ArticleCommunications medicine2025
Long-term risk of malignancies in persons with ischemic heart disease treated with trimetazidine dihydrochloride.
Article in Communications medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundMetabolic reprogramming of energy processes is a cellular hallmark of various cancers. Whether trimetazidine, an anti-ischemic agent that preferentially potentiates cellular glucose oxidation, alters the long-term risk of malignancies is unknown.
methodsIn this multi-center, retrospective cohort study, we studied the effect of trimetazidine on new-onset malignancies in 200,563 ischemic heart disease patients (mean age 70.8 years, 46.6% female) using the Hong Kong Clinical Data Analysis and Reporting System (CDARS), comparing trimetazidine users (n = 16,873) to nitrate users (n = 183,690, as control) over at least 30 days. The primary endpoint was defined as the estimated effect of trimetazidine on the overall new-onset occurrence of any malignancies a priori specified, diagnosed 90 days or more after the cohort entry.
resultsOver a mean follow-up duration of 8.36 (6.42) years, the incidence rate of new-onset malignancies amongst trimetazidine users is significantly lower compared to the non-users (8.76 vs 12.3 per 1000-person years, trimetazidine to control incidence ratio, 0.71). Trimetazidine use is associated with improved event-free survival from new-onset malignancies (Mean survival: 231 [0.53] versus 225 [0.21] months, Chi-square = 161, P < 0.001). Multivariable Cox regression demonstrates an independently lower risk of new-onset malignancies associated with trimetazidine use, with (adjusted HRs, 0.71, 95% CI, 0.66-0.77, P < 0.001) and without (adjusted HRs, 0.71, 95% CI, 0.68-0.75, P < 0.001) propensity score matching. Subgroup analyses of new-onset malignancies including lung, colorectal, hepatobiliary & pancreatic, breast, stomach & oesophageal, renal & genito-urinary, prostate, and hematological malignancies, show similar risk reductions.
conclusionsModulation of metabolic reprogramming may represent a new therapeutic target for cancer prevention.
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