Mechanisms of mitral valve motion during diastole

Yellin, Edward L.; Peskin, Charles S.; Yoran, Chaim; Koenigsberg, Mordecai; Matsumoto, Mitsuhiro; Laniado, Shlomo; McQueen, David M.; Shore, D.; Frater, Robert W.M.

doi:10.1152/ajpheart.1981.241.3.h389

Cited by 48 publications

(45 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…As demonstrated by Greenberg et al (4), intraventricular pressure gradients can even be assessed by color Doppler echocardiography. In 2-D models of nonischemic ventricles, it appears that the intraventricular flow field is represented by a number of vortexes that expand in a circular fashion from the mitral tip region (20). However, during the early phase of filling, while transmitral flow is accelerating, the dominant flow vectors are directed toward the apex (7).…”

Section: Mechanisms Of Delayed Early Diastolic Mitral-toapical Flow Pmentioning

confidence: 99%

“…Yellin et al (20) described intraventricular vortexes that occurred during LV filling due to shear between blood and mitral leaflet surface. The flow reversal described in the present study, however, started during isovolumic relaxation and therefore cannot be attributed to a similar mechanism.…”

Section: Mechanisms Of Delayed Early Diastolic Mitral-toapical Flow Pmentioning

confidence: 99%

See 1 more Smart Citation

Postsystolic shortening of ischemic myocardium: a mechanism of abnormal intraventricular filling

Urheim¹,

Edvardsen²,

Steine³

et al. 2003

American Journal of Physiology-Heart and Circulatory Physiology

View full text Add to dashboard Cite

Acute myocardial ischemia has been associated with abnormal filling patterns in the left ventricular (LV) apex. We hypothesized that this may in part be due to postsystolic shortening of ischemic apical segments, which leads to reversal of early diastolic apical flow. Fourteen open-chest anesthetized dogs were instrumented with micromanometers in the LV apex and left atrium and myocardial sonomicrometers in the anterior apical LV wall. Intraventricular filling by color Doppler and wall motion by strain Doppler echocardiography (SDE) were assessed from an apical view. Measurements were taken before and after 5 min of left anterior descending coronary artery (LAD) occlusion. In four dogs, we measured the pressure difference between the LV apex and outflow tract. At baseline, peak early diastolic flow velocities in the distal one-third of the LV were directed toward apex (9.2 Ϯ 1.6 cm/s). After LAD occlusion, the velocities reversed (Ϫ2.3 Ϯ 0.4 cm/s, P Ͻ 0.01), indicating that blood was ejected from the apex toward the base during early filling. This interpretation was confirmed by wall motion analysis, which showed postsystolic shortening of apical myocardial segments. The postsystolic shortening represented 9.7 Ϯ 1.7% (P Ͻ 0.01) and 14.2 Ϯ 2.4% (P Ͻ 0.01) of end-diastolic segment length by SDE and sonomicrometry, respectively. Consistent with the velocity changes, we found reversal of the early diastolic pressure gradient from the LV apex to outflow tract. In the present model, acute LAD occlusion resulted in reversal of early diastolic apical flow, and this was attributed to postsystolic shortening of dyskinetic apical segments. The clinical diagnostic importance of this finding remains to be determined. strain-Doppler echocardiography; two-dimensional color Doppler; myocardial ischemia; diastolic filling ASSESSMENT OF LEFT VENTRICULAR (LV) intracavitary filling by Doppler echocardiography is one of several noninvasive approaches for studying LV diastolic function. In the normal LV, the initial intraventricular filling wave propagates rapidly toward the apex, and, as demonstrated by color M-mode Doppler, there is near simultaneous onset of filling velocities along the entire LV inflow tract (7). However, in patients with reduced LV ejection fraction or impaired diastolic function, the early diastolic apical filling may be markedly delayed, and this can be measured as slowing of mitral-to-apical flow propagation (1, 13). This has been attributed to a decrease in rate of LV relaxation, which causes a decrease in the driving pressure for mitral-to-apical flow (1, 12, 13), to loss of "apical suction" (12), and enhanced vortex formations due to changes in LV and mitral valve geometry (10).There is, however, very limited insight into how regional wall motion interacts with intraventricular flow. A common finding in ischemic myocardium is postsystolic (postejection) shortening and consequently delayed onset of diastolic lengthening (8,16,17). Therefore, in the ischemic ventricle, there may be substantial regional async...

show abstract

Section: Mechanisms Of Delayed Early Diastolic Mitral-toapical Flow Pmentioning

confidence: 99%

Section: Mechanisms Of Delayed Early Diastolic Mitral-toapical Flow Pmentioning

confidence: 99%

Postsystolic shortening of ischemic myocardium: a mechanism of abnormal intraventricular filling

Urheim¹,

Edvardsen²,

Steine³

et al. 2003

American Journal of Physiology-Heart and Circulatory Physiology

View full text Add to dashboard Cite

show abstract

“…7,29,32 Changes in mitral flow are measured by the peak E velocity and deceleration time. The peak E velocity is mainly dependent on the initial driving pressure across the mitral valve,7,8 28,29,31,34 which is determined by left atrial pressure and the rate of ventricular relaxation. The deceleration time, or rate of deceleration of flow, is dependent on continued ventricular relaxation and ventricular compliance.…”

Section: Overall Relation Of Hemodynamics To Doppler Velocitiesmentioning

confidence: 99%

Relation of pulmonary vein to mitral flow velocities by transesophageal Doppler echocardiography. Effect of different loading conditions.

