Key result
Medicated patients with schizophrenia had significantly longer native myocardial T1 time compared with matched healthy controls (effect size d=0.89; p=0.02).
Why the study?
Preclinical evidence shows antipsychotics cause myocardial fibrosis and inflammation, but whether this occurs in patients with schizophrenia is unknown.
Does schizophrenia treated with antipsychotic drugs associate with myocardial fibrosis/inflammation and altered cardiac structure/function compared to matched healthy controls?
Case-Control (n=31)
Does schizophrenia treated with antipsychotic drugs associate with myocardial fibrosis/inflammation and altered cardiac structure/function compared to matched healthy controls?
Standardized Mean Difference: 0.89
p-value: p=0.02
Patients with schizophrenia taking antipsychotics exhibit early diffuse fibro-inflammatory myocardial changes and altered cardiac structure independent of established CVD risk factors.
Hypothesis-generating for myocardial changes in schizophrenia; larger prospective studies needed before clinical adoption.
Cardiovascular disease (CVD) is a major cause of excess mortality in schizophrenia. Preclinical evidence shows antipsychotics can cause myocardial fibrosis and myocardial inflammation in murine models, but it is not known if this is the case in patients. We therefore set out to determine if there is evidence of cardiac fibrosis and/or inflammation using cardiac MRI in medicated patients with schizophrenia compared with matched healthy controls. 31 participants (14 patients and 17 controls) underwent cardiac MRI assessing myocardial markers of fibrosis/inflammation, indexed by native myocardial T1 time, and cardiac structure (left ventricular (LV) mass) and function (left/right ventricular end-diastolic and end-systolic volumes, stroke volumes, and ejection fractions). Participants were physically fit, and matched for age, gender, smoking, blood pressure, BMI, HbA1c, ethnicity, and physical activity. Compared with controls, native myocardial T1 was significantly longer in patients with schizophrenia (effect size, d=0.89; p=0.02). Patients had significantly lower LV mass, and lower left/right ventricular end-diastolic and stroke volumes (effect sizes, d=0.86-1.08; all p-values <0.05). There were no significant differences in left/right end-systolic volumes and ejection fractions between groups (p>0.05). These results suggest an early diffuse fibro-inflammatory myocardial process in patients that is independent of established CVD-risk factors and could contribute to the excess cardiovascular mortality associated with schizophrenia. Future studies are required to determine if this is due to antipsychotic treatment or is intrinsic to schizophrenia.
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Pillinger et al. (2019) conducted a case-control in Schizophrenia (n=31). Schizophrenia treated with antipsychotic drugs vs. Matched healthy controls was evaluated on Native myocardial T1 time (d=0.89, p=0.02). Medicated patients with schizophrenia had significantly longer native myocardial T1 time compared with matched healthy controls (effect size d=0.89; p=0.02).
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