Ischemic cardiomyopathy pathophysiology?

[Daitong]

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Hi,

I am having a bit of trouble understanding why CAD/ischemia would result in cardiomyopathy- from my understanding, the CAD results in O2 supply/demand mismatch, but then the heart dilates to pump more to increase O2 supply?

But ultimately we still end with decreased ability to pump when you have dilated cardiomyopathy, so why does it dilate? Is it bc DCM temporarily provides ischemic relief due to the Frank-starling effect, but then gives out ultimately?

Best,

 

[deleted500612]

Hi,

I am having a bit of trouble understanding why CAD/ischemia would result in cardiomyopathy- from my understanding, the CAD results in O2 supply/demand mismatch, but then the heart dilates to pump more to increase O2 supply?

But ultimately we still end with decreased ability to pump when you have dilated cardiomyopathy, so why does it dilate? Is it bc DCM temporarily provides ischemic relief due to the Frank-starling effect, but then gives out ultimately?

Best,

It's a maladaptive response to fluid overload. Ischemia --> lack of ATP generation --> contractile dysfunction --> decreased EF --> increased ESV + EDV = ventricular volume overload --> eccentric hypertrophy of cardiomyocytes in attempt to accommodate increased volume.

Just remember:
pressure overload (afterload is too high) --> concentric hypertrophy (hypertrophic cardiomyopathy)
volume overload (preload is too high) --> eccentric hypertrophy (dilated cardiomyopathy)

 

[Instatewaiter]

Hi,

I am having a bit of trouble understanding why CAD/ischemia would result in cardiomyopathy- from my understanding, the CAD results in O2 supply/demand mismatch, but then the heart dilates to pump more to increase O2 supply?

But ultimately we still end with decreased ability to pump when you have dilated cardiomyopathy, so why does it dilate? Is it bc DCM temporarily provides ischemic relief due to the Frank-starling effect, but then gives out ultimately?

Best,

The term Ischemic cardiomyoapthy tend to be used not for actively ischemic CM but rather from dead myocardium from prior MI and resultant scar. Therefore, part of the myocardium doesn't work because it is just scar tissue after it died in the myocardial infarction rather than contracting myocardium.

With actively ischemic myocardium you have myocadial dysfunction secondary to lack of ATP creation (lack of blood flow to the area). This first affects relaxation since this is the energy dependent portion of the cardiac myocyte cycle (so diastolic dysfunction). Later you get a wall motion abnormality. This in turn affects your stroke volume. You get volume overloaded leading to dilation over time.