Timing Of Aortic Valve Closure Research Articles

Quantification of mitral papillary muscle function using speckle tracking echocardiography in apparently healthy population

Abstract Funding Acknowledgements Type of funding sources: None. Introduction Cardiac mitral papillary muscle is a structure that has been long ignored. Recently, growing evidence from case reports showed an important role in the pathophysiology of many cardiac pathologies such as hypertrophic cardiomyopathy and dilated cardiomyopathy. To our knowledge, there isn’t any approved standard technique nor any methodological descriptive study of papillary muscle function in the apparently healthy population. Purpose To investigate mitral papillary muscle function in apparently healthy population by speckle tracking echocardiography (STE) using a proposed standard method. Methods We prospectively performed standard transthoracic echocardiography(TTE) in an apparently healthy cohort. Posterior mitral papillary muscle(PPM) was visualized on a modified three chamber view. The anterior papillary muscle(APM) was visualized on a modified 4 chamber view. To measure the value of the papillary muscles longitudinal strain, tracing of PPM and APM was done by a drag and click technique using an ECHOPAC software. Good quality tracing was ensured before approving the measurements. Each papillary muscle was divided into three segments by the software. 2D longitudinal strain curves of each papillary muscle consisted in 3 solid lines of the three segments and a dashed line that represented the mean longitudinal strain of the whole papillary muscle. This latter line was used to derive peak values, post systolic shortening (PSS) and systolic stretch (SS). Time of aortic valve closure was determined on the LV outflow pulsed doppler. Results Our study included 57 apparently healthy individuals between May 2021 and August 2021. Two patients were excluded due to lack of echogenicity. 71.19% (n = 44) were male. Mean age was 36 ± 14 yrs. 15.7% (n = 9) had history of hypertension and 7% (n = 4) were diabetic. 3.5% (n = 2) had history of stroke. 91.2% (n= 52) had functional status NYHA class I, 12.2% (n = 7) had functional status class II. All of our cohort had a left ventricular ejection fraction (LVEF) above 55%, did not have diastolic dysfunction and were on sinus rhythm. PPM peak strain value was -15.49 ±4.69 %. PSS was present in 98.2% (n = 56) and SS in 62.5%(n = 36) of cases. Anterior papillary muscle (APM) had a peak strain value of -15.61 ± 3.66, PSS was present in 78.5% (n = 45) and SS in 51.7% (n = 29). Conclusion Mitral papillary muscles echocardiographic study is feasible in routine scans with modified apical views. Post systolic shortening and systolic stretch are present in the majority of individuals. Abstract Figure. posterior papillary muscle strain curve Abstract Figure. anterior papillary muscle strain curve

Pressure constrained mitral annular dysfunction determines severity of regurgitation in Barlow's disease – a 3D echocardiographic study

Abstract Background Barlow's disease provides both diagnostic and therapeutic challenges. The impact of systemic blood-pressure on severity of regurgitation is still unclear. Purpose We hypothesized that mitral annulus behaves passively with enlargement during ventricular systole, and secondly, we tested the hypothesis that severity of regurgitation correlates to systemic blood-pressure (BP) of the patient. Methods Ten patients with Barlow's disease were compared with 10 healthy controls. Brachial blood-pressure was measured according to guidelines. Transthoracic 3D echo was obtained from an apical view (38.6±8.2 frames per second). Data was analyzed using a holographic display. We measured commissure width (CW), septallateral length (SL) and mitral annular surface area throughout the cardiac cycle. Aortic flow ejection time was derived from continuous Doppler across the aortic valve. Timing of aortic valve closure was visually assessed by 3D echo. Onset and end of mitral regurgitation was derived from continuous wave Doppler of transmitral flow. Results Systolic BP in controls and patients were 122±5 and 133±12 mmHg, respectively (p<0.05). Enddiastolic volume was 87±7 ml/m2 (controls) and 100±14 ml/m2 (Barlow), p<0.02. Left ventricular EF in controls and patients were 59±5 and 62±5%, respectively, p=NS. Barlow patients had moderate or severe late systolic regurgitation with mean regurgitation volume of 51±18 ml. Annular surface area, CW and SL behaved passively with enlargement during ventricular systole (Figure 1). Peak systolic surface area, CW and SL in healthy controls and Barlow patients were 8.7±0.5 vs 20.7±3.2 cm2 (p<0.001), 30.1±1.5 vs 49.5±4.9 mm (p<0.001) and 30.9±1.5 vs 44.9±3.3 mm (p<0.001). Peak annular surface area and regurgitation volume in patients showed a positive correlation with systolic BP (y = 0.156x − 0.077, r=0.60 and y = 1.136x − 99.7, r=0.80, respectively). Conclusions We have demonstrated pressure constrained mitral annular dysfunction in Barlow's disease, indicating that systemic blood pressure may modify the severity of regurgitation. The study provides novel insights into mechanisms of mitral regurgitation and potential therapeutic actions in the future. Figure 1 Funding Acknowledgement Type of funding source: Foundation. Main funding source(s): Grieg Foundation

