Right Ventricular Dynamics in Tricuspid Regurgitation: Insights into Reverse Remodeling and Outcome Prediction Post Transcatheter Valve Intervention
Abstract
1. Introduction
2. Pathophysiological Landscape of Right Ventricular Remodeling in Tricuspid Regurgitation
2.1. Biomechanical Adaptations and Maladaptive Changes
2.2. Molecular Mechanisms of RV Maladaptive Remodeling
3. Assessing Right Ventricular Function and Evidence of Reverse Remodeling Post Transcatheter Interventions
3.1. Advanced Imaging for RV Function Assessment
3.2. Mechanisms and Manifestations of RVRR After TTVI
4. Predicting Outcomes and the Role of Artificial Intelligence
4.1. Clinical Importance of Outcome Prediction in TTVI
4.2. Biomechanical and Molecular Markers for RVRR Prediction
4.3. Leveraging Neural Networks and AI for Prognostication
5. Conclusions and Future Perspectives
Author Contributions
Funding
Conflicts of Interest
Abbreviations
AI | Artificial intelligence |
CMR | Cardiac magnetic resonance imaging |
CT | Computed tomography |
eGFR | Estimated glomerular filtration rate |
IGFBP-2 | Insulin-like growth factor binding protein 2 |
LV | Left ventricular/left ventricle |
miRNAs | MicroRNAs |
mPAP | Mean pulmonary arterial pressure |
NT-proBNP | N-terminal pro–B-type natriuretic peptide |
PASP | Pulmonary artery systolic pressure |
PDK | Pyruvate dehydrogenase kinase |
RA | Right atrial/right atrium |
ROS | Reactive oxygen species |
RV | Right ventricular/right ventricle |
RVEDV | Right ventricular end-diastolic volume |
RVEF | Right ventricular ejection fraction |
RV GLS | Right ventricular global longitudinal strain |
RV-PA | Right ventricular-pulmonary arterial |
RVESV | Right ventricular end-systolic volume |
RVRR | Right ventricular reverse remodeling |
T-TEER | Transcatheter tricuspid valve edge-to-edge repair |
TAPSE | Tricuspid annular plane systolic excursion |
TR | Tricuspid regurgitation |
TTVI | Transcatheter tricuspid valve interventions |
TTVR | Transcatheter tricuspid valve replacement |
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Category | Molecular Factor | Role in Maladaptive Remodeling | Potential for RVRR |
---|---|---|---|
Oxidative Stress and Metabolism | Reactive Oxygen Species (ROS) | Increased production; early failure of antioxidant defenses (SOD, GPX) in RV vs. LV; greater mitochondrial ROS generation. Leads to damage and apoptosis. | Reduction in oxidative stress (e.g., with antioxidants like EUK-134) improves RV systolic function. |
PGC1α | Decreased expression, leading to impaired fatty acid oxidation, reduced mitochondrial mass/number, decreased oxidative capacity, increased ROS, mitochondrial DNA damage. | Upregulation could restore metabolic function. | |
HIF-1α | Activation associated with complex II-mediated ROS production in RVH; impaired angiogenic response (decreased VEGF, unchanged capillarity). | Modulation could improve angiogenesis and reduce ROS. | |
Pyruvate Dehydrogenase Kinase (PDK) | Increased expression mediates shift to aerobic glycolysis (Warburg effect), reducing ATP efficiency and RV contractility. | Pharmacologic inhibition improves RV contractility. | |
Fatty Acid Metabolism (Dysfunctional) | Decreased fatty acid oxidation, increased lipid accumulation, production of toxic intermediates (ceramide, palmitate), lipotoxic cardiomyopathy. | Restoration of fatty acid oxidation. | |
Angiogenesis and Epigenetics | MicroRNAs (miR-143/145, miR-34, miR-379, miR-503, miR-126, miR-486) | Dysregulation in RV failure (vascular tone, apoptosis, endothelial proliferation, VEGF pathway inhibition). | Targeted delivery (e.g., miR-126) shows increased RV vascularity/function. Circulating miR-486 is a diagnostic biomarker for maladaptive RV remodeling. |
IGFBP-2 (Insulin-Like Growth Factor Binding Protein 2) | Elevated levels at baseline predict non-development of RVRR and persistent TR/RV dilation after M-TEER. | Lower levels associated with RVRR. | |
