Left ventricular systolic function and contractility
ecgwaves.com · Clinical Echocardiography
Chapter 1: Left Ventricular Function
Left ventricular function and its echocardiographic assessment
Cardiac function depends on a large number of parameters, including atrial function, valvular function, and ventricular function. A large body of science has demonstrated that these parameters are highly interdependent and rather complex. Indeed, myocardial mechanics constitute a whole research field. Cardiac function is also dependent on circulatory, pulmonary, renal and neurohormonal factors. These factors, which influence cardiac function primarily by affecting ventricular function, include blood pressure, venous return, pulmonary gas exchange efficiency, the concentration of catecholamines, angiotensin, hemoglobin, etc. A vivid example of how cardiac function can be affected by targeting peripheral mechanisms is illustrated by the use of ACE inhibitors and beta-blockers in heart failure; these drugs antagonize neurohormonal mechanisms and improve cardiac function and survival dramatically in heart failure (Yancy et al).
Acquiring a basic understanding of cardiac function requires an understanding of myocardial mechanics. This section covers all clinically relevant aspects of myocardial mechanics, with emphasis on echocardiographic aspects. The bulk of the discussion concerns left ventricular function, which has been studied intensely over several decades. Left ventricular function correlates strongly with total and cardiovascular mortality (Curtis et al). Among patients with coronary heart disease, left ventricular function is actually a stronger predictor of death than the atherosclerotic burden. Assessment of the size, mass, geometry, and function of the left ventricle is fundamental for the diagnosis and prognosis of most cardiac diseases, including coronary artery disease, heart failure, arrhythmias, structural heart disease, etc.
Over the years, a large number of parameters have been introduced to assess left ventricular function. The majority of these parameters can be calculated or approximated using two-dimensional echocardiography. The most widely adopted parameter is the ejection fraction (EF). The concept of ejection fraction was introduced by Braunwald and colleagues in 1962 (Braunwald et al) and it has since then been the dominating method for assessing ventricular function. For better or worse, ejection fraction has become virtually synonymous with left ventricular function.
An obvious drawback with the use of the ejection fraction is that it only assesses systolic function. Research in recent years has demonstrated that left ventricular diastolic function is also fundamental to global cardiac function. Diastolic dysfunction results in a special type of heart failure, referred to as heart failure with preserved ejection fraction (HFPEF). HFPEF may be more common than heart failure with reduced ejection fraction (HFREF, Redfield et al).
Echocardiography is the principal modality for investigating left ventricular systolic function and diastolic function. M-mode, 2D echocardiography and Doppler are all used to examine various parameters. Three-dimensional (3D) echocardiography has become increasingly common, and may be as precise as cardiac MRI (magnetic resonance imaging) for calculating ejection fraction.
References
Yancy et al: 2017 ACC/AHA/HFSA Focused Update of the 2013 ACCF/AHA Guideline for the Management of Heart Failure. A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Failure Society of America
Curtis et al: The association of left ventricular ejection fraction, mortality, and cause of death in stable outpatients with heart failure. JACC.
Braunwald et al: Determination of fraction of left ventricular volume ejected per beat and of ventricular end-diastolic and residual volumes. Experimental and clinical observations with a precordial dilution technic. Circulation.
Redfield et al: Heart Failure with Preserved Ejection Fraction. NEJM 2016.
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Chapter 2: Myocardial Mechanics: Structure and Function of Myocardial Fibers
Structure and contractile function of myocardial fibers
The left ventricular wall can be subdivided into several layers. These layers are similar to those seen in arteries throughout the circulatory system (Figure 1). The ventricular wall consists of an inner lining (endocardium), a thick muscle layer (myocardium) and an outer lining (epicardium). These layers are analogous to tunica intima, tunica media, and tunica adventitia, respectively.
Figure 1. Layers of the left ventricular wall, pericardium and ventricular cavity.
The endocardium
The endocardium lines the atria, ventricles and the heart valves. Similar to vascular endothelium, the endocardium contains an underlying basement membrane and a small layer of loose connective tissue. The endocardium joins the endothelium that lines the greater vessels connected to the heart.
The epicardium
The outermost layer of the ventricular wall is the epicardium, which contains fibroelastic connective tissue, blood vessels, lymphatics and adipose tissue.
The myocardium
The thick muscular layer between the endocardium and the epicardium is called myocardium. It contains cardiac muscle fibers, connective tissue and a very high density of capillaries. The muscle fibers are organized into several sheets that wrap around the ventricle with varying orientation. As explained below, this enables the ventricle to contract in several directions simultaneously.
The subendocardium is the muscle layer closest to the endocardium. The subendocardium has the poorest prerequisites in the case of myocardial ischemia. All myocardial infarctions affect the subendocardium (hence the term subendocardial infarction). Myocardial infarctions affecting only the subendocardium are usually caused by subtotal coronary artery occlusions. This is discussed in detail in the chapter NSTEMI (Non ST Elevation Myocardial Infarction).
