B49-11 Fatal Synergy: Refractory Atrial Fibrillation and Mixed Cardiogenic-Septic Shock in Chronic Severe Mitral Regurgitation With MRSA Bacteremia

Abstract Introduction Mitral regurgitation (MR) remains a major cause of morbidity and mortality, particularly when compounded by atrial fibrillation (Afib) and heart failure. Severe chronic MR induces chronic left atrial (LA) volume overload and dilation, fostering atrial fibrosis, conduction heterogeneity, and eventual permanent Afib. Once Afib with rapid ventricular response (RVR) supervenes, the regurgitant volume worsens, LA pressures escalate, and cardiac output declines precipitously, establishing a self-perpetuating regurgitant-arrhythmic loop. We present a 75-year-old man with long-standing severe MR and chronic Afib who developed refractory Afib with RVR and mixed cardiogenic and septic shock in the setting of MRSA bacteremia, culminating in multiorgan failure and death. Case Description A 75-year-old male with severe MR, heart failure with preserved EF 50-55%, chronic Afib on apixaban, hypertension, hyperlipidemia, and BPH with a chronic indwelling Foley presented after a mechanical fall and inability to rise. He was initially managed with empiric piperacillin-tazobactam for presumed urosepsis. Echocardiography revealed severe LA enlargement, posterior leaflet prolapse with severe MR, and moderate tricuspid regurgitation. Cardiology identified early cardiogenic shock secondary to severe MR and Afib with RVR. Amiodarone and furosemide were started. Within 24 hours, the patient’s heart rate increased to 180-200 bpm, refractory to escalating amiodarone therapy, and was cardioverted seven times (150-200 J). He developed acute hypoxemic respiratory failure requiring intubation, central and arterial line placement, and escalating vasopressor support, including norepinephrine, vasopressin, and esmolol. Blood cultures grew MRSA in three of four bottles, and urine cultures later revealed Pseudomonas aeruginosa and Enterococcus faecalis. Antimicrobial coverage with vancomycin and piperacillin-tazobactam was maintained. Given active bacteremia, mechanical circulatory support (intra-aortic balloon pump or Impella) and surgical valve intervention were contraindicated. Over the next 48 hours, the patient developed mixed cardiogenic and septic shock, lactic acidosis, and shock liver. Despite maximal pharmacologic support, perfusion declined. The patient was transitioned to hospice care and pronounced deceased. Discussion This case illustrates a rare and devastating convergence of end-stage valvular disease, electrical instability, and systemic infection, yielding refractory circulatory collapse. This structural remodeling promotes persistent Afib, which in turn exacerbates regurgitant volume, setting up a vicious cycle of volume overload and contractile inefficiency. The presence of MRSA bacteremia introduced a critical barrier to intervention. Surgical or transcatheter valve replacement, the only definitive therapy, was contraindicated due to active infection, and mechanical support devices risked seeding and further dissemination. Despite optimal medical management with amiodarone, cardioversion, diuresis, and vasopressors, hemodynamic deterioration was inevitable. This abstract is funded by: None