2024 SCAI SHOCK

Clipping Shock: MitraClip's Rescue from Flecainide Toxicity and Severe Mitral Regurgitation-Induced Cardiogenic Shock

Presenter

Zeryab Khan, OhioHealth Doctors Hospital- Cardiology Fellow, Columbus, OH
Zeryab Khan1, Jordan Luli, D.O.1, Cody Carter, D.O.1, Rayan El-Zein1, Lindsay Castle, D.O.2, Kevin Stiver, M.D.2, Laura D. Flannery, MD, FSCAI3 and Carlos E. Sanchez Soto, M.D., FSCAI2, (1)OhioHealth Doctors Hospital- Cardiology Fellow, Columbus, OH, (2)OhioHealth Riverside Methodist Hospital, Columbus, OH, (3)OhioHealth, Columbus, OH

Title
Clipping Shock: MitraClip's Rescue from Flecainide Toxicity and Severe Mitral Regurgitation-Induced Cardiogenic Shock

Introduction
Transcatheter mitral edge-to-edge repair (MTEER), as highlighted in TEER SHOCK and currently being investigated in CAPITOL MINOS, has emerged as a crucial treatment for severe mitral regurgitation (MR) in high-risk surgical patients experiencing cardiogenic shock (CS) 5,6. This case underscores the role of selecting appropriate mechanical circulatory support (MCS) and overcoming anatomical challenges in a patient with flecainide toxicity and severe MR-CS, managed successfully with MTEER.

Clinical Case


A 72-year-old female with severe primary MR, HFpEF, and AF presented with dyspnea, weakness, and edema. Prior to this admission, she had been hospitalized thrice in the past year for heart failure exacerbation and been evaluated for surgical mitral valve repair. Due to her limited social support, she postponed having the surgery. Initial assessment, BP was 90/68 mmHg, HR 77 bpm with wide complex arrhythmia suggestive of flecainide toxicity. She had JVD, a holosystolic murmur, pulmonary edema, and bilateral lower extremity edema. Labs showed elevated creatinine (1.6 mg/dL), NT-Pro BNP (27,000 pg/mL), and lactate (6.0 mmol/L). TTE showed EF 66%, severe MR due to a flail posterior leaflet. RHC revealed CPO 0.47 Watts, PAPi 1.5, SVR 2700 dyne·s·cm⁻⁵, and PCWP 21 mmHg with large V-waves.

Initial management with IABP, bicarbonate, nipride and dobutamine was ineffective, necessitating escalation to Impella CP. Transesophageal echocardiography (TEE) identified a focal flail posterior mitral segment with severe anteriorly directed mitral regurgitation. TEE-guided MitraClip implantation involved three clips: an XTW MitraClip at A2-P2, an NTW MitraClip at A3-P3, and a third NT MitraClip between the prior clips to address residual prolapse. Post-procedure, residual MR was moderate with a mean gradient of 3 mmHg and newly reduced EF of 20%. Hemodynamics improved significantly: CPO 0.94 Watts and SVR 900 dyne·s·cm⁻⁵ and she was able to wean from support. Following discharge on GDMT with scheduled Heart Failure follow-up, her 30-day transthoracic echocardiogram revealed an ejection fraction of 54%, mild to moderate mitral regurgitation with a mean gradient of 7 mmHg, and a stable appearance of the MitraClips. The patient experienced notable clinical improvement.

Discussion


Our case highlights the role of strategic MCS integration and anatomical assessment in pre-MTEER phase for achieving favorable outcomes. The primary role of MCS in MR-CS is to optimize hemodynamics during the procedure to avoid potential cardiovascular collapse and arrest. It also facilitates unloading of left ventricle, which can enhance the visualization of the mitral valve anatomy, improve accuracy of clip positioning, and facilitate easier grasping and clipping. Notably, primary MR due to a flail leaflet, as seen in our patient, presents unique challenges compared to secondary MR, making optimization critical to success 1,2. Despite anatomical complexity, the use of strategic multi-clip deployment as seen in other reported cases showed significant hemodynamic improvement and successful weaning from MCS in our patient 3,4. The successful outcome in our patient relied on pre-procedural planning and multidisciplinary heart team discussion. Further research is needed to assess the role of MCS with MTEER including long term mortality and functional status.