Response

To the Editor:

We thank Pal et al for raising several important questions regarding septic cardiomyopathy. They note that most patients with right ventricular (RV) dysfunction had concomitant left ventricular (LV) dysfunction and that the challenge of determining if one ventricular dysfunction preceded the other. We observed substantial overlap among LV systolic dysfunction, LV diastolic dysfunction, and RV systolic dysfunction, which is consistent with previous comparable reports of early septic cardiomypoathy.^{1, 2, 3} We agree that our data are unable to answer whether LV dysfunction preceded RV dysfunction; however, given the distribution of overlapping and isolated ventricular dysfunction, it is clear that there is no single pathway for the cascade of organ failure that is seen in septic cardiomyopathy. Pal et al also comment that 28 days may be within the early-phase of sepsis. Although we disagree with the designation of 28 days as early-phase sepsis, we agree with the need for long-term outcome assessments in critically ill patients, who may incur complications, such as pneumonias, in the convalescent phase of sepsis.

We feel obliged to address the concern about seemingly contradictory findings of echocardiography in sepsis. The cited publication studied the ratio of RV basal diameter to LV end-diastolic diameter, which may be less indicative of systolic function and more indicative of loading conditions than the parameters studied in our article.⁴ The two other large studies that investigated comparable measurements of contractility (tricuspid annular plane systolic excursion, fractional area change, free wall strain) in similar populations have demonstrated comparable associations between RV systolic dysfunction and mortality rates.^2,3 Regardless, the observation that echocardiographic parameters change in the critically ill patient is absolutely correct and should be emphasized when the septic cardiomyopathy literature is being interpreted.

Determining causality in the setting of septic multiorgan dysfunction syndrome is challenging. It is unknown whether ventricular dysfunction is a primary contributor to death, or if it is an epiphenomenon of increased pulmonary hypertension or myocardial depression from circulating cytokines. Although we suspect that most of patients in our study did not have significant RV dysfunction at baseline, this suspicion remains unsubstantiated. We agree with Pal et al that assessment of biomarkers and repeating echocardiography in survivors are important aspects to consider in future investigation.