P1754 Regional left ventricular longitudinal myocardial dysfunction in mitral valve prolapse could be primary

Abstract Background Regional left ventricular dysfunction in patients with mitral valve prolapse (MVP) and normal ejection fraction has been described by different Authors, and recent data point to a dysfunction (prevalently longitudinal strain) of the myocardium of the LV base secondary to dilatation of the mitral annulus. Purpose To investigate degree and extent of regional LV dysfunction and its mechanisms in patients with MVP, severe regurgitation and normal global systolic function, compared to patients with equivalent degree of regurgitation but functional etiology (FMR). Methods Speckle-tracking echocardiography was performed in 30 controls (N), and in severe primary (MVP, n= 50) or functional (FMR, n= 20) mitral regurgitation, to measure global, regional and segmental longitudinal peak systolic strain (LPSS, %), and time delay of peak maximum strain (TTPd, ms, calculated as time to peak maximum strain - time of aortic valve closure). Maximum and minimum mitral annulus diameters and area were measured with 3D echo. We also evaluated as recommended: LV end-diastolic volume index (EDVi, ml/m2), ejection fraction (EF, %), and left atrial end-systolic volume index (LAESVi, ml/m2) with 2D echo; LV stroke volume index, and non-invasive pulmonary systolic (PSP, mmHg) and diastolic pressures (PDP), mmHg) with Doppler echo. Results Age, heart rate, BSA and systolic blood pressure were similar between groups. Atrial fibrillation was present in 34% of MVP and 71% of FMR patients. LV EF was normal in MVP and reduced in FMR (43 ± 14 % vs N, p<.001). LV EDVi (MVP: 77 ± 20 ml/m2; FMR: 107 ± 35, both p<.001 vs N) and LAESVi (MVP: 91 ± 26 ml/m2; FMR: 80 ± 30, both p<.001 vs N) were similarly increased (volume overload) in MVP and FMR, as were PSP (MVP: 42 ± 23 ml/m2; FMR: 52 ± 25, both p<.001 vs N) and PDP (MVP: 16 ± 6 ml/m2; MVP: 15 ± 5, both p<.001 vs N). In FMR, LPSS was reduced globally (-12.8 ± 3.3, p<.001 vs N and MVP) and similarly at LV base, papillary and apical levels. In contrast, in MVP global (-19.4 ± 3.7%) and apical (-23.4 ± 4.5%) LPSS were normal, whereas LV base (-12.3 ± 5.8%, p=.003 vs N) and papillary (-17.1 ± 4%, p=.024 vs N) LPSS were reduced; further, LPSS reduction was localized to the anterior (-16 ± 4, p=.028 vs N), lateral (-17 ± 5, p=.006 vs N) and posterior (-16 ± 6, p=.007 vs N) segments, and was associated with an increased TTPd in the same segments in MVP but not in FMR patients. At multivariate analysis, degree and localisation of regional myocardial dysfunction in patients with MVP was not related to the prolapsing scallop, dimension of the mitral annulus, degree of volume overload or pulmonary pressures, or stroke volume index. Conclusions In patients with MVP, severe regurgitation and normal EF, there is a specific dysfunction pattern of regional LV longitudinal function which appears to be primary and not dependent on the degree of preload increase, mitral annulus dilatation, or localization of the prolapsing scallop.

