Acute left ventricular dilation and septic shock-induced myocardial dysfunction.

In their recent article on septic myocardial dysfunction, Dr, Bouhemad and colleagues (1) demonstrate acute and reversible left ventricular (LV) dilation in patients with septic shock-induced cardiac dysfunction. According to the authors, this LV dilation was missed in several previous studies (especially by Vieillard-Baron and coworkers) essentially because patients with septic shock were considered as a single homogeneous population, whereas their data demonstrate that the concept of preload recruitment applies only to the subgroup of patients with (and, supposedly, in response to) systolic LV ejection impairment. This conclusion, however, was drawn from a selected group of eight patients only (those with increased troponin I and fractional area changes 50%) among 45 septic shock patients studied, and Figure 3 of their article actually shows that only two of those patients had LV end-diastolic area (LVEDA) 15 cm/m at day 1. In our opinion, the main information in the present data is confirmation that major LV dilation is not common or typical feature of septic heart. In opposition with authors’ statement, we doubt that a more aggressive fluid therapy would have resulted in even greater LV dilation in their patients: a 100% increase in LV enddiastolic volume, as initially described by Parker et al (2). In our study, quoted by Dr. Bouhemad and colleagues as one having reported “normal” values of LVEDA at the beginning of septic shock, initial measurements (LVEDA 9.6 3.6 cm/ m) were obtained when 13 of 15 patients were still fluid responsive (3). After successive 250 –500 mL volume loading steps were repeated in all patients until no increase in stroke volume was obtained, final measurements (12.8 3.7 cm/m) were consistent with moderate LV dilation occurring in some patients (3, 4) but were only marginally larger than those obtained before this last volume loading step, that is, at “optimal” preload (12.2 3.4 cm/m). Thus, as expected from physiology, fluid loading plays a crucial role in the occurrence of LV dilation, but distensibility of septic LV, even if moderately increased in some patients, is limited when preload has already been recruited by optimal fluid loading. The second point we would like to discuss is whether the data really support the view that LV dilation occurs as an adaptation in response to the impairment of systolic LV ejection allowing maintenance of cardiac output. This statement was based on the correlation found between LVEDA and aortic velocity time integral in group 2. However, in accordance with definition of LV systolic dysfunction in the study (an LV ejection fraction 50%), it is a negative correlation between LVEDA and fractional area change (the higher values of LVEDA associated with the lower values of FAC) that would support the “adaptation hypothesis. ” This correlation was not reported in the article, but it can be deduced from Figure 3 that such correlation did not exist in group 2. This absence of correlation is in fact consistent with previous findings showing that LV end-diastolic volume is not affected by changes in LV ejection fraction and cardiac output that occur with time in septic shock patients, notably when inotropic support or vasoconstrictor dosages are modified (5). It has been shown in an animal model of resuscitated septic shock that LV dilation developed early, before occurrence of systolic depression (6). Cellular mechanisms such as reduced myofilament responsiveness to Ca via increased phosphorylation of contractile proteins, which constitute a cellular basis for both increased LV distensibility and systolic depression, have been demonstrated in experimental sepsis (7). Accordingly, levosimendan, a Ca sensitizer, decreased LV enddiastolic volume and increased LV ejection fraction in patients with septic myocardial depression (8). Taken together, these data suggest that moderate LV dilation, secondary to increased LV distensibility and fluid administration, is not an adaptive mechanism but rather part of septic myocardial dysfunction. The data presented by Dr. Bouhemad and colleagues are consistent with this alternative hypothesis. The authors have not disclosed any potential conflicts of interest.