Evaluation of Systolic Function of the Left Ventricle

Transcription

1 Evaluation of Systolic Function of the Left Ventricle Roxy Senior MD DM FRCP FESC FACC and Vinay Kumar Bhatia PhD MRCP Department of Cardiovascular Medicine, Northwick Park Hospital and Institute for Medical Research, Harrow Middlesex, UK Address for correspondence: Dr R Senior MD DM, FRCP, FESC, FACC Consultant Cardiologist and Director of Cardiac Research, Department of Cardiovascular Medicine, Northwick Park Hospital, Watford Road, Harrow Middlesex, HA1 3UJ United Kingdom. Tel: +44 (0) Fax: +44 (0) roxy.senior@virgin.net 1

2 Introduction The assessment of left ventricular function is one of the most clinically important and frequently requested tasks in echocardiography. We are witnessing a progressive development in echocardiographic methods and techniques including the use of higher frequency transducers, tissue Doppler, harmonic imaging and trans-pulmonary or left sided contrast agents. Initial attempts to assess left ventricular function included only M-mode measurements, such as the left ventricular internal dimension in diastole and systole, from which parameters such as fractional shortening and velocity of circumferential shortening could be derived. With the advent of two-dimensional echocardiography, area measurements and their derived volume calculations were also employed. Doppler echocardiography, by providing information on intracardiac blood flow, gives valuable information on systolic flow parameters and more recently diastolic function. There are several recently developed Doppler methodology based algorithms, such as strain rate imaging, that are substantially more sophisticated with respect to determining ventricular function. M-Mode Linear Measurements Measurements directly from two-dimensional echocardiography or two-dimensionally directed M-mode echocardiography have supplanted isolated M-mode recordings. The resolution of M-mode echocardiography for precise identification of timing is superior to that of two-dimensional echocardiography. Although one can argue that the spatial resolution of a dedicated M-mode beam is superior to that of two-dimensional echocardiography, in practice, the ability to visualize the entire left ventricle and to ensure a true minor-axis dimension (i.e. truly perpendicular to the long axis of the left ventricle) mitigates these potential advantages. Refinements in imaging processing have allowed greater levels of gray-scale registration with a substantially refined visualization of both the right and left sides of the ventricular septum and the blood pool to tissue boundary. It is now common practice to measure the actual visualized thickness of the ventricular septum and other chamber dimensions as defined by the actual tissue-blood interface rather than the distance between the leading edge echoes as was previously performed (Table 1). The location of these measurements is schematized in Figure 1 and further demonstrated in Figure 2. 2

3 Table 1: Linear Measurements of Left Ventricular Size and Function Parameter Formula Abbreviation Units LV internal dimension in diastole (cm) LVIDd mm LV internal dimension in systole (cm) LVIDs mm Fractional shortening (LVIDd LVIDs)/LVIDd FS % or 0.XX Meridional wall stress in systole PR/h σ m mm Hg or dyne-cm 2 Cubed LV volume in diastole (LVIDd) 3 cm 3 or ml Cubed LV + myocardial volume (IVS + LVIDd + PW) 3 cm 3 or ml Velocity of circumferential shortening* (LVIDd-LVIDs)/(LVIDd x ET) VCf circumference/sec * measured from the apical four chamber view; ET ejection time; IVS intraventricular septal thickness; PR pressure x radius ; PW posterior wall There are several limitations of linear measurements of the left ventricle for determining ventricular performance. One of the most obvious is that many forms of acquired heart disease, especially coronary artery disease, will result in regional variation in ventricular function. By definition, an M-mode assessment provides information regarding size and contractility along a single line. This may either underestimate the severity of dysfunction if only a normal region is interrogated or overestimate the abnormality if the M-mode beam transits exclusively through the wall motion abnormality. A second limitation of the M-mode assessment is that it often does not reflect the true minor-axis dimension. This phenomenon is illustrated in Figure 2 and is very common in elderly patients in whom there is angulation of the ventricular septum. There are several additional parameters of ventricular performance than can be derived from linear measurements. In many instances, this requires digitization of an M-mode for calculation of derived parameters. These include rates of systolic wall thickening of the posterior wall and calculation of velocity of circumferential shortening. The latter can be calculated, if the minor axis is assumed to represent a circle of known diameter, by determining the rate of change of that circumference and is typically standardized by normalizing to heart rate. An additional linear measurement that has been employed in the past is the descent of the base. During ventricular contraction, the base of the heart moves toward the apex and the magnitude of this motion is directly proportional to systolic function. Typically, M-mode interrogation is undertaken of the lateral mitral valve annulus and the amount of excursion toward the transducer is then determined (Figure 3). There is a relative linear correlation between the degree of annular excursion during systole and global systolic function. This technique may nowadays be considered to be superseded by direct measures of ventricular volume and ejection fraction. Of note, this is the same principle used in Doppler tissue imaging (DTI) of the annulus for determination of diastolic and systolic function. 3

