Heart transforming from WPW to healthy rhythm

When a Wobbly Heart Isn't Just a Rhythm Problem: Understanding WPW and Hidden Cardiomyopathy

"Discover how Wolff-Parkinson-White syndrome can lead to unexpected heart muscle weakness and what can be done about it."


Heart failure (HF) often stems from a complex interplay of factors, with dyssynchrony – poorly coordinated heart contractions – playing a significant role. While often associated with conditions like dilated ventricles or conduction system diseases, dyssynchrony's impact on heart function and a patient's well-being is well-documented.

Cardiac resynchronization therapy (CRT) has emerged as a valuable tool for managing HF symptoms and improving outcomes by addressing electrical conduction abnormalities. However, ineffective heart contractions and subsequent HF can arise from various other underlying causes.

This article delves into a unique case of severe, symptomatic dilated cardiomyopathy resulting from a right anterolateral accessory pathway (AP). Successful ablation of this pathway led to remarkable improvements in heart function and symptom resolution, highlighting the importance of understanding the diverse electromechanical mechanisms contributing to cardiomyopathy.

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How WPW Presents

In a 2021 study of Wolff-Parkinson-White syndrome, patients were 42.8 ± 16.2 years old on average, 39.9% were women, and 95.9% were symptomatic. Tachycardia was documented in 84.4% of patients. Mayo Clinic identifies a heart rate above 100 beats per minute as the most common symptom of WPW syndrome. In children, ventricular dysfunction was reported in 4.5% of WPW cases in a 2025 study, occurring more often with right anteroseptal and anterior pathways.

Conventional Treatment

The two main treatment approaches described for WPW syndrome are pharmacotherapy and electrophysiologic study with radiofrequency catheter ablation. Earlier surgical work reported that a closed-heart technique appeared safe and effective, but noted a potential limitation when subendocardial atrioventricular pathways were present. Cardiac resynchronization therapy also carries procedure-related risks, including lead-placement complications, stroke, and organ damage. These limitations show why treatment selection depends on the pathway and the procedure being considered.

From Observation to Diagnosis

Drs. Wolff, Parkinson, and White fully described the syndrome in 1930, although earlier case reports had already documented its essential features. WPW syndrome results from an extra electrical connection between the atria and ventricles that is present at birth. Supraventricular tachycardia is best diagnosed by documenting a 12-lead ECG during tachycardia, although monitoring strips or recorders may also identify it. These developments connected the syndrome's congenital electrical substrate with a practical diagnostic method.

The Case: Unmasking WPW-Related Cardiomyopathy

Heart transforming from WPW to healthy rhythm

A 24-year-old chef presented with intermittent atypical chest pain and dyspnea. Initial examinations, including social and family history, revealed no significant contributing factors. However, an ECG unveiled a sinus rhythm, a shortened PR interval, and preexcitation patterns with positive delta waves, indicative of Wolff-Parkinson-White (WPW) syndrome.

Despite the absence of reported arrhythmias, a subsequent echocardiogram revealed a concerningly low ejection fraction of 22% and a dilated left ventricle. The septum displayed significant dyskinesis, and the basal inferior wall exhibited akinetic behavior, raising concerns about underlying cardiomyopathy.

  • Key Findings
  • Dilated left ventricle with significantly reduced ejection fraction.
  • Septal dyskinesis and akinetic basal inferior wall.
  • ECG evidence of WPW syndrome without reported tachyarrhythmias.
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When WPW Affects Function

Recent case reports describe cardiac dysfunction associated with WPW and improvement after treating the accessory pathway. One report documented reversal of WPW-induced dilated cardiomyopathy through resynchronization followed by accessory-pathway ablation. Another case of type-C WPW syndrome found that radiofrequency catheter ablation played a critical role in improving cardiac function. A separate report described successful ablation as a form of cardiac resynchronization therapy in a patient with dilated cardiomyopathy.

