A male in his 40's with no previous heart history presented with palpitations. There were no symptoms or evidence of hypoperfusion. A 12-lead was recorded during the tachycardia:
The tachycardia resolved on its own with no therapy. The post conversion ECG is below.
Had it not spontaneously converted, what therapy would be appropriate?
Answer: this is RVOT, right ventricular outflow tract ventricular tachycardia, and it is usually sensitive to adenosine. (I have been waiting for a case of this for years, and here it is!) This is one of the "idiopathic" (though no longer actually idiopathic) VT types that occur in the absence of structural heart disease. They generally have a relatively narrow QRS, less than 140 ms, whereas most VT has a QRS greater than 140 ms. Here is a fine article discussing these and other types of VT in the absence of structural heart disease:
JACC 2012: Ventricular tachycardia in the absence of structural heart disease
BMJ: 2019: Ventricular Tachycardia in the absence of structural heart disease.
Adenosine would be appropriate here, as it generally is for regular, monomorphic, wide complex tachycardia, as long as you recognize that not all wide complex tachycardia that converts with adenosine is SVT with aberrancy. This is the exception to that rule. In other words, conversion with adenosine does not prove SVT.
The 12-lead ECG in RVOT VT has
1. LBBB pattern
2. wide septal r-wave
3. Inferior axis.
4. The transition from S-wave to R-wave in the precordial leads depends on how far anterior (RV outflow tract vs. LV outflow tract) the origin of the VT is.
Here is a short quote from the article:
"Patients may be asymptomatic but often present with palpitations, chest pain, dyspnea, presyncope, and even syncope. In general, Outflow Tract Arrhythmia occur more frequently with exertion or emotional stress, and may have a diurnal variation. Women may have an increase in symptoms related to changes in hormonal status. In general, the prognosis of truly idiopathic OTA is benign. Long-term follow-up studies have provided evidence that the vast majority of patients do not develop structural heart disease or SCD. However, as already noted, a small percentage of patients with very frequent VAs may have LV dysfunction over time, and rare reports have documented cardiac arrest and Polymorphic VT in patients who were initially thought to have “benign” Outflow Tract Arrhythmia."
Here are 2 more relevant posts, which include the approach to wide complex tachycardia: 1) SVT with aberrancy 2) verapamil-sensitive posterior fascicular VT
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| There is a regular, wide complex tachycardia at rate of 170 bpm, with QRS duration of 124 ms. There are no p-waves, no AV dissociation, no concordance (QRS in precordial leads are not all in the same direction). There is inferior axis (all positive in II, III, aVF, and all negative in lead aVR. There is an initial wide septal r-wave in V1 and V2 (greater than 40 ms). There is a left bundle branch block morphology, except that the initial r-wave is wider than 40 ms. What is the diagnosis? |
The tachycardia resolved on its own with no therapy. The post conversion ECG is below.
 |
| There is lead reversal, making it appear as if there are Q-waves in leads I and aVL. Otherwise it is normal. |
Had it not spontaneously converted, what therapy would be appropriate?
Answer: this is RVOT, right ventricular outflow tract ventricular tachycardia, and it is usually sensitive to adenosine. (I have been waiting for a case of this for years, and here it is!) This is one of the "idiopathic" (though no longer actually idiopathic) VT types that occur in the absence of structural heart disease. They generally have a relatively narrow QRS, less than 140 ms, whereas most VT has a QRS greater than 140 ms. Here is a fine article discussing these and other types of VT in the absence of structural heart disease:
JACC 2012: Ventricular tachycardia in the absence of structural heart disease
BMJ: 2019: Ventricular Tachycardia in the absence of structural heart disease.
Adenosine would be appropriate here, as it generally is for regular, monomorphic, wide complex tachycardia, as long as you recognize that not all wide complex tachycardia that converts with adenosine is SVT with aberrancy. This is the exception to that rule. In other words, conversion with adenosine does not prove SVT.
The 12-lead ECG in RVOT VT has
1. LBBB pattern
2. wide septal r-wave
3. Inferior axis.
4. The transition from S-wave to R-wave in the precordial leads depends on how far anterior (RV outflow tract vs. LV outflow tract) the origin of the VT is.
Here is a short quote from the article:
"Patients may be asymptomatic but often present with palpitations, chest pain, dyspnea, presyncope, and even syncope. In general, Outflow Tract Arrhythmia occur more frequently with exertion or emotional stress, and may have a diurnal variation. Women may have an increase in symptoms related to changes in hormonal status. In general, the prognosis of truly idiopathic OTA is benign. Long-term follow-up studies have provided evidence that the vast majority of patients do not develop structural heart disease or SCD. However, as already noted, a small percentage of patients with very frequent VAs may have LV dysfunction over time, and rare reports have documented cardiac arrest and Polymorphic VT in patients who were initially thought to have “benign” Outflow Tract Arrhythmia."
Here are 2 more relevant posts, which include the approach to wide complex tachycardia: 1) SVT with aberrancy 2) verapamil-sensitive posterior fascicular VT
I definitely buy a simple LA-RA reversal on that second ECG (after spending way too much time running through the possibilities), but how do you account for the inverted T-waves in the inferior leads? Just a baseline ectopic atrial rhythm?
ReplyDeleteI'm not sure which leads are reversed, but I do know that lead II should be upright (look something like V5) and it does not. So the QRS axis is not what it should be, therefore the T axis is not what it should be.
DeleteBelieve it or not, I had a case of this 1 week after you posted this. I have the EKGs if you would like them.
ReplyDeleteSure. Send them on!
DeleteCould this actually be a case of LVOT VT arising from the right coronary cusp? This is evident by the early transition (V2-V3) and the overall positive QRS complex in lead I.
Deletehttp://content.onlinejacc.org/article.aspx?articleid=1127734
Repetitive Monomorphic Ventricular Tachycardia Originating From the Aortic Sinus Cusp Electrocardiographic Characterization for Guiding Catheter Ablation
Feifan Ouyang, MD,* Parwis Fotuhi, MD,* Siew Yen Ho, PHD,† Joachim Hebe, MD,*
Marius Volkmer, MD,* Masahiko Goya, MD,* Mark Burns, MD,* Matthias Antz, MD,*
Sabine Ernst, MD,* Riccardo Cappato, MD,* Karl-Heinz Kuck, MD
If encountered without other information, it appears that it could be. In this case, the EP study showed RVOT. And for non-EP physicians who encounter such a patient, it does not make a big difference in management. Thanks for the excellent comment!
DeleteSteve Smith
Excellent!!!, the best part is that conversion with adenosine does not prove SVT.
ReplyDelete