Diastolic Heart Failure – part 4 ppsx

7 Myocardial Velocities as Markers of Diastolic Function Jarosław D. Kasprzak and Karina A. Wierzbowska-Drabik 99 Relationship Between Myocardial Velocities and Diastolic Function Cardiac diastolic dysfunction caused by ventricular abnormalities in relaxation, increased stiffness, or a combination of both is an important cause of morbidity in patients with heart disease. A direct evaluation of diastolic function requires invasive simultaneous high-fi delity measurements of left ventricular (LV) pressures and volumes. This experimental and physiologic standard is rarely feasible in a clinical setting as it requires cardiac catheterization with specialized measurements and is thus poorly suited for repetitive assessment or screening purposes. Therefore, in clinical practice, noninvasive methods, such as echocardiography and, recently, magnetic resonance imaging (MRI) are principal tools for the assessment of global and local myocardial function. Doppler echocardiography is currently a wide- spread noninvasive method used for the assessment of cardiac physiology. Pulsed wave Doppler measurements of ventricular fi lling velocities and pulmonary vein fl ow are now widely available and routinely used to estimate LV diastolic function. An important limitation of this approach, however, is its dependence on loading conditions, with an increase in the velocity of early mitral infl ow and pseudonormalization of the fi lling pattern due to a compensatory increase in left atrial pressure as LV diastolic dysfunction progresses (Figure 7.1). Doppler fl ow measurements are also limited by providing only a global insight into ventricular dysfunction. However, ventricular fi lling is physi- ologically determined by suction, that is, instantaneous pressure gradients created initially by relaxation of the myocardium after the closure of the aortic valve and, later in the cardiac cycle, by the balance between active contraction force of atria if present and late diastolic ventricular pressures, determined by ventricular wall properties. A diastolic increase in global ventricular volume depends on the elongation of the longitudinal and circumferential fi bers and is therefore refl ected by their local velocities. In addition, a novel concept of ventricular function perceived as a single ventricular myocardial band has offered an intriguing explanation of systolic and diastolic velocity coupling 1 ; this has increased interest in novel parameters of myocardial function (e.g., LV torsion dynamics). Its characteristics can also be derived from the measurements of ventricular velocities. 2 Clinical Methods of Assessing Myocardial Velocities Tissue Doppler Echocardiography A newer Doppler modality, tissue Doppler echocardiography (TDE), was introduced in early 1990s as a robust tool for assessing local myocardial velocities and, thus, function. 3 This modality was developed for the assessment of LV function and has become a fundamental clinical tool used for noninvasive determination of systolic and diastolic myocardial velocities. The technique differs from standard blood fl ow–aimed Doppler mainly 100 J.D. Kasprzak and K.A. Wierzbowska-Drabik by different fi lter settings allowing recording of lower velocity and higher intensity signals, typical for ultrasound waves returned from moving myocardium. Tissue Doppler echocardiography allows direct recording of myocardial velocities (Figures 7.1 and 7.2), thus providing quantitative information for analysis of myocardial motion that is less dependent on the quality of gray-scale two- dimensional echocardiography data. Color TDE allows recording of regional velocities with high temporal resolution (exceeding 200 frames per second in high-end echocardiographic systems) from selected large regions of myocardium. The data can be stored in digital format and reformatted for display in different color formats or used for recalculation of local velocity curves (Figure 7.3). The advantage of color TDE is the availability of simultaneous recordings from numerous sam- pling points within the myocardium in a single heartbeat. However, it only provides local mean velocities as opposed to the pulsed wave tissue Doppler mode, which records peak instantaneous velocities. Pulsed TDE allows the measurement of regional myocardial velocities in a single location at a time as defi ned by sample volume placement, with the advantage of the highest temporal resolution. Positioning of the sample volume in the mitral annulus in apical views provides integrated information about systolic and diastolic velocities along the chosen aspect of the ventricular wall. Mitral annulus motion can be recorded by TDE with high feasibility and reproducibility. 