TY - JOUR
T1 - Evidence for enhanced free radical activity in chronic congestive heart failure secondary to coronary artery disease
AU - McMurray, J.
AU - McLay, J.
AU - Chopra, M.
AU - Bridges, A.
AU - Belch, J. J. F.
N1 - Funding Information:
From the Departments of Medicine, Clinical Pharmacology and Cardiology, Ninewells Hospital and Medical School, Dundee, and the Department of Cardiology, Western Infirmary, Glasgow, Gl 16NT, Scotland, United Kingdom. This study was supported by the British Heart Foundation. Manuscript received August 21, 1989; revised manuscript received January 3, 1990, and accepted January 4.
PY - 1990/5/15
Y1 - 1990/5/15
N2 - Free radicals may be involved in the genesis of certain types of acute myocardial dysfunction ("reperfusion injury" and "stunning").1,2 Free radicals could also be implicated in the development and progression of chronic myocardial impairment. Underlying coronary artery disease may predispose to stunning. Repeated episodes of stunning may lead to permanent myocardial dysfunction.3 Additional factors could also favor free radical generation in congestive heart failure (CHF). Many other organ beds such as the kidneys and skeletal muscle undergo hypoperfusion/reperfusion cycles in patients with CHF, especially during exercise. Lactic acidosis may enhance hyperoxia in these tissues.4 Adrenergic activity is increased in CHF.5 Catecholamines may augment free radical generation by increasing mitochondrial respiration and undergoing autooxidation.6,7 In support of these possibilities antioxidant therapy has been shown to protect against catecholamine cardiomyopathies in animals.8,9 We have therefore measured malondialdehyde-like material in patients with CHF. This may give some indication of lipid peroxidation, an injurious process to membranes mediated by free radicals.10 We have also measured plasma thiol concentration. Thiols are thought to act as free radical scavengers and reduction in plasma thiol levels may reflect oxidative stress.11.
AB - Free radicals may be involved in the genesis of certain types of acute myocardial dysfunction ("reperfusion injury" and "stunning").1,2 Free radicals could also be implicated in the development and progression of chronic myocardial impairment. Underlying coronary artery disease may predispose to stunning. Repeated episodes of stunning may lead to permanent myocardial dysfunction.3 Additional factors could also favor free radical generation in congestive heart failure (CHF). Many other organ beds such as the kidneys and skeletal muscle undergo hypoperfusion/reperfusion cycles in patients with CHF, especially during exercise. Lactic acidosis may enhance hyperoxia in these tissues.4 Adrenergic activity is increased in CHF.5 Catecholamines may augment free radical generation by increasing mitochondrial respiration and undergoing autooxidation.6,7 In support of these possibilities antioxidant therapy has been shown to protect against catecholamine cardiomyopathies in animals.8,9 We have therefore measured malondialdehyde-like material in patients with CHF. This may give some indication of lipid peroxidation, an injurious process to membranes mediated by free radicals.10 We have also measured plasma thiol concentration. Thiols are thought to act as free radical scavengers and reduction in plasma thiol levels may reflect oxidative stress.11.
UR - http://www.scopus.com/inward/record.url?scp=0025307914&partnerID=8YFLogxK
U2 - 10.1016/0002-9149(90)90985-A
DO - 10.1016/0002-9149(90)90985-A
M3 - Review article
C2 - 2337039
AN - SCOPUS:0025307914
SN - 0002-9149
VL - 65
SP - 1261
EP - 1262
JO - The American Journal of Cardiology
JF - The American Journal of Cardiology
IS - 18
ER -