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Quetiapine in psychiatric practice: A narrative review on clinical efficacy, cardiac safety, and emerging therapeutic innovations
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Received: ,
Accepted: ,
How to cite this article: Koshy R, Perera PS, Jaxon A, George RT, Augusthy A, Thomas DS. Quetiapine in psychiatric practice: A narrative review on clinical efficacy, cardiac safety, and emerging therapeutic innovations. Arch Biol Psychiatry. doi: 10.25259/ABP_28_2025
Abstract
Quetiapine is an atypical antipsychotic widely prescribed for schizophrenia, bipolar disorder, and major depressive disorder, with off-label use for insomnia. Its active metabolite, norquetiapine, contributes additional antidepressant and anxiolytic benefits. In addition, recent advances have explored the development of electrochemical sensors to monitor quetiapine levels, as well as novel applications in delirium management in intensive care units and as an adjunct in breast cancer therapy. However, despite its clinical utility, quetiapine carries significant cardiovascular and metabolic risks, highlighting the importance of electrocardiogram and metabolic monitoring, particularly in vulnerable populations or in the context of overdose. This literature review gives an updated synthesis of the most recent data while critically assessing quetiapine’s therapeutic potential and safety profile. Important conclusions highlight that while low-dose quetiapine can effectively address insomnia and mood symptoms, careful patient selection and monitoring are essential to minimize adverse effects. By integrating pharmacological characteristics, emerging applications, and cardiovascular risk data, this review offers a comprehensive perspective to inform safe and effective quetiapine use in diverse clinical settings.
Keywords
Norquetiapine
Quetiapine advancements
Quetiapine cardiac effects
Quetiapine
Quetiapine side effects
INTRODUCTION
Quetiapine is approved as a first-line treatment for bipolar mania and depression, as well as an adjuvant for major depressive disorder. In 1997, the Food and Drug Administration authorized quetiapine, a commonly used second-generation antipsychotic (SGA). It was initially developed as a treatment for schizophrenia.[1] In addition to its antipsychotic effects, quetiapine exhibits sedative, hypnotic, and anxiolytic effects due to its significant affinity for serotonergic, histaminergic, and muscarinic receptors. Antipsychotics have generally been associated with an increased risk of cardiovascular morbidity and sudden cardiac death. Compared to other antipsychotics, quetiapine has not been associated with clinically significant QT prolongation; however, it has been demonstrated to cause weight gain and significant increases in triglyceride, total, and low-density lipoprotein cholesterol levels, all of which are important risk factors for the development of cardiovascular disease morbidity.[2]
Despite all of the indications, daily doses should not exceed 800 mg. It has a short half-life of 6–7 h, is rapidly absorbed, and reaches peak concentrations in 1–2 h. It is mostly removed by CYP3A4’s hepatic metabolism, with metabolites being expelled in the urine and stool. It functions as a noradrenaline reuptake inhibitor, muscarinic M1 antagonist, dopamine D2, serotonin 5HT2A (5-HT2C, 5-HT7), and 5HT1-A partial agonist. Quetiapine is less likely to cause extrapyramidal symptoms than other atypical antipsychotics.[3] However, there have been various cardiotoxicities associated with this drug.
The aim of this literature review is to critically discuss the clinical applications of quetiapine and to assess the adverse impact of this medicine on the cardiovascular system. The aim of a literature review is not to reveal new experimental findings, but to present, discuss, and analyze the available research to achieve a clear and exact idea regarding the beneficial aspects of this drug and its adverse side effects.
In examining the literature, this review will take into consideration the views of both patients and doctors to gain more insights into the practical difficulties that individuals face in the use of quetiapine, as well as understanding the reasons behind the possible association of the chemical, in whatever dosage, with terminal cardiovascular side effects. The main idea is to provide an overall overview of how the compound’s therapeutic effects have to be balanced against its cardiovascular safety risks.
In evaluating the related literature, the value of this paper will be based on the opportunity to evaluate the viewpoints of both the patient and the physician in relation to the resultant problems that can arise when taking the discussed drug. Thereby, the key focus will be on defining the ways in which, despite the relatively moderate dosages that can be effective when taking quetiapine, severe or terminal cardiovascular side effects can arise. The need for this study is that, through the assessment of both patient and physician perspectives, as well as clinical and pharmacovigilance information, this review will offer a more comprehensive insight into the occurrence of serious cardiovascular events despite standard therapeutic use. Ultimately, this research is imperative for the development of safer prescribing practices and future research regarding the cardiovascular risk associated with quetiapine.
