The patient WJT was 76 years old when he sustained two concussions within approximately 10 days: the first on 26th September and the second on 6th October 2016. These were later medically diagnosed as a concussion or mTBI. Because of his symptoms of increased ectopy and change in perception of cognitive function, WJT contacted us with concerns about his increased ectopy and malaise. WJT reported that these symptoms had been progressing over the past 5-6 months since his concussions. Symptoms included cognitive "deterioration," "not feeling well," headache, "lack of energy and fatigue," "irritability," signs of depression, and "acute audio sensitivity and poor visual acuity" which were the two most extreme, persistent and troubling symptoms that WJT experienced.
On 28th March 2017, he undertook a 24-hour Holter monitor which showed a high burden of ventricular ectopy at 9.4% (9,350/99,836 beats). This is in stark contrast to his 24-hour Holter in 2013 where there were negligible ectopic beats (Table 1; Figure 1). The patient was started on a beta-blocker Metoprolol daily 47.5 mg, but he was advised to stop taking angiotensin receptor blocker Losartan as his blood pressure would not sustain taking both medications.
In the coming months (May 2017), he performed another resting echocardiogram and exercise stress echocardiogram. Resting echocardiogram revealed that the left ventricle was normal in size and had low-normal systolic function with an estimated EF of 50%. There was considerable beat-to-beat variability depending on the degree of ectopy. Measurements included LVEDD = 5.1 cm; ESD = 3.1 cm; IVS = 1.1 cm; LVPW = 1.1 cm; and EF 50%. The patient completed 8 minutes of the Bruce protocol achieving 95% maximal predicted heart rate with blood pressure rising from rest at 138/70 to 182/85 mmHg at the termination of exercise. Again, adverse cardiac symptoms did not limit this test. WJT felt well throughout the stress test, and the resting monomorphic ventricular ectopy was resolved at peak stress. The ECG showed LBBB throughout the assessment. The impression of the stress echocardiogram at peak exercise suggested that there was an acceptable augmentation of wall thickening in all myocardial segments without clear evidence for ischaemia. Image quality was good. Thus, the exercise stress echocardiograph demonstrated a mild nonischaemic cardiomyopathy as previously known without significant ischaemia at stress and no significant change from 2013.
Although his May-June 2017 echocardiographic assessments and follow-up showed only minor changes from November 2013, the high percentage of ventricular ectopy (9.4%) was problematic for the patient. He stated that he had periods of depression. He did not feel right and expressed concerns about his cognition; again, this was likely a result of his two back-to-back concussions. Based on his description of symptoms that he was experiencing, it is likely that he had been suffering from postconcussion syndrome. The goal at this point was to try to suppress the significant number of ectopic beats. During the ensuing time period, WJT continue with the Metoprolol 47.5 mg daily and was referred for another 24-hour Holter monitoring.
The patients 24-hour Holter (6th July 2017) showed another significant increase in ventricular ectopy at 18.1% (Table 1; Figure 1). This was a significant increase from 9.4% recorded only 3 months prior on 28th March 2017. This increased ventricular ectopy also matched his persistent symptoms associated with postconcussion syndrome. Furthermore, there was a significant increase in both bigeminy and trigeminy ventricular ectopic beats (Figure 1) that was not apparent before his concussion head injury. To manage the significant increase in ventricular ectopy, the patient was prescribed Amiodarone 200 mg dose to suppress the high rate of ventricular ectopy that we believed was symptomatic and likely to be aggravating the preexisting modest LV dysfunction and his postconcussion symptoms. Patient WJT remained on Amiodarone from July 2017 to October 2017.
Within days of Amiodarone administration, our patient began feeling better, and interestingly, and remarkably, the patient reported that his intermittent cognitive impairment and mTBI/postconcussion symptomology that he experienced after his head injury had completely resolved. However, what patient WJT found to be most remarkable was that within days, "my most troubling concussion symptoms totally disappeared and simultaneously I could no longer physically detect any pronounced ventricular ectopic beats," which he was very sensitive to.