et al. 1990

View full text Add to dashboard Cite

It has previously been demonstrated that predictable changes occur in mitral flow velocities under different loading conditions. The purpose of this study was to relate changes in pulmonary venous and mitral flow velocities during different loading conditions as assessed by transesophageal echocardiography in the operating room. Nineteen patients had measurements of hemodynamics, that is, mitral and pulmonary vein flow velocities during the control situation, a decrease in preload by administration of nitroglycerin, an increase in preload by administration of fluids, and an increase in afterload by infusion of phenylephrine. There was a direct correlation between the changes in the mitral E velocity and the early peak diastolic velocity in the pulmonary vein curves (r=0.61) as well as a direct correlation between the deceleration time of the mitral and pulmonary venous flow velocities in early diastole (r=0.84).This indicates that diastolic flow velocity in the pulmonary vein is determined by the same factors that influence the mitral flow velocity curves. A decrease in preload caused a significant reduction in the initial E velocity and prolongation of deceleration time, and an increase in preload caused an increase in E velocity and shortening of deceleration time. An increase in afterload produced a variable effect on the initial E velocity and deceleration time and was dependent on the left ventricular filling pressure. The change in systolic forward flow velocity in the pulmonary vein was directly proportional to the change in cardiac output (r=0.60). The pulmonary capillary wedge pressure correlated best with the flow velocity reversal in the pulmonary vein at atrial contraction (r=0.81). Use of pulmonary vein velocities in conjunction with mitral flow velocities can help in understanding left ventricular filling. (Circulation 1990;81:1488-1497 Abnormalities of diastolic function of the heart play an integral role in many disease entities.'2 Because of the complexity of the multiple, interrelated processes contributing to diastolic function, there is no clinical tool available for its assessment.3 It has been proposed that Doppler echocardiography might provide information concerning diastole because of its ability to noninvasively measure blood flow velocities across the mitral valve.45 We, as well as others,6-9 previously demonstrated that predictable changes occur in the mitral flow velocities under different loading conditions. This has resulted in understanding the significance of changes in these velocities and has allowed the development of a conceptual framework for interpretation of the various velocity curves.'0 Pulmonary vein velocities have recently been used in conjunction with mitral flow velocities to increase our understanding of ventricular filling.11-13 However, because of the location of the pulmonary vein in the far field from a precordial apical window, it can be difficult to place the sample volume within the pulmonary vein to obtain the true velocities through the pulmonary vein. Th...

show abstract

“…'3 These approaches are based on the principle that the falling ventricular pressure contributes to the generation of the atrioventricular pressure difference that accelerates the blood across the mitral valve. 19 To analyze the effect of changes in one parameter when all other parameters were held constant (an approach that is difficult if not impossible in the conscious dog), we have included as an Appendix a series of computational studies using a lumpedparameter electric analog of early filling dynamics.…”

mentioning

confidence: 99%

Left ventricular filling dynamics: influence of left ventricular relaxation and left atrial pressure.

Ishida¹,

Meisner²,

Tsujioka³

et al. 1986

Circulation

568

166

View full text Add to dashboard Cite

Peak rapid filling rate (PRFR) is often used clinically as an index of left ventricular relaxation, i.e., of early diastolic function. This study tests the hypothesis that early filling rate is a function of the atrioventricular pressure difference and hence is influenced by the left atrial pressure as well as by the rate of left ventricular relaxation. As indexes, we chose the left atrial pressure at the atrioventricular pressure crossover (PCO), and the time constant (T) of an assumed exponential decline in left ventricular pressure. We accurately determined the magnitude and timing of filling parameters in conscious dogs by direct measurement of phasic mitral flow (electromagnetically) and high-fidelity chamber pressures. To obtain a diverse hemodynamic data base, loading conditions were changed by infusions of volume and angiotensin LI. The latter was administered to produce a change in left ventricular pressure of less than 35% (A-1) or a change in peak left ventricular pressure of greater than 35% (A-2). PRFR increased with volume loading, was unchanged with A-1, and was decreased with A-2; T and PCO increased in all three groups (p < .005 for all changes). PRFR correlated strongly with the diastolic atrioventricular pressure difference at the time of PRFR (r = .899, p < .001) and weakly with both T (r = .369, p < .01) and PCO (r = .601, p < .001). The correlation improved significantly when T and PCO were both included in the multivariate regression (r = .797, p < .0001). PRFR is thus determined by both the left atrial pressure and the left ventricular relaxation rate and should be used with caution as an index of left ventricular diastolic function.Circulation 74, No. 1, 187-196, 1986. RELAXATION ABNORMALITIES are one of the earliest manifestations of cardiac dysfunction and frequently precede systolic dysfunction in many disease states.'' Early filling function has been evaluated in a variety of diseases, e.g., coronary artery disease, hypertrophic cardiomyopathy, hypertensive heart disease, aortic valve disease, and congestive cardiomyop-

show abstract

Mechanisms of mitral valve motion during diastole

Cited by 48 publications

References 0 publications

Postsystolic shortening of ischemic myocardium: a mechanism of abnormal intraventricular filling

Postsystolic shortening of ischemic myocardium: a mechanism of abnormal intraventricular filling

Relation of pulmonary vein to mitral flow velocities by transesophageal Doppler echocardiography. Effect of different loading conditions.

Left ventricular filling dynamics: influence of left ventricular relaxation and left atrial pressure.

Contact Info

Product

Resources

About