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Many patients with septic shock and increased cardiac troponin I (cTnI) do not exhibit significant left ventricular systolic dysfunction. We hypothesized that an isolated and reversible impairment of ventricular relaxation may be associated with the increase in cTnI.Prospective, observational study.Surgical intensive care unit in a university hospital.Total of 54 patients with septic shock.Fractional area change, early diastolic velocity of mitral annulus, flow propagation velocity of early diastolic mitral inflow, cTnI, tumor necrosis factor-α, interleukin (IL)-6, -1β, -8, and -10 were measured at days 1, 2, 3, 4, 7, and 10 after onset of septic shock. Patients were classified into three groups: normal cTnI (group 1), increased cTnI and fractional area change <50% (group 2), and increased cTnI and fractional area change >50% (group 3).A total of 22 patients had an increase in cTnI, 11 with both systolic and diastolic dysfunctions and 11 with isolated impairment of left ventricular relaxation. At day 1, early diastolic velocity of mitral annulus and flow propagation velocity of early diastolic mitral inflow were significantly lower and tumor necrosis factor-α, IL-8, and IL-10 significantly higher in groups 2 and 3 compared with group 1. With resolution of septic shock, early diastolic velocity of mitral annulus and flow propagation velocity of early diastolic mitral inflow measured in patients of groups 2 and 3 returned progressively to values observed in group 1, with a parallel normalization of tumor necrosis factor-α, IL-8, and IL-10.Isolated and reversible impairment of left ventricular relaxation, associated with transient increases in cTnI, tumor necrosis factor-α, IL-8, and IL-10, was observed in 20% of patients with septic shock.