Coronary artery disease (CAD) remains a leading cause of global morbidity and mortality, mostly attributable to atherosclerosis, oxidative stress, and inflammation. L-carnitine (LC), a naturally occurring amino acid derivative involved in mitochondrial fatty acid transport, has been proposed as a cardioprotective adjunct due to reported antioxidant and anti-inflammatory effects. This systematic review, published in Inflammopharmacology, aimed to integrate mechanistic findings with clinical outcomes related to LC supplementation in CAD while critically assessing inconsistencies across the literature.

A systematic literature search of PubMed and Google Scholar was conducted through July 2025. Eligible publications included animal studies, case reports, randomized controlled trials, cross-sectional and observational studies, retrospective analyses, and prior systematic reviews or meta-analyses that examined LC effects on cardiac function, inflammation, oxidative stress, or clinical outcomes in CAD. Non-English articles, studies outside scope, and those without translations were excluded. Twenty-one studies met inclusion criteria. 

Across mechanistic endpoints, LC supplementation was associated with reductions in oxidative stress indices, inflammatory markers, and biomarkers of myocardial injury. Several clinical trials also reported improvements in left ventricular function and lipid profiles. Regarding clinical outcomes, meta-analyses indicated reductions in ventricular arrhythmias, all-cause mortality, and anginal episodes among CAD patients receiving LC. However, findings were inconsistent for heart failure progression and myocardial reinfarction, with no uniform benefit demonstrated across studies.

Overall, LC supplementation demonstrated potential cardioprotective signals in CAD, though variability across outcomes and study designs limits definitive conclusions. Further large-scale, long-term randomized trials are needed to clarify its role across diverse CAD populations.