Study of Oxygen Deprived V307L Mutated Cardiac Ventricular Cell

Introduction: Arrhythmia is an irregular heartbeat. Arrhythmias occur when the electrical signals that coordinate the heartbeat do not work properly. Cardiac arrhythmia can develop as a result of tissue damage, medication exposure, or genetic mutation. Bradycardia and tachycardia are caused by poor signaling. Heart arrhythmias are often categorized according to how quickly the heart beats. The average heartbeat is between 70 and 80 beats per minute. The difference between tachycardia and bradycardia is the speed of the heartbeat. Some cardiac arrhythmias can be fatal. A person's heart rate might be rapid or sluggish, though, and that is normal. For instance, the heart rate may rise during physical activity or fall during sleep. Surgery, medical treatments, implanted devices, and anti-arrhythmic medications are all used in treatment. An analysis of the changes in output based on changes in input constitutes a computational study, which is essentially the modeling of a biological system as a set of differential equations. To comprehend the impact of oxygen deprivation in a cardiac ventricular cell with the V307L mutation, simulation research is conducted. The action potential duration is longer in cells with oxygen deprivation than it is in cells with the V307L mutation. The oxygen deprivation in V307L mutant cells was investigated under heterozygous, homozygous, and wild-type conditions. It has been found that the Action Potential Duration (APD) of oxygen-deprived heterozygous and homozygous cells is roughly 250 ms, leading us to draw the conclusion that, although oxygen deprivation causes a longer APD and the V307L mutation causes a shorter APD, the combination of the two causes Short QT Syndrome. The spike of the action potential shows a minor alteration. Objectives: To Study the effect of V307L mutation in a cardiac ventricular cell, To Study the effect of oxygen deprivation in a cardiac ventricular cell, and To Study the effect of oxygen deprivation in V307L mutated cardiac ventricular cell. Methods: The investigation, acquisition, and advancement of knowledge regarding physiological systems are made possible through mathematical modelling. As a result, modelling is an effective technique for gaining access to the oxygen depreviated V307L cardiac ventricular cell. Additionally, using models to mimic various scenarios allows for the reconstruction of experiments and comparison of the results. The genetic mutation effect is simulated by adding the alterations to the slow delayed rectifier potassium current (IKs). In particular, the IKs expression was modified to take into consideration the experimental values of SQT2-linked KCNQ1 V 307 L mutation as noted by Bellocq et al. There are four mutation states of interest, viz. 2wild-type (WT). Results: The percentage difference of the APD in wild-type (WT) and Het mutation is presented in Table II. The findings show that there is almost similar percentage of change in APD of M-cells when fac = 0.6 to that of the endocardial and epicardial cells. Nonetheless, the longer the fac value, the more the APD of M-cells extends. With the increase in APD, the absolute difference of APD decreases as well as the percentage change in a WT and Het case. Conclusions: A computational study is carried out to understand the effect of oxygen deprivation in V307L mutated cardiac ventricular cell. In V307L mutated cell the action potential duration is shorter and in Oxygen deprived cell the action potential duration is longer. Heterozygous, homozygous and wild type conditions of V307L mutated cell were considered and oxygen deprivation in both the conditions of mutated cells were studied. It is observed that Action Potential Duration of oxygen deprived heterozygous and homozygous cells are approximately 250ms and so we may conclude that oxygen deprivation results in longer Action Potential Duration, V307L mutation gives shorter Action Potential Duration, Combination of both have Short QT Syndrome (SQTS) in Action Potential Duration when compared to the normal cells.