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J Thorac Cardiovasc Surg 2003;125:220
© 2003 The American Association for Thoracic Surgery

Letters to the Editor

Reply

Gus J. Vlahakes, MD

Massachusetts General Hospital, 55 Fruit St—BUL 119, Boston, MA 02114-2696

Reply to the Editor:

My colleagues and I appreciate the questions raised by Danton in his letter to the Editor. The relationship between maximum right ventricular (RV) function and systemic pressure was suggested in 1955 by Peter Salisbury.Go 1 On the basis of this early study, weGo 2 demonstrated that, at the onset of RV failure, the RV free wall becomes ischemic, and this ischemia and failure can be reversed by raising systemic pressure. Although we believed that the entire matter was simply an issue of RV perfusion, additional studies from our laboratory began to cast doubt on this hypothesis. Page and associates,Go 3 using a model in which the right coronary circulation perfuses only the RV free wall, demonstrated that the maximal pressure developed by the right ventricle is determined primarily by maximal developed left ventricular (LV) pressure, and not by right coronary perfusion pressure. The issue of RV free wall versus left heart contribution was further explored by Damiano and colleaguesGo 4 in a model in which the RV free wall was electrophysiologically isolated from the rest of the heart. They demonstrated two distinct contributions to global RV function: one derived from RV free wall contraction and one derived from contraction of the left side of the heart. On the basis of these studies, we undertook the study recently published by Klima and coworkersGo 5 to investigate further the nature of left heart contribution to RV function.

Putting together the findings of our recent study with the prior work has led us to conclude that approximately half of RV function is derived from the contribution of the free wall, which is dependent on perfusion pressure, combined with a significant contribution from the left side of the heart, that is, via the interventricular septum. Furthermore, in our study, even when no LV preload was introduced into the left ventricle, the ventricle still developed pressure because of blood returning to the left side of the heart through the thebesian vessels; in our preparation, peak developed LV pressure closely correlated with aortic pressure, irrespective of left heart output. Although we do not deny the role of RV free wall ischemia in the pathogenesis of RV failure, we do maintain that the process is complex with multiple determinants.

Irrespective of mechanism, our study supports the physiologic principle that developed LV pressure, and hence systemic pressure, must be maintained when treating patients with RV failure.

References

  1. Salisbury PF. Coronary artery pressure and strength of right ventricular contraction. Circ Res. 1955;3:633-8.[Abstract/Free Full Text]
  2. Vlahakes GJ, Turley K, Hoffman JIE. The pathophysiology of failure in acute right ventricular hypertension: hemodynamic and biochemical correlations. Circulation. 1981;63:87-95.[Abstract/Free Full Text]
  3. Page RD, Harringer W, Hodakowski GT, Guerrero JL, LaRaia PJ, Austen WG, et al. Determinants of maximal right ventricular function. J Heart Lung Transplant. 1992;11:90-8.[Medline]
  4. Damiano RJ Jr, LaFollette P Jr, Cox JL, Lowe JE, Santamore WP. Significant left ventricular contribution to right ventricular systolic function. Am J Physiol. 1991;261:H1514-24.[Abstract/Free Full Text]
  5. Klima UP, Lee M-Y, Guerrero JL, LaRaia PJ, Levine RA, Vlahakes GJ. Determinants of maximal right ventricular function: role of septal shift. J Thorac Cardiovasc Surg. 2002;123:72-80.[Abstract/Free Full Text]




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