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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