MATERIAL AND METHODS
A comprehensive literature search was done across databases such as PubMed, Google Scholar, and Embase for papers published from 2008 to 2025. We conducted the search on databases using keywords such as quetiapine, quetiapine fumarate, norquetiapine, insomnia, cardiotoxicity, cardiac effects, side effects, sedative, corrected QT (QTc) prolongation, and quetiapine advancements. This study was conducted from June 2025 to September 2025. Narrative reviews, case reports for evidence, meta-analysis, and controlled trials were considered during the search method.
This narrative review was done by finding evidence, which was undertaken in a structured but flexible way. The titles and abstracts retrieved from the initial search were screened for relevance to the pharmacological properties, sedative effects, cardiac safety, and adverse effects of quetiapine.
The articles were then screened for inclusion in the review according to the following inclusion criteria: studies involving quetiapine or its active metabolite, norquetiapine; studies assessing cardiac outcomes, including changes in the QTc interval, arrhythmias, or cardiotoxicity; studies investigating sedative responses or off-label use in insomnia; and studies offering clinical, pharmacological, or mechanistic information. Narrative reviews, case reports, observational studies, meta-analyses, randomized controlled trials, and preclinical studies were regarded as providing a comprehensive understanding of the subject.
RESULTS
Quetiapine composition and mode of action
Quetiapine is a psychoactive substance that is a member of the dibenzothiazepine derivative chemical class. It is found as a fumarate salt in tablets. With a log P of 0.45, quetiapine fumarate is soluble in water. It is thermally stable up to 200°C and has a melting point of 176°C.[4] Depending on the patient’s characteristics, the severity of the illness, etc., it is given in pills, solutions, or suspensions at varying dosages. It is a dopamine D1 and D2 receptor (DRD1 and DRD2) antagonist and a serotonin 5-HT2 receptor antagonist (HTR2) with affinity for other receptors, including histamine H1, muscarinic M1, M3, and M5, α1-adrenergic, and other serotonin receptors, though its exact mode of action is still up for debate.[5] In addition to quetiapine, its active metabolite, norquetiapine have affinities to dopamine D1 and D2 receptors and brain serotonin 5-HT2A, which are thought to support its clinical antipsychotic effectiveness while lowering the risk of extrapyramidal side effects. In addition, quetiapine is widely used at lower doses in routine clinical practice for insomnia, anxiety, and psychomotor agitation, most likely because of its sedative effect from H1 histamine receptor antagonism, anxiolytic effect from norepinephrine reuptake inhibition, and serotonergic 5-HT1A agonism.[6]
Applications of quetiapine
Insomnia
Quetiapine works well as a medication to promote sleep. A good night’s sleep is necessary for improved performance and wellness.[7] Lower dosages of quetiapine (around 25–100 mg daily) are known to mediate sedative effects by predominantly affecting alpha 1 and alpha 2 adrenergic receptors as well as histaminergic (H1) receptors.[8] In doing so, quetiapine can lengthen overall sleep duration and enhance sleep architecture. N2 sleep has been found to rise, and some research indicates that sleep efficiency has improved.[9] Furthermore, the half-life of the parent molecule of quetiapine is 7 h, and the drug’s oral bioavailability in tablet form is nearly 100% of its oral solution bioavailability. Hence, it takes 1–2 h for the immediate-release form to reach its maximum plasma concentration at just 50 mg, which is in line with the receptor profile for potent hypnotic effects even at the lowest therapeutic doses.[1,8] This property of quetiapine makes it ideal for patients with insomnia to help regulate their sleep schedules. The reason quetiapine is typically prescribed at lower dosages for insomnia is that norquetiapine has a high affinity for norepinephrine transporter (NET) and increases synaptic norepinephrine levels, which can sometimes diminish the sedative effects of quetiapine at higher dosages [Figure 1].[1]
- Applications of quetiapine. NET: Norepinephrine transporter, SN: Salience network, BPSD: Behavioral and psychological symptoms of dementia.
