This is one of the first case-control studies to apply the relatively novel technology of STE in the diagnosis and monitoring of sepsis-induced myocardial depression in the adult population. There are two important conclusions. The first part of our study involved comparing the strain values in patients with septic shock and patients with sepsis only. We observed a significant difference in the measured GLS (–14.5 % vs –18.3 %, P < 0.001) between the two groups of patients. The strain value of –18.3 % in our control group is comparable to the previously reported range of –17 % to –23 % in normal healthy subjects [13, 14]. This is in contrast to patients with septic shock, where myocardial impairment is present, evidenced by the depressed strain value of –14.5 % in our study group. Importantly, conventional echocardiographic parameters of left ventricular function, including LVEF, FS, and LIMP, all failed to detect a difference between the two groups of patients. Our data mirror the findings from a pediatric population, reported by Basu et al. [15], where the GLS was –14.4 % in the septic group and –23.3 % in the control group (P < 0.001). Again, there was no significant difference in LVEF and FS between the two groups of patients.
Recent research has provided preliminary data indicating that strain may be sensitive to acute changes in load [16]. We undertook efforts to minimize the interplay of other hemodynamic variables on the measurement of cardiac strain. The cardiac preload in the study group was higher (7.4 mmHg vs 5.9 mmHg, P = 0.017), by a negligible absolute value of 1.5 mmHg, evidencing that these patients with hypotension have been adequately volume-resuscitated prior to echocardiographic analysis. All patients in the study group were instituted on vasopressors, with comparable afterload indices between the two groups (systemic vascular resistance 1090 dynes•sec/cm5 vs 1194 dynes•sec/cm5, P = 0.303; systemic vascular resistance index 1807 dynes•sec/cm5/m2 vs 1976 dynes•sec/cm5/m2, P = 0.333).
The second part of this study involved serial echocardiographic examinations in the group of patients with septic shock. In the patients who could be weaned off vasopressors by 72 hours, we observed a difference in strain values obtained at diagnosis and recovery (–14.6 % vs –16.0 %, P = 0.026). Nonsurvivors did not exhibit the improvement in myocardial strain at 72 hours (–15.3 % vs –15.8 %, P = 0.563). This supports the current understanding of septic cardiomyopathy as a reversible form of myocardial impairment during the sepsis syndrome.
The diagnosis of sepsis-induced myocardial impairment has been difficult without the availability of a sensitive and specific bedside diagnostic tool. One of the commonest measures of left ventricular function, LVEF, is affected to a significant degree by the changing preload and afterload in sepsis. Vieillard-Baron, in a series of echocardiography studies, showed that when performed at different times after the onset of septic shock, echocardiography yields different incidences of left ventricular dysfunction [17, 18]. In the first 6 hours of resuscitation, there was an 18 % incidence of decreased left ventricular ejection fraction; this rose to 40 % after 24 hours, and 60 % after 2–3 days. The postulation to explain this phenomenon was the increase in afterload with time, secondary to the vasopressors used for resuscitation, or the natural resolution of the disease. The authors concluded, in a review on septic cardiomyopathy [19], that the measurement of LVEF “actually reflects the (left ventricular) afterload rather than the intrinsic contractility”.
STE has emerged as a direct, angle-independent, and highly reproducible measurement of left ventricular function. Its application in conditions such as heart failure with preserved ejection fraction [20] has shown it to offer incremental and prognostic value in the assessment of left ventricular performance. GLS is the most commonly used strain-based measure of left ventricular global systolic function, and its use has been included in international echocardiography guidelines [8]. With the development in software technology, basic strain measurements may now be performed at the bedside, and our experience has shown it to be feasible with patients in septic shock admitted to the intensive care unit.
We managed to show how STE may be useful as a tool for diagnosis as well as disease monitoring in sepsis-induced myocardial impairment. It enables the detection of subtle left ventricular dysfunction early in the course of illness, which is not otherwise detected by measurement of LVEF alone, and further discriminates the reversibility of this condition in patients who subsequently recover. In demonstrating similar preload and afterload parameters in our study and control groups, we have eliminated possible interference by these factors in the measurement of strain. The proper identification and description of sepsis-induced myocardial impairment may have important therapeutic implications, guiding the use of cardioprotective strategies such as β-blockers in the management of patients with septic shock [21].
Our study has several limitations. First, the sample size was small, especially in the subgroup analyses. Second, as the timing of the reassessment echocardiogram as either when the patient came off inotropic or vasopressor support, or at 72 hours, was decided arbitrarily, we were unable to prove the complete reversibility of strain measurements to normal values upon recovery. Third, we did not have a resuscitation protocol for the choice and dose of inotropes and vasopressors. Finally, our data were not compared to more objective modalities of quantifying ventricular function, such as cardiovascular magnetic resonance imaging or radionuclide ventriculography.