Effects of Lurasidone on Left Ventricle Systolic Functions

Lurasidone is an atypical antipsychotic drug used both on patients with schizophrenia or bipolar disorder. It improves patients' clinical symptoms through dopamine D2 and serotonin 5-HT2A receptor antagonism. However, the effect of antipsychotic drugs on cardiac functions is an important parameter for patient safety during the treatment process. Although the existing literature on the cardiac effects of lurasidone is limited, atypical antipsychotic are known to cause corrected QT interval prolongation, arrhythmias and suppression on cardiac functions. Studies show that these cardiac side effects are mostly related to clozapine which is a D2 and 5-HT2A antagonist such as lurasidone. Though not fully understood, it is thought that cardiac events due to antipsychotic drugs occur because of type 1 hypersensitivity and rising levels of pro-inflammatory cytokines. It might also be related to ischemia that free oxygen radicals initiate at the molecular level. D2 receptors play a critical role in the regulation of heart rate and vascular tone. D2 receptor antagonism may increase the risk of hypertension by changing systemic vascular resistance and heart rate. In addition, inhibition of D2 receptors may lead to loss of the vasodilator effects of dopamine, leading to impaired cardiovascular homeostasis. Similarly 5-HT2A receptors have important effects of cardiac functions. 5-HT2A receptor antagonism, together with imbalances in serotonin levels, may increase heart rate and affect vascular tone, leading to vasoconstriction. It is possible that the increase in systemic vascular resistance and cardiac inotropy through receptor antagonism may cause deterioration in cardiac functions and should be considered in clinical follow-up. There are a limited number of studies examining the potential effects of lurasidone on cardiac functions. For example, one study reported that lurasidone treatment did not cause a significant prolongation of the QTc interval, while another study reported that the overall cardiac safety profile of lurasidone use was quite favorable. However, more data are needed to compare cardiac side effects between lurasidone and other antipsychotics and how these effects should be managed in clinical practice. The aim of this study is to gain information about the possible cardiac effects of the lurasidone molecule by evaluating left ventricular systolic function with the help of periodic transthoracic echocardiography. In particular, clarifying the potential risks of lurasidone on cardiac health and the clinical significance of these risks is important both to increase patient safety and to optimize treatment processes.