Not Every Case Causes Dysfunction

Ventricular dysfunction is not an inevitable consequence of WPW syndrome. A study of children reported that left-ventricular dysfunction from sustained or incessant tachyarrhythmia is rarely seen, particularly outside infancy. Cleveland Clinic describes WPW as an extra electrical pathway that allows signals to travel too quickly, but that description alone does not establish cardiomyopathy. The available evidence therefore supports distinguishing electrical risk from demonstrated ventricular failure.

Evolving Resynchronization Options

Comparative pacing research has expanded beyond conventional biventricular pacing. Multiple clinical studies reported that left bundle branch area pacing had electrical resynchronization comparable to His-bundle pacing while being superior in some measured respects. Left bundle branch area pacing and left-ventricular or conduction-system approaches are being compared with His-bundle pacing and conventional biventricular pacing. The WiSE CRT system offers an endocardial alternative intended to remove lead complications and provide greater freedom in selecting the pacing site.

Further investigation via cardiac magnetic resonance imaging confirmed abnormal septal motion without delayed myocardial enhancement. Given these findings, the patient was referred to an electrophysiologist for further evaluation and potential intervention.

Unlocking Recovery: Ablation and the Road to a Healthier Heart

Electrophysiological studies pinpointed the earliest ventricular electrogram at the 10 o'clock position of the tricuspid annulus, confirming the presence of a right anterolateral accessory pathway. Radiofrequency ablation successfully eliminated the pathway, restoring normal electrical conduction.

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Risk Is Not Always Obvious

Asymptomatic ventricular preexcitation does not mean that risk is absent. An ACC review reports that one meta-analysis estimated the overall lifetime risk of sudden cardiac death in asymptomatic WPW patients at 3% to 4%, with most cases occurring between ages 10 and 40 years. Expert guidance also notes that people with WPW syndrome may experience palpitations, dizziness, or fainting because of the extra electrical pathway. Risk assessment therefore requires attention to both symptoms and the pathway's electrical behavior.

Technology and Market Expansion

Recent cardiac resynchronization research reports a trend toward reduced mortality with CRT-D devices compared with ICDs. Market projections also point to expanding investment: the Wolff-Parkinson-White syndrome market is projected to grow at a 5.88% compound annual growth rate from 2025 to 2035. Separately, the cardiac resynchronization therapy market was valued at $5.1 billion in 2025 and is projected to reach $8.2 billion by 2033, according to one market analysis. These projections describe technology and market momentum, not guaranteed improvements for every patient.

A Congenital and Genetic Spectrum

WPW syndrome is one of the most common causes of fast-heart-rate problems in infants and children, according to MedlinePlus. Diagnostic risk is not uniform: a WPW pattern or syndrome is considered high risk for sudden cardiac death when preexcitation persists during induced atrial fibrillation. WPW is also among the preexcitation disorders found to have a genetic component. These features make age, rhythm behavior, and family or genetic context relevant to broader assessment.

Unexpected Presentation

WPW can affect people without a known underlying heart condition. One report described malignant arrhythmia and aborted sudden cardiac death as the first presentation in a previously asymptomatic 17-year-old patient. Another case involved a 13-year-old girl with shortness of breath, cough, wheezing, tachycardia, and left bundle branch block. These cases illustrate why symptoms may initially resemble ordinary respiratory or rhythm complaints while still requiring cardiac evaluation.

Follow-up assessments three months post-ablation revealed remarkable improvements. The patient reported increased exercise tolerance, and an echocardiogram showed a normalized PR interval and an ejection fraction that had rebounded to 57% with improved left ventricular dimensions and wall motion.

This case underscores the importance of considering WPW syndrome as a potential cause of cardiomyopathy, even in the absence of incessant tachycardia. Early referral to an electrophysiologist for evaluation and potential ablation can lead to significant improvements in cardiac function and overall quality of life.

