Medicated patients with schizophrenia exhibited significantly longer native myocardial T1 times compared to matched healthy controls (1212.38 vs 1190.96 ms, d = 0.89), indicating early diffuse myocardial fibrosis or inflammation.
Case-Control (n=31)
Single-blind
No
Do medicated patients with schizophrenia have evidence of cardiac fibrosis, inflammation, or altered cardiac structure and function on MRI compared to matched healthy controls?
Medicated patients with schizophrenia exhibit early diffuse fibro-inflammatory myocardial changes and altered cardiac structure on MRI compared to matched controls, independent of traditional cardiovascular risk factors.
Standardized Mean Difference: 0.89
Absolute Event Rate: 1212.38% vs 1190.96%
p-value: p=0.02
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. Thirty-one 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). 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.
Pillinger et al. (Fri,) conducted a case-control in Schizophrenia (n=31). Antipsychotic treatment in schizophrenia vs. Matched healthy controls was evaluated on Native myocardial T1 time (d = 0.89, p=0.02). Medicated patients with schizophrenia exhibited significantly longer native myocardial T1 times compared to matched healthy controls (1212.38 vs 1190.96 ms, d = 0.89), indicating early diffuse myocardial fibrosis or inflammation.