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• W4240420002 abstract "We thank Drs Orso and Copetti for their comments on our recent review in CHEST, summarizing the current understanding of molecular mechanisms and clinical implications of septic cardiomyopathy.1Martin L. Derwall M. Al Zoubi S. et al.The septic heart: current understanding of molecular mechanisms and clinical implications.Chest. 2019; 155: 427-437Abstract Full Text Full Text PDF PubMed Scopus (143) Google Scholar We agree with the authors that, among many factors/mechanisms causing sepsis-induced cardiac dysfunction, adrenergic overstimulation, due to endogenous elevated catecholamine levels and exogenous catecholamine administration, is thought to play a debatable role in the pathophysiology of septic cardiomyopathy. Indeed, blockade of β1-adrenergic receptor signaling and/or enhancement of cardiac β2-adrenergic receptor signaling could be potential therapeutic strategies to inhibit inflammation in the septic heart.2Drosatos K. Lymperopoulos A. Kennel P.J. et al.Pathophysiology of sepsis-related cardiac dysfunction: driven by inflammation, energy mismanagement, or both?.Curr Heart Fail Rep. 2015; 12: 130-140Crossref PubMed Scopus (125) Google Scholar Of note, despite the beneficial effects shown by experimental and a few (small) clinical trials, β-adrenergic blockade therapy in septic shock is not yet established, as results are conflicting3Suzuki T. Suzuki Y. Okuda J. et al.Sepsis-induced cardiac dysfunction and β-adrenergic blockade therapy for sepsis.J Intensive Care. 2017; 5: 22Crossref PubMed Scopus (73) Google Scholar: In particular, landiolol, a selective β1-blocker with a 4-min half-life, showed detrimental effects on cerebral oxygenation when therapy is aimed at attaining a certain heart rate.4Kurita T. Kawashima S. Morita K. et al.Use of a short-acting β1 blocker during endotoxemia may reduce cerebral tissue oxygenation if hemodynamics are depressed by a decrease in heart rate.Shock. 2017; 47: 765-771Crossref PubMed Scopus (10) Google Scholar Moreover, another study revealed that enteral metoprolol (a selective β1-blocker) therapy in patients with septic myocardial depression leads to a significant increase in the required doses of catecholamines.5Schmittinger C.A. Dünser M.W. Haller M. et al.Combined milrinone and enteral metoprolol therapy in patients with septic myocardial depression.Crit Care. 2008; 12: R99Crossref PubMed Scopus (78) Google Scholar In our opinion, further experimental and clinical research is required to elucidate a valid strategy to target the hyperactivation of the sympathetic nervous system during septic shock. This clearly includes not only β-adrenergic receptors but also α-adrenergic receptors (eg, the α2-adrenergic receptor), as there are increasing experimental data showing that α2-adrenergic blockade attenuates septic cardiomyopathy by increasing cardiac norepinephrine concentration and inhibiting cardiac endothelial activation.6Yu X. Wang Y. Yang D. et al.α2A-Adrenergic blockade attenuates septic cardiomyopathy by increasing cardiac norepinephrine concentration and inhibiting cardiac endothelial activation.Sci Rep. 2018; 8: 5478Crossref PubMed Scopus (14) Google Scholar We were encouraged to perform a concise review including treatment advances based on randomized controlled clinical trials, and thus our review focused on treatment strategies with existing robust clinical evidence. As mentioned in our article, we agree with Drs Orso and Copetti that adequately powered and well-performed randomized controlled trials are necessary to clarify the debatable role of β-blockers in septic cardiomyopathy therapy. The Septic Heart: Current Understanding of Molecular Mechanisms and Clinical ImplicationsCHESTVol. 155Issue 2PreviewSeptic cardiomyopathy is a key feature of sepsis-associated cardiovascular failure. Despite the lack of consistent diagnostic criteria, patients typically exhibit ventricular dilatation, reduced ventricular contractility, and/or both right and left ventricular dysfunction with a reduced response to volume infusion. Although there is solid evidence that the presence of septic cardiomyopathy is a relevant contributor to organ dysfunction and an important factor in the already complicated therapeutic management of patients with sepsis, there are still several questions to be asked: Which factors/mechanisms cause a cardiac dysfunction associated with sepsis? How do we diagnose septic cardiomyopathy? How do we treat septic cardiomyopathy? How does septic cardiomyopathy influence the long-term outcome of the patient? Each of these questions is interrelated, and the answers require a profound understanding of the underlying pathophysiology that involves a complex mix of systemic factors and molecular, metabolic, and structural changes of the cardiomyocyte. Full-Text PDF Adrenergic Overstimulation: A Neglected Mechanism of Sepsis-Related CardiomyopathyCHESTVol. 155Issue 3PreviewWe read with great interest the paper by Martin et al1 about septic cardiomyopathy in a recent issue of CHEST (February 2019). In particular, we were impressed by the examination of the etiopathologic mechanisms of sepsis-related cardiomyopathy. However, we think the effect produced by adrenergic stimulation in determining cardiac dysfunction in patients with sepsis has not been addressed. Continuous adrenergic overstimulation constitutes, in the stage immediately after the initial compensation phase, an activation of beta-1 receptors. Full-Text PDF" @default.
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• W4240420002 doi "https://doi.org/10.1016/j.chest.2018.10.018" @default.
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