An incidental finding in a 40 year old

Authored by Dr Lisanne Schoutens (FY2 Doctor, John Radcliffe Hospital, Oxford)

A fit and well 40 year old man was referred to cardiology clinic due to an incidental finding on his ECG. He has no significant cardiac or other past medical history and takes no regular medications. He is adopted, and his family history is unknown. In clinic, his observations and bloods were all normal. Echocardiogram demonstrated a structurally normal heart and good biventricular function

 

ECG interpretation:

This ECG shows a regular sinus rhythm with a ventricular rate of approximately 72 beats per minute. The PR interval is measured by the automated ECG machine at over 120ms. In fact the QRS complex is broad at also just over 120ms, with a slurred initial upstroke and a dominant R wave in lead V1, and the PR interval is actually shorter than 120 ms.

The combination of a short PR interval and slurred initial upstroke of the QRS complex points towards a diagnosis of pre-excitation. As the patient is asymptomatic this is NOT Wolff-Parkinson White syndrome – the syndrome was defined by the three physicians as the finding of this type of ECG AND symptoms of palpitations most likely due to re-entrant tachycardia involving the accessory pathway that causes the ECG findings.

 

Explanation of ECG findings:

Wolff-Parkinson-White syndrome is the most common type of ventricular pre-excitation syndrome. It is characterised by the presence of an accessory conductive pathway which directly connects from the atria to the ventricles. During sinus rhythm, electrical impulses are conducted through both the accessory pathway and the atrioventricular node. Conduction through the accessory pathway may be faster than conduction through the atrioventricular node, because the tissue in the accessory pathway depolarises by means of a fast inward sodium current, whereas the tissue in the atrioventricular node uses a slow inward calcium current. This leads to early onset of ventricular excitation and a short PR interval on the ECG.

The accessory pathway inserts directly into the ventricular myocardium and electrical activity then spreads through direct muscle fibre-to-muscle fibre conduction. This is slower than conduction through the specialised His-Purkinje conductive system. The initial upstroke of the QRS complex is therefore slurred: the ‘delta wave’, and the duration of the QRS complex is prolonged.

Electrical activity is also conducted through the atrioventricular node and the His-Purkinje fibres. Once this reaches the ventricular myocardium, it contributes to a later phase of ventricular excitation. The overall shape of the QRS complex is the result of a ‘fusion’ between the early slow ventricular excitation resulting from conduction through the accessory pathway, and the late ventricular excitation from conduction through the atrioventricular node and His-Purkinje conductive system.  Depending upon how rapidly they each conduct the ECG may have more of a slurred upstroke and delta wave or not.

 

Wolff-Parkinson-White syndrome:

An accessory pathway is a congenital abnormality that occurs in approximately 2-4 in 1000 people. It may be associated with other cardiac abnormalities including Ebstein’s anomaly, mitral valve prolapse, and hypertrophic cardiomyopathy.

The majority of patients with ECG findings of pre-excitation are asymptomatic, but a small percentage develop tachyarrythmias and may present with palpitations, dizziness, syncope, chest pain or sudden cardiac death. This is then labelled as Wolff-Parkinson-White syndrome. This can either be due to atrioventricular re-entry tachycardia using the accessory pathway, or due to supraventricular arrhythmias such as atrial fibrillation and atrial flutter. These may be conducted to the ventricles via the accessory pathway, leading to very fast ventricular rates with risk of ventricular fibrillation and sudden death.

The faster the pathway can conduct the more dangerous it is. If the conduction through the pathway is intermittent on the ECG (i.e. sometimes there is a delta wave and sometimes there is not) an/or with exercise the delta wave disappears (i.e. the AV node conducts faster than the accessory pathway) then it is felt that the pathway probably will not conduct fast enough to allow rapidly conducted AF – the potential life threatening arrhythmia with this condition. However, this is not totally reliable and modern management is to offer all people with the pre-excitation on their ECG a cardiac electrophysiology study to formally assess how fast the pathway conducts. Then if it conducts rapidly and/or sustains tachycardia then the pathway will be ablated. For this reason anyone with a pre-excited ECG, whether symptomatic (WPW) or not, should be referred to a cardiologist specialising in electrophysiology and ablation.

