Lipid peroxidation is not increased in heart failure patients on modern pharmacological therapy.
BACKGROUND
Previous studies support a role of oxygen-free radicals in the development of congestive heart failure (CHF). The aim of this study was to investigate whether lipid peroxidation is increased in CHF patients on modern pharmacological therapy and whether there is a positive correlation between plasma levels of markers of lipid peroxidation and severity of heart failure (HF). Plasma malondialdehyde (MDA) and isoprostanes are often used as markers of lipid peroxidation and oxidative stress. We also studied whether long-term treatment with isosorbide-5-mononitrate (IS-5-MN) in combination with standard HF therapy affects P-MDA levels in patients with evidence of left ventricular (LV) dysfunction following acute myocardial infarction (AMI).


METHODS
Ninety-two patients with clinical or echocardiographic evidence of LV-dysfunction following AMI were randomized to treatment with either IS-5-MN or placebo. In a subgroup of 83 patients with available plasma MDA, echocardiography, right-heart catherization, and plasma natriuretic peptides were evaluated. Control subjects were 80 healthy blood donors. A second study group consisted of 56 patients with CHF, evaluated with respect to LV function, brain natriuretic peptide and markers of oxidative stress (P-MDA and 8-isoprostane). The second control group comprised 50 healthy subjects.


RESULTS
Lipid peroxidation measured by P-MDA and 8-isoprostane was not increased in patients with LV dysfunction treated with standard HF therapy. No positive correlation was found to the severity of HF. Long-term IS-5-MN therapy did not influence P-MDA concentrations.


CONCLUSIONS
Although results from many experimental and clinical studies suggest that oxidative stress is increased in HF, this may not be true for patients treated with beta blockers and inhibitors of the renin-angiotensin system.
Tingberg
Erik
E
Department of Cardiology, University Hospital, SE-221 85 Lund, Sweden. erik.tingberg@skane.se
Ohlin
Ann-Kristin
AK
Gottsäter
Anders
A
Ohlin
Hans
H
D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D047228:Angiotensin II Type 1 Receptor Blockers / Q000097:blood; D000806:Angiotensin-Converting Enzyme Inhibitors; D009320:Atrial Natriuretic Factor / Q000097:blood; D002216:Captopril / Q000627:therapeutic use; D015897:Comorbidity; D003692:Delayed-Action Preparations; D015237:Dinoprost / Q000031:analogs & derivatives / Q000097:blood; D005260:Female; D006333:Heart Failure / Q000000981:diagnostic imaging / Q000188:drug therapy* / Q000453:epidemiology / Q000378:metabolism*; D006439:Hemodynamics; D006801:Humans; D007548:Isosorbide Dinitrate / Q000008:administration & dosage / Q000031:analogs & derivatives* / Q000627:therapeutic use; D015227:Lipid Peroxidation; D019808:Losartan / Q000627:therapeutic use; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood; D020097:Natriuretic Peptide, Brain / Q000097:blood; D020030:Nitric Oxide Donors / Q000008:administration & dosage / Q000627:therapeutic use*; D018384:Oxidative Stress / Q000502:physiology; D017257:Ramipril / Q000627:therapeutic use; D013318:Stroke Volume; D014463:Ultrasonography; D018487:Ventricular Dysfunction, Left / Q000097:blood* / Q000453:epidemiology
D047228:Angiotensin II Type 1 Receptor Blockers; D000806:Angiotensin-Converting Enzyme Inhibitors; D003692:Delayed-Action Preparations; D020030:Nitric Oxide Donors; D020097:Natriuretic Peptide, Brain; C075750:8-epi-prostaglandin F2alpha; D008315:Malondialdehyde; D009320:Atrial Natriuretic Factor; D002216:Captopril; D015237:Dinoprost; D007548:Isosorbide Dinitrate; D019808:Losartan; D017257:Ramipril; C030397:isosorbide-5-mononitrate