Diastolic Suction During Acute Coronary Occlusion
To the Editor:
We congratulate Bell et al on the recent publication of their study1 that presents evidence indicating a decrease in forces responsible for diastolic suction during an acute occlusion of the left anterior descending coronary artery in dogs. Their experimental preparation is elegant, and we agree with their principal interpretation of their data: the acute loss of regional cardiac contractile function due to myocardial ischemia can result in a decrease in the mechanical generation and storage of elastic forces available to induce ventricular suction during early diastole.
In our view, the authors’ introductory remark that “One determinant of filling that may be altered during coronary occlusion but has not previously been studied is the ability of the LV to fill by suction” is an incomplete representation of the literature. In a previous publication,2 we described in detail the form of intraventricular pressure gradients found in the normal canine left ventricle during early diastole. In that report, we argued that the pattern of these early diastolic pressure gradients could only be present in a structure that filled by the process of mechanical suction. In a follow-up to that study, we hypothesized that any condition that interferes with regional systolic function might be expected to interfere with the process of diastolic suction and thereby modify the normal pattern of the early diastolic intraventricular pressure gradient. To test this hypothesis,3 we measured the intraventricular pressure gradient in dogs before and after occlusion of the left anterior descending coronary artery and found a strong relationship between the magnitude of the intraventricular pressure gradient and left ventricular systolic function. We concluded that loss of functional myocardium available to store energy during systole and release it during diastole in the form of elastic recoil impairs the process of diastolic suction. Thus, we respectfully suggest that the present work by Bell et al represents evidence complementary to our own, emphasizing again the important link between systolic function and the process of diastolic suction.
In addition, we question the authors’ conclusion that because fully relaxed pressure was positive during coronary occlusion, this “resulted in a situation in which a force causing suction was no longer present under operating conditions.” To use atmospheric pressure to define the presence or absence of ventricular suction, meticulous care is needed to exclude hydrostatic pressure artifacts in the measurements. In another study,4 we demonstrated that inaccuracies of pressure measurement of up to 5 mm Hg may be introduced by certain methods of zeroing micromanometers. Errors of this magnitude may lead to misinterpretation when the presence or absence of ventricular suction is defined in this way. Bell et al do not describe this important aspect of their experimental technique. In addition, by defining and discussing suction only in terms of the presence of subatmospheric pressure, the authors have ignored other plausible arguments that define suction as filling (+dV) in the presence of decreasing pressure (−dP).5 6 By that definition, suction is a mechanism that is always operative during the early diastolic filling phase, despite the absence of subatmospheric pressure, even in severely dysfunctional ventricles. This implies that our present notions about the concept of ventricular suction, and thus of equilibrium volume, are incomplete.
- Copyright © 1998 by American Heart Association
Bell SP, Fabian J, Watkins MW, LeWinter MM. Decrease in forces responsible for diastolic suction during acute coronary occlusion. Circulation. 1997;96:2348–2352.
Courtois M, Kovacs SJ, Ludbrook PA. The transmitral pressure-flow velocity relationship: the importance of regional pressure gradients in the left ventricle during diastole. Circulation. 1988;78:661–671.
Courtois M, Kovacs SJ, Ludbrook PA. The physiologic early diastolic intraventricular pressure gradient is lost during acute myocardial ischemia. Circulation. 1990;81:1688–1696.
Courtois M, Fattal PG, Kovács SJ, Tiefenbrunn AJ, Ludbrook PA. Anatomically and physiologically based reference level for measurement of intracardiac pressures. Circulation. 1995;92:1994–2000.
Katz LN. The role played by the ventricular relaxation process in filling the ventricle. Am J Physiol. 1930;95:542–553.
Kovacs SJ. Diastolic filling and the equilibrium volume of the ventricle. Int J Cardiovasc Med Sci. 1997;1:109. Abstract.
We are pleased to respond to Courtois et al in regard to our article, “Decrease in Forces Responsible for Diastolic Suction During Acute Coronary Occlusion.”R1 We are familiar with their elegant work elucidating diastolic intraventricular gradients during coronary occlusionR2 and cited it originally. It was deleted at the suggestion of a reviewer (with whom we agree) who indicated that intraventricular gradients do not necessarily implicate suction and are not a measure of the force causing suction. In our view and that of others,R3 suction represents conversion of potential energy produced during contraction to kinetic energy during filling. An indication that potential energy is present at end systole is a negative transmural pressure after relaxation, ie, the chamber is below equilibrium volume and “under compression” due to stored elastic energy. Our preparation, in which the ventricle relaxes at end-systolic volume without filling, provides a measure of that restoring force. Courtois et al contend that suction always operates during filling regardless of end-systolic volume, offering as proof the presence of intraventricular gradients and the decline in ventricular pressure early during filling. This concept differs from ours because it does not require energy storage at end systole. Although the gradient increases in parallel with restoring forces,R4 one must be present for inflow to proceed from mitral annulus to apex, regardless of the mechanism of filling. The argument that decreasing ventricular pressure requires an “active” process neglects the fact that with an open mitral valve, the ventricle is part of an open system that includes the left atrium and pulmonary circulation. Pressure and volume changes elsewhere in the system could account for the pressure decline.
The question posed about pressure measurement refers to their articleR5 advocating referencing of pressures to the uppermost level of fluid. This eliminates hydrostatic pressure and results in lower measured pressures than with conventional reference points. Our pressures were referenced to the midpoint of the mitral valve plane, defined by external landmarks. As a practical matter, in our preparation it is impossible to define the position of the uppermost level of fluid within the ventricle because of dynamic motion during each cardiac cycle, which is modified by the various interventions used. Equilibrium volume in dogs of the size we used is ≈10 to 20 mL. The hydrostatic pressure in an ellipsoid of this volume with its long axis oriented horizontally is quite small. We therefore opted to use a consistent reference, understanding that this might slightly underestimate restoring forces. Since our design was to compare coronary occlusion to baseline conditions, this approach does not alter our conclusions.
Bell S, Fabian J, Watkins MW, LeWinter MM. Decrease in forces responsible for diastolic suction during acute coronary occlusion. Circulation. 1997;96:2348–2352.
Courtois M, Kovacs SJ, Ludbrook PA. The physiologic early diastolic intraventricular gradient is lost during acute myocardial ischemia. Circulation. 1990;81:1688–1696.
Nikolic SD, Yellin EL, Tamura K, Vetter H, Tamura T, Meisner JS, Frater RWM. Passive properties of canine left ventricle: diastolic stiffness and restoring forces. Circ Res. 1988;62:1210–1222.
Nikolic SD, Feneley MP, Pajaro OE, Rankin JS, Yellin ES. Origin of regional pressure gradients in the left ventricle during early diastole. Am J Physiol. 1995;268:H550–H557.
Courtois M, Farral PG, Kovacs SJ, Teifenbrunn AJ, Ludbrook PA. Anatomically and physiologically based reference level for measurement of intracardiac pressures. Circulation. 1995;92:1994–2000.