J Thorac Cardiovasc Surg 1998;116:368-369
© 1998 Mosby, Inc.
Impact of coronary venous pressure elevation on left ventricular function: Implications for the Fontan circulation
Robert J. M. Klautz, MD, PhD,
Gerda L. van Rijk-Zwikker, MD, PhD,
Paul Steendijk, PhD,
Jim Wilde, MD,
David F. Teitel, MD,
Jan Baan, PhD
Reply to the Editor:
We would like to thank Dr. Mehlhorn for his comment on our article, published in the October 1997 issue of this Journal (J Thorac Cardiovasc Surg 1997;114:560-7). His first concern was that we did not mimic the clinical setting of the Fontan circulation and therefore ignored the adverse effects of increased central venous pressure on myocardial fluid dynamics. In our study we did not intend to mimic the Fontan circulation but were only interested in determining whether it is useful to divert the coronary sinus to the (low pressure) left atrium. To answer this question, we investigated the isolated effects of acute elevation of coronary sinus pressure on coronary flow and left ventricular function. Numerous reports have shown that this elevation of coronary sinus pressure alone is responsible for decreased coronary flow and concomitant limitation of left ventricular function. We did not find such an effect. That other factors play a role in the patient with a Fontan circulation is beyond doubt. Indeed, every patient with a Fontan circulation has an inherent elevation of central venous pressure, regardless of whether the coronary sinus is diverted to the left atrium, and thus is subject to potential effects on lymphatic drainage of the myocardium. We fully agree with Dr. Mehlhorn that myocardial edema may play an important role in decreased left ventricular function, as was mentioned in our article, but this was not the subject of our study.
The second concern Dr. Mehlhorn addresses is the duration of elevation of coronary venous pressure. As mentioned in our article, this is indeed a point of concern. In our opinion, it is very difficult to conclude from short-term animal studies using longer periods of elevated coronary sinus pressure that deterioration of myocardial function is indeed caused by the elevation of coronary sinus pressure and not by the deterioration of the animal preparation, which is a known problem in these kinds of experiments. We believe that (long-term) animal studies, not designed to mimic the patient with a Fontan circulation but aimed at answering specific questions, will help us understand what mechanisms play an important role in affecting the left or, rather, the systemic ventricle in the Fontan setting.
Department of CardioThoracic SurgeryUniversity Hospital Rotterdam/Dijkzigt,
The Netherlands
