Literature DB >> 7588920

Neurohormonal changes after acute myocardial infarction. Relationships with haemodynamic indices and effects of ACE inhibition.

S G Foy1, I G Crozier, A M Richards, M G Nicholls, J G Turner, C M Frampton, H Ikram.   

Abstract

To determine the neurohormonal response to angiotensin-converting enzyme (ACE) inhibition after acute myocardial infarction, 36 patients presenting within 6 h of the onset of chest pain were studied in a single regional cardiology service. In this double-blind study, 13 patients were randomized to receive captopril, 12 patients received enalapril, and 11 patients received placebo, for 12 months. In patients receiving placebo, acute myocardial infarction was associated with activation of the renin-angiotensin-aldosterone and sympathetic nervous systems, and stimulation of plasma brain natriuretic peptide and atrial natriuretic peptide levels. ACE inhibition did not significantly alter circulating levels of norepinephrine, brain natriuretic peptide or atrial natriuretic peptide. Compared with placebo, enalapril induced a steep decline in plasma ACE activity, and plasma angiotensin II levels were reduced by both ACE inhibitors. Using grouped data, circulating levels of brain natriuretic peptide at the zero sampling time were significantly higher than atrial natriuretic peptide values. Brain natriuretic peptide levels at 72 h were significantly correlated with the radionuclide left ventricular ejection fraction measured 5 days and 3 months after infarction. Similar associations were observed for atrial natriuretic peptide and norepinephrine. We confirm activation of the renin-angiotensin-aldosterone and sympathetic nervous systems after acute myocardial infarction. The atrial natriuretic peptide and brain natriuretic peptide and sympathetic nervous system responses to acute myocardial infarction were not significantly modified by ACE inhibition. Brain natriuretic peptide and atrial natriuretic peptide levels were significantly correlated with the left ventricular ejection fraction measured 5 days and again 3 months after myocardial infarction, and may prove a useful prognostic index.

Entities:  

Mesh:

Substances:

Year:  1995        PMID: 7588920     DOI: 10.1093/oxfordjournals.eurheartj.a060995

Source DB:  PubMed          Journal:  Eur Heart J        ISSN: 0195-668X            Impact factor:   29.983


  6 in total

1.  Increased cardiac sympathetic nerve activity following acute myocardial infarction in a sheep model.

Authors:  D L Jardine; C J Charles; R K Ashton; S I Bennett; M Whitehead; C M Frampton; M G Nicholls
Journal:  J Physiol       Date:  2005-03-17       Impact factor: 5.182

Review 2.  The renin-angiotensin-aldosterone system and cardiac ischaemia.

Authors:  H Ikram
Journal:  Heart       Date:  1996-11       Impact factor: 5.994

3.  Ventricular expression of natriuretic peptides in Npr1(-/-) mice with cardiac hypertrophy and fibrosis.

Authors:  Leigh J Ellmers; J W Knowles; H-S Kim; O Smithies; N Maeda; V A Cameron
Journal:  Am J Physiol Heart Circ Physiol       Date:  2002-08       Impact factor: 4.733

4.  Ischemia-reperfusion injury leads to distinct temporal cardiac remodeling in normal versus diabetic mice.

Authors:  Megumi Eguchi; Young Hwa Kim; Keon Wook Kang; Chi Young Shim; Yangsoo Jang; Thierry Dorval; Kwang Joon Kim; Gary Sweeney
Journal:  PLoS One       Date:  2012-02-08       Impact factor: 3.240

5.  The heart as an endocrine organ.

Authors:  Tsuneo Ogawa; Adolfo J de Bold
Journal:  Endocr Connect       Date:  2014-04-15       Impact factor: 3.335

6.  Correlation of plasma catestatin level and the prognosis of patients with acute myocardial infarction.

Authors:  Dan Zhu; Hong Xie; Xinyu Wang; Ying Liang; Haiyi Yu; Wei Gao
Journal:  PLoS One       Date:  2015-04-07       Impact factor: 3.240

  6 in total

北京卡尤迪生物科技股份有限公司 © 2022-2023.