4 Indirect M-Mode Markers of Left Ventricular Function These include an increased E-point septal separation and gradual closure of the aortic valve during systole. The magnitude of opening of the mitral valve, as reflected by E-wave height, correlates with transmitral flow and, in the absence of significant mitral regurgitation, with left ventricular stroke volume. The internal dimension of the left ventricle correlates with diastolic volume. As such, the ratio of mitral excursion to left ventricular size reflects the ejection fraction Normally, the mitral valve E point (maximal early opening) is within 6 mm of the left side of the ventricular septum. In the presence of a decreased ejection fraction, this distance is increased (Figure 4). Inspection of the aortic valve opening pattern can also provide indirect evidence regarding systolic function of the left ventricle. If left ventricle forward stroke volume is decreased, there may be a gradual reduction in forward flow in late systole, which results in gradual closing of the aortic valve in late systole. This results in a rounded appearance of the aortic valve in late systole (Figure 5). Two- dimensional measurements Two-dimensional echocardiography provides inherently superior spatial resolution for determining left ventricular size and function. Its role in obtaining linear measurements has already been discussed. A number of different two-dimensional echocardiography views have been used to provide information regarding ventricular systolic function, some of which rely exclusively on area measurements and others of which rely on calculation of volume from the two-dimensional image. Table 2 outlines the commonly used two-dimensional measurements and their derived calculations. Table 2: Area-/Volume-Based Measurements for Ventricular Size and Function Parameter Abbreviations Formula Units Short axis diastolic area (at mid LV) ASx d cm 2 Short axis systole area (at mid LV) ASx s cm 2 Fractional area change FAC (ASx d ASx s )ASx d % or 0.XX Four-chamber LV area in diastole ALV 4c-d cm 2 Four-chamber LV area in systole ALV 4c-s cm 2 LV volume in diastole a LVV d ml LV volume in systole a LVV s ml Stroke volume SV LVV d = LVV s ml Ejection fraction EF SV/LVV d % or 0.XX a Determined by Simpson rule, area length method etc ; LV left ventricle 4

