Objective: To determine the frequency and spectrum of myocardial dysfunction in patients with severe sepsis and septic shock using transthoracic echocardiography and to evaluate the impact of the myocardial dysfunction types on mortality. Patients and Methods: A prospective study of 106 patients with severe sepsis or septic shock was conducted from August 1, 2007, to January 31, 2009. All patients underwent transthoracic echocardiography within 24 hours of admission to the intensive care unit. Myocardial dysfunction was classified as left ventricular (LV) diastolic, LV systolic, and right ventricular (RV) dysfunction. Frequency of myocardial dysfunction was calculated, and demographic, hemodynamic, and physiologic variables and mortality were compared between the myocardial dysfunction types and patients without cardiac dysfunction. Results: The frequency of myocardial dysfunction in patients with severe sepsis or septic shock was 64% (nϭ68). Left ventricular diastolic dysfunction was present in 39 patients (37%), LV systolic dysfunction in 29 (27%), and RV dysfunction in 33 (31%). There was significant overlap. The 30-day and 1-year mortality rates were 36% and 57%, respectively. There was no difference in mortality between patients with normal myocardial function and those with left, right, or any ventricular dysfunction. Conclusion: Myocardial dysfunction is frequent in patients with severe sepsis or septic shock and has a wide spectrum including LV diastolic, LV systolic, and RV dysfunction types. Although evaluation for the presence and type of myocardial dysfunction is important for tailoring specific therapy, its presence in patients with severe sepsis and septic shock was not associated with increased 30-day or 1-year mortality. M yocardial dysfunction in sepsis is one of the most complex organ failures to characterize because of the dynamic adaptation of the cardiovascular system to the disease process, host response, and resuscitation. The pathophysiology of this entity is complex and multifactorial. Systemic, extracellular, and cellular mechanisms have been described, including maldistribution of coronary blood flow, cytokine-induced (tumor necrosis factor ␣, interleukin 1␤, interleukin 6) neutrophil activation and myocardial injury, complement (C5a)-triggered myocyte contractile failure, calcium handling dysregulation, and cytopathic hypoxia due to mitochondrial dysfunction.

Whereas both leaflets tethering is related to preoperative ischemic MR, both leaflets tethering but with predominant contribution from augmented and progressive PML tethering is related to recurrent/persistent ischemic/functional MR late after surgical annuloplasty.

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