Sachin S. Goel, MD, FACC, FSCAI
Medical Director, Structural Heart Interventions
Houston Methodist DeBakey Heart & Vascular Center
Associate Professor, Weill Cornell Medical College
Associate Professor of Cardiology, Houston Methodist Academic Institute
Associate Clinical Member, Houston Methodist Research Institute
Houston, Texas
ssgoel@houstonmethodist.org

Anita W. Asgar, MD, MSc
Section Chief, Interventional Cardiology
Bluhm Cardiovascular Institute
Medical Director, Structural Heart Program
Northwestern Medicine
Chicago, Illinois
anita.asgar@gmail.com

Himanshu Agarwal, MD, FACC, FSCAI
Assistant Professor, Creighton University School of Medicine
Director, Structural Heart Program
Director, Interventional Cardiology and Cardiac Catheterization Laboratories
CHI Creighton University School of Medicine–Bergan Mercy Hospital
Omaha, Nebraska
himanshu.agarwal@commonspirit.org

Anu Tunuguntla, MD, FACC, FSCAI
Interventional & Structural Cardiologist
Medical Director of Cardiac Cath Lab & Structural Heart Program
CHI Health Nebraska Heart
Omaha, Nebraska
anuradha.tunuguntla@commonspirit.org

How do you differentiate between patients with functional mitral regurgitation (MR) who may benefit from transcatheter repair versus those best managed with medical therapy alone?

Dr. Goel: I focus on several key factors:

  • Severity and symptom burden: Patients with moderate-to-severe or severe functional MR who remain symptomatic (eg, New York Heart Association class II-IV) despite optimized guideline-directed medical therapy (GDMT) (quadruple therapy) are candidates for intervention.
  • Left ventricular function and remodeling: Assessment of left ventricular ejection fraction (LVEF) and dimensions is critical. The COAPT trial showed that patients with a LVEF between 20% and 50% benefited from mitral transcatheter edge-to-edge repair (M-TEER).
  • Pulmonary hypertension and right ventricular function: Significant pulmonary hypertension or right ventricular dysfunction may influence outcomes and candidacy. We work closely with our heart failure team to try and optimize GDMT to lower pulmonary artery pressures before considering intervention.
  • Anatomic Suitability: Imaging, such as transesophageal echocardiography (TEE), must confirm favorable valve anatomy for M-TEER.
  • Comorbidities: Patients with advanced/end-stage chronic obstructive pulmonary disease who are oxygen dependent may benefit less from M-TEER or not benefit at all.

Overall, this is a multidisciplinary decision that needs to take into consideration patient symptoms, cardiac function, pulmonary hypertension, and patient anatomy.

What is one lesson you’ve learned from a challenging mitral case that has shaped your practice?

Dr. Goel: One key lesson from a challenging M-TEER case is the critical importance of intraprocedural integration of echocardiographic and hemodynamic data. Although color Doppler remains essential for assessing residual MR and transmitral gradients, it must be interpreted alongside pulmonary vein Doppler and invasive left atrial pressure measurements to obtain a comprehensive assessment of procedural success. In some cases, color Doppler may suggest more-than-mild residual MR; however, significant improvement in systolic pulmonary vein flow (from reversal at baseline to upright and dominant wave postclip) and > 50% reduction in left atrial V-wave amplitude often indicate a favorable hemodynamic response. This integrated approach is especially valuable in patients with complex or technically challenging imaging, where reliance on color Doppler alone may be misleading.

What imaging techniques do you rely on most for planning and executing mitral interventions, and what are your typical strategies for handling suboptimal imaging cases?

Dr. Asgar: High-quality imaging is the backbone of M-TEER—from case selection to final clip release. Preprocedurally, three-dimensional TEE with multiplanar reconstruction (MPR) defines mechanism and lesion location: central A2 to P2 versus commissural/bileaflet disease, flail gap/width, leaflet lengths and mobility, coaptation depth/length, annular calcification, and baseline transmitral valve area/gradient. CT is optional but helpful for annular calcification mapping and transseptal planning in anatomically tortuous atria. In cases of difficult imaging, the challenges may be patient related or anatomic. Patient challenges include large hiatal hernias, previous esophagectomy, esophageal stricture, or anything that prevents adequate TEE imaging, while anatomic challenges may include important shadowing due to calcification, mechanical valves, or anatomic variations.

When imaging is suboptimal, apply a structured approach:

  • Optimize TEE imaging: Position the patient tilted to the left by using a pressure bag under the right shoulder. This can be inflated as required to adjust the position. Increase frequency for near-field leaflet edges, adjust depth/sector, lower color scale (40-60 cm/s) for vena contracta, and minimize artifact with careful gain and dynamic range.
  • Change windows/planes: Use the transgastric basal short axis for grasping, rotate to avoid acoustic shadowing from calcification or prior clips, and avoid foreshortening that underestimates coaptation gap. Two-dimensional (2D) x-plane imaging may be preferable to single plane where anatomic locations are challenging. Three-dimensional MPR may not be helpful if baseline 2D imaging is challenging, as frame rates and imaging resolution are decreased in MPR. To improve MPR, keep sectors small to focus on a particular area and preserve frame rates.
  • Augment with hemodynamics: Left atrial v. wave trends and pulmonary vein flow can validate effective reduction when color jets are eccentric or poorly visualized.
  • Add intracardiac echocardiography (ICE) or switch to TEE/ICE hybrid: Three-dimensional ICE improves leaflet-edge visualization, chordal interference detection, and leaflet insertion confirmation when esophageal views are limited (eg, poor tolerance, prior esophageal surgery).
  • Escalate pragmatically: Consider brief ventilation to hold or lower tidal volume, and reposition the patient; consider staging or alternative therapies if visualization remains inadequate.

