MI in transplanted heart

[Convalaria]

---

Members do not see this ad.

A 66 yo man who has a history of congestive heart failure and successful heart transplant 4 y ago suddenly becomes unconscious while watching TV. At ED he is declared dead on arrival. His wife says that he showed no sign of distress or pain before loosing consciousness. He spent the afternoon before his death playing baseball with his grandchild. At autopsy, examination shows early signs of myocardial ischemia in the posterior interventr.septum and thickened RV wall. What caused death?

The correct answer is A. Concentric intimal thickening of coronal arteries.

But because of thickened RV I chose C. High pulmonary vascular resistance. Others answers are irrelevant.
If it is intimal thickening of coronal arteries, then why would he have RV hypertrophy?

Thanks in advance!

 

[Szent]

Maybe he did have Pulmonary HTN leading to RV hypertrophy, but thats unlikely the cause of death. The more likely cause of death is Coronary Artery Disease = Intimal Thickening.

 

[Untraditional]

A 66 yo man who has a history of congestive heart failure and successful heart transplant 4 y ago suddenly becomes unconscious while watching TV. At ED he is declared dead on arrival. His wife says that he showed no sign of distress or pain before loosing consciousness. He spent the afternoon before his death playing baseball with his grandchild. At autopsy, examination shows early signs of myocardial ischemia in the posterior interventr.septum and thickened RV wall. What caused death?

The correct answer is A. Concentric intimal thickening of coronal arteries.

But because of thickened RV I chose C. High pulmonary vascular resistance. Others answers are irrelevant.
If it is intimal thickening of coronal arteries, then why would he have RV hypertrophy?

Thanks in advance!

Do you mean "coronary"?

Anyway, if he has CHF and if its left sided this would cause a pressure hypertrophy of the RV (afterload yields concentric hypertrophy) which would increase O2 demand. Since the arteries are undergoing intimal thickening and we have a posterior infarct you can infer that the RCA became occluded.

Hypertrophy was due to CHF.
Death was due ischemia of the hypertrophied ventricle secondary to the intimal thickening.

Maybe I'm oversimplifying but I don't see how the transplant bit is relevant to the answer. Could they be going for some kind of immune mediated fibrinoid necrosis?

 

[Convalaria]

Do you mean "coronary"?

Anyway, if he has CHF and if its left sided this would cause a pressure hypertrophy of the RV (afterload yields concentric hypertrophy) which would increase O2 demand. Since the arteries are undergoing intimal thickening and we have a posterior infarct you can infer that the RCA became occluded.

Hypertrophy was due to CHF.
Death was due ischemia of the hypertrophied ventricle secondary to the intimal thickening.

Maybe I'm oversimplifying but I don't see how the transplant bit is relevant to the answer. Could they be going for some kind of immune mediated fibrinoid necrosis?

yep, coronary, sorry, mistyped.

Explanation said that this intimal thickening of coronary arteries may be as a part of chronic rejection.
I think I didn't pay enough attention that they asked the cause of the death, not about the cause of hypertrophy RV. Hate when this happens.

Thank you, guys

 

[frankyazz]

Do you mean "coronary"?

Anyway, if he has CHF and if its left sided this would cause a pressure hypertrophy of the RV (afterload yields concentric hypertrophy) which would increase O2 demand. Since the arteries are undergoing intimal thickening and we have a posterior infarct you can infer that the RCA became occluded.

Hypertrophy was due to CHF.
Death was due ischemia of the hypertrophied ventricle secondary to the intimal thickening.

Maybe I'm oversimplifying but I don't see how the transplant bit is relevant to the answer. Could they be going for some kind of immune mediated fibrinoid necrosis?

That is what I was thinking regarding the transplant... Chronic transplant rejection with fibrinoid necrosis causing occlusion and decreased blood supply. Due to this, there was ischemia, and the hypertrophy of the RV (for whatever reason), would increase the O2 demand thus exacerbating the condition.

 

[frankyazz]

yep, coronary, sorry, mistyped.

Explanation said that this intimal thickening of coronary arteries may be as a part of chronic rejection.
I think I didn't pay enough attention that they asked the cause of the death, not about the cause of hypertrophy RV. Hate when this happens.

Thank you, guys

You beat me!

 

[Szent]

Yeah, after a bit of rereading myself the use of 'concentric' to describe intimal thickening would indicate something other than atherosclerotic CAD. Good luck!

 

[frizzles]

A 66 yo man who has a history of congestive heart failure and successful heart transplant 4 y ago suddenly becomes unconscious while watching TV. At ED he is declared dead on arrival. His wife says that he showed no sign of distress or pain before loosing consciousness. He spent the afternoon before his death playing baseball with his grandchild. At autopsy, examination shows early signs of myocardial ischemia in the posterior interventr.septum and thickened RV wall. What caused death?

The correct answer is A. Concentric intimal thickening of coronal arteries.

But because of thickened RV I chose C. High pulmonary vascular resistance. Others answers are irrelevant.
If it is intimal thickening of coronal arteries, then why would he have RV hypertrophy?

Thanks in advance!

transplanted hearts don't have innervation so you can't feel angina. and the most common complication after 1 year is called chronic allograft vasculopathy or something like that. it has to do with immune attack that leads to infarction

 

[iCY]

RV hypertrophy could just be a distractor? or perhaps he did have pulmonary HTN that caused RV thickening leading to a missmatch between blood supply/demand leading to an MI.

Honestly the RV thickening really doesn't matter. If you analyze the acute onset of symptoms & the localization to the right coronary artery (posteriro IV septum) the cause of DEATH was an MI. pulmonary HTN would not just kill you like that out of the blue, you would have signs of right sided CHF first.

 

[hotchik]

transplanted hearts don't have innervation so you can't feel angina. and the most common complication after 1 year is called chronic allograft vasculopathy or something like that. it has to do with immune attack that leads to infarction

Isn't that interesting? I didn't know that before studying for step 1 (although it makes sense and should've figured it out lol)

 

[Phloston]

transplanted hearts don't have innervation so you can't feel angina. and the most common complication after 1 year is called chronic allograft vasculopathy or something like that. it has to do with immune attack that leads to infarction

You nailed it.

I read this question and was actually surprised because CAV (coronary allograft vasculopathy) is NOT high-yield, but it showed up in USMLE Rx, and I remember having been blown away that it's B-cell-, NOT T-cell-, mediated.

You've gotta figure that classic chronic rejection of a heart transplant would be more diffuse, leading to either fibrosis, with loss of diastolic function and resultant restrictive cardiomyopathy, or mixed fibrosis-myocardial apoptosis, w/ diminished systolic function, leading to a dilated cardiomyopathy. However, that's CD4/CD8-mediated.

Atherosclerotic development in a transplanted heart leading to MI within a few years post-op is unlikely. If the patient gets an MI within a few years following a heart transplant, it's VERY likely to be CAV.

If I recall correctly from USMLE Rx, it had to do with antibody production, from B-cells (plasma cells), targeted against intimal/medial components of the vasculature. If the patient could feel pain, it would supposedly present like angina.