4 Functional Parameters Derived from Myocardial Velocities Myocardial velocity measurement using echocardiography allows for the recalculation of deriva- tive parameters. Among them the most important are the markers of myocardial deformation — strain and strain rate. The main limitation of TDE is that myocardial velocities have limited ability to refl ect function in one particular region due to tethering between segments. 5 Thus, the recorded velocity refl ects both active contraction in the segment under investigation and passive motion resulting from tethering. Furthermore, regional NOR Myocardial velocities Mitral flow velocities AbR PSN RES FIGURE 7.1. Corresponding traces of mitral flow velocities and myocardial velocities in a normal individual and in patients with different stages of diastolic dysfunction. Notably, there is no increase in early diastolic myocardial velocity with progressive diastolic dysfunction. Mitral early diastolic flow velocity, however, increased progressively and shows typical pseudonormalization (third panels from left). NOR, normal filling; AbR, abnormal relaxation profile; PSN, pseudonormalized filling; RES, restrictive filling pattern. 7. Myocardial Velocities 101 FIGURE 7.2. Typical recording of myocardial velocities using the pulsed wave tissue Doppler technique. The main components are systolic wave (S′), early diastolic wave (E′), and late diastolic wave (A′). Brief isovolumic bi-directional velocity (with predominant positive component) is seen before S′. FIGURE 7.3. Diastolic regional asynchrony of the left ventricle. Color tissue echocardiography recording allows the reconstruction of myocardial velocity curves from basal septal and lateral segments of the left ventricle showing the delay of early relaxation velocity from the basal septum. Late diastolic velocities are syn- chronous. AVO, aortic valve opening; AVC, aortic valve closure; MVO, mitral valve opening; MVC, mitral valve closure. 102 J.D. Kasprzak and K.A. Wierzbowska-Drabik velocity is determined by cardiac translational motion. The motion of the mitral annulus refl ects integrated longitudinal shortening and lengthening of myocardium located between the apex and the measurement site. For example, in the setting of apical infarction, velocities in the basal portion of the ventricle will also be diminished, which may lead to misdiagnosis of dysfunction in these segments. On the other hand, the contraction of normal regions causes passive motion registered in neighboring nonviable myocardium. Recently introduced techniques based on TDE — strain and strain rate imaging — may overcome these limitations (Figure 7.4). 6,7 FIGURE 7.4. Normal left ventricular strain (top) and strain rate (bottom) curves recalculated from tissue Doppler velocities. Examples of the strain curves are from the basal lateral segment of the left ventricle. Cardiac cycle markers are shown on the graph. AVO, aortic valve opening; AVC, aortic valve closure; MVO, mitral valve opening; MVC, mitral valve closure. 7. Myocardial Velocities 103 Strain is a measure of deformation, occurring whenever myocardium contracts or relaxes. During the contraction of the ventricle, myocardium shortens longitudinally and circumferen- tially (negative strain) and thickens radially (positive strain). Diastole is characterized by reverse values of strain. Strain rate describes how fast myocardial shortening or lengthening occurs. It is calculated from myocardial Doppler velocities (V1 and V2) measured at two locations separated by a distance (L). During contraction, when myocardial shortening occurs, these two locations are getting closer, and, when the two locations are moving apart, lengthening takes place. Strain rate is defi ned as the instantaneous spatial velocity gradient 8,9 with the unit of s −1 : Strain rate SR (s −1 ) = (V2 − V1)/L Strain (or myocardial deformation, ε) repre- sents the fractional or percentage change in dimension and is calculated as change in length (L − L 0 ) divided by original length (L 0 ). 