Meticulous imaging—and a clear bailout plan—prevents single-leaflet device attachment, iatrogenic stenosis, and residual MR.

What’s your approach to managing intraprocedural complications, such as significant residual MR or device migration?

Dr. Agarwal: Managing intraprocedural complications during mitral interventions requires rapid recognition and a systematic approach. When faced with significant residual MR, the key is to define the mechanism, whether inadequate leaflet grasp, malalignment, or leaflet injury. Real-time imaging with TEE or ICE is essential to guide troubleshooting. In many cases, repositioning or deploying an additional device can optimize results, whereas leaflet tear or severe tissue injury may necessitate bailout strategies such as further device implantation, valve-in-valve/valve-in-ring transcatheter mitral valve replacement (TMVR), or, when unavoidable, surgical conversion.

Device migration or embolization poses a different challenge and demands immediate, decisive action. If the device remains partially anchored, retrieval and redeployment may be possible; if embolized, percutaneous snaring through large-bore access is typically the first-line approach, with urgent surgical intervention if instability or obstruction occurs. Success in these situations hinges on preparation (having retrieval tools, backup devices, and surgical standby readily available) and seamless coordination among the interventionalist, imager, anesthesiologist, and surgeon to ensure patient safety and the best possible outcome.

To summarize, the key to managing complications in mitral interventions is early recognition, stepwise troubleshooting, and always being complication-ready, with a multidisciplinary team.

How do you coordinate postprocedural care for mitral patients, particularly regarding heart failure management and anticoagulation?

Dr. Tunuguntla: For mitral interventions, we run an integrated, protocolized pathway that pairs the structural team with primary/heart failure cardiologists. Patients leave the lab with decongestion targets to help aid medication titration (eg, daily weight/loop diuretic plan, 48-72–hour nurse call, 7-14–day clinic visit with blood work [N-terminal pro-brain natriuretic peptide, CHEM-7]). Patients also have a 30-day clinic visit appointment made with limited 2D echocardiogram for MR surveillance and labs. This office visit is explicitly used to accelerate GDMT with angiotensin receptor‐neprilysin inhibitor/angiotensin converting enzyme inhibitor/angiotensin receptor blocker, evidence-based Β-blocker, mineralocorticoid receptor antagonist, and sodium-glucose cotransporter 2 inhibitor, given that outcomes after M-TEER coincide with how aggressively and successfully GDMT is optimized. Observational and registry analyses show that uptitrating GDMT after M-TEER is associated with lower all-cause mortality and fewer heart failure hospitalizations, supporting a “fast-track GDMT” approach even when MR is corrected.1 In COAPT-like populations, durable reductions in heart failure hospitalizations out to 5 years further underscore that device therapy should be coupled with continued GDMT optimization rather than de-escalation.

Antithrombotic therapy is tailored to procedure and rhythm. After M-TEER and in the absence of another indication for anticoagulation, we often use only low-dose aspirin given the low device thrombosis risk. If the patient has atrial fibrillation or another thromboembolic indication exists, we continue oral anticoagulation and generally avoid antiplatelet therapy. In contrast, TMVR carries a higher early valve thrombosis risk (approximately 6%-8% in contemporary series), so we recommend at least 3 months of vitamin K antagonist (VKA) anticoagulation, with longer duration individualized to anatomy and thrombotic/bleeding risk. For surgical bioprosthetic mitral valve replacement or mitral repair, we discharge patients on VKA (target international normalized ratio [INR], approximately 2.5) for around 3 months and then transition to antiplatelet therapy if no other indication for oral anticoagulation exists. For patients with rheumatic mitral stenosis or mechanical prostheses and atrial fibrillation, we recommend VKA rather than a direct oral anticoagulant. We operationalize this with a standardized discharge order set and a nurse-led follow-up call at 3 to 5 days to confirm adherence and INR/bleeding checks.

1. Adamo, M, Tomasoni, D, Stolz, L. et al. Impact of transcatheter edge-to-edge mitral valve repair on guideline-directed medical therapy uptitration. J Am Coll Cardiol Intv. 2023;16: 896-905. doi: 10.1016/j.jcin.2023.01.362

Disclosures
Dr. Goel: Consultant to Abbott, Medtronic, Edwards Lifesciences, and Boston Scientific Corporation.
Dr. Asgar: Consultant to Abbott.
Dr. Agarwal: Proctor/speakers bureau and consultant for Abbott, Edwards Lifesciences, Medtronic, and Boston Scientific Corporation.
Dr. Tunuguntla: None.