Relationship between premature ventricular complexes and Neutrophil– Lymphocyte Ratio in asymptomatic healthy young men

Background: There is no clear mortality benefit from premature ventricular beat (PVC) suppression in asymptomatic patients. In addition, It has been showed that evidence for structural heart disease consistent with non-ischemic scarring possibly due to inflammation in patients with PVCs. This situation suggests that the mechanisms by which PVCs can be also generated with include clinical and subclinical inflammation. The neutrophil–lymphocyte ratio (NLR) is an easy, cheap, non-invasive, and universally available laboratory marker used to evaluate clinical and subclinical systemic inflammation. We investigated the NLR in asymptomatic healthy young men with PVC (structural heart disease excluded with cardiac magnetic resonance imaging) compared with controls. Methods: 21 asymptomatic (or atypical complaint) healthy young men with PVCs were recruited into the study as they attended to Diyarbakır Military Hospital for screening from January 2013 to December 2014. The control group consisted of 922 male. Instead of Lown's grading of PVCs, we considered as endpoints > 153 PVC over 24 h (in Holter Electrocardiogram). Data were analysed with the SPSS software version 15.0 for Windows. Results: There were no significant differences between the 2 groups with respect to age, gender, body mass index, smoking, as well as glucose, creatinine, total cholesterol, triglyceride, LDL-C, HDL-C, haemoglobin levels, white blood cell count, and red cell distribution width. The NLR was significantly higher among the men with PVC than that of the control group (2.6 ±0.8 vs 2.1 ± 0.7, respectively; P = 0.002). Conclusions: We found that the NLR is significantly elevated in asymptomatic healthy young men with PVC compared with control group. The increased NLR values might indicate subclinical and clinical inflammation in asymptomatic healthy young men with PVC, and we must consider that there can also be inflammation in the one of the mechanisms of PVCs in humans