Amisulpride and symptomatic bradycardia: a case report

Huang, Li-Chung; Huang, Li‐Chun; Tseng, Shih-Yen; Hou, Yuh‐Ming; Hsiao, Chih‐Cheng

doi:10.1016/j.genhosppsych.2013.12.005

Cited by 11 publications

(11 citation statements)

References 15 publications

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“…In previous studies, it has been observed that subpopulations of SCZ patients manifested a significant decrease in resting heart rate and disease progressed to sinus bradycardia after taking SGAs, while other patients taking the same medicines did not show any abnormalities in heart rhythm. Similar phenomena have been reported by researchers around the world without studying the mechanisms that drive them [13]. Sinus bradycardia is defined as a mean sinus rate of less than 60 beats per minute and is a commonly observed arrhythmia.…”

Section: Introductionsupporting

confidence: 67%

Genome-wide association study of antipsychotic-induced sinus bradycardia in Chinese schizophrenia patients

Weng

Wang

et al. 2021

PLoS ONE

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Second-generation antipsychotics (SGAs) play a critical role in current treatment of schizophrenia (SCZ). It has been observed that sinus bradycardia, rare but in certain situations life threatening adverse drug reaction, can be induced by SGAs across different schizophrenia populations. However, the roles of genetic factors in this phenomenon have not been studied yet. In the present study, a genome-wide association study of single nucleotide polymorphisms (SNPs) was performed on Chinese Han SCZ patients to identify susceptibility loci that were associated with sinus bradycardia induced by SGAs. This study applied microarray to obtain genotype profiles of 88 Han Chinese SCZ patients. Our results found that there were no SNPs had genome-wide significant association with sinus bradycardia induced by SGAs. The top GWAS hit located in gene KIAA0247, which mainly regulated by the tumor suppressor P53 and thus plays a role in carcinogenesis based on resent research and it should not be a susceptibility locus to sinus bradycardia induced by SGAs. Using gene-set functional analysis, we tested that if top 500 SNPs mapped genes were relevant to sinus bradycardia. The result of gene prioritization analysis showed CTNNA3 was strongly correlated with sinus bradycardia, hinting it was a susceptibility gene of this ADR. Our study provides a preliminary study of genetic variants associated with sinus bradycardia induced by SGAs in Han Chinese SCZ patients. The discovery of a possible susceptibility gene shed light on further study of this adverse drug reaction in Han Chinese SCZ patients.

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Section: Introductionsupporting

confidence: 67%

Genome-wide association study of antipsychotic-induced sinus bradycardia in Chinese schizophrenia patients

Weng

Wang

et al. 2021

PLoS ONE

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“…Bradycardia: Some cases also reported antipsychotic impacts on lowering the HR, particularly SGAs such as risperidone[ 12 ], quetiapine[ 13 ], amisulpride[ 14 ], olanzapine[ 15 ], and paradoxically clozapine[ 16 ]. These cases were mostly elderly patients with signs abated after discontinuation of drugs.…”

Section: Clinical Manifestations Of Antipsychotics Cardiotoxicitymentioning

confidence: 99%

“…Quetiapine-induced bradycardia has also been reported in elderly patients, in which settings, a time sequential improvement was achieved after decreasing the drug dosage[ 13 ]. A male patient developed symptomatic bradycardia during usage of amisulpride (400-800 mg/d), which dramatically improved after the complete termination of amisulpride usage[ 14 ]. An 84-year-old patient presented with conscious depression, bradycardia (40 beats/min), hypotension, miosis, and hypothermia after 2.5 mg/day olanzapine therapy, and his condition improved with supportive therapy[ 15 ].…”

Section: Clinical Manifestations Of Antipsychotics Cardiotoxicitymentioning

confidence: 99%

Antipsychotics cardiotoxicity: What's known and what's next

Li¹,

Tang²,

Li³

2021

WJP

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Chronic use of antipsychotic medications entails a dilemma between the benefit of alleviating psychotic symptoms and the risk of troubling, sometimes life-shortening adverse effects. Antipsychotic-induced cardiotoxicity is one of the most life-threatening adverse effects that raises widespread concerns. These cardiotoxic effects range from arrhythmia to heart failure in the clinic, with myocarditis/cardiomyopathy, ischemic injuries, and unexplained cardiac lesions as the pathological bases. Multiple mechanisms have been proposed to underlie antipsychotic cardiotoxicity. This review aims to summarize the clinical signs and pathological changes of antipsychotic cardiotoxicity and introduce recent progress in understanding the underlying mechanisms at both the subcellular organelle level and the molecular level. We also provide an up-to-date perspective on future clinical monitoring and therapeutic strategies for antipsychotic cardiotoxicity. We propose that third-generation antipsychotics or drug adjuvant therapy, such as cannabinoid receptor modulators that confer dual benefits — i.e. , alleviating cardiotoxicity and improving metabolic disorders — deserve further clinical evaluation and marketing.

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“…Another case of amisulpride therapeutic dose-induced asymptomatic bradycardia has also been reported (Prikryl et al, 2011). More than that, the recent report pointed out amisulpride can even cause symptomatic bradycardia (Huang et al, 2015). Cardiovascular side effects of amisulpride even in therapeutic dose may need stringent monitoring.…”

mentioning

confidence: 92%