10 The reference noninvasive method that provides quantitative data about myocardial deformation in multiple planes is tagged MRI. In 1998, Heimdal et al. 11 introduced a clinical method to calculate strain rate from regional Doppler velocity gradients. Later, Urheim et al. 12 reported noninvasive measurements of strain by TDE, calculated as the time integral of strain rate. Clinically, strain can be calculated by several different formulas, but it is most often reported as Lagrangian strain (defi ned as current length divided by original length, or percent change in length). Regional diastolic longitudinal strain may be interpreted as regional lengthening fraction and radial strain as regional thinning fraction. Comparing the two parameters, strain rate is less load dependent and appears to be a better measure of local contractility than strain, 13 closely related to dP/dt max . On the other hand, strain rate imaging is more angle dependent than other Doppler techniques. Because of its load dependency, 14 strain (similar to ejection fraction) is still not a perfect measure of contractility or effi cacy of diastole, but its local assessment provides valuable insight into timing and amplitude of systolic and diastolic events. Another related modality derived from TDE myocardial velocity data is tissue tracking. 15 Using tissue tracking, tissue displacement is recalculated as the time integral of local velocities and color coded in consecutive phases of cardiac motion; however, there is little experience regarding the assessment of diastole. Tissue Doppler echocardiography data can also be converted into color-coded maps of cardiac cycle intervals (e.g., tissue synchronicity imaging 16 ) that can be applied to detect diastolic phase abnormalities. The current echocardiographic modalities used in humans for the study of local myocardial function are summarized in Table 7.1. Two-Dimensional Echocardiographic Velocity and Strain Measurements — Speckle Tracking Echocardiography The Doppler technique has signifi cant limitations mainly related to the ability to detect only the velocity component parallel to the ultrasound beam. Therefore, alternative strain measurement techniques are being sought. Recent progress in computing allows calculation of myocardial velocities and strain based on the detection of motion of a recognizable image pattern between consecutive image frames. This approach has no angle dependency and thus offers the potential to monitor myocardial strain in two dimensions. Human studies were performed using the comparison of adjacent radiofrequency signals 17 and speckle tracking techniques. 18 These studies confi rm that myocardial speckles are highly reproducible tissue ultrasound refl ectors that can be analyzed similar to magnetic resonance tags. Various software implementations of the technique are currently available, for example, under the trade names 2-Dimensional Strain (Figure 7.5) and Velocity Vector Imaging (Figure 7.6). 19 It has been shown that the method also allows the calculation of novel indexes potentially useful for the assessment of diastolic physiology, such as ventricular torsion. 20,21 Currently the technique is undergoing human validation, and signal to noise ratio versus frame rate tradeoff appears to be the main issue. In the future, the tracking algorithms may be applied to obtain three-dimensional velocity and deformation estimates. 22 104 J.D. Kasprzak and K.A. Wierzbowska-Drabik Magnetic Resonance Imaging An alternative method for measuring local myocardial velocities is MRI. Phase-contrast MRI has been used to measure transmitral and pulmonary vein fl ow. Phase-contrast MRI allows velocity encoding of moving structures in any direction at 14–18 ms temporal resolution and thus obtaining myocardial velocity estimates. Preliminary experience with a retrospective electrocardiographi- cally triggered Flash phase-contrast MRI technique with a velocity coding of 30 cm/s has been reported. 