This study aimed to investigate the electrocardiographic (ECG) and biochemical changes induced by azithromycin administration in rats and to evaluate the potential protective effect of L-carnitine. Twenty-four male Wistar Albino rats were randomly divided into four groups (n=6): Control, Azithromycin (30 mg/kg/day, orally, 14 days), Azithromycin + L-Carnitine (100 mg/kg/day, i.p., 14 days), and L-Carnitine. ECG recordings were obtained and serum high-sensitivity cardiac troponin T (hs-cTnT), conventional cardiac enzymes (aspartate aminotransferase [AST], creatine kinase [CK], and lactate dehydrogenase [LDH]) and lipid profile (total cholesterol, triglycerides, high-density lipoprotein [HDL], and low-density lipoprotein [LDL]) were measured. In contrast to the prevailing view in the literature, significant shortening of QT and corrected QT (QTc) intervals was detected in the azithromycin group compared to the control group (78.00±6.07 ms and 175.08±16.37 ms, respectively; p<0.001). ST segment elevation was observed in 100% of the azithromycin group, while L-carnitine co-administration reduced this rate to 50% (p<0.05). Biochemically, hs-cTnT levels in the azithromycin group showed approximately a 6-fold increase compared to the control group (3861.50±2087.96 pg/mL; p<0.05); L-carnitine treatment significantly suppressed this elevation. No significant difference was found between groups in conventional enzymes and lipid profile (p>0.05). Azithromycin has been linked to an increased risk of adverse cardiac events, including potential myocardial injury, which?in the acute period?is characterized by QT shortening and ST elevation rather than QT prolongation. L-carnitine appears to confer partial protection against this cardiotoxicity by preserving myocardial integrity. hs-cTnT was found to be a more sensitive marker in reflecting myocardial damage compared to conventional enzymes and lipid parameters.