Oxidative stress in cardiovascular disease: molecular basis of its deleterious effects, its detection, and therapeutic considerations.
OBJECTIVE
The adoption of immediate reperfusion strategies to treat acutely occluded coronary arteries and the emergence of high-resolution molecular biology techniques have drawn attention to oxidative stress and reactive oxygen species generation in the cardiovascular system. Recent evidence suggests that oxidative stress is a common denominator in many aspects of cardiovascular pathogenesis. This review outlines the current understanding of reactive oxygen species generation and their role in cardiovascular pathophysiology, including atherogenesis, acute myocardial infarction, and congestive heart failure.


RESULTS
Recent studies highlighting endothelial dysfunction as a response to oxidative stress are of particular interest, as are the findings linking myocardial lipid accumulation (cardiac lipotoxicity) and peroxidation to congestive heart failure. Finally, newer methods to detect reactive oxygen species, including urine assays for measurement of 8,12 iPGF2alpha VI along with nuclear magnetic resonance, can help quantitate the reactive oxygen species burden noninvasively.


CONCLUSIONS
The body of current evidence from in vitro studies indicates that oxidative stress plays a major role in cardiovascular disease but the details of molecular events in vivo and in particular in humans remains to be determined. This could partly explain the failure of antioxidant therapy in preventing cardiovascular morbidity and mortality in major clinical trials. The emerging technologies, including MRI, can help delineate the events leading to reactive oxygen species generation and dissipation in humans, and potentially provide a more precisely targeted therapy for the population at risk.
Molavi
Behzad
B
Department of Internal Medicine, Division of Cardiovascular Medicine, University of Arkansas for Medical Sciences and the Central Arkansas Veterans Healthcare System, Little Rock, Arkansas 72205-7199, USA. molavibehzad@uams.edu
Mehta
Jawahar L
JL
D000208:Acute Disease; D000975:Antioxidants / Q000378:metabolism / Q000627:therapeutic use; D001161:Arteriosclerosis / Q000378:metabolism / Q000503:physiopathology; D002318:Cardiovascular Diseases / Q000378:metabolism / Q000503:physiopathology*; D006801:Humans; D015425:Myocardial Reperfusion; D018384:Oxidative Stress / Q000502:physiology*; D017382:Reactive Oxygen Species / Q000009:adverse effects / Q000378:metabolism
D000975:Antioxidants; D017382:Reactive Oxygen Species