A study published ahead-of-print in Circulation Arrhythmia and Electrophysiology has found that Brugada syndrome ECG is more prevalent among patients with schizophrenia than patients without schizophrenia. Use of sodium-channel blocking antipsychotics is not attributable to this prevalence.
“Emerging evidence indicates that schizophrenia and acute psychosis may impact on cardiac electrophysiology,” report Marieke T Blom (Heart Center, Department of Cardiology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands) and others. However, “The causes for sudden cardiac death-risk in schizophrenia are unresolved.” In this study, the authors aimed to establish whether ECG markers of risk of sudden cardiac death-particularly Brugada-ECG pattern-are more prevalent in schizophrenia patients than in non-schizophrenic controls.
In this cross-sectional study, the authors compared ECGs of a cohort of 275 schizophrenia patients from the Department of Severe Mental Illness, Mental Health Care Center, North Holland to ECGs of two cohorts of non-schizophrenia patients. One cohort (n=179), with participants without psyhcopathology from the ongoing longitudinal Netherlands study of depression and anxiety (NESDA) was age comparable with the schizophrenia group. The other control cohort (n=1,168) was 20 years older than the study cohort with participants randomly selected from the population in a region of the Netherlands (Hoorn study).
“Several studies suggested that schizophrenic patients have higher biologic age relative to their calendar age with commensurately increased prevalence of cardiovascular and metabolic disorders,” Blom et al write, for this reason they studied this second cohort.
Blom et al report that 32 patients (11.6%) in the schizophrenia group had Brugada-ECG at baseline (one had type 1 Brugada-ECG and 32 had type 2/3). This was significantly more than the two non-schizophrenia groups where no patients had type 1 Brugada ECG, while 2 (1.1%) patients (NESDA group) and 28 (2.4%) patients (Hoorn group) had type 2/3 Brugada-ECG. Furthermore, patients with schizophrenia had longer QT-interval, an increased proportion of mild or severe QTc-prolongation and higher heart rates than non-schizophrenic patients. Increased QTc-prolongation was, however, largely explained by confounding factors, including use of QTc-prolonging (antipsychotic) drugs.
“Many researchers ascribe sudden cardiac death in schizophrenia to antipsychotics,” note the authors. In this study, prevalence of Brugada-ECG was not attributed to the use of sodium-channel blocking medication (including antipsychotics). Therefore, “Future studies are required to establish the causes for the increased prevalence of Brugada-ECG or Brugada syndrome in schizophrenia,” Blom et al suggest.
“If proven in future studies that increased prevalence of Brugada-ECG in schizophrenia reflects increased prevalence of Brugada syndrome, this finding could contribute to a better understanding of excess sudden cardiac death-risk in schizophrenia patients,” the authors write. Due to the lack of data of family history of sudden cardiac death in the schizophrenia group, Blom et al comment, they could not establish a higher prevalence of Brugada syndrome in schizophrenia.
Hanno Tan, lead investigator of the study, (Department of Cardiology, Heart Center Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands) told Cardiac Rhythm News that one important implication for clinical practice is that “Brugada syndrome should be considered in families in which both sudden unexplained death and schizophrenia occur.”
