The Septic Heart

Septic 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. The afterload-related cardiac performance, together with speckle-tracking echocardiography, could provide methods to improve the diagnostic accuracy and guide therapeutic strategies in patients with septic cardiomyopathy. Because there are no specific/causal therapeutics for the treatment of septic cardiomyopathy, the current guidelines for the treatment of septic shock represent the cornerstone of septic cardiomyopathy therapy. This review provides an up-to-date overview of the current understanding of the pathophysiology, summarizes the evidence of currently available diagnostic tools and treatment options, and highlights the importance of further urgently needed studies aimed at improving diagnosis and investigating novel therapeutic targets for septic cardiomyopathy. Septic 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. The afterload-related cardiac performance, together with speckle-tracking echocardiography, could provide methods to improve the diagnostic accuracy and guide therapeutic strategies in patients with septic cardiomyopathy. Because there are no specific/causal therapeutics for the treatment of septic cardiomyopathy, the current guidelines for the treatment of septic shock represent the cornerstone of septic cardiomyopathy therapy. This review provides an up-to-date overview of the current understanding of the pathophysiology, summarizes the evidence of currently available diagnostic tools and treatment options, and highlights the importance of further urgently needed studies aimed at improving diagnosis and investigating novel therapeutic targets for septic cardiomyopathy. ResponseCHESTVol. 156Issue 3PreviewWe thank Dr Sanfilippo and colleagues for their comments on our review summarizing the current understanding of molecular mechanisms and clinical implications of septic cardiomyopathy.1 We fully agree with the authors that one of the main challenges in the definition of septic cardiomyopathy is the evaluation of cardiac function in the setting of highly variable preload and afterload conditions, as well as the lack of longitudinal echocardiography data starting from premorbid heart function. 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 The Challenging Diagnosis of Septic CardiomyopathyCHESTVol. 156Issue 3PreviewWe read with interest the “septic heart” review in the February issue of CHEST.1 The authors highlight the urgent need for a clear definition of septic cardiomyopathy. The main challenges in this definition are the evaluation of the cardiovascular context (in particular, evaluation of cardiac function in the setting of highly variable preload and afterload conditions), and the lack of longitudinal echocardiography data starting from premorbid heart function with serial echocardiographic evaluations performed during the course of the critical illness and eventually following recovery. Full-Text PDF ResponseCHESTVol. 155Issue 3PreviewWe 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.1 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. Full-Text PDF