23,24 However, the values obtained at lower frame rates available with current MRI tech- nology are only moderately correlated with TDE data, and thus their clinical relevance remains yet unsettled. More data are available regarding the three- dimensional evaluation of myocardial deformation using myocardial tagging by MRI. 25 The data are usually obtained using electrocardiographi- cally gated, segmented k-space, fast gradient-echo pulse sequences with spatial modulation of mag- netization to generate a grid tag pattern that can be followed to analyze deformation 26 and TABLE 7.1. Echocardiographic modalities used to study myocardial motion. Modality Parameters Comments Myocardial velocities by Myocardial velocities measured in individual segments Assesses local myocardial function; possible pulsed wave TDE* detection of early changes (e.g., ischemic dysfunction during stress echocardiography) Mitral annulus velocities Peak diastolic annulus velocities and early to late Stratifies diastolic dysfunction and diagnoses by pulsed wave TDE* diastolic velocity ratio pseudonormalization. Reflects total longitudinal function of the selected ventricular wall and diastolic asynchrony of the left ventricle. Ratio of peak early diastolic mitral inflow velocity to Thoroughly validated for noninvasive estimation of left peak early diastolic mitral annulus velocity (E/E′) ventricular filling pressure and prognostic stratification Myocardial strain by Color-coded two-dimensional or curved M-mode) Measures deformation present in actively contraction or TDE display of myocardial deformation (shortening and elongating myocardium. Detects abnormalities in amplitude lengthening) and timing of regional myocardial function independent of passive heart motion. Attempts to assess atrial function Myocardial strain rate Color-coded (two-dimensional or curved M-mode) Less load-dependent measure of contractility than strain. by TDE display of rate of myocardial shortenting or Reproducibility problems, high sensitivity to noise lengthening (instantaneous spatial velocity gradient) Myocardial Color-coded (two-dimensional or curved M-mode) Detects abnormalitites in amplitude and timing of regional displacement by TDE display of temporal sequence of myocardial myocardial function (e.g., tissue tracking) displacement in systole or diastole Myocardial strain and Non-Doppler myocardial motion detection by Detects motion regardless of its direction and allows velocity by speckle computerized tracking of speckle patterns in B-mode calculation of strain components in orthogonal directions tracking images (two-dimensional strain). Recently validated; good echocardiography (STE) correlation between STE and sonomicrometry or magnetic resonance imaging tagging for systolic strain Myocardial velocity Non-Doppler myocardial velocity detection by Composite method incorporating the principle of speckle vector imaging computerized tracking of speckle patterns in B-mode tracking echocardiography; calculation of instantaneous image, displayed by arrows corresponding to velocity vectors relative to an operator-selected reference instantaneous velocity vectors point Left ventricular torsion Local left ventricular rotation can be measured by Potential tool for measuring systolic twist and diastolic by speckle tracking myocardial speckle tracking. Twist (torsion) is untwist of the left ventricle echocardiography calculated as difference between rotation of apex and base *Comparable data can be reconstructed from high temporal resolution acquisitions of a cardiac cycle using color mode tissue Doppler echocardiography (TDE). Color mode provides mean velocities, whereas pulsed mode provides peak velocities. 7. Myocardial Velocities 105 FIGURE 7.5. Quantitative analysis of left ventricular longitudinal strain recorded using the speckle tracking technique (two- dimensional strain) from an apical four-chamber view. Individual strain curves are calculated from six individual locations selected within the apical four-chamber view. At bottom left, the color strain data are reformatted into curvilinear M-Mode (the contour FIGURE 7.6. Vector velocity imaging of myocardial velocities in a patient with cardiomyopathy. Vectors represent instantaneous velocities and direction (left panel, vector length is proportional to instantaneous velocity) and can be displayed as a velocity graph in the time domain (top right panel) or as a curved color M-Mode graph (bottom right panel). (Courtesy of Siemens.) of the left ventricle is straightened onto the vertical axis, and the horizontal axis, time, corresponds to the single cardiac cycle duration). Diastolic strain shows early diastolic increase due to early filling and a smaller degree of late diastolic increase after left atrial contraction. SL, longitudinal strain; ES, end-systole. 106 J.D. Kasprzak and K.A. Wierzbowska-Drabik calculate local strain. Another MRI option offer- ing similar features is displacement encoding with stimulated echoes (DENSE). 