The Pacing Effects on Myocardial Mechanics of the Right Ventricle Using Two-Dimensional Strain Imaging

Objective: Our study aimed to assess the 6 months effect of right ventricular apical (RVA) pacing on RV longitudinal systolic strain (LSS) using two-dimensional speckle tracking echocardiography (2D STE). Background: RVA pacing differs from the natural conduction through His-Purkinje fibers in having slower conduction velocity as well as altering the normal myocardial sequences of activation. Despite the fact that numerous studies have investigated the effects of RVA pacing on the LV, data on the effects on the RV function remain scarce. 2-D STE permits an objective and quantitative assessment of segmental and global myocardial function and has been validated against tagged MRI. We used 2-D STE to evaluate the RV LSS in response to RVA pacing. Methods: This case-control study was carried out on 60 subjects (30 patients implanted with DDD devices for 3rd degree AV block + 30 age and sex matched controls) in the period between February 2018 and February 2020 in the Cardiology Department, Faculty of Medicine, Menoufia University. The patients were evaluated 6 months after their implantation using conventional echo, M Mode, Doppler and 2D STE. 2D STE was used to identify the LSS of RV myocardial segments at the time of aortic valve closure. Statistical analysis was conducted using SPSS software v 20. Results: Results revealed that RVA pacing resulted in a statistically significant reduction of the global RV LSS in patients with DDD pacemakers vs controls (P Conclusion: RVA pacing reduces the RV free wall and the global RV LSS. Apical segments were the most affected.

Longitudinal Movement of the Common Carotid Artery Wall: New Information on Cardiovascular Aging

Putative changes in the multiphasic pattern of longitudinal movement of the common carotid artery wall in the normal aging process are unknown. The aim of this study was to explore the phases, and resulting patterns, of the longitudinal movement of the intima–media complex of the human common carotid artery with respect to age and gender. One hundred thirty-five healthy non-smoking patients of different ages were investigated using in-house-developed ultrasound methods. The patterns of longitudinal movement seen in middle-aged and older patients were markedly different from those commonly seen in young patients, including the appearance of two additional phases of motion and, thus, new complex patterns. The displacement and maximum velocity of one of the phases, occurring at the time of aortic valve closure, increased quadratically with age in both men and women.

The Effect of Exercise on the Timing of Aortic Valve Closure with Respect to the ECG Tracing

Objective: The temporal relationship between electrical repolarization of the heart and mechanical relaxation is not well quantified. In this study we examined the timing of the aortic valve (AoV) closure with respect to the electrical repolarization at rest and following exercise in young healthy subjects. Methods: We measured the period from the apex of the T wave (aT) to the beginning of the second heart sound (S2-aT) and the period from the apex of the T wave to the end of the T wave (eT-aT). Results: At rest, AoV closure occured immediately after the end of the T wave as evidenced by a ratio of (S2-aT)/(eT-aT) greater than 1. The mean time delay between the end of the T wave and AoV closure was 15.5ms which was only 4% of the QT interval duration. After exercise, AoV closure occured just before the end of the T wave (but after the peak of the T wave) as evidenced by the ratio of (S2-aT)/(eT-aT) being between 0 and 1. The mean time difference between the end of the T wave and AoV closure was - 4.4ms, which was only 1% of the QT interval duration. In combination, the QT and RR intervals account for some of the inter-subject variability. Conclusions: AoV closure closely approximates the end of T wave in healthy subjects indicating existence of electromechanical coupling during left ventricular relaxation. Clinically the end of T wave could, therefore, be used as a surrogate for AoV closure in healthy subjects.

Comparison of septal strain patterns in dyssynchronous heart failure between speckle tracking echocardiography vendor systems

