Abnormal electrical conduction through the heart is associated with dangerous heart rhythms that can cause sudden death. At present, the exact causes of these abnormal heart rhythms are unknown, however research has shown that genetics plays a significant role in an individual's risk profile. Genes are made of DNA, and they provide instructions to make proteins which influence growth and development of all cells in the body. Small changes in the make up of a gene can alter its function or change the way it provides information to the body. It is becoming increasingly understood that a person's risk of sudden death is due to many small variations in genes combined rather than one single change. Electrocardiograms (ECGs) are a non-invasive method of recording electrical activity within the heart. Different time points on the ECG refer to when the bottom chambers of the heart (ventricles) contract to pump blood around the body, or relax to their resting state. The QRS interval on an ECG is related to ventricle contraction, while the JT interval is specific for when the ventricles return to their resting state. The QT interval refers to the period from the beginning of the QRS interval to the end of the JT interval. Another important marker which is calculated from many leads on an ECG is spatial QRS-T angle. This represents electrical conduction in the heart in a three dimensional manner during ventricle contraction and relaxation and could represent different biological processes compared with other ECG parameters. Changes in the duration of these ECG parameters are associated with the development of abnormal heart rhythms and sudden cardiac death. Previous smaller studies have identified genetic changes (variants) influencing the duration of QT, JT and QRS intervals however a large proportion of the genetic contribution to these ECG markers remains unexplained. This is likely due to the size of previous studies and lack of power to detect rare variants. We will conduct the largest study to date, for QT, JT and QRS intervals which will have greater power to detect variants that are as yet unidentified including less common or rare variants which may have a greater effect on the duration of these ECG traits. We will also perform a study to determine the genetic contribution to spatial QRST angle, which has never been studied before. As it offers a global assessment of cardiac ventricular conduction compared with other ECG traits, we anticipate we will identify new pathways and biological mechanisms for the generation of abnormal heart rhythms. Significant genetic variants identified from these studies will be extensively investigated using publically available datasets to map variants to pathways in cardiac function and arrhythmia generation. These analyses will help to improve our understanding of the role of these genetic variants in causing abnormal heart rhythms and could give insights into how to prevent or treat them in the future. We will also test for association between genetic variants and clinical outcomes including hospital admissions for abnormal heart rhythms, changes in heart chamber dimensions on scans and the risk of heart attacks or death. At present, current markers for predicting abnormal heart rhythms and sudden death are not specific or sensitive enough to be used to test the general population. This research is designed to identify new genetic contributions to abnormal heart rhythms in order to improve risk prediction for sudden cardiac death and other adverse cardiac events. It will help identify people in the general population who would benefit from early treatment or monitoring to prevent disease. The results will aid physician decision making and help us understand what influences the health of the general population and their risk of significant cardiac disease.