A Circulating Myocardial Depressant Substance is Associated with Cardiac Dysfunction and Peripheral Hypoperfusion: Discussion

In: Septic Shock

8 Nov 2014

Further, this in vivo myocardial depression was correlated significantly with the extent of myocardial cell shortening observed using an in vitro model of myocardial cell performance. This correlation suggests that the degree of in vitro myocardial cell depression reflects the pathophysiologic events responsible for the in vivo myocardial depression. These findings confirm and extend the observations made in a previous set of studies.
The present study provides new data regarding the incidence of circulating MDS in patients with septic shock. As part of an ongoing prospective study of human septic shock, 50 patients admitted to our critical care unit were suspected of having septic shock based on the presence of fever and hypotension. review

Of the 50 patients, 16 turned out not to have sepsis; of these only one patient, with severe cardiogenic shock, met our criteria for circulating MDS. The remaining 34 patients subsequently met microbiologic criteria confirming the diagnosis of shock secondary to sepsis. Of the 34 confirmed septic shock patients, 14 (41 percent) had a circulating MDS.
With positive in vitro depression defined at —20 percent, the MDS positive patients clearly have depressant activity, but some patients with 0 to —20 percent depression may also have significant circulating biologic depressant activity. Biologic assays frequently lack precise discriminating capability. A highly significant correlation does exist between the in vitro myocardial cell assay and the in vivo EF in the 14 MDS-positive patients. To analyze the sensitivity of the existing biologic assay will require isolation and purification of the MDS molecule(s) and development of a radioimmunoassay or an enzyme-linked immunosorbent assay (ELISA).
Previous studies by our group and others have demonstrated clearly that the myocardial depression of human septic shock is not associated with reduction in coronary blood flow nor with net myocardial lactic acid production. Thus, it is very unlikely that myocardial ischemia causes the myocardial dysfunction of human septic shock.

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