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The negative impact of oxidative stress in chronic cardiac failure and coronary heart disease calls for a new pathophysiologic and therapeutic approach.

Oxidative stress, when associated with ECG aspects of "coronary disease", indicates an accelerated course of atherosclerosis in the onset phase (by cellular involvement, migration, proliferation, etc.) and an additional thrombogenic risk in the "ischemic disease" phase, when associated with chronic cardiac failure, it indicates a progressive form with "replacement fibrosis". The therapy that reduces the oxidative stress can slow down the physiopathologic process, and clinically improves the patients' condition and prognosis.