VPDs are the most common arrhythmia that confront us in cardiology clinics .While it can be a totally benign manifestation in some , it may signify a sinister condition in others. ECG is the easiest and surest way to identify VPD.However a shrewd echocardiographer can detect the VPDs while imaging the heart.It is often missed if one do not concentrate on the mitral valve motion.
Note :The VPD convert the typical M pattern into a inverted U pattern in mitral valve.
One of the important hemodynamic side-effect of VPD is intermittent mitral regurgitation.
Effect of VPD on mitral valve opening .
By conventional thinking VPDs are expected to impact more on the mitral valve closure than it’s opening .In reality it has indirect influence on mitral valve opening as well. The retrograde conduction(VA conduction) of the VPD determine the timing of atrial contraction and hence the mitral valve opening. If the VPD gets blocked retrogradely within AV node , the normal sinus impulse will activate the atria in an antegrade fashion .Note , he atrial activity occur randomly when multiple VPDs occur.This makes the cardiac cycle too complex to assess especially the diastole. (In fact true physiological diastole may not occur here !)
If the mitral valve opening is interfered by a VPD (Early diastole is the favorite time for VPDs to appear ! ) .When it occurs the AML is suddenly pushed upon superiorly by the premature ventricular activity and hence resets the mechanical diastole. Please note electrical resetting of atrium is different from mechanical resetting.
It is also possible atria and ventricle contract simultaneously .This is the time , a cannon wave may occur inside LA .VPDs can result in pulmonary venous canons and may even elevate pulmonary venous pressure if this occurs repetitively .
Another possibility is , VPDs may not initiate a ventricular contraction at all .It may be simply be an electrical event. That’s why we changed the name of extra systole and premature contraction into just premature depolarisations.
Why is it important to know about M Mode motion of VPDs
Cardiologists continue to engage wide qrs tachycardias in the wrong side of their brain for many decades .The ECG debate about wide qrs tachycardia is expected to continue for generations . ! Few smart cardiologists would rapidly put the echo probe over the mitral valve and able to differentiate instantly a VT form SVT with fair degree of accuracy.
Detection of regular M shaped mitral AML will exclude a VT with a high degree of precision .(AV dissociation by echo )*
Even presence of trivial MR* (More often diastolic ) which occur irregularly will definitely indicate it is VT . SVT hemodynamically can not result in this MR is gives us evidence for AV dissociation
* No reference for these observed indices in our lab. (Class 1 Level C expert opinion( No one calls me as expert though ! )
What is the mechanism of VPD induced mitral regurgitation ?
It is well-known VPDs can cause mitral regurgitation .Not every VPD cause MR.
- The timing is important .
- It can be either systolic or diastolic MR .
- If VPD occur in early diastole (After the T wave , the MR jet will collide with diastolic mitral flow. )
- Paradoxical septal motion induced by VPDs can alter the pap muscle alignment transiently and result in MR
- We dot not know how a LV apical VPD differ from RVOT VPD in the genesis of MR.
- Logic would suggest RVOT VPDs are unlikely to result in MR as there is a time lag for the impulse to reach the LV base
What is the effect of VPD and Aortic valve opening ?
While every VPD promptly hits the mitral valve , aortic valve may or may not open with VPDs .Again timing and focus of VPD could be important.This is the reason during multiple VPDs only few open the aortic valve , that explains pulse deficit. (The so called missed beat )
Final message
Anterior mitral leaflet (AML) is the most mobile structure of the heart . Hence , it is not surprising to note sudden unexpected ventricular contraction will have maximum impact on this valve .
When VPDs occur in clusters or at random it has a complex effect on the mitral valve motion. This is responsible for palpitation , minimal mitral regurgitation and rarely trouble some pulmonary venous cannons and raise in pulmonary venous pressure .
Careful analysis of AML motion can give us useful clues to differentiate VT from SVT during wide qrs tachycardia
Dr.S.Venkatesan MD 