Though heart is primarily known as a mechanical organ , in reality it is a vital electrical organ as well . The entire mesh of electrical pathway from SA node to Purkinje fiber would easily cross a mile or two .Maintaining and protecting such a delicately woven network needs lots of electrical sense . It is not surprising to note , VT or VF can be induced virtually in every human heart if stimulated rapidly. Electrocution induced by VF is the typical example.Cardiac surgeons do it regularly before surgery .
So , inducible VT in the EP lab need to be defined in a strict manner .
- VT must be triggered by a single stimuli (or two )
- Multiple sites should not be stimulated(ideally single site , at most two )
- It should be sustained.
- Only mono-morphic VT has significance
- Induced p0lymorphic VT has no clinical value.
- Pharmacological stimulus such as isoprenaline can be used but reduces specificity.
*If a VT rapidly degenerate into VF it usually means a polymorphic VT while unstable irregular polymorphic VT could be same as VF )
How do you make sure what we induce in EP lab is same as the clinical VT ?
This is the most difficult task for electro -physiologists. In real life setting VT is often induced by ischemia hypoxia , local acidosis and electrolytic imbalance. However rarely mind this issue . In EP lab we induce it with artificial electrodes . Does it make sense to compare these two totally different set of triggers in real life and a virtual EP life . Ideally to confirm ischemic VT one has to induce ischemia in EP lab and look for VT . (Adenosine stress ? ) Further , only re -entrant VTs can be induced in EP lab by programmed stimulation . Automatic VTs can not be induced by stimulation .
The chances of inducing a VT in EP lab is directily proportional to the aggression of the electro physiologists and patience of the patient ! One can afford to use more aggressive protocols only if a clinical VT was recently the documented .
Electrical stress testing of heart
It may be tempting to refer induction of VT in EP lab as electrical stress testing for the heart. But fundamentally there is a difference between this and the conventional EST . Unlike exercise stress test the inducibility of VT highly unpredictable . It has far too many variables . (The surface area of contact , number , Intensity , site of stimuli , scar location , irritability of viable myocardium , inertness of scarred myocardium , and finally the cellular milieu etc )
Thoughts to ponder over Is it not “a fundamentally a wrong concept” to give importance to inducible VT ?
Why should we treat a clinically non relevant inducible VT ? We do not know yet whether inducible VT in other wise normal LV function has any long-term significance . Currently it makes no sense to intervene in VT if the LV function is good and the episodes are not clinical but only inducible.
Note: If there is severe LV dysfunction (EF < 30 % ) one can implant an ICD without an EP study . ( Of course to state more dramatically without even single documented VT !) MADIT 2
Final message .
A VT which is inducible in EP lab has no meaning , if the LV function is normal , while even a non-existent (potential )VT in the setting of severe LV dysfunction is vitally important !
Though we differentiate cardiac function into mechanical and electrical for academic purposes , it is astonishing to note how the heart is able to function as a single unit . We know today , the ultimate outcome of VT is not dictated by electrical status of the heart rather , the mechanical ability to with -stand sudden dis-organized ventricular contractions ( A ventricle with good contractile function has inherent capacity to extinguish most episodes of VT .(Myocytes with inbuilt biological ICDs ?)
It is a million dolor question why some VT remain as non- sustained while others rapidly degenerate into fast VT and VF thereafter
Reference
The two contrasting studies
The MUSTT (1999) trial exposed the limitation of clinical utility of inducible VT . Multicenter Unsustained Tachycardia Trial (MUSTT) Investigators
While MADIT 2 (2002)which recommends an ICD in every patients with severe LV dysfunction following MI without even a EP study .
Dr.S.Venkatesan MD 
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