AimTo analyze inter-vendor differences of speckle tracking echocardiography (STE) in imaging cardiac deformation in patients with dyssynchronous heart failure. Methods and resultsEleven patients (all with LBBB, median age 60.7years, 9 males) with implanted cardiac resynchronization therapy devices were prospectively included. Ultrasound systems of two vendors (i.e. General Electric and Philips) were used to record images in the apical four chamber view. Regional longitudinal strain patterns were analyzed with vendor specific software in the basal, mid and apical septal segments. Systolic strain (SS), time to peak strain (TTP) and septal rebound stretch (SRS) were determined during four pacing settings, resulting in 44 unique strain patterns per segment (total 132 patterns). Cross correlation was used to analyze the comparability of the shape of 132 normalized strain patterns. Correlation of strain patterns of the two systems was high (R2 median: 0.68, interquartile range: 0.53–0.82). Accordingly, strain patterns of intrinsic rhythm were recognized equally using both systems, when divided into three types. GE based SS (18.9±4.7%) was significantly higher than SS determined by the Philips system (13.4±4.3%). TTP was slightly but non-significantly lower in GE (384±77ms) compared to Philips (404±83ms) derived strain signals. Correlation of SRS between the systems was poor, due to minor differences in the strain signal and timing of aortic valve closure. ConclusionsThe two systems provide similar shape of strain patterns. However, important differences are found in the amplitude, timing of systole and SRS. Until STE is standardized, clinical decision making should be restricted to pattern analysis.

Left ventricular twist angle: echocardiographic assessment of amplitude and timing in normal and disease conditions

Purpose: The current concept of myocardial function incorporates complex rotational mechanics. Speckle Tracking Echocardiography (STE) allows for left ventricular (LV) twist deformation assessment, but quantitative data are often variable and little is known of torsional timing. The aim was to evaluate the LV twist angle and sequence of rotation in severe systolic dysfunction, less pronounced disease and in normal conditions. Methods: 101 subjects were studied (mean age 48.1±15 years, 46% women). Of these, 33 patients (PTS) demonstrated severe LV systolic dysfunction with EF ranging from 14 to 34%, mean 26.7% (Group 3); 33 PTS showed LV EF ranging from 37 to 69%, mean 55.5% (Group 2); and 35 subjects were healthy volunteers with EF between 62 and 67%, mean 65.2% (Group 1). Concurrent net LV twist angle was calculated using two-dimensional STE short axis images as the absolute apex-to-base difference in LV rotation at time of aortic valve closure (AVC). Time to peak apical and basal rotation was also measured as well as AVC independent peak LV twist angle, indicating the maximal torsional deformation without isochronal occurrence. Results: LV twist angle at AVC was significantly lowest in Group 3, showing a mean value of 5.6±5.0° (p<0.001), but no difference was found between Group 1 and 2, with measurements of 13.3±4.7° and 16.1±6.3°, respectively. In general, peak rotation was different from the values measured at AVC and did not occur simultaneously at basal and apical level. Therefore, LV twist angle at AVC was lower than peak twist angle in 96% of subjects. However, both measurements showed good correlation, with coefficients of 0.87, 0.9 and 0.87 in Group 3, 2 and 1, respectively. The absolute difference between time to peak apical and basal rotation was significantly larger in Group 3 as compared to Group 1, showing mean values of 96.8±81.2 ms and 44.3±41.0 ms, respectively (p=0.01). Conclusions: LV twist angle at aortic valve closure shows significant decrease in patients with severe LV systolic dysfunction, but due to a potential compensatory mechanism is comparable between patients with less pronounced disease and healthy subjects. Measurements of LV twist angle at aortic valve closure and at maximal amplitude show good correlation, though there is a temporal gradient of LV peak rotation between basal and apical level. This absolute timing difference is larger in patients with severe LV systolic dysfunction as compared to healthy subjects.

THE PRELIMINARY STUDY OF EVALUATION OF LEFT VENTRICULAR BULK ROTATION AND UNTWISTING IN HEART TRANSPLANT PATIENTS AT POSTOPERATIVE 3 MONTHS BY TWO-DIMENSIONAL ULTRASOUND SPECKLE TRACKING IMAGING

ObjectivesTo evaluate the change of left ventricular bulk rotation and untwisting in heart transplant patients at postoperative 3 months by two-dimensional ultrasound speckle tracking imaging (STI).MethodsThere were 15 heart transplant...