5 Two-dimensional images are used to determine ventricular volume, from which stroke volume and ejection fraction are than calculated. The most common method for determining ventricular volumes is the Simpson s rule or the method of disks. This technique requires recording an apical four or two chamber view from which the endocardial border is outlined in end-diastole and end-systole. The ventricle is then mathematically divided along its long axis into a series of disks of equal height. Individual disk volume is calculated as height multiplied by disk area where height is assumed to be the total length of the left ventricular long axis divided by the number of segments or disks. The surface area of each disk is determined from the diameter of the ventricle at that point. The ventricular volume is then represented by the sum of the volume of each of the disks, which are equally spaced along the long axis of the ventricle. This methodology is illustrated in Figure 6. If a ventricle is symmetrically contracting, then either the four or two chamber view will then reflect the true ventricular volume. In any view, foreshortening of the ventricular apex will result in inaccurate assessment of the left ventricular ejection fraction and most often in overestimation of the ejection fraction. If there is asymmetry of the ventricular geometry or a systolic wall motion abnormality, a single-plane view will have reduced accuracy for the reasons previously mentioned. In this instance, a biplane determination of volume will increase accuracy and is recommended by the American Society of Echocardiography. There are several limitations to using Simpson s rule measurements of left ventricular volumes. Firstly, apical views must be used and myocardial dropout is always a potential problem. The use of tissue harmonic imaging and contrast echocardiography can decrease but not always eliminate this problem. For accurate volume determination, the transducer must be at the true apex and the ultrasonic cross-sectional beam must be though the center of the left ventricle. These conditions are frequently not met resulting in an artifactual small left ventricular volume. There are several clues that help to determine whether the transducer is at the true apex. In the normal ventricle, the apex does not move from apex to base during filling or emptying of the chamber. Additionally, the true apex is the thinnest area of the left ventricle. If the visualized apex has the same thickness as the surrounding walls and appreciable motion in systole, it is likely to be a tangential cut through the left ventricle rather than a true on-axis view. In an effort to automate and simplify volume determination, instrumentation is commercially available that will automatically identify and track the endocardial border of the left ventricle. The endocardial borders, which are automatically tracked, are then likewise subject to calculation of volume using the methodology described above, thereby providing an instantaneous ventricular volume display. The stroke volume and ejection fraction can be calculated from the maximal and minimal volumes (Figure 7). A further refinement of this methodology is the ability to export the instantaneous ventricular volume and then combine it with instantaneous determination of systolic pressure. This allows the creation of a pressure volume loop which has been shown to provide load-independent information regarding ventricular contractility. A final refinement of the determination of ventricular volume involves the application of three-dimensional echocardiography. Three-dimensional imaging or reconstruction obviously reduces the limitation on single or biplane imaging which has the potential to either disproportionately represent or underestimate a wall motion abnormality. By creating a three-dimensional image set, all regions of the ventricular myocardium will be incorporated in the volume determination. Numerous studies have demonstrated the superiority of threedimensional imaging for determining ventricular volume especially in abnormally shaped ventricles. 5

6 Regional left ventricular function The most common form of acquired heart disease encountered in western modern medicine is coronary artery disease along with its sequelae of myocardial ischemia, infarction, and chronic remodelling. By definition, the early phases of coronary artery disease result in segmental or regional abnormalities rather than global abnormalities. Evaluation of segmental or regional function requires a different set of analysis algorithms and tools from those used for global function (Table 3). Table 3: Methods for Evaluation of Regional Wall Motion Abnormalities Visual/subjective Descriptive: normal, hypokinetic, akinetic, dyskinetic normal myocardial thickness versus scar Location: anterior, lateral, inferior, posterior, apex, basal, mid, apical segments Semi-quantiative WMS or WMSI Normal = 1 ) Hypokinetic = 2 ) Scored for each segment Akinetic = 3 ) Dyskinetic = 4 ) WMSI = n = N n= 1 WMS N Quantitative Anatomy based Radian change Regional area change Center-line chordal shortening (applied t short axis or apical views) Doppler tissue imaging Local velocity Velocity gradient (endocardial epidcardial) Myocardial displacement Myocardial strain Strain rate imaging WMS, wall motion score; WMSI, wall motion score index Normal ventricular contraction consists of simultaneous myocardial thickening and endocardial excursion toward the center of the ventricle. There is some regional 6