27 However, application of these techniques to the assessment of diastolic dysfunction is limited to preclinical studies, 28 including specifi c aspects of diastolic physiology such as LV untwisting. 29 Clinical Interpretation of Myocardial Velocities Easily available noninvasive measurements of local myocardial velocities were rapidly incorpo- rated into diagnostic strategies for many cardiac pathologies. Normal LV myocardium presents with a distinct sequence of myocardial velocities depicted by pulsed wave or reconstructed color- coded tissue Doppler (see Figures 7.1 and 7.3). The main velocity components are the systolic wave (S′ or Sm) corresponding to ventricular ejection, early diastolic wave (E′ or Em) corresponding to early ventricular fi lling, and late diastolic wave (A′ or Am) during atrial contraction, corresponding to the late phase of ventricular fi lling. Additionally, brief velocities can be recorded during isovolumic contraction immediately before S′ (usually predominantly directed toward the apex) and during isovolumic relaxation immediately before E′ (usually predominantly away from the apex). The appearance and direction of the isovolumic phase velocities is quite variable, their signifi cance is unclear, and diagnostic utility is controversial. Peak acceleration during isovolumic relaxation was proposed as a load-independent measure of diastolic function. Peak septal acceleration during isovolumic relaxation correlated better than peak lateral wall acceleration with both pressure- derived peak negative dP/dt (r = −0.80) and tau (tau is the time constant for LV isovolumic pressure fall (r = −0.87) but not with left atrial pressure. 30 However, peak acceleration during the diastolic fi lling period did correlate (r = −0.81) with mean left atrial pressure. 31 There is a myocardial velocity gradient between the LV base and apex for both the systolic S′ and the diastolic E′ and A′ velocity waves. Both S′ and E′ wave velocities decrease with age, whereas the A wave velocity increases. Perez-David et al. 32 studied age-related changes in myocardial velocities in subendocardial, mesocardial, and subepi- cardial layers of myocardium. The decrease in early diastolic peak velocity was the most pro- nounced aging-related change. Color M-mode tissue Doppler imaging multilayer analysis showed also that subendocardium is more susceptible to age-related changes involving diastolic function. Yamada et al. 33 evaluated the effect of aging on diastolic LV wall motion velocity in 80 healthy persons with pulsed tissue Doppler imaging. In both posterior wall and ventricular septum, peak E′ diastolic wall motion velocities correlated inversely with age, and the peak atrial A′ wall motion velocities correlated directly with age. Mitral annular velocities, refl ecting the dynamics of the longitudinal axis of the heart, appear to be less dependent on loading conditions than mitral infl ow velocities, which makes them potentially useful as markers of diastolic physiology. In an experimental study, Hasegawa et al. 34 examined the effect of progressive diastolic dysfunction produced by rapid pacing on the dynamics of LV fi lling and the mitral annulus motion. Velocity of the early wave of mitral infl ow decreased with mild diastolic dysfunction but progressively increased in response to elevations in left atrial pressure. In contrast, E′ progressively declined with worsening of heart failure, despite the increases in left atrial pressure and the left atrial to LV pressure gradient, accurately refl ecting the progressive slowing of LV relaxation as heart failure developed. Consistent with the experimental fi ndings of Firstenberg et al. 35 Hasegawa et al. found that in the presence of normal LV relaxation, E′ is sensitive to changes in the left atrial to LV pressure gradient, but, with slowed relaxation, the dependence of E′ on the pressure gradient is greatly reduced. When LV relaxation is slowed, E′ occurs after LV pressure equals or later in diastole when LV pressure again exceeds left atrial pressure, and it is much less dependent on the pressure gradient. Numerous studies have assessed the impact of preload on myocardial diastolic velocities. The simplest parameter that can be derived from pulsed tissue Doppler recording is E′ diastolic mitral annular velocity, which at fi rst was reported as a load-independent index of LV diastolic function. According to later studies, acute reduction of preload (usually hemodialysis model) was 7. Myocardial Velocities 107 observed to affect not only mitral infl ow parameters but also tissue E′ wave velocity and mitral- to-apical fl ow propagation velocity. 