Key result
Electroconvulsive therapy did not cause a relevant increase in high-sensitive cardiac troponin I, but resulted in higher mean NT-proBNP levels of uncertain clinical relevance.
Why the study?
Does electroconvulsive therapy cause myocardial damage as measured by hscTnI and NT-proBNP in patients undergoing the procedure?
Observational (n=23)
Does electroconvulsive therapy cause myocardial damage as measured by hscTnI and NT-proBNP in patients undergoing the procedure?
Electroconvulsive therapy does not appear to cause acute myocardial damage as measured by hsTnI, though it may lead to increases in NT-proBNP of unclear clinical significance.
Answers are grounded in this paper and cite their sources.
ECT may not cause myocardial injury; leaves open the relevance of NT-proBNP rises and need for prospective safety studies.
Electroconvulsive therapy (ECT) is a remarkably safe procedure. However, there might exist a subgroup of patients with an increased risk for cardiovascular events. The cardiac-specific enzymes high-sensitive cardiac troponin I (hscTnI) and N-terminal pro-B-type natriuretic peptide (NT-proBNP) were measured before and after ECT in 23 patients. No relevant increase of hscTnI after ECT was found. Mean NT-proBNP levels were higher after ECT and in three patients a new NT-proBNP elevation after ECT was identified. In conclusion, our small study did not find any evidence for myocardial damage due to ECT by measuring hsTnI, but an increase of NT-proBNP, whose clinical relevance could only be speculated, yet.
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Kranaster et al. (2018) conducted an observational in Patients undergoing electroconvulsive therapy (n=23). Electroconvulsive therapy (ECT) vs. Before ECT (baseline) was evaluated on Myocardial damage assessed by high-sensitive cardiac troponin I (hscTnI) and N-terminal pro-B-type natriuretic peptide (NT-proBNP). Electroconvulsive therapy did not cause a relevant increase in high-sensitive cardiac troponin I, but resulted in higher mean NT-proBNP levels of uncertain clinical relevance.
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