Monocyte-to-High-Density-Lipoprotein Ratio Is Associated with Ventricular Arrhythmia in Patients with Implantable Cardioverter-Defibrillators: A Cross-Sectional Study

Background: Residual arrhythmic risk persists in recipients of implantable cardioverter-defibrillators (ICDs) despite guideline-based selection, and inexpensive markers that refine this risk are needed. The monocyte-to-high-density-lipoprotein ratio (MHR) integrates a pro-inflammatory (monocyte) and an anti-inflammatory/antioxidant (HDL) signal in a single index derived from routine blood work. We examined whether MHR is associated with ventricular arrhythmia in ICD patients. Methods: In this cross-sectional study we assessed 382 ICD recipients attending a device outpatient clinic and classified them by a composite ventricular arrhythmia outcome (non-sustained ventricular tachycardia, sustained ventricular tachycardia, or ventricular fibrillation) documented on device interrogation. MHR and comparator inflammatory markers were measured at the same visit. Discrimination was assessed by receiver operating characteristic (ROC) analysis, the optimal threshold by the Youden index, and independence by multivariable logistic regression; internal validity was examined with repeated cross-validation, bootstrap optimism correction, and calibration testing. Results: The ventricular arrhythmia outcome was present in 58 patients (15.2%). MHR was higher in patients with the outcome (median 16.3 vs. 12.3, p < 0.001) and discriminated it with an area under the curve (AUC) of 0.756 (95% CI 0.673–0.828). At the optimal threshold of 15.71, sensitivity was 63.8% and specificity was 83.3%, with a negative predictive value of 92.8%; the outcome was present in 40.7% of patients above versus 7.2% below this cut-off. MHR remained independently associated with the outcome after adjustment for age, left ventricular ejection fraction, etiology, and renal function (odds ratio 1.23 per unit, 95% CI 1.16–1.32; p < 0.001) and outperformed high-sensitivity C-reactive protein (DeLong p < 0.001). Discrimination was preserved in both ischaemic and non-ischaemic cardiomyopathy without interaction by etiology (p = 0.67). The model was stable on internal validation (cross-validated AUC 0.761; optimism 0.021; Hosmer–Lemeshow p = 0.66). Conclusions: MHR is independently associated with documented ventricular arrhythmia in ICD patients and, being derived from routine tests, may warrant prospective evaluation as a low-cost adjunct for risk stratification.