Plasma corticotrophin releasing hormone, vasopressin, ACTH and Cortisol responses to acute myocardial infarction

Abstract

Within 6 hours of a myocardial infarction, mean plasma CRH, AVP and cortisol values were very significantly raised above mean control values, while ACTH was very significantly reduced. During the 3 days following an acute myocardial infarction, plasma CRH, AVP and cortisol fell substantially, and this pattern was not influenced by angiotensin converting enzyme inhibitors. By contrast, plasma ACTH showed a significant increase with time. This suggests that the usual relationships between CRH, AVP and ACTH, and between ACTH and cortisol are disturbed in patients admitted to hospital with myocardial infarction. Maximum levels of AVP observed in 12 patients exceeded 50 pmol/l, which may be sufficiently high to interfere with tissue perfusion. It is postulated that V1 AVP receptor antagonists may have a therapeutic application in limiting infarct size.

Relation of morning serum cortisol to prothrombotic activity in women with stable coronary artery disease

“…Basal cortisol levels in stable CAD are unlikely influenced by the acute phase of MI because cortisol rise during AMI usually returns to normal within one week post-MI [4,26]. In stable CAD, possible correlates of elevated basal cortisol levels are depressed mood [27] and, as previously shown in the sample of women patients investigated in this study, feelings of vital exhaustion [9].…”

“…During the first hours of an acute myocardial infarction (AMI), hyperactivity of the HPA axis is evident as regards cortisol spillover [3][4][5]. Higher cortisol levels in AMI patients at hospital admission predicted extent of myocardial damage [5,6], risk of recurrent non-fatal MI [7], and mortality [6].…”

Morning and afternoon serum cortisol level in patients with post-myocardial infarction depression

“…An immediate increase in cortisol after MI has been previously reported [15,16]. In the (aforementioned) studies cortisol concentration normalised during the first 72 h after MI.…”

Hypothalamo–pituitary–adrenal axis response to coronary artery embolization: an ovine model of acute myocardial infarction

“…Myocardial viability appears to be associated with the presence of collateral blood flow within the infarct bed (Sabia et al 1992). Blockade of the plasma catecholamine (The Norwegian Multicenter Study Group 1981) and angiotensin (Pfeffer et al 1992, Foy et al 1994, GISSI-3 1994, ISIS-4 1995 responses to myocardial infarction in humans has been shown to improve patient survival. It is clear from this study in sheep that plasma AVP rises almost immediately with onset of infarction, and if AVP V, receptor blockade is to be considered as a means of improving tissue perfusion, treatment may best be administered early.…”