The answer to this question is not easy , as one would tend to believe . In fact this question , takes it for granted revascularisation will improve the LV dysfunction in patients with severe LV dysfunction.
The truth is , we are not sure about the mechanisms . How revasculariastion will have an effect on chronically dying or dead myocardium ? (Acutely dying myocardium is a different story, where revascualrisation has a profound effect , that is called salvaging the myocardium )
This issue is of great clinical significance in end stage ischemic heart disease .A typical myocardial segment in ischemic cardiomyopathy has millions of the dead cells interwoven with dying cells with occasional clusters if live cells scattered all over .Once the process of myocardial apotosis sets in , myocardial cell death does not result in segmental destruction instead an universal cell death.(Paracrine signals of cell death that spills over to adjacent segments ) The current standards of revascualrisation (PCI and CABG) aims to provide blood flow in a segmental fashion. Even if the blood flow is restored in an obstructive vessel it is not clear , how it is going to enter the chronically atrophied myocytes.
Meanwhile , many studies are available suggesting coronary revascularisation does indeed improve LV dysfunction. These evidence has never been conclusive .Real world experience would also confirm this simple fact , that angina relief is definite following revascularisation but not dyspnea relief in patients with LV dysfunction .
So , when seeking the guidelines for revascularisation ( PCI or CABG ) in patients with CAD one need to ask this specific question
Does the patient has
B.Angina and dyspnea
If the answer is C , assess the patient again , rule out systemic causes of dyspnea (Anemia, renal function etc) rethink or postpone revascularisation.If primary or secondary LV muscle dysfunction has set in revascularisation has little value.