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(Circulation. 1998;98:2098-2102.)
© 1998 American Heart Association, Inc.

Correspondence

Diastolic Suction During Acute Coronary Occlusion

Michael Courtois, MA; Sándor J. Kovács, PhD, MD; ; Philip A. Ludbrook, MD

Washington University School of Medicine, St Louis, Mo

Response

Stephen B. Bell, BA; ; Martin M. LeWinter, MD

The University of Vermont, Department of Medicine, Cardiology Unit, Burlington, VT

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."¹ We are familiar with their elegant work elucidating diastolic intraventricular gradients during coronary occlusion² 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,³ 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,⁴ 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 article⁵ 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.

References

1. Bell S, Fabian J, Watkins MW, LeWinter MM. Decrease in forces responsible for diastolic suction during acute coronary occlusion. Circulation. 1997;96:2348–2352.[Abstract/Free Full Text]
   
2. Courtois M, Kovacs SJ, Ludbrook PA. The physiologic early diastolic intraventricular gradient is lost during acute myocardial ischemia. Circulation. 1990;81:1688–1696.[Abstract/Free Full Text]
   
3. 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.[Abstract/Free Full Text]
   
4. 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.[Abstract/Free Full Text]
   
5. 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.
   

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