Sudden cardiac arrest (SCA) is a worldwide public health problem and is the main cause of death from cardiovascular disease. Drugs, including noncardiac drugs (drugs to treat noncardiac conditions), may impact on the risk of the occurrence of SCA. This may be due to the ability of these drugs to modify the cardiac ion channels whose concerted activity underlies the cardiac action potential (AP) and the heart’s electrical properties. Several noncardiac drugs have been documented that could impact VF/SCA risk by interacting with cardiac ion channels such as IKr and INa (as an off-target effect). Thus, knowledge about the electrophysiological mechanism whereby a drug increases SCA risk (by blocking INa or IKr or by impacting on another ion channel) is important to design rational prevention strategies to avoid drug-induced SCA. In this thesis, we explored the possible mechanism whereby anti-epileptic drugs (carbamazepine, gabapentin, lamotrigine, levetiracetam, pregabalin, and valproic acid) and opioids (tramadol, codeine, and fentanyl) increase the risk of SCA, and sulfonylurea antidiabetics (glibenclamide, gliclazide, glimepiride, and tolbutamide) decrease the risk of SCA, on a cellular level. In the end, we found anti-epileptic drugs (carbamazepine, lamotrigine, and valproic acid) and opioid (tramadol) have effect on cardiac ion channels properties reflecting on APs. Sulfonylurea antidiabetics were studied on ischemia-induced shortening of action potential duration in human induced pluripotent stem cell-derived cardiomyocytes and found only glibenclamide significantly rescued this shortening.