The Time Constant of Left Ventricular Relaxation

Left ventricular (LV) diastolic dysfunction induces the increase of LV diastolic pressure and subsequently of left atrial and pulmonary capillary pressures independent of systolic function, resulting in the onset of heart failure. In the early 1990s, several clinical studies demonstrated that diastolic dysfunction is an independent prognostic factor in patients with heart failure with reduced ejection fraction (EF).1,2 In the past decade, many clinical studies have clarified that heart failure with preserved EF (HFPEF) accounts for ≈40% of heart failure and that its prognosis is as poor as heart failure with reduced EF.3 With the growing interest in HFPEF, the important role of diastolic dysfunction in the pathogenesis of heart failure has been realized again, because it is plausible that LV diastolic dysfunction is one of the principal causes for this phenotype of heart failure.4 Article see p 268 Major determinants of LV diastolic function are relaxation and stiffness.5 Despite the clinical requisite for their evaluation in understanding the pathophysiology of each patient with heart failure, there are no established indices for the noninvasive assessment of these factors. An invasive measure of LV pressure is required for the evaluation of LV relaxation, and the simultaneous recording of LV pressure and geometry is necessary for the assessment of LV stiffness. LV relaxation abnormality is likely to precede LV stiffening or systolic dysfunction during the development of chronic heart failure and has been assigned as a sensitive sign of LV dysfunction. Peak negative value of the first derivative of LV pressure (peak−dP/dt) has been used as a quantitative index for LV relaxation, but it depends on many other hemodynamic and functional factors. Weiss et al6 showed that the time course of isovolumic pressure decrease subsequent to peak−dP/dt is exponential and proposed the time …

Mechanisms of Preejection and Postejection Velocity Spikes in Left Ventricular Myocardium

Normal left ventricular myocardium demonstrates distinct spikes in the velocity trace before and after left ventricular ejection. We tested the hypothesis that the preejection and postejection velocity spikes reflect early systolic shortening and late systolic lengthening that are interrupted by mitral and aortic valve closure, respectively. In 11 anesthetized dogs, timing of valve closure was determined by pressure variables; left ventricular dimensions were determined by sonomicrometry. Myocardial shortening started 20+/-10 ms (mean+/-SD; P<0.001) before mitral valve closure and was interrupted at the time of mitral valve closure (time difference, 4+/-7 ms). Similarly, myocardial lengthening started 31+/-15 ms (P<0.001) before aortic valve closure and was interrupted at the time of aortic valve closure (time difference, 0+/-3 ms). Prevention of mitral (n=4) and aortic (n=4) valve closure by stenting the valves abolished the preejection and postejection velocity spikes, respectively. Echocardiographic measurements of patients (n=15) with severe mitral regurgitation showed that the preejection velocity spike was reduced after prosthetic valve replacement (43+/-25 versus 32+/-15 mm/s; P=0.036), indicating that preejection shortening was larger with a leaking valve. Similarly, late systolic lengthening was reduced in patients (n=15) with severe aortic regurgitation after prosthetic valve replacement; minimum postejection velocity spike was increased from -32+/-11 to -17+/-11 mm/s; P=0.0003). Asynchronous onset of contraction/relaxation and atrioventricular interaction were investigated as alternative mechanisms of the velocity spikes in dogs and patient groups but were found implausible. This study supports the hypothesis that normal left ventricular preejection and postejection velocity spikes are attributed to valve closures that interrupt early systolic shortening and late systolic lengthening, respectively.

Automatic timing of aortic valve closure in apical tissue Doppler images

Ultrasound color tissue Doppler imaging (TDI) can be used to estimate velocities of moving left ventricular cardiac tissue. Aortic valve closure (AVC) can be observed as a notch in apical TDI velocity/time curves occurring after ejection, but before early relaxation. This work sought to evaluate automatic and automated algorithms using TDI for timing AVC. Mitral valve position and the time point of early relaxation were extracted and used to accomplish the task. To test the algorithms, phonocardiogram of the second heart sound was recorded simultaneously with TDI and used as a reference method. The algorithms were tested on apical views of 16 healthy subjects. In 98% of the cardiac cycles, the automatic algorithm estimated the time point of AVC within 25 ms of the reference. Automatic detection of AVC might save manual effort and provide a marker separating ejection and diastole for further automated analysis. (E-mail: sveinaaa@ntnu.no)

658 Automatic timing of aortic valve closure using tissue Doppler imaging

658 Automatic timing of aortic valve closure using tissue Doppler imaging

Propagation of spontaneously actuated pulsive vibration in human heart wall and in vivo viscoelasticity estimation

