Key result
Trimetazidine added to optimal medical therapy significantly reduced oxidative stress, inflammation, and major acute cardiovascular events in patients with NSTE-ACS (P<0.05).
Why the study?
Trimetazidine increases mitochondrial adenosine triphosphate production, but its impact on oxidative stress, inflammation, endothelial dysfunction, and long-term prognosis in CAD needed evaluation.
Does trimetazidine added to optimal medical therapy improve oxidative stress, endothelial dysfunction, inflammation, and long-term prognosis in patients with inadequately controlled coronary artery disease?
Cohort (n=570)
Does trimetazidine added to optimal medical therapy improve oxidative stress, endothelial dysfunction, inflammation, and long-term prognosis in patients with inadequately controlled coronary artery disease?
p-value: p=<0.05
The addition of trimetazidine to optimal medical therapy may reduce oxidative stress and improve long-term clinical outcomes, particularly in patients with non-ST-elevation acute coronary syndrome.
May support adjunctive use in NSTE-ACS; leaves open need for randomized confirmation.
BACKGROUND: In coronary artery disease (CAD), reduction of perfusion in coronary arteries is followed by increases of oxidative stress and decreases of adenosine triphosphate reserve. In this condition, trimetazidine (TMZ), a metabolic anti-ischemic agent, seems to be an ideal therapeutic agent because it increases mitochondrial adenosine triphosphate production. STUDY QUESTION: To evaluate the impact of TMZ on oxidative stress, inflammation, endothelial dysfunction, and long-term prognosis in CAD. STUDY DESIGN: Patients with CAD with symptoms not adequately controlled were enrolled consecutively for a period of 18 months. MEASURES AND OUTCOMES: Five hundred seventy patients with CAD were enrolled in a prospective study and divided into 4 groups in relation with the type of CAD and the addition of TMZ to optimal medical therapy (OMT). The impact of TMZ added to OMT on oxidative stress (total antioxidant status, antioxidized low-density lipoprotein antibodies, and antimyeloperoxidase antibodies), endothelial dysfunction (flow-mediated dilatation and von Willebrand factor activity), and inflammation (C-reactive protein and fibrinogen) at 6 months and on long-term prognosis in CAD in comparison with OMT at 5 years of follow-up was evaluated. RESULTS: At 6 months, TMZ added to OMT significantly decreased the incidence of oxidative stress in CAD (P < 0.03) and reduced endothelial dysfunction and inflammation only in non-ST-elevation acute coronary syndrome (NSTE-ACS, P < 0.04). TMZ added to OMT with or without interventional/surgical vascularization led to decreased readmission for NSTE-ACS and heart failure (P < 0.05) in all patients with CAD and a significantly reduced incidence of cardiovascular death, acute myocardial infarction, and stroke (P < 0.05) in patients with NSTE-ACS at 5 years of follow-up. CONCLUSIONS: In patients with NSTE-ACS, TMZ added to OMT with or without interventional and/or surgical reperfusion reduced oxidative stress, endothelial dysfunction, inflammation, and major acute cardiovascular events, whereas in patients with chronic coronary syndrome, TMZ decreased oxidative stress and readmission for ACS and heart failure.
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Bobescu et al. (2021) conducted a cohort in Coronary artery disease (CAD) (n=570). Trimetazidine (TMZ) added to optimal medical therapy vs. Optimal medical therapy (OMT) alone was evaluated on Oxidative stress, endothelial dysfunction, inflammation at 6 months, and long-term prognosis (cardiovascular death, acute myocardial infarction, and stroke) at 5 years (p=<0.05). Trimetazidine added to optimal medical therapy significantly reduced oxidative stress, inflammation, and major acute cardiovascular events in patients with NSTE-ACS (P<0.05).
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