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Pseudo ventricular hypertrophy and pseudo myocardial infarction in Wolff-Parkinson-White syndrome
1Division of Cardiology, Creighton University Medical Center, Omaha, NE 68131-2044, USA. ikhan@cardiac.creighton.edu
Insights
Wolff-Parkinson-White syndrome alters ventricular activation, mimicking heart conditions on ECGs. These ECG patterns, including pseudo ventricular hypertrophy and infarction, are not indicative of actual heart disease in WPW patients.
Area of Science:
- Cardiology
- Electrophysiology
- Medical Diagnostics
Background:
- Wolff-Parkinson-White syndrome (WPW) is characterized by an accessory pathway enabling pre-excitation of the ventricles.
- Altered ventricular activation sequences in WPW can lead to electrocardiogram (ECG) findings that mimic other cardiac pathologies.
Observation:
- The anatomical location of the accessory pathway significantly influences the resulting ECG patterns.
- Right-sided pathways can simulate left ventricular hypertrophy, while left-sided pathways may mimic right ventricular hypertrophy.
- Specific pathway locations can generate ECG findings suggestive of anterior, lateral, or inferior myocardial infarction.
Findings:
- WPW syndrome can produce electrocardiogram (ECG) abnormalities that are often mistaken for ventricular hypertrophy and myocardial infarction.
- The specific pseudo-hypertrophy and pseudo-infarction patterns are directly related to the electrophysiological properties of the accessory pathway.
- These ECG manifestations are artifacts of altered conduction, not indicators of structural heart disease or ischemic events.
Implications:
- Diagnosis of ventricular hypertrophy and myocardial infarction should be approached with caution in patients with known or suspected WPW syndrome.
- Understanding the ECG variations in WPW is crucial for accurate diagnosis and appropriate patient management.
- ECG interpretation in WPW requires careful consideration of the underlying electrophysiological abnormality to avoid misdiagnosis.
Abstract:
In Wolff-Parkinson-White syndrome, the sequence of ventricular activation is altered and depending on the anatomic site of the accessory conduction pathway may result in pseudo ventricular hypertrophy and pseudo myocardial infarction patterns on electrocardiogram. The right-sided accessory pathway may direct the depolarization vector towards left amplifying R-wave amplitude in left-sided limb-leads simulating left ventricular hypertrophy. The left-sided accessory pathways may give rise to prominent R-waves in right precordial leads simulating right ventricular hypertrophy. The right lateral accessory pathways may simulate anterior infarction because of prominent Q-waves in right precordial leads. The left lateral accessory pathways directing depolarization vector towards right may cause Q-waves in lateral limb-leads simulating high lateral myocardial infarction. In posteroseptal accessory pathway, the ventricular depolarization vector is directed superiorily giving rise to prominent Q-waves in inferior limb leads simulating inferior myocardial infarction. Therefore, ventricular hypertrophy and myocardial infarction should not be diagnosed from the electrocardiograms of Wolff-Parkinson-White syndrome.