Though myocardial viscoelasticity is essential in the evaluation of heart diastolic properties, it has never been noninvasively measured in vivo. By the ultrasonic measurement of the myocardial motion, we have already found that some pulsive waves are spontaneously excited by aortic-valve closure (AVC) at end-systole (T0). These waves may serve as an ideal source of the intrinsic heart sound caused by AVC. In this study, using a sparse sector scan, in which the beam directions are restricted to about 16, the pulsive waves were measured almost simultaneously at about 160 points set along the heart wall at a sufficiently high frame rate. The consecutive spatial phase distributions, obtained by the Fourier transform of the measured waves, clearly revealed wave propagation along the heart wall for the first time. The propagation time of the wave along the heart wall is very small (namely, several milliseconds) and cannot be measured by conventional equipment. Based on this phenomenon, we developed a means to measure the myocardial viscoelasticity in vivo. In this measurement, the phase velocity of the wave is determined for each frequency component. By comparing the dispersion of the phase velocity with the theoretical one of the Lamb wave (the plate flexural wave), which propagates along the viscoelastic plate (heart wall) immersed in blood, the instantaneous viscoelasticity is determined noninvasively. This is the first report of such noninvasive determination. In in vivo experiments applied to five healthy subjects, propagation of the pulsive wave was clearly visible in all subjects. For the 60-Hz component, the typical propagation speed rapidly decreased from 5 m/s just before the time of AVC (t = T0 - 8 ms) to 3 m/s at t = T0 + 10 ms. In the experiments, it was possible to determine the viscosity more precisely than the elasticity. The typical value of elasticity was about 24-30 kPa and did not change around the time of AVC. The typical transient values of viscosity decreased rapidly from 400 Pa x s at t = T0 - 8 ms to 70 Pa x s at t = T0 + 10 ms. The measured shear elasticity and viscosity in this study are comparable to those obtained for the human tissues using audio frequency in in vitro experiments reported in the literature.

Comparative measures of systolic ejection during treadmill exercise by impedance cardiography and Doppler echocardiography

Measurements of systolic ejection dynamics by impedance cardiography were compared with simultaneous Doppler echocardiography in normal subjects and coronary artery disease patients. Patients with chest pain admitted for elective coronary angiography were monitored by simultaneous impedance cardiography and Doppler echocardiography before, during, and after treadmill exercise. Ensemble-averaged ECG, impedance cardiogram (ICG), the first derivative of ICG (d Z/d t), and Doppler waveforms were analyzed to identify systolic ejection variables. The timing of aortic valve opening was well correlated ( r = 0.78) the timing of peak ejection velocity was very well correlated ( r = 0.86), and the timing of aortic valve closure was moderately correlated ( r = 0.69 and r = 0.73) in these subjects. The thoracic electrical impedance acceleration and normalized impedance acceleration indices were moderately correlated with Doppler model acceleration ( r = 0.74, r = 0.79). The impedance cardiogram waveforms are of complex origin and are related to both aortic blood velocity and aortic blood acceleration. Users of d Z/d t timing features for determining aortic valvular events might consider alternative impedance features to improve ejection time accuracy.

Dissociation between left ventricular untwisting and filling. Accentuation by catecholamines.