36–38 Effects of the reduction of preload on left and right ventricular myocardial velocities in healthy subjects was assessed by Pela et al. 39 Lower body negative pressure caused progressive preload reduction that resulted in a signifi cant decrease of E′ and A′ myocardial velocities at the mitral and tricuspid annulus but without changing the E′/A′ ratio. On the other hand, during physiologic preload-alter- ing maneuvers, which included Trendelenburg, reverse Trendelenburg, and amyl nitrate inhala- tion, Doppler tissue early diastolic velocities were not signifi cantly affected, in contrast to standard transmitral Doppler fi lling indices. This suggests, within certain limits, a degree of load indepen- dence that is advantageous for a practical index of diastolic dysfunction. 40 Bruch et al. 41 documented an impact of increased stroke volume on mitral annulus motion measured by TDE. Systolic and early diastolic mitral annular velocities were elevated in the increased stroke volume group (due to mitral disease) compared with the controls and were signifi cantly reduced in the group with reduced stroke volume (after myocardial infarction, dilated cardiomyopathy, or hypertensive heart disease). The advantages of TDE for the assessment of local diastolic function have been most widely applied in the following fi elds: • Improved grading of diastolic dysfunction • Identifi cation of elevated fi lling pressures • High sensitivity detection of early stage myocardial disease • Evaluation of regional diastolic asynchrony • Differentiation between restrictive and constric- tive physiology of diastolic dysfunction • Prognostic stratifi cation The interest in the signifi cance of local myocardial velocities led to a series of clinically oriented studies, especially in coronary artery disease — by defi nition a regional entity. Even though not routinely used for the detection of ischemia, change in diastolic velocity parameters, including decrease of peak early diastolic velocity and decrease of tissue E′/A′ ratio, have been documented in segments supplied by stenotic arteries. In contrast, no differences in myocardial function were observed between well-perfused segments in patients with coronary artery disease and controls. 42 The number of abnormally relaxing segments was shown to determine the global mitral infl ow profi le. The subjects with coronary artery disease and normal mitral infl ow had on average 3.7 ± 2.7 segments with impaired regional diastolic function, and patients with delayed relaxation profi le had 10.3 ± 3 segments, which gave distinct statistical signifi cance (p < 0.001). 42 In the study by Moreno et al., 43 pulsed tissue Doppler was useful in differentiating between viable and nonviable segments in patients with three-vessel coronary artery disease. In another study, viable segments presented higher early diastolic velocities than nonviable segments and a lower prevalence of E/A ratio <1. The assessment of regional myocardial early diastolic velocities was also performed during dobutamine infusion. Greater than 2 cm/s decrease of early diastolic velocity for the examined segment had a higher diagnostic accuracy for ischemia (84% sensitivity and 93% specifi city) than two-dimensional echocardiography (78% sensitivity and 71% specifi c- ity) or even radionuclide scintigraphy (61% sensitivity and 86% specifi city). 44 Tissue Doppler echocardiography was also used for intraopera- tive monitoring of LV function during coronary grafting with left internal mammary artery using transesophageal echocardiography. 45 Immediately after mammary artery grafting, the peak systolic and late diastolic anterior wall velocities increased, indicating improvement in the systolic but con- comitant impairment in the diastolic function of the grafted anterior wall. Myocardial Velocities and Grading of Diastolic Dysfunction The left ventricle fi lls in diastole in response to the pressure gradient from the left atrium to the left ventricle early in diastole after mitral valve opening and late in diastole during atrial systole. With mild diastolic dysfunction, transmitral E is reduced due to a slowing of the rate of LV relaxation. In more advanced levels of diastolic dysfunction, E returns to its normal values (pseudonormalization) due to the effect of 108 J.D. Kasprzak and K.A. Wierzbowska-Drabik increasing left atrial pressure, which increases the early diastolic transmitral pressure gradient. With even more severe dysfunction, the peak E rate may be higher than normal. 