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LETTER TO THE EDITOR
TRANSMURAL VS. TRANSMITRAL PRESSURE GRADIENTS
Existence of diastolic transmural pressure gradients (
Ptransmural) is not questioned; however, Ptransmural are the results, not the causes, of suction. Even short-axis ventricular slices with zero Ptransmural spring apart when cut (see Viewpoint, Ref. 22). Furthermore, in contrast to open-chest settings, Ptransmural and transmitral gradients are not interchangeable in closed-chest settings.
If dPLV/dVLV<0 and the atrium is intact, the recoil overcomes residual unrelaxed elements and the endocardium recoils faster than the aspirated blood can enter. Suction is the resultant sum of tissue-motion generated forces on the blood, and therefore includes any effects that Ptransmural may have on the tissue.
The duration and magnitude of dPLV/dVLV<0 determines the extent of suction. Thus suction exists with LV dilatation, but the duration of suction and the associated aspirated volume is diminished relative to healthy hearts because ESV is barely below Vdiastasis = Vequilibrium.
When atrial pressure rises such that PLA>Pperi, the atrium exerts outward force on the pericardium, and although this may increase the atrioventricular pressure gradient it does not cause suction. Indeed, ventricles can fill without atria (see Viewpoint, Ref. 28). Instead, suction is powered by elastic energy stored by titin (Viewpoint, Ref. 11) and other sources (3, 6) and involves recoiling tissue-generated PLA-PLV being converted to motion of blood.
MECHANISMS OF SUCTION
Our Viewpoint unifies two definitions of suction: one invoking dPLV/dVLV<0 and the other relying on ESV<VEq. We show that the laws of statics and dynamics, independent of specific ventricular recoil mechanisms, establish that suction-initiated filling brings the ventricle to mechanical equilibrium at Vdiastasis.
RELIABILITY OF MEASUREMENTS
Functional imaging elegantly elucidates details inaccessible to catheters, but these details are consequences of ventricular suction. Demonstration of ventricular suction only requires that dPLV/dVLV<0. Indeed Pasipoularides (5), in agreement with others, observes RV pressures decreasing as RV filling proceeds.
IS DIASTASIS HEMODYNAMIC STASIS?
Conclusions from Carlsson et al. (1a) regarding diastasis must consider heart rate (HR), because diastasis is lost when HR > 80 (2). Indeed, in contrast to the two lower HR subjects from Carlsson et al., the remaining six subjects had HR 
80 and lack diastasis.
Intracavity flow exists during early diastole (3), although by diastasis there is no net volume change and intracavity swirling diminishes to minimal levels (Fig. 2E; Ref. 7).
When L-waves are present, or in other cases where LV volume continuously changes, Vdiastasis is not achieved. However, these cases are exceptions to the rule, and most ventricles possess diastasis (see online supplemental video).
Load variation impacts transmitral gradients, transmitral flow, and Vdiastasis. We stress that while Vdiastasis is a static equilibrium state for a particular beat, specific Vdiastasis values are expected to vary with load. Thus filling pressure variation may not directly correlate with changes in suction.
CONCLUSION
The physiological mechanisms governing diastole remain an active field of research. Future and current work regarding diastolic function must abide by the constraint that all hearts are mechanical suction pumps (dPLV/dVLV<0) at mitral valve opening and initiate filling at a volume below their equilibrium volume (ESV<Vequilib=Vdiastasis).
FOOTNOTES
Address for reprint requests and other correspondence: S. J. Kovács, Cardiovascular Biophysics Laboratory, Washington Univ. Medical Center, 660 South Euclid Ave Box 8086, St. Louis, MO 63110 (e-mail: sjk{at}wuphys.wustl.edu)
REFERENCES
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