7 heterogeneity of this motion with the proximal inferoposterior and lateral walls contracting somewhat later than the septum and inferior wall. There is also heterogeneity of the degree of endocardial excursion and myocardial thickening with greater absolute and percentage changes from diastole to systole at the base when compared with the apex. These changes may be exaggerated with myocardial ischemia. Figure 8 schematizes the currently recommended wall segment model for description of regional wall motion. Most previous schemes have used a 16-segment model which includes a portion of the true apex in each of the four distal segments. A shortcoming of the 16- segment model is that if an abnormality is isolated to the apex, it is represented in each of four separate segments (segments 13-16), thus resulting in a disproportionate contribution to the wall motion score especially if the abnormality was limited to the true apex. More recently, a 17 th segment has been proposed that represents the true apex. Addition of the 17 th segment allows more precise communication with investigators and clinicians dealing with other imaging modalities which have traditionally recognized a true apical segment. Depending on the size of an apical wall motion abnormality it may either enhance the accuracy of the wall motion score, if the abnormality is confined to the true apex, or result in overestimation if it involves portions of the four distal segments. When portions of the distal segments are involved, they will also be given an abnormal wall motion score which again may result in disproportionate weighting of an apical wall motion abnormality. When describing regional wall motion abnormalities, it is important not only to characterize their location but also their extent and severity. When dealing with coronary artery disease, the location of a wall motion abnormality is predictive of the location of the coronary culprit lesion. Figure 8 also depicts the relationship of the predefined 16 segments of the left ventricle to the traditional distribution of the left anterior descending, circumflex, and right coronary arteries. It should be emphasized that there can be substantial overlap in the more distal distributions of these arteries as well as in the posterior circulation in general. Additionally, after coronary artery bypass surgery, the location of wall motion abnormalities may be atypical depending on the location of the myocardium perfused by the residual native arteries and by bypass grafts. In clinical practice, one often encounters atypical wall motion abnormalities, one of which is tardokinesis or a segment with delayed systolic contraction. This phenomenon may be difficult to appreciate in real time and is best noted by viewing the segment with M-mode, a frame-by-frame cine loop and trimming the cine loop to display only the first half of systole or with tissue Doppler imaging or strain rate imaging. Another confusing segmental wall motion finding is early relaxation. A given segment appears to relax or move outward before the rest of the chamber. Thus far, this finding has not correlated with any pathology and is generally considered to be a normal variation. It is noted most often with stress echocardiography at high heart rates. The same analysis methods noted for tardokinesis may help identify this wall motion pattern. Non-ischaemic Wall Motion Abnormalities Several conditions result in wall motion abnormalities unrelated to ischemia or coronary artery disease and are catergorised in Table 4. 7

8 Table 4: Non-ischaemic Regional Wall Motion Abnormality Conduction system based Left bundle branch block Ventricular pacing Premature ventricular contractions Ventricular pre-excitation (Wolf-Parkinson-White syndrome) Abnormal ventricular interaction Right ventricular volume overload Right ventricular pressure overload Pericardial constriction Miscellaneous After cardiac surgery Congenital absence of the pericardium Posterior compression Ascites Hiatal hernia Pregnancy Doppler Evaluation of Global Left Ventricular Function Clinicians have used Doppler spectral profiles to evaluate global left ventricular function since the early 1970s. The earliest, conceptually simplest, and still probably one of the more clinically useful methods for following left ventricular function is to evaluate the time velocity integral (TVI) of the left ventricular outflow tract or ascending aorta. Basically, the principle is that if the cross-sectional area of the chamber is known, then the product of that cross-sectional area and the mean velocity of flow equals the volumetric flow. In a pulsatile flow system such as the beating heart, in which the flow velocity is confined to mechanical systole, the volume calculated equals the forward ventricular stroke volume in the aorta. This forward stroke volume can then be multiplied by the heart rate to obtain cardiac output. Typically, the areas evaluated for determination of systolic flow and hence global left ventricular performance have been the left ventricular outflow tract, with the Doppler interrogation taking place from the apex of the heart or occasionally the ascending aorta using a right parasternal approach Figures 9 and 10. Using either approach (and in the absence of aortic insufficiency), the calculated stroke volume should accurately reflect actual volume of flow for the analyzed beat. However, two points are worthy of mention: firstly, this methodology assumes a flat velocity profile when in actual fact the flow profile is parabolic and therefore the mean velocity by this technique may not reflect the true cross sectional velocity. Secondly, because the formula for cross sectional area involves the square of the radius, any error in measuring the LVOT diameter will result in a substantial error in the flow calculation. Myocardial Performance Index The myocardial performance index (MPI) is an expression of global ventricular performance. It is a simple index that includes both systolic and diastolic parameters and can be applied to 8

