwent bystander (in the aisle) CPR for about 20 minutes while forcing the plane to land. Altogether, she received seven shocks via AED. At the time of our evaluation, she was alert and in no distress. She did not carry a family history of SCD but reported “she had an issue with heart valve”. Her initial ECG showed atrial fibrillation with a heart rate of 135 bpm, QTc of 515 ms and no findings suggestive of myocardial injury. Her initial workup showed a potassium level of 3.2 mmol/L and no other significant laboratory abnormalities. Her TTE revealed thickened mitral valve leaflets with bileaflet prolapse and severe (4+) central MR. In addition, mitral annular disjunction (MAD) was noted. Her LVEF was 65% with normal wall motion. A left heart catheterization demonstrated normal coronary arteries. Following, a cardiac MRI confirmed MAD at the P3 scallop only, dilated mitral annulus and with a disjunction gap of 7 mm. Furthermore, there was no intramyocardial or annular late gadolinium enhancement (LGE) noted. An ICD was implanted for secondary prevention and she was then referred for mitral valve repair. With this case, we aim at increasing awareness of MAD and SCD. Currently, clinicians rely mostly on anecdotal evidence. While there is increasing literature suggesting the arrhythmogenic nature of MAD, the pathophysiology and implications are still debated. Interestingly, a subject of recent debate, our patient did not have any LGE suggesting no scar/fibrosis that would serve as a nidus for ventricular arrhythmias. Further, a threshold disjunction gap distance of clinical significance has yet to be determined. The benefit of surgical correction remains unclear. Indeed, further prospective studies are required to delineate MAD and help guide early management and its’ ultimate impact on prognosis