His follow-up 24-hour Holter monitor (25th October 2017) confirmed an absence of ventricular ectopy (0%; 1/89,189 beats). The resolution of the ventricular ectopy was successfully managed with Amiodarone, as was his postconcussion symptoms. He remained stabilised on the 200 mg dose of Amiodarone.
Because of the concern regarding the long-term side effects of Amiodarone, his dosage was dropped 100 mg and kept for 3 months and then dropped again to 50 mg thereafter (February 2018). WJT felt completely well on the 50 mg dose of Amiodarone for a good period of time (March to June 2018). Despite the substantial dose reduction, he remained free of any important ventricular ectopy with a very low burden of ventricular dysrhythmia (0.1%; 87/100, 487 beats) on his most recent 24-hour Holter monitor (23rd May 2018). At this time, the patient was stopped from taking Amiodarone completely and prescribed his longstanding Losartan 25 mg. His follow-up 24h-hour Holter monitor on 16th October 2018 showed that ventricular ectopy was 0.2% (167/98,937 beats). At this time, no further postconcussion symptoms were reported.
This was a retrospective study that was approved by a University Research Ethics Board (REB #2018-113), and all work was conducted in accordance with the Declaration of Helsinki (1964). The patient WJT provided his written informed consent to have all of his medical records available for this case study report. Patient WJT DOB is 23rd September 1940, and he was 76 years of age at the time of his two concussions within 10 days of each (26th September and 6th October 2016).
The data were acquired from all medical records from 1997 to 2018 and put into Microsoft Excel spreadsheet (Microsoft Office, Microsoft Corporation, Seattle, USA) for ease of data management and interpretation. The ventricular and supraventricular (atrial) data were taken from the 24-hour Holter monitor (Phillips Holter Monitoring Recorder, Phillips, New Zealand). Heart rate variability (HRV) data were taken from the printed Holter monitor report. We attempted to get the raw ECG data to conduct our own HRV analysis, but this was not possible due to restrictions of the manufacturer. HRV was not conducted during the preconcussion 24-hour Holter monitoring (4th November 2013). However, the HRV software was consistent for all recording dates after the concussions. Fast Fourier transformation using Welch's periodgram method for frequency-domain and time-domain spectral analyses was used to determine HRV metrics.
The results for this case study report are presented in Tables 1 and 2 and Figures 1 and 2. As noted in Table 1 and Figure 1, there was a significant increase in ventricular (VE) and supraventricular (SVE) ectopy within months of the patient sustaining his two concussions in September and October 2016. In addition to the VE and SVE, single prematureatrial contractions (PACs) and bigeminy and trigeminy beats were also significantly increased following the concussion incidents.  Table 2 and Figure 2 represent the heart rate variability (HRV) data. HRV was observed through spectral power analysis frequencies, being ultra-low frequency (0-0.003 Hz), very low frequency (VLF; 0.003-0.04 Hz), low frequency (LF; 0.04-0.15 Hz), and high frequency (HF; 0.15-0.4 Hz). Results showed that the LF : HF ratio, as assessed by the power of LF to HF, decreased with the reduction of ventricular ectopic beats.
The nonlinear analysis of the ECG has been used to derive HRV, by analyzing the variation in the R to R peaks of the ECG waveform. HRV has been used to reflect sympathetic and parasympathetic control and neurocardiac autonomic function. Changes in HRV are due to alterations in both low (LF) and high (HF) frequency, and research has shown that there is an increase in the LF : HF ratio in individuals with persistent ventricular ectopic beats. For our patient, ventricular ectopic events were highest on 28th March 2017 (9.4% ventricular ectopy) and 6th July 2017 (18% ventricular ectopy). Furthermore, this increase in the LF : HF ratio with an increase in ventricular ectopy does suggest a potential impairment in the sympathovagal balance of HRV. However, over the following one-year period, the LF : HF ratio decreased from 1.32 to 1.13 (Figure 2), suggesting a decreased reliance on LF dominance, and improved HRV/ANS function. LF power is a net effect of several intrinsic modulatory factors from both sympathetic and parasympathetic branches of the ANS, vagally mediated baroreflex, and even some respiratory influences at lower respiratory rates. All other time-domain analysis variables were unchanged from 28th March 2017 to 21st February 2018.