Signaling Pathways | PI3K/Akt/mTOR pathway | Inactivated in pathological hypertrophy (pressure overload). | Activated in physiological hypertrophy (exercise-induced); enhances ventricular hypertrophy and function, suppresses apoptosis; gene therapy with constitutively active PI3K can improve function. |
Modality | Strengths | Parameters Measured | Utility for RVRR | Limitations |
---|---|---|---|---|
Echocardiography (2D and 3D) | First-line, widely available, real-time, non-invasive. 2D strain (speckle tracking) is angle-independent, sensitive for early dysfunction, good reproducibility. 3D echo provides comprehensive anatomical and volumetric assessment. | TAPSE, RVFAC, RVMPI, RV-Sa (conventional). RV peak systolic strain (RVPSS), RV global longitudinal strain (RV GLS). RV volumes (RVEDV3D, RVESV3D), RVEF3D (3D echo). | Early detection of myocardial deformation impairment. Quantifies RV volume unloading and structural remodeling. Measures improvement in RV FW-GLS and RV-PA coupling (TAPSE/PASP). | 2D methods limited by suboptimal acoustic windows, geometric assumptions, and inability to capture complex 3D anatomy. 2D-TAPSE alone may fail to predict outcomes. |
Cardiac Magnetic Resonance Imaging (CMR) | Gold standard for volumetric quantification of RV. Excellent endocardial definition, no ionizing radiation. Quantitative TR measurement via phase-contrast imaging. Can assess regional RV performance with tissue tagging. | RV volumes (end-diastolic, end-systolic), RVEF, RV mass. TR regurgitant volume, TR fraction. Regional shortening. | Precise quantification of RV volume reduction and changes in EF. Baseline RVESV (CMR-derived) is a strong predictor of RVRR. | Impractical for some patients (inability to stay supine, implanted devices). Less available than echo. |
Cardiac Computed Tomography (CT) | Detailed anatomy of TV and RV. Full-cycle CT captures complex RV anatomy and annular plane dynamics. AI-augmented software automates post-processing and quantification. | RV volumes (RVEDV, RVESV), RVEF. CT-based 3D-TAPSE (anterior, posterior, septal, lateral), iTAPSE, iTAPSE volume. | Substantial reduction in RV-EDV after TTVR (35%). Posterior iTAPSE and iTAPSE volume are independent predictors of cardiovascular outcomes after TTVI. | Ionizing radiation. Contrast use. |
Biomechanical Change/Marker | Observed Change | Impact on RV |
---|---|---|
Tricuspid Regurgitation (TR) Severity Reduction | Immediate and significant reduction in TR grade (e.g., to ≤2+ in 83% of patients at 6 months, 41% reduction in vena contracta, 50% in TR volume, 54% in EROA). Optimal procedural results (residual TR ≤ 1+) associated with more pronounced RVRR. | Reduces RV volume overload and wall stress, improving cardiac efficiency. |
RV Volume Reduction (Reverse Remodeling) | Biphasic pattern: early RV volume unloading (RVEDV reduction, e.g., −9.7% at discharge, −35% after TTVR) and later structural remodeling (RVESV reduction, e.g., −5.4% at 6 months). Average RV and TV dimensions decrease significantly. | Improved RV geometry, reduced wall stress, and enhanced cardiac output. Associated with improved survival. |
RV Ejection Fraction (RVEF) | May initially decline post-TTVI but gradually increases over time, returning to baseline values by 2 years. Effective RVEF improves immediately post-procedure. | Reflects improved pump function and overall RV efficiency. |
RV Global Longitudinal Strain (RV GLS) | Initial decline followed by late recovery to pre-procedural baseline values. Improvement in RV FW-GLS is a definition of RVRR (>10% improvement). | Direct assessment of myocardial deformation, indicating improved contractility and less impairment. |
RV-Pulmonary Artery (RV-PA) Coupling (TAPSE/PASP ratio) | Significant improvement (e.g., from 0.36 to 0.42). Improvement in RV-PA coupling is a definition of RVRR (>10% improvement). | Reflects improved RV efficiency in handling afterload, crucial for prognosis. |