Bipolar disorder (BD)
According to a study finding, using sertraline and quetiapine together considerably lowered Hamilton anxiety scale and Hamilton depression scale scores when compared to using sertraline alone, which may have a synergistic effect on lowering depressive and anxious symptoms. In stroke patients, sertraline and quetiapine medications greatly reduced symptoms of anxiety, depression, and mood disorders. Nevertheless, this investigation found no evidence that quetiapine administration in combination affects the likelihood of developing BD in patients with a lengthy history of anxiety disorder.[10] Studies on how lithium or quetiapine affects indicators of gray matter network characteristics in manic patients in vivo are scarce. We hypothesized that six weeks of lithium or quetiapine treatment would result in changes in the global topological metrics as well as regional nodal centralities of key brain regions of the salience network (SN) such as the insula and anterior cingulate cortex, and that these changes would be related to reductions in the severity of mania symptoms, since both drugs have been shown to have effects on brain anatomy and function in prior research.[11] The Food and Drug Administration (FDA) has approved quetiapine for the treatment of adult patients with BD and schizophrenia.[12] A primary limitation noted is that there is no substantiation that quetiapine administration affects the liability of developing bipolar disorder in cases with a long history of affective disorder.[10] Likewise,exploration regarding the use of quetiapine on Argentine matter network characteristics in manic cases in vivo remains scarce.[11] Therefore, while quetiapine is FDA-approved for BD, its role in altering disorder progression in high-threat affective populations remains unproven.[10,11]
Dementia
Quetiapine is a better option for treating Behavioral and Psychological Symptoms of Dementia (BPSD) in Lewy body dementia and Parkinson’s disease with dementia, since it has fewer extrapyramidal adverse effects than other atypical antipsychotic drugs (except for clozapine). The Brief Psychiatric Rating Scale (BPRS), Clinical Global Impression of Change (CGI-C), and Neuropsychiatric Inventory (NPI) all show no evidence of quetiapine’s ability to treat psychosis or agitation. The literature that is now available does not support the use of quetiapine in the treatment of BPSD; instead, there are safer medications such as carbamazepine, citalopram, memantine, and cholinesterase inhibitors, as well as more effective medications like risperidone.[13] The limitation of quetiapine in this environment is that the detailed Psychiatric Rating Scale, CGI-C, and NPI show no substantiation of its capability to treat psychosis or agitation in these cases. Furthermore, current literature does not support its use for BPSD, as they are safer, and many other effective drugs such as risperidone, citalopram, and memantine are available too. Accordingly, quetiapine should only be considered when the threat of extrapyramidal side effects from other antipsychotics outweighs its lack of proven efficacity in treating dementia-related agitation.[13,14]
Post-traumatic stress disorder
Two studies found quetiapine to be useful in treating flashbacks, while one study found it to be effective in treating anxiety. In every study that examined them, quetiapine also showed promise in reducing symptoms of psychosis and depression. The entire dose range of quetiapine (25–800 mg/d) is included in the research. Nonetheless, the five studies’ dose mean values, which vary from 100 to 258 mg/d, are typically modest, indicating that quetiapine may still be useful for treating symptoms at low to moderate levels.[12]The limitation of quetiapine in this environment is that the detailed Psychiatric Rating Scale, CGI-C, and NPI show no substantiation of its capability to treat psychosis or agitation in these cases. Furthermore, current literature does not support its use for BPSD as they are safer, and many other effective drugs such as risperidone, citalopram, and memantine are available too (new-3). Accordingly, quetiapine should only be considered when the threat of extrapyramidal side effects from other antipsychotics outweighs its lack of proven efficacy in treating dementia-related agitation [Table 1].[13]
| Condition | Typical dosage | Primary mechanism/benefits | Key limitations and notes |
|---|---|---|---|
| Insomnia | Low (25–100 mg) | Antagonist at H1, alpha 1, and 2 receptors; increases sleep duration and N2 sleep. | High doses may decrease sedation due to norquetiapine’s NET affinity. |
| Bipolar disorder | Variable | FDA-approved; reduces mania and depressive symptoms; synergistic with sertraline. | No evidence that it prevents the development of BD in patients with long-term affective disorders. |
| Dementia (BPSD) | Low | Preferred for Lewy Body/Parkinson’s due to low extrapyramidal side effects. | Lacks proven efficacy for psychosis or agitation; risperidone or citalopram are often preferred. |
| PTSD | 100–258 mg (Mean) | Effective for flashbacks, anxiety, and depressive symptoms within PTSD clusters. | Requires further clinical verification; most effective at low-to-moderate doses. |
NET: Norepinephrine transporter, FDA: Food and Drug Administration, BD: Bipolar disorder, BPSD: Behavioral and psychological symptoms of dementia, PTSD: Post-traumatic stress disorder.
Cardiotoxicity of quetiapine
A SGA medication, quetiapine, is frequently used to treat a range of mental illnesses due to its excellent safety record.[15]At lower dosages, quetiapine effectively treats insomnia by causing sedative effects and substantial occupancy of the H1 and 5-HT2C receptors.[7] Coma, respiratory depression, hypotension, tachycardia, and QTc interval prolongation on the electrocardiogram (ECG) are all frequently linked to quetiapine overdose.[3] It must be taken with other medications for quetiapine poisoning to be lethal. Although cardiac arrhythmias, coma, and death have occasionally been documented, sedation or hypotension and tachycardia are the usual symptoms of an acute overdose [Figure 2].[16]
- Adverse effects of quetiapine. QTc: Corrected QT interval, ECG: Electrocardiogram.
