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 .
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 .
*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 .
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 ?)
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 .