## 4 Discussion  
As the early detection of SCA is critical, yet not well established, the overall intention of this study was to determine the earliest time-frame prior to the onset of SCA in which ECG changes pertaining \begin{table}
\begin{tabular}{c c c c} \hline
**Time Period** & **Accuracy** & **Sensitivity** & **Specificity** \\ \hline
9 min prior & 69.8\% & 62.8\% & 76.8\% \\
8 min prior & 72.8\% & 70.0\% & 75.7\% \\
7 min prior & 71.4\% & 65.3\% & 77.5\% \\
6 min prior & 68.8\% & 64.7\% & 72.8\% \\
5 min prior & 68.5\% & 61.8\% & 71.2\% \\
4 min prior & 70.3\% & 64.5\% & 76.2\% \\
3 min prior & 70.7\% & 57.5\% & 83.8\% \\
2 min prior & 71.1\% & 62.3\% & 79.8\% \\
1 min prior & 68.5\% & 57.8\% & 79.2\% \\ \hline \end{tabular}
\end{table} 
Table 1: _Cont._  
\begin{table}
\begin{tabular}{c c c c c c c} \hline  & \multicolumn{3}{c}{**Linear SVM**} & \multicolumn{3}{c}{**Non-Linear SVM**} \\ \cline{2-7}
**Time Period** & **Accuracy** & **Sensitivity** & **Specificity** & **Accuracy** & **Sensitivity** & **Specificity** \\ \hline
3 h prior & 61.8\% & 50.5\% & 73.5\% & 78.4\% & 75.8\% & 80.2\% \\
2 h prior & 68.7\% & 63.7\% & 73.7\% & 77.8\% & 84.3\% & 71.2\% \\
1 h prior & 75.3\% & 73.5\% & 76.0\% & 77.1\% & 77.5\% & 7  
to SCA can be detected. Statistical comparison of the importance of each feature in comparison to a normal patient population, with a focus on time-based detection was also pertinent to this study. **Heart Rate. ** The first feature investigated in this study was mean resting heart rate, where patients in the SCA cohort exhibited a higher mean resting heart rate compared to the normal patient cohort. This correlated with literature findings, however, a larger difference between the SCA and normal cohort was observed in this study compared to previously conducted studies (18.9 vs. 7.5 bpm increase in the SCA cohort) [22]. The mean heart rate was then found to gradually increase and decrease between 3 h prior to SCA onset before exhibiting a sudden drop during SCA onset. There was a statistically significant difference in the mean resting heart rate observed between the two cohorts at 3 h and 6 min prior to SCA onset. However, after further statistical analysis statistical significance was only achieved at 3 h prior to SCA onset and as the \(p\)-value obtained was close to the cutoff value of 0.05, the findings should be considered as only marginally significant. The mean resting heart rate is an important marker as it both contributes to and reflects cardiovascular pathophysiology [23]. Heart rate is controlled by neural influences, where under normal physiological conditions the resting heart is under parasympathetic control, as proven in studies involving the pharmacological blockade of the autonomic influences with atropine [24]. The initial increase in heart rate observed occurs as a result of the patient's underlying cardiovascular disease, where there is a chronic imbalance between the sympathetic and parasympathetic control of the heart. The late decrease observed just prior to SCA onset may be attributed to two mechanisms. The first suggested mechanism is vagal withdrawal, which occurs as a result of contraction-perfusion mismatch and, consequently missed baroreflex input. A high heart rate results in a decrease in the diastolic perfusion time resulting in hemodynamically-insufficient ventricular contractions [25]. Overall, it leads to deleterious effects on the overall cardiac output and ultimately results in hemodynamic collapse and the functional deterioration of the heart. The second suggested mechanism is due to premature ventricular contraction-mediated disturbance of the cardiac cycle. The increased sympathetic output due to CVD results in the heightened electrical instability of the heart. This in turn gives rise of premature ventricular contractions (PVC), which are early depolarizations originating from the ventricle [26]. PVCs result in the delayed activation of the ventricular myocardium as depolarizations from the sinoatrial node are unable to reach the ventricles.