Biventricular Interaction | Reduction in RV volume overload improves biventricular interaction, alleviating leftward bowing of the septum and improving early LV filling. Increased LV forward stroke volume (e.g., 30% increase). | Enhanced overall cardiac output and systemic perfusion. |
Model Type | Input Data Types | Key Input Parameters (Examples) | Risk Stratification (Example Cut-Offs) | Model Output | Utility/ Significance |
---|---|---|---|---|---|
Survival Tree-Based Model | Preprocedural clinical, laboratory, echocardiographic, and hemodynamic data. | Mean pulmonary artery pressure (mPAP), NT-proBNP levels, Right Atrial (RA) area, Estimated Glomerular Filtration Rate (eGFR). | Low-Risk: mPAP ≤ 28 mmHg AND NT-proBNP ≤ 2728 pg/mL (2-year survival: 85.5%) High-Risk: mPAP > 28 mmHg AND RA area > 32.5 cm2 AND eGFR ≤ 51 mL/min (2-year survival: 52.6%) | 2-year survival rate. | Effectively stratifies patients into distinct risk categories, comparable to TRI-Score and outperforms EuroScore II in identifying high-risk patients. Informs patient selection and personalized treatment. |
Penalized Cox Proportional Hazard Regression, Random Survival Forest (RSF), Extreme Gradient Boosting | 27 clinical and echocardiographic features from echocardiography reports and electronic medical records. | Heart rate, right ventricular systolic pressure (RVSP), blood pressure, diuretic use, age, BMI, chronic kidney disease, prior cardiac surgery, signs of congestion/hypoperfusion (AST, creatinine, hyponatremia), LV ejection fraction, LV end-diastolic dimension. | Identifies top contributing features for mortality prediction. | 1-year and 3-year mortality prediction (C-index 0.74–0.75 for 1-year). | Good overall performance in predicting long-term mortality in TR patients. Conditional RSF often ranks highest. |
Deep Learning for RVEF Prediction from 2D Echo | 2D apical 4-chamber view echocardiographic videos. | Video frames processed by convolutional networks. | Reduced RVEF < 45% (significantly worse 1-year survival: 80.3% vs. 92.1%). | Predicted RVEF. | Refines prognostication, superior to conventional 2D TAPSE in predicting 1-year mortality. Can screen for patients needing intensified follow-up. |
AI-augmented CT analysis for 3D-TAPSE | Full cardiac cycle CT images (axial thin slices). | 3D tricuspid annulus dynamics (anterior, posterior, septal, lateral TAPSE measurements, iTAPSE volume). | Posterior iTAPSE > 4.5 mm/m2 (1-year combined endpoint: 17.2% vs. 63.6%). iTAPSE volume > 9 mL/m2 (1-year combined endpoint: 16.4% vs. 57.1%). | CT-based 3D-TAPSE values, prediction of hospitalization and mortality. | Automates complex measurements, provides incremental predictive value over 2D-TAPSE, refines risk stratification. |
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Doldi, P.M.; Thienel, M.; Willy, K. Right Ventricular Dynamics in Tricuspid Regurgitation: Insights into Reverse Remodeling and Outcome Prediction Post Transcatheter Valve Intervention. Int. J. Mol. Sci. 2025, 26, 6322. https://doi.org/10.3390/ijms26136322
Doldi PM, Thienel M, Willy K. Right Ventricular Dynamics in Tricuspid Regurgitation: Insights into Reverse Remodeling and Outcome Prediction Post Transcatheter Valve Intervention. International Journal of Molecular Sciences. 2025; 26(13):6322. https://doi.org/10.3390/ijms26136322
Chicago/Turabian StyleDoldi, Philipp M., Manuela Thienel, and Kevin Willy. 2025. "Right Ventricular Dynamics in Tricuspid Regurgitation: Insights into Reverse Remodeling and Outcome Prediction Post Transcatheter Valve Intervention" International Journal of Molecular Sciences 26, no. 13: 6322. https://doi.org/10.3390/ijms26136322
APA StyleDoldi, P. M., Thienel, M., & Willy, K. (2025). Right Ventricular Dynamics in Tricuspid Regurgitation: Insights into Reverse Remodeling and Outcome Prediction Post Transcatheter Valve Intervention. International Journal of Molecular Sciences, 26(13), 6322. https://doi.org/10.3390/ijms26136322