As the name suggests dilated cardiomyopathy would imply cardiac chambers will dilate at least some time in the course of the disease .It can be minimalmild or massive. A new entity called non dilated cardiomyopathy is also gaining wider acceptance . (That will be dealt seperately )
Logic would suggest the first chamber to dilate in DCM should be the left ventricle because it is facing the direct load of systemic blood. But we also know whenever LV is stressed left atrium comes to it’s assistance .
Left atrium does this by total self sacrifice ( by all means!) increases it’s force of contractionelevating it’s mean pressure or even increasing it’s rate (AF) .
Like most other critical questions in cardiology , the factors that determine LV dilatation in DCM , is also poorly understood !
Is it the after load ?
Is it the muscle mass ? or it’s turgid or flabbiness ?
Is it the interstitial integrity?
Is it the blood volume ?(LVEDV , LV residual volume )
When the issue is complex it is usual to make the the unknown genetic defects , the scapegoat !
As of now the most important determinant of LV dilatation could be the behavior of the desminsthe gap junctions and myosins the titins etc
If the LV of a DCM patient refuses or resists dilatation what might happen ? Is it good or bad for the patient ?
Here is a catch . A LV that does not dilate obviously should be be good for the patient is in’t ? Medicine is not that simple.
When LV fails to dilate it means it has become too stiff and rigid and pass on the burden to to LA which faces the music. And in the process it dilates.This is the reason we observe diastolic dysfunction in vast number of DCM patients.( Currently it is estimated > 75% DCM will have significant diastolic dysfunction )
So now we can imagine how complex the sequence of hemodynamic stress in DCM that determine the chamber enlargement.( RARV dimension in DCM is a separate issue !)
So now answer this question : Which chamber dilates first in DCM ?
Any of the above
Both of the above dilate simultaneously
The answer must be 3 .
Why recognising this sequence of chamber enlargement in DCM is important ?
It gives us an opportunity to assess the dominant mechanism of LV dysfunction.There are reports where some DCMs have more diastolic dysfunction than systolic dysfunction .This will have important therapeutic implication.Further many of the infiltrative disorders of LV can have features of both DCM & RCM .
When a RCM begins to dilate it is usually a harbinger of terminal heart failure. But, it need not be always true . A small restrictive LV when dilates may acquire a slightly improved diastolic properties as the LV becomes more placid . And , if it happens the LA size may regress.
The role of LV restriction devices likeAcron meshDor procedureplication in refractory DCM is not well defined. All these modalities actually adds a small dose of diastolic dysfunction in these patients who have grossly dilated ventricles. This fact is very important as presence of any preexisting significant diastolic dysfunction in DCM makes the role of LV restrictive devices and surgery a big question mark !