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| http://dx.doi.org/10.1016/j.hrcr.2015.05.005 | DOI Listing |
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Distinguishing Wolff-Parkinson-White Syndrome From Fasciculoventricular Pathway Using QRS-T Angle Analysis.
Pacing Clin Electrophysiol
January 2025
Division of Pediatric Electrophysiology, Pediatric Medical Care Center, Osaka City General Hospital, Osaka, Japan.
Article Synopsis
- Wolff-Parkinson-White (WPW) syndrome and fasciculoventricular pathway (FVP) both show delta waves on an ECG, but distinguishing between them, especially WPW type B, can be complex due to similar features.
- A study analyzed 40 WPW patients and 54 FVP patients to assess the QRS-T angle, resulting in a significantly larger QRS-T angle in the WPW group (45.7°) compared to FVP (17.8°).
- The research suggests that the QRS-T angle could be a useful marker for differentiating WPW syndrome from FVP, with a cut-off value of 22°
Causes of paradoxical response include Pure His capture and inadvertent intermittent direct atrial capture. In the index case , we postulate that the likely mechanism of paradoxical prolongation could be due to decrement in the AV node due to the shortening of HH interval which happened as a result of a narrower H + Vc beat .
View Article and Find Full Text PDFHide and seek: Masking of preexcitation from a slow-conducting, decremental right lateral accessory pathway due to preexcitation via a fasciculoventricular pathway.
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Division of Pediatric Cardiology, Department of Pediatrics West Virginia University School of Medicine and West Virginia University Children's Heart Center Morgantown West Virginia USA.
Masking of preexcitation from a slow-conducting, decremental AP due to preexcitation via an FV pathway.
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Department of Cardiology, Tongren Municipal People's Hospital, Tongren, Guizhou, China.
A 23-year-old male with a history of ventricular pre-excitation and atrial flutter presented for evaluation after recurrent syncope. The possible mechanism of syncope erroneously attributed to pre-excited atrial flutter with fast heart rates in the first hospitalization. The patient was found to have advanced heart block and PRKAG2 genetic mutation in the second hospitalization.
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