Neuroendocrine changes in acute myocardial infarction

McAlpine, Howard M.; Cobbe, Stuart M.

doi:10.1016/0002-9343(88)90206-9

Cited by 71 publications

(29 citation statements)

References 33 publications

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“…[1][2][3] All 3 groups in the present study were examined under the same laboratory conditions to avoid confounding influences related to circadian variation, 29 alcohol, 30 visceral distension, and a large meal. 31,32 In addition, all groups were closely matched to avoid confounding factors such as age, gender, 13 race, 33 body weight, 34 and heart rate.…”

Section: Discussionmentioning

confidence: 99%

“…Both groups were closely matched to avoid interfering effects on sympathetic nerve activity by factors including arterial pressure, 25,37 peak serum CK levels, and degree of left ventricular dysfunction. 1,2 In addition, both groups received similar therapy. Such considerations make it unlikely that confounding factors would have unequivocally explained the similarity of the magnitude of sympathetic hyperactivity between ant-AMI and inf-AMI.…”

Section: Graham Et Al Sympathetic Drive and Site Of Infarctionmentioning

confidence: 99%

“…ympathetic hyperactivity has been shown to occur early after acute myocardial infarction (AMI), [1][2][3][4] although very little is known about whether its magnitude differs between anterior wall (ant-AMI) and inferior wall (inf-AMI) infarction. This information is important because it may be relevant to the prognosis after AMI and to the mechanisms of associated sympathetic activation.…”

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confidence: 99%

“…1,2,13 However, although the prognosis after ant-AMI is poorer than after inf-AMI, 5,8,14,15 it is as yet unknown whether sympathetic nerve hyperactivity occurs to a greater extent in the former than the latter. The only available information has been derived from experimental studies in animals.…”

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confidence: 99%

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Sympathetic Drive in Anterior and Inferior Uncomplicated Acute Myocardial Infarction

et al. 2004

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Background-The sympathetic activation that follows acute myocardial infarction (AMI) has been associated with increased morbidity and mortality. Because the prognosis after anterior AMI (ant-AMI) is worse than that after inferior AMI (inf-AMI), we planned to determine whether the magnitude of sympathetic hyperactivity differs between the two. Methods and Results-Thirty-nine patients with uncomplicated AMI, comprising 2 matched groups of 17 patients with ant-AMI, and 22 patients with inf-AMI were examined. Measurements were obtained 2 to 4 days after AMI and compared with 20 normal subjects (NC) who were matched in terms of age and body weight to the AMI groups. Resting muscle sympathetic nerve activity was quantified from multiunit bursts (MSNA) and from single units (s-MSNA). Both groups of AMI patients were matched with regard to hemodynamic variables, left ventricular function, and infarct size. Both groups had greater (at least PϽ0.01) sympathetic nerve activity than NC (60Ϯ4.3 bursts/100 cardiac beats and 68Ϯ4.9 impulses/100 cardiac beats), but the magnitude of sympathetic nerve hyperactivity in ant-AMI (81Ϯ4.0 bursts/100 cardiac beats and 91Ϯ4.9 impulses/100 cardiac beats) was similar (PϾ0.05) to that in inf-AMI (80Ϯ3.2 bursts/100 cardiac beats and 90Ϯ4.0 impulses/100 cardiac beats) Conclusions-Both ant-AMI and inf-AMI resulted primarily in a similar magnitude of sympathetic nerve hyperactivity.These findings suggest that the worse prognosis after ant-AMI compared with after inf-AMI would not be related primarily to the degree of sympathetic hyperactivity.

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Section: Discussionmentioning

confidence: 99%

Section: Graham Et Al Sympathetic Drive and Site Of Infarctionmentioning

confidence: 99%

mentioning

confidence: 99%

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Sympathetic Drive in Anterior and Inferior Uncomplicated Acute Myocardial Infarction

et al. 2004

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“…31 Acute myocardial infarction is accompanied by activation of numerous systemic and local neurohumoral factors, including the renin-angiotensin system. 32,33 Furthermore, reperfusion of the acutely infarcted area (as obtained experimentally by removal of a coronary ligature and clinically by thrombolytic agents) produces a surge in reactive oxygen species, causing tissue damage beyond that inflicted by ischaemia 34 and partially attributed to activation of local humoral factors, including A II. Inhibition of ACE was shown to minimize the extent of this damage, 35,36 although it is unclear how much of this benefit should be attributed to A II suppression and how much to potentiation of bradykinin.…”

Section: Oxidative Stressmentioning

confidence: 99%

Angiotensin II as a cardiovascular risk factor

Gavras

2002

J Hum Hypertens

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A renin-angiotensin level that is inappropriately high for the systemic blood pressure and the state of sodium balance is now recognized to be one of the modifiable cardiovascular risk factors. Angiotensin acts both as a circulating hormone and as a locally acting paracrine/autocrine/intracrine factor. The adverse effects of angiotensin on the heart include the mechanical results of elevated resistance to the pumping function of the myocardium, as well as the effects of neurohumoral abnormalities on various cardiac structures. In addition, cardiac damage follows acute ischaemic injury or chronic energy starvation due to coronary artery disease, attributable to either mechanical obstruction Keywords: angiotensin II; renin-angiotensin system; cardiovascular disease; myocardial infarction Myocardial ischaemiaAngiotensin II (A II) is one of the major systemic pressor hormones (others include noradrenaline, vasopressin and endothelin). The idea that excessive levels of circulating A II can cause myocardial infarctions originated from an early experiment in which exogenous infusion of A II produced widespread areas of myocardial necrosis in rabbits. 1 Clinical observations in patients subjected to extreme stimulation of the renin-angiotensin system during haemodialysis revealed that these patients were prone to coronary death. This was attributed to intense coronary vasoconstriction, because focal myocardial necrosis was described in areas with no detectable coronary obstructive lesions. 2 These experiments were later replicated and amplified by other investigators. 3,4 It was found that an excess of endogenous or exogenous A II can damage the myocardium via several additional mechanisms, such as increased sarcolemmic permeability and death of cardiac myocytes, or increased permeability and destruction of coronary microvascular endothelial cells. All these eventually lead to the replacement of contractile myocardium by fibrotic tissue.Angiotensin II exerts a preferential pressor action on the coronary, renal, cerebral and adrenal vasculaCorrespondence: H Gavras, Department of Medicine, Boston University School of Medicine, 715 Albany Street, Boston, MA 02118, USA. E-mail: hgavrasȰbu.edu (atherosclerotic and/or thrombotic) or functional stenosis (vasospasm). Activation of the renin-angiotensin system has several haemodynamic and humoral consequences, all of which may damage the myocardium. These include acute myocardial ischaemia, left-ventricular hypertrophy, arrhythmias, alterations in the coagulation-fibrinolysis equilibrium, increased oxidative stress, and pro-inflammatory activity. A brief review of some of the mechanisms by which activation of the renin-angiotensin system can inflict damage on the heart is presented.

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