46,47 Transmitral fl ow is determined by multiple parameters such as fi lling pressure, LV elastic recoil and myocardial relaxation, atrial function, and the compliance of receiving chambers. In addition, fl ow can be modifi ed by mitral valve abnormalities or pericardial constraint. Thus, many additional parameters, including early diastolic ventricular fi lling propagation velocity, pulmonary venous fl ow velocities and duration, responses to preload modifi cations by Valsalva maneuver, nitroprusside administra- tion, and leg elevation, have been proposed to improve the defi nition of diastolic physiology. The ability of TDE to record myocardial velocities in vivo has been well validated for this application. In the setting of normal LV relaxation, peak early mitral annular velocity (E′) precedes peak early transmitral fl ow (E) recorded by pulsed wave Doppler. In impaired relaxation E′ follows E. 48 Rodriguez et al. 49 suggested that in patients with diastolic dysfunction elastic recoil related to mitral annular motion is lost. Hemodynamic refl ection of the elastic recoil, the minimal pressure recorded in the left ventricle, tends to be low in subjects with normal recoil. 50 Nagueh et al. 51 aimed to identify the hemodynamic determinants of the mitral annulus diastolic velocities measured by tissue Doppler in an experimental study in dogs. The authors observed a positive relation between E′ and the transmitral pressure gradient (r = 0.57, p = 0.04) and strong correlations with the time constant (tau) for LV isovolumic pressure fall (r = −0.83, p < 0.001), peak LV −dP/dt (r = 0.8, p < 0.001) and minimal LV pressure (r = −0.76, p < 0.01). The relation between E′ and the transmitral pressure gradient was abolished in the settings when tau was longer than 50 ms. The late diastolic velocity of the mitral annulus also had signifi cant positive relations with left atrial dP/dt, left atrial relaxation, and inverse correlation with LV end-diastolic pressure. Also in patients, in contrast to the curvilinear relationship of traditional Doppler indices with the severity of myocardial disease as they progress from normal to restrictive physiology, tissue Doppler parameters show a uniphasic decline in velocities (Figure 7.2): the peak velocity of the mitral annulus during early diastole is reduced in patients with impaired relaxation. The E′ declines with age and in LV hypertrophy and is perceived as a useful index of LV relaxation, inversely related to the time constant of relaxation. 52 Patients with diastolic dysfunction often have increased endo- cardial and perivascular fi brosis, which alter E′ velocity. 53 Contrary to E, E′ remains reduced in patients with pseudonormalized or restrictive fi lling patterns, despite elevated left atrial pressure. This has been demonstrated in a classic study by Sohn et al., 54 which opened way to every- day clinical use of myocardial diastolic velocities and was confi rmed in various patient popula- tions. 55–57 Chapter 13 provides a comprehensive review of how to estimate LV fi lling pressure by TDE and other echocardiographic modalities. Abnormal Diastolic Velocities as Early Markers of Subclinical Myocardial Disease Diastolic velocities were proposed in many pathologies as early markers of disease affecting myocardial function. In young, obese, otherwise healthy women, concentric LV remodeling was found to be related with decreased systolic and diastolic functions. Obese women (body mass index >30 kg/m 2 ) had lower systolic and diastolic myocardial velocities than nonobese, and both parameters were negatively correlated with body mass index. In multivariate analysis, body mass index was the only independent predictor of systolic and diastolic myocardial velocities. 58 Regional changes in myocardial systolic and diastolic velocities can be detected by TDE in patients with hypertrophic cardiomyopathy. A signifi cantly decreased myocardial function in basal septum was observed in hypertrophic cardiomyopathy patients compared with hyper- tensives. 59 Although regional function is most abnormal in markedly hypertrophied walls, the impairment is also seen in segments not affected by hypertrophy and in patients with a mutation for hypertrophic cardiomyopathy but without clear phenotypic changes. 