What pathway location adds to the picture

These findings suggest that the measured change in pumping function after ablation may depend on where the accessory pathway is located. They do not show that ablation produces the same improvement for every pathway or every patient.[1]

Pre-excitation can be associated with ventricular dysfunction even when sustained arrhythmias are absent; the proposed link is that activation through the extra pathway can make ventricular contraction less coordinated. This offers a possible mechanism, not proof that it explains every case of dysfunction.[2]

How the comparison evidence varies

The infant series included infants with dilated cardiomyopathy, whereas the adult pilot enrolled patients with regional wall-motion abnormalities and performed ablation before magnetic resonance imaging in some participants. The populations and assessment sequence therefore differ, limiting direct comparison with the case described here.[3] [4]

What remains unresolved about WPW-related dysfunction

  • Do changes in ventricular function after ablation persist over time, given reports that dysfunction may progress and the lack of prospective studies noted in that account?[5]
  • How much do pathway location and underlying myocardial changes each contribute to dysfunction or its persistence after ablation? The available observations describe differences, but do not separate their effects.[1] [4]

About this Article -

Written with AI assistance from published research, and reviewed by the Mystum team. See our About page for more information.

Everything You Need To Know

1

How can Wolff-Parkinson-White (WPW) syndrome, primarily known for causing rapid heartbeats, lead to heart muscle weakness?

Wolff-Parkinson-White (WPW) syndrome is typically associated with rapid heartbeats due to an extra electrical pathway in the heart. However, in rare cases, continuous pre-excitation caused by the accessory pathway can lead to dilated cardiomyopathy, weakening the heart muscle and reducing its ability to pump blood effectively. This situation can occur even without noticeable arrhythmias.

2

What does it mean when a patient with Wolff-Parkinson-White (WPW) syndrome is diagnosed with dilated cardiomyopathy, and how does it affect the heart?

Dilated cardiomyopathy in the context of Wolff-Parkinson-White (WPW) syndrome means the left ventricle becomes enlarged and weakened. The heart's pumping efficiency, measured by ejection fraction, is significantly reduced. Specific areas, like the septum and basal inferior wall, may exhibit abnormal or absent movement (dyskinesis and akinesis), respectively, impairing overall heart function.

3

How does radiofrequency ablation help in cases where Wolff-Parkinson-White (WPW) syndrome has led to heart muscle problems?

Radiofrequency ablation targets and eliminates the accessory pathway in Wolff-Parkinson-White (WPW) syndrome. By restoring normal electrical conduction, ablation can reverse the negative effects of continuous pre-excitation on the heart muscle. In cases where WPW has led to dilated cardiomyopathy, successful ablation can lead to significant improvements in heart function and symptom relief, as the heart no longer has to compensate for the abnormal electrical activity.

4

Is Cardiac Resynchronization Therapy a solution for Cardiomyopathy arising from Wolff-Parkinson-White?

Cardiac resynchronization therapy (CRT) is typically used to improve heart function in heart failure patients by coordinating the contractions of the left and right ventricles using biventricular pacing. It addresses dyssynchrony commonly found with dilated ventricles or conduction system diseases. In the described case involving Wolff-Parkinson-White (WPW) syndrome, radiofrequency ablation targeting the accessory pathway was used instead of CRT to treat heart muscle weakness.

5

What is an 'accessory pathway' in Wolff-Parkinson-White (WPW) syndrome, and how does its location impact treatment strategies?

An accessory pathway (AP) in Wolff-Parkinson-White (WPW) syndrome is an extra electrical connection between the atria and ventricles, bypassing the normal AV node pathway. In this particular instance, the accessory pathway was located on the right side of the heart (right anterolateral). Ablation of this specific pathway restored normal electrical conduction, allowing the heart to beat more efficiently and reversing the cardiomyopathy caused by the abnormal electrical activity. The exact location of the AP is critical for electrophysiologists to target during ablation.

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