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CASE REPORT
Year : 2012  |  Volume : 1  |  Issue : 2  |  Page : 127-129

Incidental finding of Wolff-Parkinson-White syndrome in emergency department


Department of General Medicine, Siddhartha Medical College, Vijayawada, Andhra Pradesh, India

Date of Web Publication11-Jul-2012

Correspondence Address:
Talluri Venkata Siva Pradeep
Post Graduate Student, Department of General Medicine, Government Siddhartha Medical College, Vijayawada, Andhra Pradesh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2277-8632.98366

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  Abstract 

A middle-aged male patient was admitted into our Emergency medical department with a history of suicidal consumption of an unknown toxic substance mixed with alcohol. During evaluation features of Wolff-Parkinson-White (WPW) syndrome were identified in his ECG. Pathophysiology, complications and treatment of WPW syndrome are discussed and the literature is reviewed.

Keywords: Accessory pathway, catheter ablation, tachyarrhythmias, Wolff-Parkinson-White syndrome


How to cite this article:
Rao K S, Seshaiah K V, Rao D S, Pradeep TV. Incidental finding of Wolff-Parkinson-White syndrome in emergency department. J NTR Univ Health Sci 2012;1:127-9

How to cite this URL:
Rao K S, Seshaiah K V, Rao D S, Pradeep TV. Incidental finding of Wolff-Parkinson-White syndrome in emergency department. J NTR Univ Health Sci [serial online] 2012 [cited 2019 Oct 23];1:127-9. Available from: http://www.jdrntruhs.org/text.asp?2012/1/2/127/98366


  Introduction Top


Wolff-Parkinson-White syndrome (WPW) is uncommon in general population (0.15-0.25%) and sometimes it is identified in ECG during routine evaluation of patients attended to Emergency or outpatient department. Patients with WPW syndrome may be asymptomatic or may have episodes of tachyarrhythmias, with a risk of sudden cardiac death (SCD).


  Case Report Top


A 33-year-old male patient was admitted into emergency medical department with a history of suicidal consumption of an unknown toxic substance mixed with alcohol [Figure 1]. Patient was in altered sensorium. His vitals were normal. Except altered mental status, other systemic examination was unremarkable. His ECG findings were short PR interval (80 ms), Slurred onset of the QRS (delta wave), widening of QRS (> 120 ms) and secondary ST-T changes. ECG findings are suggestive of WPW syndrome, most common form of the pre-excitation syndromes [Figure 2].
Figure 1: Photograph of the patient

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Figure 2: ECG of the patient

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On second day of hospitalization patient recovered completely. He was re-examined with complete history taking from the patient. He never suffered from any episode of palpitations or syncope. No positive family history. His routine investigations including X-ray chest were normal. 2D Echocardiogram was unremarkable.

This is a case of asymptomatic WPW syndrome (manifest pre-excitation). These asymptomatic patients usually do not require evaluation or treatment; but they need periodic follow-up, as there is a risk of tachyarrhythmias or SCD. This patient was discharged on seventh day with an advice of periodic follow-up.


  Discussion Top


WPW syndrome is caused by the presence of an abnormal accessory electrical conduction pathway between the atria and the ventricles.

Accessory pathways (APs) are fibres that connect the atria or AV node to the ventricle outside the normal AV nodal-His-Purkinje conduction system. These pathways can conduct impulses in the forward and / or reverse direction and are potential substrates for re-entrant tachycardias. In some cases, the pathways are only able to conduct in the retrograde direction; they do not produce any ventricular pre-excitation and are said to be concealed [Figure 3]a and b.
Figure 3: (a) Manifest AP, (b) Concealed AP

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Background

Cardiologists Louis Wolff (1898-1972), John Parkinson (1885-1976) and Paul Dudley White (1886-1973) are credited with the definitive description of this disorder in 1930.

Classic ECG Findings

WPW syndrome is commonly diagnosed on the basis of the ECG in an asymptomatic individual. [1] The three basic features are [Figure 4].
Figure 4: ECG features of WPW syndrome

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  • PR interval less than 120 ms during sinus rhythm.
  • QRS complex duration more than 120 ms with a slurred, slowly rising onset of the QRS in some leads (delta wave).
  • Secondary ST-T wave changes that are generally directed in an opposite direction to the major delta and QRS vectors.
Pathophysiology

The most common bypass tract is an accessory atrioventricular (AV) pathway otherwise known as bundle of Kent. Other variants of APs include atriofascicular, fasciculoventricular, nodofascicular and nodoventricular. [1] Nodofacsicular pathways are referred to as Mahaim fibres and typically manifest a normal PR interval with a delta wave. [2]

The location of the APs in descending order of frequency is 53% in left free wall, 36% in posteroseptal, 8% in right free wall and 3% in anteroseptal.

