Background Hypertrophic cardiomyopathy (HCM) and obstructive sleep apnoea (OSA) are independently associated with increased risk of arrhythmic events. Oximetry based studies suggest a high prevalence of OSA in HCM. Signal Average ECG (SAECG) is a non-invasive method of detecting late ventricular potentials which are low-amplitude, high-frequency signals occurring in the terminal portion of the QRS complex, analysis of which may aid in predicting the risk of reentry ventricular arrhythmias and sudden cardiac death. SAECG parameter profiles in HCM with concurrent OSA have not been previously studied.

Methods In this prospective study, 84 patients with HCM (24 of whom had previously diagnosed OSA and were treated for this) underwent SAECG analysis. The 60 HCM patients with no prior history of OSA underwent polysomnography assessment to determine their OSA status and severity. The final sample included 58 males (69%). An Apnea Hypopnea Index (AHI) >5/Hr was considered diagnostic for OSA (5–15 mild, 15–30 moderate, >30 severe).

Results 62 (74%) subjects were found to have OSA (15 mild, 9 moderate, 14 severe, 24 treated). Subjects with OSA were older with higher BMI. For analysis, subjects were split into those without sleep apnoea, those with sleep apnoea and those with sleep apnoea on treatment. No significant differences were found between groups in filtered QRS duration nor terminal QRS duration however the root mean square voltage of the terminal 40 ms of the QRS segment was significantly lower in the sleep apnoea group (mean 36 msec) when compared to the non-OSA group (mean 56 msec, p=0.028) and lower still in the treated OSA group (mean 30 msec, p=0.007). Similarly, the mean voltage of the terminal 40 msec of the filtered QRS segment was significantly lower in the sleep apnoea group (mean 26μv) when compared to the non-OSA group (mean 39μv, p=0.034) and again was lower still in the treated OSA group (mean 22μv, p=0.007). Those subjects with sleep apnoea and with sleep apnoea on treatment were also found to have a higher prevalence of atrial fibrillation and a higher prevalence of family history of sudden death.

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Abstract 19 Figure 1

Conclusion Abnormal SAECG patterns with significantly reduced root mean square voltages and terminal 40 msec voltages are seen in those patients with HCM and concurrent OSA. These changes do not appear to reverse with treatment of OSA and in fact appear to shorten further still. The SAECG may prove useful as a marker of underlying sleep apnoea and also may provide utility in predicting an individual with HCM’s risk of developing arrhythmia particularly atrial fibrillation and potentially ventricular arrhythmia.

Conflict of Interest Nil