Use of left ventricular filling and ejection patterns in assessing severity of chronic mitral and aortic regurgitation

Osbakken, Mary D.; Bové, Alfred A.

doi:10.1016/0002-9149(84)90636-2

Cited by 24 publications

(7 citation statements)

References 25 publications

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“…By use of these methods, a modulus of regional chamber stiffness (kc) was calculated from echocardiographically determined dimension data. By fitting all the coordinates of pressure versus dimension measured from the end of the early filling period to end diastole by Equation 1, kc becomes a single numerical value that represents the entire P-versus-wnD2/4CSA curve. kC generally reflects the shape or steepness of the curvilinear P-versus-wrD2/ 4CSA relation but does not reflect this relation's position along the abscissa.…”

Section: Simultaneous LV Echocardiography and Catheterizationmentioning

confidence: 99%

Changes in diastolic function during development and correction of chronic LV volume overload produced by mitral regurgitation.

et al. 1993

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Background. Mitral regurgitation (MR) causes an augmentation in left ventricular (LV) diastolic function, increasing early diastolic filling rate and decreasing LV stiffness. Whether these changes in diastolic function persist, return to normal, or become abnormal after mitral valve replacement (MVR) is unknown.Methods and Results. Simultaneous LV echocardiography and catheterization studies were performed in six dogs in the baseline state (baseline), 3 months after creation of MR (chronic MR), and 3 months after MVR. Chronic MR caused LV dilation (end-diastolic dimension increased from 4.5±0.1 cm in baseline to 5.8+0.1 cm in chronic MR,p<0.05) and eccentric LV hypertrophy (LV-to-body weight ratio increased from 3.6±0.2 g/kg in baseline to 4.9±0.4 g/kg in chronic MR, p<0.05). Chronic MR caused an increase in LV early diastolic filling rate (peak rate of increase in minor-axis dimension increased from 11±1 cm/sec in baseline to 18+1 cm/sec in chronic MR,p<0.05), did not change the time constant of myocardial relaxation (T was 31±4 msec in baseline and 30±2 msec in chronic MR), and caused a decrease in the modulus of regional chamber stiffness from 7.7± 1.2 in baseline to 2.4±0.03 in chronic MR,p<0.05. MVR caused the resolution of LV dilation (end-diastolic dimension returned to normal [4.8±0.2 cm]), but three months after MVR, regression of LV hypertrophy was incomplete (LV-to-body weight ratio remained

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Section: Simultaneous LV Echocardiography and Catheterizationmentioning

confidence: 99%

Changes in diastolic function during development and correction of chronic LV volume overload produced by mitral regurgitation.

et al. 1993

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“…Similar observations have been made in studies of LV systolic ejection patterns in humans. [42][43][44] Others have suggested that ejection of blood into the left atrium in mitral regurgitation is not prolonged because the regurgitant blood flow is nearly complete by the time of zero systolic flow as approximated by the aortic dicrotic notch.3"1145,46 An examination of the timing of systolic events in our patients with mitral regurgitation demonstrates that minimum ventricular volume does indeed occur well after both end systole and zero systolic flow, suggesting that regurgitant flow does continue into protodiastole as shown by Braunwald.41 If one examines the timing of these systolic events between patient groups, however, the time to minimum ventricular volume is similar in all patient groups, whereas end systole is achieved more rapidly in patients with mitral regurgitation than in control patients or in patients with aortic regurgitation.…”

Section: Hemodynamic Datamentioning

confidence: 99%

Dissociation of end systole from end ejection in patients with long-term mitral regurgitation.

Brickner

Starling

1990

Circulation

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To determine whether left ventricular (LV) end systole and end ejection uncouple in patients with long-term mitral regurgitation, 59 patients (22 control patients with atypical chest pain, 21 patients with aortic regurgitation, and 16 patients with mitral regurgitation) were studied with micromanometer LV catheters and radionuclide angiograms. End systole was defined as the time of occurrence (Tmax) of the maximum time-varying elastance (Emax), and end ejection was defined as the time of occurrence of minimum ventricular volume (minV) and zero systolic flow as approximated by the aortic dicrotic notch (Aodi). The temporal relation between end systole and end ejection in the control patients was Tmax (331±42 [SD] msec), minV (336±36 msec), and then, zero systolic flow (355+±23 msec). This temporal relation was maintained in the patients with aortic regurgitation. In contrast, in the patients with mitral regurgitation, the temporal relation was Tmax (266±49 msec), zero systolic flow (310±37 msec, p<0.01 vs. Tmax), and then, minV (355+±37 msec,p<0.001 vs. Tmax andp<0.01 vs. Aodi). Additionally, the average Tmax occurred earlier in the patients with mitral regurgitation than in the control patients and patients with aortic regurgitation (p<0.01, for both), whereas the average time to minimum ventricular volume was similar in all three patient groups. Moreover, the average time to zero systolic flow also occurred earlier in the patients with mitral regurgitation than in the control patients (p<0.01) and patients with aortic regurgitation (p<0.05). Because of the dissociation of end systole from minimum ventricular volume in the patients with mitral regurgitation, the end-ejection pressure-volume relations calculated at minimum ventricular volume did not correlate (r= -0.09), whereas those calculated at zero systolic flow did correlate (r= 0.88) with the Emax slope values. We conclude that end ejection, defined as minimum ventricular volume, dissociates from end systole in patients with mitral regurgitation because of the shortened time to LV end systole in association with preservation of the time to LV end ejection due to the low impedance to ejection presented by the left atrium. Therefore, pressure-volume relations calculated at minimum ventricular volume might not be useful for assessing LV chamber performance in some patients with mitral regurgitation. (Circulation 1990;81:1277-1286

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“…Mitral and aortic regurgitation are associated with a large E wave [7,8] but neither were present at baseline nor immediately following exercise. Therefore, by excluding these factors that can alter the A/E ratio (systolic dysfunc tion, tachycardia, valvular regurgitation), the observed changes were presumably a reflection of increased left ventricular filling pressure secondary to a primary dia stolic abnormality.…”

Section: Case Reportmentioning

confidence: 96%

Left Ventricular Filling Patterns in Hypertensive Pulmonary Edema

Gallino¹,

Milner²,

Blunda³

et al. 1992

Am J Noninvas Cardiol

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We report a case of congestive heart failure in a hypertensive subject with concentric left ventricular hypertrophy. Doppler analysis of left ventricular filling patterns revealed a decrease in active atrial filling (A wave) during exercise, not present in a comparison assymptomatic hypertensive patient. A drop in the A wave and the A/E ratio during exercise may serve as a marker for congestive heart failure related to diastolic dysfunction.

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Use of left ventricular filling and ejection patterns in assessing severity of chronic mitral and aortic regurgitation

Cited by 24 publications

References 25 publications

Changes in diastolic function during development and correction of chronic LV volume overload produced by mitral regurgitation.

Changes in diastolic function during development and correction of chronic LV volume overload produced by mitral regurgitation.

Dissociation of end systole from end ejection in patients with long-term mitral regurgitation.

Left Ventricular Filling Patterns in Hypertensive Pulmonary Edema

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