Does an MI cause a fever

[Ramoray]

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I remember reading that following an MI you can have a fever but does a fever persist days later in a person who had an MI? especially if the MI caused circ. collapse or anything.. just curious as i saw a quesitno with fever and mi and it was not the answer but i was thinking of the association but did not remmeber or ever know. thanks

 

[GrandMasterB]

a month out- or so- does dressler's give you a fever?

 

[lasek]

I remember reading that following an MI you can have a fever but does a fever persist days later in a person who had an MI? especially if the MI caused circ. collapse or anything.. just curious as i saw a quesitno with fever and mi and it was not the answer but i was thinking of the association but did not remmeber or ever know. thanks

I also remember reading that, but dont remeber the details. I'd say that since fever is caused by inflamation (leaving out a lot of middle ground), an inflamatory process in the post-MI myocardium can produce a fever for a few days or a week. I'm just not sure if an MI will cause sufficient myocardial inflamation to produce a prolonged systemic responce such as a fever. Hope that helps a bit.

 

[Idiopathic]

It can...circulating catecholamines go way up > > > can lead to fever.

 

[lasek]

It can...circulating catecholamines go way up > > > can lead to fever.

Would catecholamines go up sufficiently though? The whole problem I'm having is if there will be enough of the pyrogens (whatever they may be) released into the system to cause a fever for more than a few days. There obviously is enough to produce a fever for a short time, but would the increase in pyrogen levels last for long? I think that the duration of the fever would depend on the magnitude of the insult. Sorry if I'm stating the obvious.

 

[Idiopathic]

Would catecholamines go up sufficiently though? The whole problem I'm having is if there will be enough of the pyrogens (whatever they may be) released into the system to cause a fever for more than a few days. There obviously is enough to produce a fever for a short time, but would the increase in pyrogen levels last for long? I think that the duration of the fever would depend on the magnitude of the insult. Sorry if I'm stating the obvious.

Well, you have to maintain heart rate in the face of decreased SV, and the way to do that is with catecholamines. A mildly inflammatory state is present also, rememer, that lasts into the next month, and is responsible for much of the remodeling.

 

[Ramoray]

Well, you have to maintain heart rate in the face of decreased SV, and the way to do that is with catecholamines. A mildly inflammatory state is present also, rememer, that lasts into the next month, and is responsible for much of the remodeling.

Thanks guys, how to catecholamines cause a fever? come to think of it i for some reason never learned much about fever. I only know the Il1, 6 inflam pathway of fever. How exactly to catacholamines do this? thanks for the help!

 

[omarsaleh66]

Thanks guys, how to catecholamines cause a fever? come to think of it i for some reason never learned much about fever. I only know the Il1, 6 inflam pathway of fever. How exactly to catacholamines do this? thanks for the help!

I think its through IL-1. Perhaps, by changing the hypothalamus setpoint so the body's temperature can get higher without the hypothalamus regulating autonomics to cool the body. Not sure tho, im kinda making this up, been a long time.

 

[lasek]

From the abstract this seems like it should be a good review of catecholamines and inflamation. And it looks like omar was right.
I dont have access to the full article. If someone has access to it, I'd be interested to read it.

Stress hormones, proinflammatory and antiinflammatory cytokines, and autoimmunity.
Ann N Y Acad Sci. 2002 Jun;966:290-303. Review.
Elenkov IJ, Chrousos GP.

(http://www.ncbi.nlm.nih.gov/entrez/...&dopt=Abstract&list_uids=12114286&query_hl=14)

Recent evidence indicates that glucocorticoids and catecholamines, the major stress hormones, inhibit the production of proinflammatory cytokines, such as interleukin (IL)-12, tumor necrosis factor (TNF)-alpha, and interferon (IFN)-gamma, whereas they stimulate the production of antiinflammatory cytokines, such as IL-10, IL-4, and transforming growth factor (TGF)-beta. Thus, systemically, an excessive immune response, through activation of the stress system, stimulates an important negative feedback mechanism, which protects the organism from an "overshoot" of proinflammatory cytokines and other products of activated macrophages with tissue-damaging potential. Conversely, in certain local responses and under certain conditions, stress hormones actually may boost regional immune responses, through induction of TNF-alpha, IL-1, and IL-8, and by inhibiting TGF-beta production. Therefore, conditions that are associated with significant changes in stress system activity, such as acute or chronic stress, cessation of chronic stress, severe exercise, and pregnancy and the postpartum period, through modulation of the systemic or local pro/antiinflammatory cytokine balance, may suppress or potentiate autoimmune diseases activity and/or progression.

 

[Ramoray]

From the abstract this seems like it should be a good review of catecholamines and inflamation. And it looks like omar was right.
I dont have access to the full article. If someone has access to it, I'd be interested to read it.

Stress hormones, proinflammatory and antiinflammatory cytokines, and autoimmunity.
Ann N Y Acad Sci. 2002 Jun;966:290-303. Review.
Elenkov IJ, Chrousos GP.

(http://www.ncbi.nlm.nih.gov/entrez/...&dopt=Abstract&list_uids=12114286&query_hl=14)

Recent evidence indicates that glucocorticoids and catecholamines, the major stress hormones, inhibit the production of proinflammatory cytokines, such as interleukin (IL)-12, tumor necrosis factor (TNF)-alpha, and interferon (IFN)-gamma, whereas they stimulate the production of antiinflammatory cytokines, such as IL-10, IL-4, and transforming growth factor (TGF)-beta. Thus, systemically, an excessive immune response, through activation of the stress system, stimulates an important negative feedback mechanism, which protects the organism from an "overshoot" of proinflammatory cytokines and other products of activated macrophages with tissue-damaging potential. Conversely, in certain local responses and under certain conditions, stress hormones actually may boost regional immune responses, through induction of TNF-alpha, IL-1, and IL-8, and by inhibiting TGF-beta production. Therefore, conditions that are associated with significant changes in stress system activity, such as acute or chronic stress, cessation of chronic stress, severe exercise, and pregnancy and the postpartum period, through modulation of the systemic or local pro/antiinflammatory cytokine balance, may suppress or potentiate autoimmune diseases activity and/or progression.

thanks lasek that was interesting and helpful. the more i study path in general it seems like everything comes down to Il 1 and TNF or one of the cytokines. i always heard the term inflamation but not until year 2 of med school did i see in every disease it is bascially the cause! thank again

 

[HiddenTruth]

Yea, I think it's a direct effect of the hypothalamus in conjunction with the inflammatory process. I mean, we all know IL-1, and 6, and PGE2 mediated increase in fever. But, the posterior nucleus of the hypothalamus also directly stimulates the sympathetic NS, and it also acts to conserve heat--> hyperthermia.

 

[lasek]

thanks lasek that was interesting and helpful. the more i study path in general it seems like everything comes down to Il 1 and TNF or one of the cytokines. i always heard the term inflamation but not until year 2 of med school did i see in every disease it is bascially the cause! thank again

I didnt notice until after being almost done with pathology, but true. I cant think of any disease that isn't related to cytokines in one way or another.