Effect of vitamin deficiency on electrocardiogram parameters

Objective: The aim of this study was evaluate the effect of vitamin deficiency on Electrocardiographic (ECG) parameters in adult patients diagnosed with vitamin deficiency. Materials and Methods: All patients over the age of 18 who applied to Cardiology, Internal Medicine and Family Medicine polyclinics between June 15, 2024 and January 15, 2025 and who required treatment due to vitamin deficiency (vitamin D, vitamin B12, folate) during their examinations were included in the study. All polyclinic patients outside the dates of June 15, 2024 and January 15, 2025, patients who applied to other polyclinics other than Internal Medicine and Cardiology Polyclinics between June 15, 2024 and January 15, 2025, patients whose vitamin values were not checked or electrocardiography was not taken after their polyclinic application, patients who did not accept to participate in the study and patients under the age of 18 were not included in the study. The patients' age, gender, weight, height, hemogram, biochemistry and ECG results were recorded. Three months later, the ECGs and blood tests of patients who were called for a polyclinic checkup with vitamin deficiency and those in a similar group with normal vitamin values were recorded again for control purposes. Results: In the group with vitamin B12 deficiency, the QTc interval was found to be significantly longer (414.42 ± 24.04 ms vs. 407.50 ± 21.45 ms; p = 0.041), while the ejection fraction (EF) was significantly higher (60.60 ± 3.28% vs. 59.05 ± 3.27%; p = 0.005). Additionally, in the B12-deficient group, the QT/QTc ratio was lower (0.913 ± 0.06 vs. 0.937 ± 0.05; p = 0.022), and the FVDFB (an indicator of ventricular diastolic function) was significantly lower (149.85 ± 19.70 vs. 158.76 ± 24.86; p = 0.017). Correlation analysis revealed negative associations between vitamin B12 levels and BMI (r = –0.209; p = 0.010), QTc (r = –0.159; p = 0.005), and EF (r = –0.224; p = 0.006). In our study, the mean age was significantly lower in the folic acid deficiency group compared to the control group (folate deficiency: 51.09 ± 16.75 years; control: 58.47 ± 12.96 years; p = 0.010). Regarding biochemical parameters, the folate-deficient group exhibited significantly lower levels of AST (17.72 ± 6.25 vs. 19.65 ± 6.31; p = 0.016), total cholesterol (181.06 ± 50.75 vs. 207.20 ± 48.76; p = 0.002), triglycerides (146.82 ± 138.10 vs. 153.24 ± 78.31; p = 0.034), and LDL cholesterol (102.24 ± 38.23 vs. 125.47 ± 41.9; p = 0.001) compared to the control group. Furthermore, positive correlations were identified between folate levels and total cholesterol (r = 0.284; p < 0.001) as well as LDL cholesterol (r = 0.312; p < 0.001). Evaluation of ECG parameters demonstrated that the S-wave amplitude was lower in the folate-deficient group (3.81 ± 2.76 vs. 4.69 ± 3.29; p = 0.057), while the R/S ratio was significantly higher (2.32 ± 1.99 vs. 1.68 ± 1.47; p = 0.047). In the vitamin D deficiency group, the mean age was also significantly lower (51.52 ± 15.69 vs. 58.42 ± 13.60; p = 0.04). Examination of chronic diseases revealed higher rates of hyperlipidemia (33.3% vs. 50.7%; p = 0.032) and coronary artery disease (25.3% vs. 41.3%; p = 0.038) in the group without vitamin D deficiency. In terms of biochemical parameters, creatinine (0.72 [0.48–1.16] vs. 0.85 [0.50–1.84]; p = 0.005), BUN (24.18 ± 8.40 vs. 31.75 ± 10.61; p < 0.001), and GGT (15 [6–48] vs. 18.80 [9–191]; p = 0.047) levels were significantly lower in the vitamin D deficiency group. Conversely, BMI (29.64 ± 5.57 vs. 27.06 ± 3.98; p = 0.02) and GFR (98.44 ± 17.16 vs. 87.20 ± 25.24; p = 0.002) were significantly higher in the vitamin D deficiency group. Assessment of ECG parameters showed that the PR interval was significantly shorter (147.83 ± 20.71 vs. 161.07 ± 23.55; p < 0.001), S-wave amplitude was lower (3 [1–17] vs. 4 [1–16]; p = 0.001), Tp-e/QTc ratio tended to be lower (0.18 [0.09–0.50]; p = 0.052), and the R/S ratio was significantly higher (1.4 [0.17–10]; p = 0.001) in the vitamin D deficiency group. Conclusion: Taken together, these results indicate that vitamin deficiencies may contribute to impaired cardiac electrical activity, thereby potentially increasing the risk of arrhythmogenesis. Keywords: Vitamin Deficiency, Electrocardiography, Family Medicine, Preventive Medicine