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Associations of schizophrenia with arrhythmic disorders and electrocardiogram traits: genetic exploration of
Jorien L Treur1, Anaïs B Thijssen1, Dirk J A Smit1
1Genetic Epidemiology, Department of Psychiatry, Amsterdam UMC, University of Amsterdam, The Netherlands.
Insights
Schizophrenia liability increases Brugada syndrome risk, suggesting a genetic link between the conditions. This finding highlights the need for cardiac monitoring in schizophrenia patients.
Area of Science:
- Genetics
- Psychiatry
- Cardiology
Background:
- Sudden cardiac death contributes to reduced life expectancy in schizophrenia patients.
- Arrhythmic disorders are implicated, but the schizophrenia-arrhythmia relationship is unclear.
Purpose of the Study:
- To investigate shared genetic liability between schizophrenia and cardiac arrhythmias.
- To explore potential causal effects between schizophrenia, arrhythmias, and electrocardiogram (ECG) traits.
Main Methods:
- Utilized large-scale genome-wide association study data for schizophrenia, atrial fibrillation, Brugada syndrome, and ECG traits.
- Assessed genetic correlations and performed functional annotation.
- Employed Mendelian randomization to explore bidirectional causal relationships.
Main Results:
- No global genetic correlation found, except between schizophrenia and Brugada syndrome (r_g = 0.14).
- Identified significant local genetic correlations between schizophrenia and cardiac traits, with overrepresented immune/viral response genes.
- Schizophrenia liability causally increases Brugada syndrome risk (beta = 0.14) and heart rate during activity (beta = 0.25).
Conclusions:
- Specific genomic regions and pathways link schizophrenia and arrhythmia, despite limited global genetic correlation.
- The causal effect of schizophrenia on Brugada syndrome necessitates enhanced cardiac monitoring and early intervention for schizophrenia patients.
Background:
An important contributor to the decreased life expectancy of individuals with schizophrenia is sudden cardiac death. Arrhythmic disorders may play an important role herein, but the nature of the relationship between schizophrenia and arrhythmia is unclear.
Aims:
To assess shared genetic liability and potential causal effects between schizophrenia and arrhythmic disorders and electrocardiogram (ECG) traits.
Method:
We leveraged summary-level data of large-scale genome-wide association studies of schizophrenia (53 386 cases, 77 258 controls), arrhythmic disorders (atrial fibrillation, 55 114 cases, 482 295 controls; Brugada syndrome, 2820 cases, 10 001 controls) and ECG traits (heart rate (variability), PR interval, QT interval, JT interval and QRS duration, n = 46 952-293 051). We examined shared genetic liability by assessing global and local genetic correlations and conducting functional annotation. Bidirectional causal relations between schizophrenia and arrhythmic disorders and ECG traits were explored using Mendelian randomisation.
Results:
There was no evidence for global genetic correlation, except between schizophrenia and Brugada syndrome (rg = 0.14, 95% CIs = 0.06-0.22, P = 4.0E-04). In contrast, strong positive and negative local correlations between schizophrenia and all cardiac traits were found across the genome. In the most strongly associated regions, genes related to immune and viral response mechanisms were overrepresented. Mendelian randomisation indicated that liability to schizophrenia causally increases Brugada syndrome risk (beta = 0.14, CIs = 0.03-0.25, P = 0.009) and heart rate during activity (beta = 0.25, CIs = 0.05-0.45, P = 0.015).
Conclusions:
Despite little evidence for global genetic correlation, specific genomic regions and biological pathways emerged that are important for both schizophrenia and arrhythmia. The putative causal effect of liability to schizophrenia on Brugada syndrome warrants increased cardiac monitoring and early medical intervention in people with schizophrenia.
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