Role of beta-blocker therapy on the sympathetic effects in stroke heart syndrome

Background: Sympathetic activation, inflammation, and neuro-endocrine response after an ischemic stroke contribute to the development of the stroke heart syndrome (SHS). One marker of SHS is a troponin “rise and fall pattern” > 30%. Among the beta-blocker drugs, the β1 antagonist class has a selective effect on the heart against sympathetic neurotransmitters. The aim of this study is to evaluate the possible role of pre-stroke chronic cardioselective β1 blocker treatment (B1B) in preventing SHS. Methods: We retrospectively analyzed data of 891 acute stroke patients admitted to the stroke unit at the University Hospital of Trieste (Italy) between 2018 and 2020. In total, 490 patients met the inclusion criteria. Clinical data, imaging characteristics and markers of cardiac injury (troponin I [TnI], N-terminal fragment of B type natriuretic peptide (NT-proBNP), and “rise and fall pattern” > 30%) and the chronic pre-stroke use of B1B were collected. We compared SHS against lack of SHS (no-SHS), subsequently examining the data through a multivariable analysis to determine possible SHS predictive factors. Results: No association between chronic B1B pre-stroke use and SHS (odds ratio [OR] 1.031; 95% confidence interval [CI] 0.636–1.672; p = 0.900) has been observed. The same result has been found in a sub-analysis on patients with chronic heart failure characterized by high NT-proBNP levels (> 900 pg/mL; n = 212), in which no association between chronic pre-stroke use of B1B and SHS (OR 0.807; 95% CI 0.449–1.451; p = 0.474) was identified. Conclusions: In our single-center retrospective cohort, a pre-stroke chronic B1B treatment seems not to prevent the development of SHS, including in patients with NT-proBNP > 900 pg/mL with chronic heart failure. These results should be confirmed by future randomized controlled trials to better understand the lack of effect of beta blockers on SHS.