9 either the left or right ventricle. The MPI incorporates three basic time intervals that are readily derived from Doppler recordings: the ejection time (ET); isovolumic contraction time (IVCT) and the isovolumic relaxation time (IVRT). From these values, the MPI can be calculated from the following formula:- MPI = ( IVCT + IVRT ) / ET Systolic dysfunction is associated with a prolongation of IVCT and a shortening of the ET. Therefore, this will result in an increase in the MPI, the normal range is 0.39 ± 0.05, and values above 0.50 are considered abnormal. The MPI may be of value in patients in whom tricuspid regurgitation is either not present or cannot be quantified to assess for pulmonary hypertension. Determination of Left Ventricular dp/dt An additional method for deriving parameters of left ventricular global function is the calculation of left ventricular dp/dt. This represents the rate of increase in pressure within the left ventricle. If confined to the early phases of systole, during isovolumic contraction, this is a relatively load-independent measure of ventricular contractility. The dp/dt has long been a standard calculation using a high-fidelity micrometer catheter in the catheterization laboratory. Using the spectral display of a mitral regurgitation jet, similar information regarding the rate of pressure development within the left ventricle can be derived. If this measurement is undertaken in the early phases of systole while the increasing ventricular pressure is less than the aortic pressure it is relatively load independent. The method by which this is performed is to record the mitral regurgitation spectral profile at a high sweep speed (typically 100 mm/sec), as shown in Figures 11 and 12. Examination of the upstroke of the velocity curve can then be used to derive instantaneous measurements. To determine the dp/dt, one calculates the time difference in milliseconds from the point at which the velocity is at 1 m/sec and 3 m/sec. The time between these two points represents the time that it takes for a 32 mm Hg change to occur in the left ventricular cavity, dp/dt is then calculated as dp/dt 32 mm Hg time (seconds). Determination of dp/dt using this method has been validated against invasive hemodynamic measurements. In addition to determining this parameter in early phases of systole, the negative dp/dt over the analogous pressure change (36 to 4 mm Hg) in diastole can also be calculated and may provide information regarding diastolic function. Either a reduced positive or negative dp/dt carries significant prognostic implications. There are contributors to left ventricular dp/dt in addition to intrinsic myocardial contractility. In the presence of marked mechanical dysynchrony, (as typified by left bundle branch block) dp/dt may be reduced not due to decreased contractility but rather as a consequence of contractile dysynchrony and inefficiency. Normal LV systolic function is correlated with a dp/dt of greater than 1000 mm Hg /s. Doppler Tissue Velocity Briefly, this technique relies on altering receiver gains and frequency filters so that the Doppler signal arising from relatively dense, slow-moving targets such as the myocardium and cardiac annulus are interrogated for their velocity. Doppler tissue imaging (DTI) can be superimposed as a colour display on 2D and M-mode, saturating the typical anatomic 9

10 structure information (Figures 13 and 14). More commonly for the determination of function, a pulsed Doppler sample volume is placed within an area of the myocardium or the annulus and the velocities at that point then displayed for quantification (Figure 15). When evaluating global performance, DTI velocities will show some regional variation based on which area of the mitral annulus is interrogated (septal vs. lateral). Although maximal accuracy may be obtained by averaging values, most laboratories standardize clinical measurements to either the septal or lateral annulus to maximize efficiency. The annular velocity in systole has shown a good correlation with the left ventricular ejection fraction over a wide range of ventricular function (Figure 16). Strain Rate Imaging and Other Derived Doppler Tissue Parameters DTI determines the direction and velocity of wall motion. There are several additional parameters of systolic function that can be derived from this velocity determination (Figure 17). The simplest to understand is displacement defined as excursion (in millimetres). This is calculated as the product of systolic velocity and duration of contraction. Figures 18 and 19 are examples of the myocardial displacement calculation in a normal subject and in the presence of a lateral wall infarction. Strain rate imaging is a newly developed variation of DTI that provides a high-resolution evaluation of regional myocardial function. Figure 17 outlines the methodology for deriving this parameter. For strain rate imaging, DTI is used to simultaneously determine velocities in two adjacent points as well as the relative distance between those two points. Strain rate is defined as the instantaneous rate of change in the two velocities divided by the instantaneous distance between the two points. Positive strain rate represents active contraction and negative values relaxation or lengthening between the two points. As with the endocardialepicardial velocity gradient, strain rate has been demonstrated to be a more sensitive and earlier indicator of regional dysfunction than many routine techniques. The images in Figures 20 and 21 were recorded in a normal subject and in a subject with anterior wall infarction respectively. Strain rate imaging has tremendous temporal resolution as well and can be used to demonstrate subtle phenomena such as post-systolic contraction. Figure 22 is a graphic representation of instantaneous strain rate over time at multiple interrogation points, demonstrating both the temporal and potential high spatial resolution of this technique. 10