Circulating Neutrophil and Monocyte Counts Are Inversely Associated With Heart Rate Variability Indices: The Maastricht Study

Background Inflammatory biomarkers, including immune cells appear associated with reduced heart rate variability (HRV), an indicator of cardiac autonomic nervous dysfunction. However, the influence of leukocytes on HRV and their relation across sex and glucose metabolism status remains unclear. Hence, we sought to investigate the cross‐sectional association between leukocytes and HRV indices and their association across sex and glucose metabolism status in a general population. Methods We retrieved cross‐sectional data of 1888 participants of the Maastricht Study who completed the baseline survey between November 2010 and December 2017. Blood leukocyte numbers (including neutrophils, monocytes, basophils, eosinophils, and lymphocytes) were determined with an automated hematology analyzer. Qualitative changes within lymphocytes were assessed with flow cytometry. HRV indices were assessed using a 24‐hour ECG. Time‐domain and frequency‐domain HRV index average scores were calculated. We regressed HRV average scores on standardized leukocytes and adjusted the models for several covariates. Results In fully adjusted models, higher neutrophil (−0.07 [−0.11 to −0.03]; false discovery rate (FDR)‐corrected P value, P FDR =0.006) and monocyte (−0.05 [−0.09 to −0.02]; P FDR =0.020) counts were associated with a lower time‐domain average score. Higher neutrophil (−0.07 [−0.11 to −0.03]; P FDR =0.006) and monocyte (−0.05 [−0.09 to −0.01]; P FDR =0.020) counts were also associated with a lower frequency‐domain HRV index average score. No effect modification by either sex or glucose metabolism status was found ( P intFDR >0.05). There were no other associations between immune cells and HRV indices. Conclusions Higher neutrophil and monocyte counts were associated with lower HRV, irrespective of sex and glucose metabolism status. This suggests a role of these cells reflecting innate immune processes and inflammatory response in cardiac autonomic nervous dysfunction.