One atypical antipsychotic medication is quetiapine. It blocks a number of neurotransmitter receptors in the brain, such as histamine (H1), dopamine (D2), serotonin (5-HT2A, 5-HT2C), alpha-adrenergic (α1, α2), and muscarinic acetylcholine (M1, M3) receptors, with minor agonism of 5-HT1A receptors. Because of its poor affinity for beta-adrenergic receptors, quetiapine inhibits the central sympathetic nervous system. Since quetiapine also binds to α2 adrenergic receptors, the increased expression of these receptors in the brainstem may cause hypotension and bradycardia.[15] Although quetiapine’s calming effect is caused by blocking histamine-1 receptors, the ether-a-go-go-related gene is channel inhibited, which can lead to arrhythmogenic consequences. This could affect the QT interval.[16]
In relation to a suicide attempt, the patient recalls swallowing a full bottle of her mother’s quetiapine 50 mg pills, or 3g (total dosage). When the ECG was performed 16 h after the initial tracing, it showed no acute ischemia alterations or ST-segment deviations, a prolonged QTc of 470 ms, and a normal sinus rhythm of 83 bpm.[3] According to the most recent diagnostic standards, a QTc interval is deemed “prolonged” if it is >450 ms for men and 470 ms for women.[17] A premature atrial beat brought on by an ectopic focus, which results in Ectopic Atrial Rhythm (EAR), near the atrioventricular (AV) junction, especially at the bottom of the atria because of the negative P wave, is compatible with the first ECG, which was taken 30 min after the quetiapine was consumed. Since a QRS complex is always present, preserving AV synchronization, it is also evident that the ectopic depolarization was successfully carried out to the ventricles. EAR is one of the conduction anomalies that might result from quetiapine’s increased cardiac muscarinic obstruction. Through muscarinic M2 receptors, the parasympathetic nervous system produces its cardiac action. If these receptors are blocked, a vagal withdrawal would provide an ectopic stimulus, which would result in an EAR.[3] By detecting QT interval prolongation early, precautionary ECG monitoring lowers the risk of ventricular arrhythmia in individuals receiving quetiapine treatment.[18] Due to the potential delayed effect of QT prolongation, which only manifested in the second trace, 17 h after the suicide attempt, this case further highlights the significance of ECG monitoring following the intake of high dosages of quetiapine.[3] A ventricular arrhythmia called torsade de pointes (TdP), which can result in sudden death, is one of the most serious effects of a prolonged QT interval.[17] There are occurrences of quetiapine-related TdP that have been documented; they have involved therapeutic dosages of the drug combined with a variety of contributing variables (like hypokalemia) or with the co-ingestion of much more likely causative medicines (like citalopram).[18]
It has also been reported that quetiapine causes cardiomyopathy. Drug-induced cardiotoxicity is largely caused by oxidative and nitrative changes to important mitochondrial proteins. An energy imbalance, mitochondrial dysfunction, stress-related signaling pathway activation, p53 accumulation, and cellular death are all consequences of oxidative stress brought on by increased free radical formation in cardiomyocytes.[19] Numerous investigations have documented the cardiotoxicity of antipsychotics from a clinical standpoint. These cardiovascular impacts include variations in blood pressure and heart rate, as well as more serious and deadly conditions such as congestive heart failure and QTc prolongation. There have also been reports of quetiapine-induced bradycardia in older people, where a time-sequential improvement was attained following a reduction in medication dosage. An exclusive article also detailed the example of a 37-year-old woman who took large doses of quetiapine and developed cardiomyopathy; she recovered over the course of the following months after stopping the medication.[20] An intriguing case study is a 75-year-old male retiree who has been treated with 200 mg of quetiapine daily for his history of depression and bipolar illness, which is characterized by severe to moderate manic episodes. When his son discovered him lying on the floor in a semi-deep coma, he was living alone with the occasional housekeeper’s assistance. Extremely severe quetiapine intoxication is reported in this case. A coma and an elevated QT-interval that resulted in a cardiac arrest were among the potential side effects mentioned; they were only alleviated by prompt medical attention. Oxygenation, ventilation, hemodynamic support, gastrointestinal lavage, and the injection of activated charcoal under continuous ECG monitoring were all components of a successful treatment [Figure 3].[21]
- Drug-induced cardiotoxicity.
