To the Editor:—

We congratulate Vieillard-Baron et al.  1for the article entitled “Early Preload Adaptation in Septic Shock? A Transesophageal Echocardiographic Study.” The authors of this study were unable to confirm the concept of early preload adaptation by left ventricular dilatation in septic shock as described by Parrillo et al.  2,3Vieillard-Baron et al.  1conclude that systolic function was the unique determinant of stroke index in septic shock. We have two comments regarding this study.

First, the conclusion is based on the validity of an accurate measurement of left ventricular end-diastolic volume by transesophageal echocardiography in patients with septic shock. Indeed, to our knowledge, the relation between the true left ventricular end-diastolic volume and the left ventricular end-diastolic volume and areas measured using transesophageal echocardiography has not been analyzed in patients with septic shock. Therefore, we are not sure about the validity of these results, and it cannot be excluded that transesophageal echocardiography techniques possibly underestimate left ventricular end-diastolic volume in this study.

Second, interestingly, the initial study of Parker et al.  2describes two groups of patients with quite different left ventricular volumes. In the subgroup with a lower systemic vascular resistance index (SVRI; 1,127 ± 159 dyn · s · cm−5· m−2), mean left ventricular volume index was normal (81 ± 9 ml/m2), whereas the other group showed left ventricular dilatation and a higher SVRI (1,559 ± 168 dyn · s · cm−5· m−2). Calculating SVRI for the patients studied by Vieillard-Baron et al.  1on the basis of the hemodynamic data provided (systolic arterial pressure = 90–110 mmHg; mean arterial pressure ≈ 60 mmHg; central venous pressure = 13 mmHg; cardiac index = 3.2 l · min−1· m−2), we obtained an SVRI of 1,175 dyn · s · cm−5· m−2. This value is comparable to the low SVRI group reported by Parker et al. , 2but more interestingly, in both studies, these groups have a normal left ventricular volume index. This comparison also suggests that there is not really a contradiction between the data of the two clinical investigations. Both Parker et al.  2and Vieillard-Baron et al.  1report a normal mean left ventricular volume in patients with septic shock and decreased afterload. 4 

In conclusion, we believe that further studies should be performed to define more precisely the concept of early preload adaptation by the left ventricle in septic shock.

1.
Vieillard-Baron A, Schmitt JM, Beauchet A, Augarde R, Prin S, Page B, Jardin F: Early preload adaptation in septic shock? A transesophageal echocardiographic study. A nesthesiology 2001; 94: 400–6
2.
Parker MM, Shelhamer JH, Bacharach SL, Green MV, Natanson C, Frederick TM, Damske BA, Parrillo JE: Profound but reversible myocardial depression in patients with septic shock. Ann Intern Med 1984; 100: 483–90
3.
Parrillo JE: Pathogenetic mechanisms of septic shock. N Engl J Med 1993; 328: 1471–7
4.
Nussbacher A, Gerstenblith G, O’Connor FC, Becker LC, Kass DA, Schulman SP, Fleg JL, Lakatta EG: Hemodynamic effects of unloading the old heart. Am J Physiol 1999; 277: H1863–71