60 Impairment of diastolic function measured by tissue Doppler was seen also in uremic patients [...]... Circulation 1993;88:221 5–2 223 52 Zile MR, Brutsaert DL New concepts in diastolic dysfunction and diastolic heart failure: Part I: diagnosis, prognosis, and measurements of diastolic function Circulation 2002;105:138 7–1 393 53 How to diagnose diastolic heart failure European Study Group on Diastolic Heart Failure Eur Heart J 1998;19:99 0–1 003 54 Vasan RS, Levy D Defining diastolic heart failure: a call for... characterization of isolated diastolic heart failure in comparison to systolic heart failure JAMA 2002;288:2 14 4 2 150 43 Kitzman DW Exercise intolerance Prog Cardiovasc Dis 2005 ;47 :36 7–3 79 44 Pina IL, Apstein CS, Balady GJ, et al Exercise and heart failure: a statement from the American Heart Association Committee on exercise, rehabilitation, and prevention Circulation 2003;107:121 0– 1225 45 Lapu-Bula R, Robert... of diastolic dysfunction in the intact heart In Lorell BH, Grossmann W, eds Diastolic Relaxation of the Heart Boston: Kluwer Academic, 19 94: 16 7–1 46 , with permission.) 8 Diastolic Versus Systolic Heart Failure an important role in the mechanisms of exercise intolerance in both SHF and DHF 129 TABLE 8.3 Prevalence of specific symptoms and signs in systolic heart failure (SHF) and diastolic heart failure. .. 2002;106:1 34 2–1 348 46 Kitzman DW, Higginbotham MB, Cobb FR, et al Exercise intolerance in patients with heart failure and preserved left ventricular systolic function: failure of the Frank-Starling mechanism J Am Coll Cardiol 1991;17:106 5–1 072 47 Sullivan MJ, Hawthorne MH Exercise intolerance in patients with chronic heart failure Prog Cardiovasc Dis 1995;38: 1–2 2 133 48 Packer M Abnormalities of diastolic. .. Korkmaz ME, Flachskampf F, Garcia M, Thomas JD Is Doppler 41 42 43 44 45 46 47 48 49 50 51 tissue velocity during early left ventricular filling preload independent? Heart 2002;87:33 6–3 39 Bruch C, Stypmann J, Gradaus R, Breithardt G, Wichter T Stroke volume and mitral annular velocities Insights from tissue Doppler imaging Z Kardiol 20 04; 93:79 9–8 06 Garcia-Fernandez MA, Azevedo J, Moreno M, Bermejo J,... of Systolic and Diastolic Heart Failure Heart failure is defined as the pathologic state in which the heart is unable to pump blood at a rate required by the metabolizing tissues or can do so only with an elevated filling pressure When the heart failure results from systolic dysfunction, the pathologic state can be called systolic heart failure (SHF) When the heart failure results from diastolic dysfunction... Mechanisms and models in heart failure: a combinatorial approach Circulation 1999;100: 99 9–1 008 Cohn JN Structural basis for heart failure Ventricular remodeling and its pharmacological inhibition Circulation 1995;91:250 4 2 507 Francis GS Pathophysiology of chronic heart failure Am J Med 2001;110 Suppl 7A:37S 46 S Effects of enalapril on mortality in severe congestive heart failure Results of the Cooperative... Circulation 2002;105:119 5–1 201 40 Baicu CF, Zile MR, Aurigemma GP, et al Left ventricular systolic performance, function, and contractility in patients with diastolic heart failure Circulation 2005;111:230 6–2 312 41 Zile MR, Baicu CF, Gaasch WH Diastolic heart failure abnormalities in active relaxation and passive stiffness of the left ventricle N Engl J Med 20 04; 350:195 3–1 959 42 Kitzman DW, Little WC,... assessment of diastolic dysfunction using Doppler echocardiography provides useful information on the severity of heart failure and the prognosis.3 1–3 5 Specifically, Brucks et al.31 examined the association of systolic and diastolic function with severity of heart failure assessed by plasma brain natriuretic peptide levels and prognosis in 1 04 heart failure patients with an EF . 2003;91 (4) :47 3 4 80. 46 . Ohno M, Cheng CP, Little WC. Mechanism of altered patterns of left ventricular fi lling during the development of congestive heart failure. Circula- tion 19 94; 89:2 24 1–2 250. 47 Cardiol 2003 ;42 : 157 4 1 583. 8 Diastolic Versus Systolic Heart Failure Hidekatsu Fukuta and William C. Little 119 Introduction Heart failure is defi ned as the pathologic state in which the heart is. peptide levels in systolic heart failure importance of left ventricular diastolic function and right ventricular systolic function. J Am Coll Cardiol 20 04; 43 :41 6 4 22. 78. Edvardsen T, Skulstad

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