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Transcript
712
Editorial Comment
The Right and Left Ventricles:
The Odd Couple*
BRUCE H. BRUNDAGE, MD, FACC
Torrance, California
The present study. Most physicians who care for patients
with acute myocardial infarction have had the unhappy
experience of struggling to save the patient with acute right
ventricular infarction. Profound hypotension or cardiogenic
shock is a welI recognized complication and on occasion,
even with apparently welI preserved left ventricular function, the patient succumbs despite all efforts (1). The report
by Goldstein and coworkers (2) in this issue of the Journal
makes important observations about the role of the ventricular septum in maintaining right ventricular stroke volume in
the presence of acute right ventricular ischemia.
The right and left ventricles are indeed an odd couple. The
right ventricle is complex in shape and is designed to be a volume
pump. The left ventricle is a prolate ellipse and required to pump
against high pressure. The two ventricles even have substantialIy
different coronary artery supplies in most persons. TraditionalIy
each chamber is often considered independently and too often the
impact ofits neighbor is not appreciated. Yet the two are wrapped
in a permanent and important relation that is further elucidated by
Goldstein et aI. (2). The impact on the interventricular septum of
a right ventricle that is pressure- or volume-overloaded, or both,
is welI recognized and has been studied extensively since the
advent of echocardiography (3). However the impact of the
septum on right ventricular performance is less well understood
and the investigative work of Goldstein and coworkers (2) has
added significantly to our knowledge and understanding.
Analysis of this study, however, raises several issues.
The most perplexing question is, Why does the right ventricular pressure exceed control values after the infusion of
dopamine? Goldstein et aI. (2) conclude that stimulation of
myocardial contractility did not enhance right ventricular
performance directly but by way of the pistonlike motion of
the ventricular septum. This explanation does not adequately explain the return of maximal positive and negative
right ventricular pressure changes over time (dP/dt) to control levels after dopamine treatment. Also, panel 4 of their
Figure 1 suggests some thickening of the right ventricular
free wall in comparison with that in panels 2and 3. Could the
*Editorials published in Journal of the American College of Cardiology
reflect the views of the authors and do not necessarily represent the views of
JACC or the American College of Cardiology.
From the Division of Cardiology, Harbor-UCLA Medical Center, Torrance, California.
Address for reprints: Bruce H. Brundage, MD, Division of Cardiology, F-9,
Harbor-UCLA Medical Center, 1000 West Carson, Torrance, California 90509.
©1992. by the American College of Cardiology
JACC Vol. 19, No.3
March I, 1992:712
marked increase in aortic pressure to 172/55 mm Hg (much
higher than the control value of 121/78) have improved
coronary perfusion pressure enough to enhance collateral
flow to the right ventricular myocardium? It is certainly well
recognized that in dogs preexisting coronary collateral channels can open rapidly when ischemia is produced.
Possible limitations. Because the transverse shape of the
canine right ventricle is a crescent, its systolic performance
might be more favorably affected by inward bulging of the
ventricular septum than would that of the human right
ventricle, which is more triangular. Thus, extrapolation of
the hemodynamic results obtained in dogs to humans may be
problematic. In this study (2) only two planes of the heart
were imaged by two-dimensional echocardiography. With
the increasing availability of new three-dimensional imaging
methods like ultrafast computed tomography and nuclear magnetic resonance imaging, future studies will be able to visualize
the right and left ventricles in their entirety and may provide
further insight into systolic ventricular interaction. To date,
however, too little attention has been paid to the geometric
differences between the canine and the human right ventricle
and the potential for producing different effects from ventricular interaction, during systole or diastole.
FinalIy, Goldstein et al. (2) performed the experiments in
the same sequence in alI dogs, right atrial and ventricular
ischemia first and septal ischemia second. Reversing the order
in some animals might have been instructive. The worsening
of right ventricular function after septal artery occlusion might
also have been a function of time. The authors also speculate
on how dopamine would have affected right ventricular performance in the absence of septal ischemia. Even though the
experimental protocol is a difficult one, as indicated by the
number of animals unable to complete alI stages, a randomization of procedural steps in future studies would be ideal.
Clinical implications. Although translating the results of
any animal laboratory study to the clinical arena always has
limitations, the findings of Goldstein et aI. (2) have important
clinical implications. Inotropic drugs have a beneficial effect
when the combination of right ventricular and septal ischemia exists and the mechanism of improvement almost
certainly involves the pistonlike effect of the ventricular
septum on the right ventricular cavity. Felix and Oscar are
indeed an odd couple but the relation works and studies such
as the one reported in this issue of the Journal (2) indicate
that we are learning more about how it works.
References
I. Cohn IN, Giuha NH, Broder Ml. Limas CJ. Right ventricular infarction:
clinical and hemodynamic features. Am J Cardiol 1974;33:209-14.
2. Goldstein JA, Tweddell JS, Barzilai B, Yagi Y, Jaffe AS, Cox JL.
Importance of left ventricular function and systolic ventricular interaction
to right ventricular performance during acute right heart ischemia. J Am
Coli Cardiol 1992;19:704-11.
3. Louie EK, Rich S, Levitsky S, Brundage BH. Doppler echocardiographic
demonstration of the differential effects of right ventricular pressure and
volume overload on left ventricular geometry and filling. J Am Coli Cardiol
1992;19:84-90.
0735-1097/92/$5.00