CHEST Guidelines-Response_chest

Response_chest_7

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In the February 2019 issue of CHEST, a paper by Martin et al. discussed septic cardiomyopathy, focusing on its etiopathologic mechanisms. A correspondence from Drs. Orso and Copetti highlights that the role of adrenergic overstimulation might be overlooked in assessing cardiac dysfunctions related to sepsis. They emphasize that continuous adrenergic stimulation activates beta-1 receptors, leading to myocardial damage, and suggests that exploring this aspect might be crucial for understanding not only the mechanisms of sepsis-induced damage but also that from other conditions like burns and trauma. They also propose that addressing this might improve therapeutic strategies for sepsis, potentially incorporating beta-blocking drugs like esmolol.<br /><br />In response, the original authors underscore the complexity surrounding adrenergic stimulation in septic cardiomyopathy and acknowledge that while experimental and small clinical trials suggest potential benefits from beta-blockade, results remain conflicting. They articulate that the complete therapeutic validity of beta-blockers for septic shock remains unverified, citing inconsistent findings about drugs like landiolol and metoprolol. They call for further research to assess strategies targeting sympathetic nervous system hyperactivation during sepsis, including a focus on both beta and alpha-adrenergic receptors.<br /><br />Overall, both correspondences agree on the need for more clinical research to verify the role of beta-blockers in septic cardiomyopathy and advocate for well-powered randomized controlled trials to better define therapy strategies. This exchange highlights ongoing debates and complexities in managing septic cardiomyopathy, underscoring the necessity for research to refine understanding and treatment approaches.

Keywords

septic cardiomyopathy

adrenergic overstimulation

beta-1 receptors

myocardial damage

beta-blockers

sepsis

therapeutic strategies

sympathetic nervous system

randomized controlled trials

cardiac dysfunctions