Efficient early diastolic filling is essential for normal cardiac function. Diastolic suction, as evidenced by a decreasing left ventricular pressure during early filling, could result from restoring forces (the release of potential energy stored during systolic deformation) dependent on myofilament relaxation. Although these restoring forces have been envisioned within individual myofibers, recent studies suggest that gross fiber rearrangement involving the connective tissue network occurs easy in diastole. This may lead to the release of potential energy stored during systole and suction-aided filling. To establish precisely the timing and extent of restoration of the systolic torsional deformation of the left ventricle with respect to early filling at baseline and with enhanced relaxation, we studied untwisting during control conditions and with catecholamine stimulation. Using noninvasive and nondestructive magnetic resonance tagging, torsional deformation of the left ventricle was measured at 20-msec intervals in 10 open-chest, atrially paced dogs, starting at aortic valve closure. Eight equiangular tags intersected the epicardium and endocardium in three short-axis imaging planes (base, mid, and apex). From the intersection points, epicardial and endocardial circumferential chord and arc lengths were measured and angular twist of mid and apical levels with respect to the base (maximal torsion and its reversal, untwisting) was calculated. Echo-Doppler provided timing of aortic valve closure and of mitral valve opening. Zero torsion was defined at end diastole. Torsion at the apical level reversed rapidly between its maximum and the time immediately after mitral valve opening: from 7.0 +/- 5.8 degrees to 3.2 +/- 5.4 degrees and 12.0 +/- 8.5 degrees to 6.9 +/- 7.8 degrees (mean +/- SD, both p less than 0.01) at the epicardium and endocardium, respectively. During the same period, no significant circumferential segment length changes occurred. As expected, after mitral valve opening, filling resulted in significant circumferential segment lengthening, whereas further reversal of torsion was small and nonsignificant. During dobutamine infusion, torsion at end systole was greater and reversal during isovolumic relaxation was much more rapid and greater in extent (p less than 0.01). Torsion reversed from 11.5 +/- 4.3 degrees to 5.7 +/- 4.8 degrees and 17.4 +/- 6.4 degrees to 6.9 +/- 7.7 degrees at epicardium and endocardium. Untwisting occurs principally during isovolumic relaxation before filling and is markedly enhanced in speed and magnitude by catecholamines. This partial return of the left ventricle to its preejection configuration before mitral valve opening could represent an important mechanism for the release of potential energy stored in elastic elements during the systolic deformation. These myocardial restoring forces would be markedly enhanced by physiological changes consequent to catecholamines such as during exercise, offsetting the concomitant shortening of the filling period.

Impairment of diastolic function by shortened filling period in severe left ventricular disease.

A dilated left ventricle with reduced ejection fraction is usually attributed to impaired systolic function. To investigate the possibility that ventricular filling might also be disturbed, M mode echocardiograms, phonocardiograms, and Doppler cardiograms were recorded in 30 patients with ventricular disease of varying cause. All but four had functional mitral regurgitation. The size of the left ventricular cavity was increased in all and peak velocity of circumferential fibre shortening was reduced. Diastolic abnormalities included a short isovolumic relaxation time, and, on digitised M mode, a reduced rate of dimension increase and of posterior wall thinning. Although the timing of aortic valve closure was normal, mitral regurgitation persisted beyond it by 95 (35) ms and beyond mitral valve opening by 60 (40) ms. This reduced the effective filling time (the interval when the mitral valve was open and mitral regurgitation was absent) to less than 200 ms in seven patients. The effective filling time correlated closely with the RR interval, the regression equation indicating a reduction of 80 ms for each 100 ms fall in RR interval. It was also independently shortened by 2 ms a year with increasing age. The effective left ventricular filling time may thus be very short in patients with left ventricular cavity dilatation and functional mitral regurgitation. It is suggested that when diastolic function is also abnormal, this short filling time may physically limit ventricular inflow. Its close relation to heart rate might contribute to the therapeutic effect of beta blockade in such patients.

Effect of oral milrinone on end-systolic relations in patients with severe congestive heart failure