Please see below the pre- and post-ablation ECGs of this patient. Note the longer PR interval, shorter QRS duration and absence of the delta wave on the post-procedure ECG.

Post-ablation ECG:

 

A 35 year old woman with palpitations

Authored by Dr Francesca Finch (FY2 doctor, John Radcliffe hospital Oxford)

HPC: A 35 year old woman was admitted with a 2 day history of palpitations associated with intermittent dizziness. Her symptoms started suddenly when she was working at her desk. She did not experience any chest pain. Observations were stable throughout.

She had a similar episode occurred 6 months previously which was self-limiting, for which she did not seek medical attention.

She is normally fit and well, with no significant past medical history or regular medications.

Blood tests were all within normal range, and bedside ECHO showed a structurally normal heart.

 

When looking at this ECG, it is easier to break it down into sections.

In the rhythm strip, there are sections of sinus rhythm (tachycardic) followed by 4 to 5 beats of regular broad complex monomorphic tachycardia. The differential diagnosis of a broad complex tachycardia is supraventricular tachycardia (SVT) with aberrancy, SVT and an accessory pathway, and ventricular tachycardia (VT).

There are also a couple of singular broad QRS complexes, which are ventricular ectopic beats.

Thee fact that the morphology of the ectopics matches the tachycardia make VT most likely. This is a focal type of arrhythmia rather than a rentrant circuit. The focus  is either firing once, producing a ventricular ectopic or multiple times, leading to a run of VT.

Next we can see that there is a LBBB morphology, indicated by the dominant S wave in V1 and broad R wave in V5-V6. This shows that the ectopics are the result of a right ventricular origin (if it was a RBBB pattern then it comes from the left ventricle).

Finally, we look at the axis of the abnormal QRS complexes. The QRS complexes are very positive in the inferior leads – the QRS is positive in leads II, III and aVF. This shows us the electrical activity is moving towards the inferior leads (the principle is that if activation is moving away from an ECG lead the QRS is initially and predominantly negative and if it is moving towards it the lead it is positive). In this case it must be originating from the outflow tract of the right ventricle (near the pulmonary valve) which is high up and heading down to the lower part of the ventricle.

Putting this altogether, this is an example of right ventricular outflow tract tachycardia.

A cardiac MRI was performed, which showed non-dilated LV, with borderline impaired systolic function. (LVEF 53). There is a small patch of fibrosis in the region of the basal inferior LV/RV junction. The RV has normal volume and systolic function

 

Right Ventricular Outflow Tract (RVOT) Tachycardia

Most VTs occur in structurally abnormal hearts. However in 10% of patients with VT, no structural heart disease, metabolic/electrolyte abnormalities or other cause such as long QT syndrome can be found. This type of arrhythmia has been described as idiopathic VT.

Idiopathic VTs can originate from multiple anatomical regions, including the left ventricular outflow tract (LVOT) and right ventricular outflow tract (RVOT), the left fascicular system, the mitral and tricuspid annuli, and the papillary muscles, or they can develop in the epicardial space. More than half of all idiopathic VTs originate from the outflow tracts (OTs), and of these, approximately 80% originate from the RVOT

Commonly occuring symptoms include palpitations, chest pain, dyspnoea, and light-headedness during episodes . Syncope can occur rarely. However some patients may have only fatigue or may be entirely asymptomatic

In general RVOT VTs have a good and benign prognosis. Treatment is tailored on an individual basis depending on the nature and severity of symptoms. Pharmacotherapy may include a beta blocker, Verapamil or Diltiazem.  Class I (IA and IC) anti-arrhythmic drugs and class III drugs, such as sotalol and amiodarone may also be used. Catheter ablation is considered in cases where pharmacological treatment is not effective or not tolerated.