# Transcatheter Paravalvular Leak Closure: A Step-by-Step Guide

**Authors:** Georgios E. Papadopoulos, Ilias Ninios, Sotirios Evangelou, Andreas Ioannides, Vlasis Ninios

PMC · DOI: 10.3390/jcdd13020096 · Journal of Cardiovascular Development and Disease · 2026-02-16

## TL;DR

This paper provides a detailed guide for transcatheter closure of paravalvular leaks, emphasizing imaging, device selection, and complication prevention.

## Contribution

A step-by-step, phenotype-driven approach to transcatheter PVL closure with standardized safety and outcome measures.

## Key findings

- Multimodality imaging and morphology-matched device selection are critical for successful PVL closure.
- Residual PVL severity is the most consistent determinant of procedural efficacy.
- High implant success is achievable in experienced programs with careful patient selection.

## Abstract

Paravalvular leak (PVL) remains a clinically important complication after surgical or transcatheter valve implantation, presenting predominantly with heart failure (HF) and/or high-shear hemolysis. While redo surgery can be definitive, contemporary candidates frequently carry prohibitive operative risk, positioning transcatheter PVL closure as a key therapeutic alternative. However, available outcome data are largely derived from observational series and registries with heterogeneity in PVL mechanisms, prosthesis types, imaging protocols, and endpoint definitions. Standardized frameworks—such as those proposed by the PVL Academic Research Consortium—support harmonized PVL grading and clinically meaningful composite endpoints that integrate imaging/hemodynamic results with patient-centered outcomes. Across datasets, the most consistent determinant of benefit is residual PVL severity: procedural efficacy is most commonly defined as achieving ≤ mild residual regurgitation without prosthetic leaflet interference, device embolization, or major complications. This review provides a step-by-step, phenotype-driven approach to transcatheter PVL closure, emphasizing multimodality imaging (TEE and cardiac CT, with adjunct CMR and PET when appropriate), access and support planning tailored to valve position, and morphology-matched device selection—often requiring modular multi-device strategies for elongated crescentic channels, particularly in hemolysis-predominant presentations. We also synthesize evidence on complications and bailout management, with a focus on preventable high-severity events (leaflet impingement, embolization, stroke/air, vascular injury, tamponade) and standardized pre-release safety checks. Collectively, contemporary practice supports high implant success in experienced programs, with clinical improvement tightly coupled to procedural endpoint quality and careful Heart Team selection.

## Linked entities

- **Diseases:** heart failure (MONDO:0005252)

## Full-text entities

- **Genes:** AVP (arginine vasopressin) [NCBI Gene 551] {aka ADH, ARVP, AVP-NPII, AVRP, VP}, GPLD1 (glycosylphosphatidylinositol specific phospholipase D1) [NCBI Gene 2822] {aka GPIPLD, GPIPLDM, PIGPLD, PIGPLD1, PLD}
- **Diseases:** air (MESH:D004618), Infection (MESH:D007239), hepatic congestion (MESH:D002311), AR (MESH:D013734), vascular injury (MESH:D057772), PVL (MESH:D019559), annular (MESH:D016460), thrombosis (MESH:D013927), anemia (MESH:D000740), ascites (MESH:D001201), cardiorenal syndrome (MESH:D059347), death (MESH:D003643), coronary compromise (MESH:D003323), Paravalvular Leak Device (MESH:D009471), pulmonary venous hypertension (MESH:D006976), tamponade (MESH:D002305), HF (MESH:D006333), renal dysfunction (MESH:D007674), Endocarditis (MESH:D004696), Ductal, Septal, and VSD (MESH:D044584), embolization (MESH:D004617), thromboembolic (MESH:D013923), hemolytic anemia (MESH:D000743), aortic regurgitation (MESH:D001022), cardiac perforation (MESH:D057112), Muscular VSD (MESH:D004310), valve dysfunction (MESH:D006349), pulmonary vascular disease (MESH:D014652), Calcification (MESH:D002114), dyspnea (MESH:D004417), cardiogenic shock (MESH:D012770), angina (MESH:D000787), pulmonary edema (MESH:D011654), ASD (MESH:D001321), injury to (MESH:D014947), annular abscess (MESH:D000038), Inflammation (MESH:D007249), dehiscence (MESH:D013529), ADO (MESH:D011681), LVOT (MESH:D000092242), hypotension (MESH:D007022), iron deficiency (MESH:D000090463), Hemolysis (MESH:D006461), PVR (OMIM:193235), MR (MESH:D008944), atrial arrhythmias (MESH:D001145), Tricuspid and Pulmonary PVL (MESH:D018785), stroke (MESH:D020521), impingement (MESH:D019534), venous congestion (MESH:D006940), Mitral PVL (MESH:D008946)
- **Chemicals:** PET (MESH:D011093), nitinol (MESH:C013616), iron (MESH:D007501)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

5 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12941249/full.md

## References

67 references — full list in the complete paper: https://tomesphere.com/paper/PMC12941249/full.md

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Source: https://tomesphere.com/paper/PMC12941249