The use of quetiapine was linked to an increased risk of stroke, hypertensive heart disease, and coronary artery disease in a study of 284,234 non-elderly individuals in the United States, which included 12,094 patients treated with quetiapine and 253,027 taking antidepressants.[22] At lesser dosages, quetiapine can have additional negative effects in addition to the dangers of sedation and daytime sleepiness. The risk of acute cardiovascular events is increased by weight gain, hyperglycemia, and dyslipidemia, as well as orthostatic hypotension and cognitive impairment, which are especially concerning in older individuals.[23] It may appear strange that quetiapine’s relationship with dyslipidemia would raise the risk (in intent-to-treat analysis) of major adverse cardiovascular events and cardiovascular death, but not of non-fatal myocardial infarction or ischemic stroke.[22] It has been demonstrated that low-dose quetiapine use raises the risk of myocardial infarction and ischemic stroke.[23]
Current updates of quetiapine
Some interesting updates on quetiapine have been reviewed in this study. First, the study done by Nazari et al.[24](2023) showcases a highly specific electrochemical sensor for the identification and detection of quetiapine that has been developed. Because quetiapine is an electroactive material, electrochemical techniques can be used to measure it. Among the techniques used to determine this substance are spectrophotometry, high-performance liquid chromatography, fluorescence spectroscopy, and polarography. C-C3N4/Li2FeMn3O8 was effectively employed as a suitable modifier in the carbon paste electrode production method for quetiapine drug quantification and identification with good performance because of its appropriate structure, high surface area, and exceptional catalytic impact.[24] Second, targeting DNA repair, apoptosis, and cancer cell migration, quetiapine provides a unique, multipronged strategy to enhance outcomes in this high-risk subtype of breast cancer.[25] Finally, given its encouraging effects in lowering agitation and delirium duration, quetiapine appears to be a sensible choice for treating delirium in intensive care unit patients. Overall, it seems to have an acceptable safety profile, with generally controllable side effects.[26]
DISCUSSION
While quetiapine is often used, the current literature supporting its efficacy and safety in the long term is still limited. A subsequent study assessing patients with chronic insomnia who received atypical antipsychotics, such as quetiapine, did show improvements in subjective and objective measures of sleep over time, suggesting possible efficacy in selected patients.[27] However, due to several limitations such as small sample size and lack of randomization, the results of this study cannot be generalized. The effectiveness of low-dose quetiapine in treating primary insomnia has not been consistently demonstrated by randomized controlled trials. Improvements in total sleep time and sleep latency were not significantly different from placebo in a double-blind, placebo-controlled study evaluating quetiapine 25 mg in patients with primary insomnia, indicating that quetiapine is not therapeutically effective at the usual hypnotic doses used to treat insomnia.[28]Furthermore, clinical reviews have indicated that the majority of studies are small, short-term, or uncontrolled and that the evidence currently available for quetiapine’s effectiveness in treating insomnia is of low quality and insufficient.[29,30]Moreover, meta-analytic results also indicate that although quetiapine may have a positive effect on subjective sleep quality and total sleep time in more general psychiatric populations, these effects are also often associated with a greater risk of adverse events and treatment discontinuation.[31] Safety issues are of particular concern when considering long-term or off-label prescribing. A systematic review of case reports has identified withdrawal symptoms such as rebound insomnia, nausea, agitation, and tachycardia after abrupt discontinuation of quetiapine, which may indicate physiological dependence and the need for gradual tapering approaches.[32] These results are of concern in light of the widespread off-label prescribing of quetiapine in older populations. In general, there is no support for the use of quetiapine in the treatment of primary insomnia in the current literature, given the lack of efficacy and the important safety issues.
CONCLUSION
Quetiapine is a dose-related psychotropic drug with a wide range of applications. At low doses, its antihistamine and α-adrenergic properties make it useful in the treatment of insomnia and as an adjunct in PTSD. At higher doses, it is still an FDA-approved drug for the management of BD and schizophrenia, often in combination with selective serotonin reuptake inhibitor (SSRIs). Some new applications are being explored in the field of oncology and intensive care unit delirium. Nevertheless, the drug’s benefits must be carefully considered in the context of its risks, such as QTc interval prolongation, arrhythmias, and long-term metabolic disturbances such as weight gain and hyperlipidemia.
Ethical approval:
Institutional Review Board approval is not required.
Declaration of patient consent:
Patient’s consent is not required as there are no patients in this study.
Conflicts of interest:
There are no conflicts of interest.
Use of artificial intelligence (AI)-assisted technology for manuscript preparation:
The authors confirm that there was no use of artificial intelligence (AI)-assisted technology for assisting in the writing or editing of the manuscript and no images were manipulated using AI.
Financial support and sponsorship: Nil.
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