The presence of an AP allows a re-entrant tachycardia circuit to be established. Characteristically, the AP has more rapid conduction but a longer refractory period than that of the AV node. In patients with WPW in which the AP participates, 95% of supraventricular tachycardias (SVTs) is due to orthodromic tachycardia and 5% is due to antidromic tachycardia.

In orthodromic tachycardia, the ECG shows no delta wave; QRS complex is normal and P-waves are typically inverted in the inferior and lateral leads. In antidromic tachycardia, ECG shows wide QRS tachycardia and often shows slurred R-wave upstroke with QRS duration longer than 160 ms. [1],[3]

Clinical Features

APs are considered congenital phenomena, may manifest in later life. It may be inherited as familial trait and may have a genetic component. It may be associated with other congenital heart defects like Ebstein's anamoly, mitral valve prolapse and cardiomyopathy. [4] WPW may be associated with PRKAG2, a protein kinase enzyme encoded by the PRKAG2 gene. [5] Prevalence of WPW is 0.1-0.3% in general population.

Males are more affected than females. WPW is found in all ages and decreases with age. The frequency of SVT increases with age. [6]

Treatment

Patients with only ECG abnormality without tachyarrythmias do not require electrophysiological evaluation or therapy. [7] Asymptomatic patients need periodic observation, as in our case. For patients with frequent episodes of symptomatic tachyarrythmias, therapy should be initiated. Two therapeutic options are pharmacological therapy and catheter ablation. Drugs which prolong conduction time and / or refractoriness in the AV node, AP or both to prevent rapid rates are used. Adenosine, propranolol, verapamil and digitalis prolong conduction time and refractoriness in AV node. Digitalis should not be used in patients with atrial fibrillation (AF), because it shortens the refractoriness in AP and speed the ventricular response. In patients with AF, drugs that prolong the refractory period in AP should be used, such as class Ia and Ic drugs. [7]

Cardioversion is the treatment of choice if there is hemodynamic impairment.

Radiofrequency catheter ablation is the treatment of choice in patients with recurrent symptomatic tachyarrythmias, poorly controlled with drugs. Prophylactic catheter ablation can also be an option for patients with high-risk profile. [8]

Prognosis

Risk stratification is best performed via EPS. WPW syndrome is associated with excellent prognosis with potential for permanent cure through ablation. The incidence of sudden cardiac death (SCD) in WPW is one in 100 symptomatic cases. The factors which increase the risk of SCD are the multiple APs, short AP refractory periods (<240 ms), AF, atrial flutter and family history of SCD.

 
  References Top

1.Rosner MH, Brady WJ Jr, Kefer MP, Martin ML. Electrocardiography in the patient with the Woll-Parkinson-White syndrome: Diagnostic and initial therapeutic isuues. Am J Emerg Med 1999;17:705-14.  Back to cited text no. 1
[PUBMED]    
2.Longo DL, Fauci AS, Kasper DL, Hauser SL, Jameson JL, Loscalzo J. Harrison's principles of internal medicine. 18th ed. New York: The McGraw Hill Companies, Inc.; 2012. p. 1889-90.  Back to cited text no. 2
    
3.Fuster V, Wayne Alexander R, O'Rourke RA. Hurst's the heart. 10 th ed. New York: The McGraw Hill Companies, Inc.; 2001. p. 815-8.  Back to cited text no. 3
    
4.Ehtisham J, Watkins H. Is Wolff-Parkinson-White syndrome a genetic disease? J Cardiovasc Electrophysiol 2005;16:1258-62.  Back to cited text no. 4
[PUBMED]  [FULLTEXT]  
5.Gollob MH. Modulating phenotypic expression of the PRKAG2 cardiac syndrome. Circulation 2008;117:134-5.  Back to cited text no. 5
[PUBMED]  [FULLTEXT]  
6.Brembilla-Perrot B, Yangni N'da O, Huttin O, Chometon F, Groben L, Christophe C. Wolff-Parkinson-White syndrome in the elderly: Clinical and electrophysiological findings. Arch Cardiovasc Dis 2008;101:18-22.  Back to cited text no. 6
    
7.Libby P, Bonow RO, Mann DL, Zipes DP. Braunwald's heart disease: A textbook of cardiovascular medicine. 8 th ed. New York: Saunders Elsevier; 2007. p. 884-93  Back to cited text no. 7
    
8.Pappone C, Santinelli V, Manguso F, Augello G, Santinellio O, Vicedomini G. A randomized study of prophylactic catheter ablation in asymptomatic patients with the Wolff-Parkinson-White syndrome. N Engl J Med 2003;349:1803-11.  Back to cited text no. 8
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4]



 

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