The new inotropic agent milrinone has both vasodilator and inotropic cardiovascular effects, but the importance of these effects in patients with severe congestive heart failure (CHF) is controversial. The left ventricular (LV) end-systolic pressure-diameter relation was used to determine the independent inotropic effect of milrinone. Seven patients with New York Heart Association class III CHF were invasively monitored with right-sided heart catheters and radial arterial lines. M-mode echocardiography was used to measure LV dimensions. The effect of a 10mg oral dose of milrinone on hemodynamic, echocardiographic and end-systolic variables was determined. End-systolic pressure was measured at the dicrotic notch of the arterial pressure tracing and end-systolic LV dimensions at the time of aortic valve closure. Methoxamine (n = 6) or nitroprusside (n = 1) was used to alter afterload so that the end-systolic pressure-diameter relation could be determined. Arterial vasodilation from milrinone was evidenced by a decrease in mean arterial blood pressure (88 ± 5 to 77 ± 2 mm Hg, p <0.025) and an increase in cardiac index (from 2.7 ± 0.2 to 3.2 ± 0.2 liters/min/m 2, p <0.025), with no change in heart rate (80 ± 5 beats/min). Milrinone decreased preload as assessed by the pulmonary artery wedge pressure (from 17 ± 2 to 10 ± 2 mm Hg, p <0.01) and end-diastolic LV diameter (from 7.4 ± 0.4 to 7.0 ± 0.4 cm, p <0.025). Milrinone caused decreases in the end-systolic pressure (from 79 ± 5 to 68 ± 2 mm Hg, p <0.01) and end-systolic LV diameter (from 6.6 ± 0.4 to 6.1 ± 0.5 cm, p <0.025). Milrinone treatment decreased end-systolic afterload as measured by end-systolic wall stress (from 106 ± 12 to 81 ± 12 g/cm 2, p <0.005), but resulted in no corresponding change in percent fractional shortening (13 ± 1 vs 13 ± 2%) or in rate-corrected velocity of circumferential fiber shortening (0.45 ± 0.05 vs 0.43 ± 0.06 circ/s). The slope of the end-systolic pressure-diameter relation was not significantly different at control (37 ± 6 mm Hg/cm) than at peak milrinone effect (46 ± 11 mm Hg/cm), nor was there a significant change in the diameter intercept (3.9 ± 0.7 vs 4.1 ± 0.7 cm). The range of pressure and diameter values over which the end-systolic pressure-diameter relation was determined, however, was limited by the markedly abnormal LV function and cardiovascular status of these patients. In conclusion, during acute oral therapy in patients with severe CHF, the predominant effect of milrinone as assessed by end-systolic relations is as a vasodilator and not as a positive inotropic agent.

Abnormal left ventricular diastolic function in chronic Chagas' disease: an echocardiographic study

Simultaneous M-mode echochardiograms and phonocardiograms were recorded in 19 patients with chronic Chagas' disease, and were digitised and compared with normal in order to study systolic and diastolic left ventricular function. Five of the patients were in New York Heart Association class 1, 9 in class 2, and 5 in class 3. Left ventricular cavity dimensions were increased in 3 and shortening fraction reduced in 1. Peak velocity of circumferential fibre shortening was below the 95% confidence limit of normal in 9. In contrast to previous echocardiographic studies, diastolic abnormalities were common, with prolongation of isovolumic relaxation time in 9 patients and reduced rate of dimension increase in 11. However, in spite of regional disease, documented angiographically in 5 of 6 patients, there was no evidence of asynchronous wall motion during relaxation seen in patients with coronary artery disease and comparable segmental abnormalities of wall motion. The relative timing of aortic valve closure and minimum cavity dimension was normal in all but 3 patients, and a significant dimension change during isovolumic relaxation in only one. Thus diastolic disturbances are common at all stages of Chagas' disease, and may represent a fundamental aspect of the pathological process as it affects the left ventricle.

Limitations of two frame method for displaying regional left ventricular wall motion in man.

Regional abnormalities of left ventricular function are frequently determined from superimposed cavity outlines at end-diastole and end-systole. The timing of end-diastole is standardised with respect to the electrocardiogram, but that of end-systole is undefined, and frequently determined by simple inspection. To examine the effect of variation in the timing of the end-systolic frame on apparent regional wall motion, 35 left ventricular angiograms from patients wit ischaemic heart disease were digitised frame by frame, and the timing of aortic valve closure and mitral valve opening superimposed on contour displays. In 15 patients, the pattern in the two frame display with end-systole taken as aortic valve closure was similar to that when it was taken as mitral valve opening. In the remaining 20, however, there were major discrepancies between the two, because of changes in cavity shape during isovolumic relaxation. These shape changes were the result of asynchronous termination of systole in different regions of the ventricle. In addition, there was a significant increase in left ventricular cavity area of 3.9 +/- 1.7 per cent during isovolumic relaxation, corresponding to an increase in calculated volume of 8.1 +/- 4.5 per cent. Estimates of ejection fraction derived from end-systole taken at end-ejection were thus consistently greater than those at mitral valve opening. These differences in the apparent pattern of regional wall motion resulting from lack of definition of end-systole are large compared with those reported after intervention angiography, or surgery. Thus, if two frame methods are to be used, the timing of end-systole must be standardised. We suggest that end-ejection be used. Changes of shape during isovolumic relaxation should be considered separately.