# Premature Ventricular Complex-Induced Cardiomyopathy, a Review: Current Insights, Diagnostic Challenges, and Therapeutic Strategies

**Authors:** Mario J. Recio-Ibarz, Teresa Olóriz, Naiara Calvo, Beatriz Jáuregui, Vanesa Alonso-Ventura, Daniel Cantero Lozano, Carlos López-Perales

PMC · DOI: 10.3390/jcm15041360 · 2026-02-09

## TL;DR

This paper reviews PVC-induced cardiomyopathy, a reversible heart condition caused by frequent premature ventricular complexes, and highlights advances in diagnosis and treatment.

## Contribution

The paper provides updated insights into diagnostic methods and therapeutic strategies for PVC-induced cardiomyopathy.

## Key findings

- PVC-induced cardiomyopathy is reversible with effective suppression of arrhythmia.
- Advances in imaging and ablation therapy have improved diagnosis and treatment outcomes.
- Artificial intelligence and computational mapping are emerging as tools for prediction and procedural guidance.

## Abstract

Premature Ventricular Complexes (PVCs) are among the most frequent ventricular arrhythmias observed in daily cardiology practice. Although often benign, sustained high ectopic activity can result in left ventricular dysfunction known as PVC-induced Cardiomyopathy (PVC-CMP), a condition that is frequently reversible when the arrhythmia is effectively suppressed. The underlying mechanisms are multifaceted, involving electromechanical dyssynchrony, contractile inefficiency, abnormal calcium cycling, neurohormonal activation, and progressive structural remodeling. The likelihood of developing PVC-CMP varies among individuals and is influenced by electrophysiological and structural factors. Diagnosis relies on prolonged rhythm monitoring, comprehensive multimodality imaging, and demonstration of ventricular recovery after reducing the ectopic burden, which, in turn, confirms causality. Over the past decade, major advances in electrocardiographic mapping, cardiac imaging, and ablation therapy have transformed this field, demonstrating excellent efficacy and safety profiles. In parallel, artificial intelligence and computational mapping are emerging as powerful tools for prediction and procedural guidance. Recognition of PVC-CMP as a distinct, treatable cardiomyopathy highlights the importance of early detection and individualized therapy, offering the prospect of complete functional recovery and the prevention of heart failure progression.

## Linked entities

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

## Full-text entities

- **Genes:** TTN (titin) [NCBI Gene 7273] {aka CMD1G, CMH9, CMPD4, CMYO5, CMYP5, EOMFC}, SLC5A2 (solute carrier family 5 member 2) [NCBI Gene 6524] {aka SGLT2}, RYR2 (ryanodine receptor 2) [NCBI Gene 6262] {aka ARVC2, ARVD2, RYR-2, RyR, VACRDS, VTSIP}, LMNA (lamin A/C) [NCBI Gene 4000] {aka CDCD1, CDDC, CMD1A, CMT2B1, EMD2, FPL}, LGALS3 (galectin 3) [NCBI Gene 3958] {aka CBP35, GAL3, GALBP, GALIG, L31, LGALS2}, DES (desmin) [NCBI Gene 1674] {aka CDCD3, CSM1, CSM2, LGMD1D, LGMD1E, LGMD2R}, PKP2 (plakophilin 2) [NCBI Gene 5318] {aka ARVD9}, PLN (phospholamban) [NCBI Gene 5350] {aka CMD1P, CMH18, PLB}, DSP (desmoplakin) [NCBI Gene 1832] {aka DCWHKTA, DP}, SCN5A (sodium voltage-gated channel alpha subunit 5) [NCBI Gene 6331] {aka CDCD2, CMD1E, CMPD2, HB1, HB2, HBBD}, REN (renin) [NCBI Gene 5972] {aka ADTKD4, HNFJ2, RTD}
- **Diseases:** fibrosis (MESH:D005355), inflammation (MESH:D007249), auriculoventricular block (MESH:D014927), LV dilatation (MESH:C565277), thyroid, hepatic, pulmonary, and dermatologic complications (MESH:D008107), injury (MESH:D014947), myocardial disease (MESH:D004194), coronary or valvular damage (MESH:D003327), mitochondrial dysfunction (MESH:D028361), Phrenic nerve/coronary injury (MESH:D000080902), tremor (MESH:D014202), Brugada syndrome (MESH:D053840), LVOT (MESH:D000092242), blurred vision (MESH:D014786), hypertension (MESH:D006973), short QT syndrome (MESH:C566506), ischemic (MESH:D002545), LGE (MESH:C564835), gastrointestinal intolerance (MESH:D005767), Diabetes (MESH:D003920), cardiovascular (MESH:D002318), Ectopy (MESH:D050030), biventricular dilation (MESH:D002311), atrioventricular block (MESH:D054537), ventricular decline (MESH:D018754), anxiety (MESH:D001007), dizziness (MESH:D004244), chronic kidney disease (MESH:D051436), discoordination (MESH:C562757), toxicity (MESH:D064420), vascular injury (MESH:D057772), arrhythmogenic (MESH:D019571), renal dysfunction (MESH:D007674), Ventricular Arrhythmias (MESH:D001145), HF (MESH:D006333), infarct (MESH:D007238), torsade de pointes (MESH:D016171), ventricular dilation (MESH:C566255), LV dysfunction (MESH:D018487), structural abnormalities (MESH:C566527), heart disease (MESH:D006331), stroke (MESH:D020521), coronary artery disease (MESH:D003324), LV remodeling (MESH:D020257), Cardiomyopathy (MESH:D009202), Scar (MESH:D002921), fatigue (MESH:D005221), arrhythmic (OMIM:212500), sleep disordered breathing (MESH:D012891), ventricular tachycardia (MESH:D017180), bronchospasm (MESH:D001986), QT prolongation (MESH:D008133), ventricular dyssynchrony (MESH:D014693), PVCs (MESH:D018879), rhythm (MESH:D021081), neurological symptoms (MESH:D009461), hypotension (MESH:D007022), cardiac tamponade (MESH:D002305), chronic (MESH:D002908), bradycardia (MESH:D001919)
- **Chemicals:** adenosine (MESH:D000241), Flecainide (MESH:D005424), bisoprolol (MESH:D017298), Class III (-), propafenone (MESH:D011405), sodium (MESH:D012964), caffeine (MESH:D002110), potassium (MESH:D011188), diltiazem (MESH:D004110), carvedilol (MESH:D000077261), natriuretic peptides (MESH:D045265), catecholamine (MESH:D002395), Mexiletine (MESH:D008801), Sotalol (MESH:D013015), hydroquinidine (MESH:C014486), quinidine (MESH:D011802), aldosterone (MESH:D000450), Dronedarone (MESH:D000077764), Amiodarone (MESH:D000638), isoproterenol (MESH:D007545), verapamil (MESH:D014700), alcohol (MESH:D000438), metoprolol (MESH:D008790), cyclic AMP (MESH:D000242), calcium (MESH:D002118), dihydropyridine (MESH:C038806), ethanol (MESH:D000431)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

4 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12942255/full.md

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Source: https://tomesphere.com/paper/PMC12942255