The Effects of Head Impacts on QTVI in Soccer Players

Abstract

The QT variability index (QTVI) provides an estimation of the temporal variability in the myocardial repolarization process and has been shown to be a valid measure of cardiac autonomic function (CAF). Published data indicate elevated QTVI values are associated with an increased risk for ventricular arrhythmias. Fatal arrhythmia appears to be the most common mechanism of sudden cardiac death (SCD) in the athletic population. While the majority of SCD's are caused by definitive cardiovascular disorders found post‐mortem, the causes of many are unknown and left to speculation. Previous research has demonstrated a relationship of concussion to changes in QTVI, conceivably putting athletes, in particular, those in contact sports, at risk for dangerous arrhythmias and subsequent SCD. No study to date has investigated the relationship of sub‐concussive impacts to QTVI. The purpose of this study is to examine how sub‐concussive head impacts (HI) affect QTVI values. College‐aged male varsity soccer athletes (n = 24) were recruited to participate in the study. HI sustained during a collegiate soccer game were observed and quantified during a 90‐minute pre‐season match and symptoms experienced due to HI were documented by questionnaire. Athletes who did not play in the game were subsequently matched with non‐athlete gender‐, age‐ and body‐weight controls. Subjects were assigned to one of three groups: athletes who played (AP); athletes who did not play (ADNP); and control (CON). The AP group was further categorized by symptoms experienced from HI: athletes who did not experience HI (AP0), those who experienced at least one asymptomatic HI (AP1), and those who experienced at least one symptomatic HI (AP2). Pre‐ and 24‐hour post‐match mean resting heart rate (HR) and mean QT interval corrected for heart rate (QTc) were measured within a 120‐second interval of a resting single‐lead electrocardiogram using Power Lab/ECG Analysis Add‐On for LabChart 8 (ADInstruments). QTVI was calculated as the logarithm of the ratio between the variances of the normalized QT and RR intervals, using the equation QTVI = Log10[(QTv/QTm2)/(RRv/RRm2)] (where QTv is the QT interval variance, QTm is the mean QT interval, RRv is the RR interval variance, and RRm is the mean RR interval). Statistical analyses included Wilcoxon matched pairs tests to determine differences between individual pre‐and post‐match QTVI's, unpaired t‐tests to determine differences between AP, ADNP and CON group means, and ANOVA to determine differences among subgroups, pre‐ and post‐match. Statistical significance was set a‐priori at P < 0.05. No demographic differences were present among groups. At 24 hours post‐match, no differences were found in the variables measured: HR, QTc and QTVI values. No differences were found among subgroups and from pre‐ to post‐match. We conclude that the head impacts sustained during the collegiate soccer match were not forceful enough to provoke a significant change in QTVI from baseline within a 24‐hour period. However, head impacts that provoked symptoms appeared to slightly increase the QTVI from baseline within 24 hours. It is possible that a 24‐hour period is not enough time to establish if QTVI's are still rising, and if so, when they peak. Future research investigating the effects of sub‐concussive HI over a period of 48 hours is warranted.