Orientation of myocardial fibers
The orientation of myocardial fibers varies, and this allows the left ventricle to contract in a highly sophisticated and effective way. Muscle fibers adjacent to the endocardium are longitudinally oriented, which results in longitudinal shortening (Figure 2A). Muscle fibers in the middle layer (mid-wall) are oriented circularly around the short-axis. Contraction in this muscle layer results in radial shortening, meaning that the diameter of the ventricular cavity decreases (Figure 2B). The muscle fibers adjacent to the epicardium are oriented approximately 60° in relation to the fibers of the mid-wall. Contraction in this layer results in a twisting motion of the entire ventricle. The basal segments are twisted clockwise, and the apex is twisted counterclockwise. The twisting contraction is called circumferential shortening (Figure 2C).
Figure 2A-2C. The orientation of myocardial muscle fibers results in longitudinal, radial and circumferential shortening (contraction).
Longitudinal, radial and circumferential shortening occur simultaneously. This results in the AV plane being pulled towards the apex (which is fixed to the diaphragm via the pericardial sack), while the myocardium travels towards the center of the cavity and the entire ventricle is twisted. Moreover, all myocardium also thickens during the contraction, which further reduces the volume of the cavity, thereby squeezing out blood into the aorta. Longitudinal contraction, radial contraction, circumferential contraction, and myocardial thickening are assessed by means of echocardiography.
These mechanisms provide a highly effective contraction that maximizes the ejection of blood (Figure 3). this is demonstrated by the fact that the muscle fibers themselves can only be shortened by about 13% of their length, but the sum of all contractions results in a reduction of the diameter and length of the ventricle by 20%, and more than 60% of the end-diastolic volume can be ejected to the aorta.
Figure 3. Myocardial contraction (shortening) occurs in three directions: longitudinally, radially and circumferentially.
Chapter 3: Ventricular Pressure-Volume Relationship: Preload, Afterload, Stroke Volume, Wall Stress & Frank-Starling’s law
Ventricular Pressure-Volume Relationship
Left ventricular pressure-volume relationship can be described by a loop diagram with volume depicted on the x-axis and left ventricular pressure on the y-axis. If left ventricular pressure and volume are measured continuously during a single cardiac cycle, the loop diagram shown in Figure 1 is obtained.
Figure 1. Left ventricular pressure-volume relationship during a single cardiac cycle.
In Figure 1 we begin in diastole, when the mitral valve opens. When the mitral valve opens, blood flows into the left ventricle. This results in a rapid increase in left ventricular volume, but only a small increase in left ventricular pressure. This is explained by the fact that the left ventricle is capable of relaxing and expanding rapidly during diastole. The term compliance is used to describe the ability of the left ventricle to relax during diastole. Compliance is fundamental to diastolic function. High compliance is desirable and means that the ventricle is capable of filling rapidly while operating at low end-diastolic pressure.
EDV (End Diastolic Volume) denotes the volume in the left ventricle, just before contraction commences. Left ventricular pressure increases when the contracting starts, and when left ventricular pressure exceeds left atrial pressure, the mitral valve closes. Upon closing of the mitral valve, left ventricular pressure increases rapidly while both the aortic valve and the mitral valve are closed. This phase is called isovolumetric contraction (IVC; Figures 1 and 2).
Figure 2. Left ventricular pressure-volume relationship and ECG waveforms during systole and diastole.
When left ventricular pressure exceeds diastolic pressure in the aorta, the aortic valve opens and blood is ejected into the aorta. Left ventricular volume decreases as the ventricle contracts and pumps blood into the aorta. After the maximum pressure is reached, the ventricle relaxes, which results in diminished left ventricular pressure. The aortic valve closes when aortic pressure exceeds left ventricular pressure.
ESV (End Systolic Volume) is defined as left ventricular volume at the closure of the aortic valve. Upon aortic valve closure, the ventricle relaxes and pressure drops rapidly, without any significant changes in volume. This phase is referred to as isovolumetric relaxation (IVR; Figures 1 and 2). When the ventricular pressure is less than the left atrial pressure, the mitral valve opens and the cycle is repeated.
Stroke volume (SV) and stroke work (SW)
Stroke volume (SV) is defined as the difference between ESV and EDV, which is equivalent to the width of the loop in Figure 1. The area within the loop is the stroke work (SW), which is discussed below.
The pressure-volume loop in Figure 1 can be moved along the black lines called EDPVR and ESPVR. EDPVR (End-Diastolic Pressure-Volume Relationship) shows the relationship between ESV and left ventricular volume. The EDPVR curve shows that the left ventricle can withstand large pressure increases but at a certain threshold, pressure rises rapidly with further volume increases. This is explained by the existence of an upper limit for ventricular compliance. The greater the left ventricular compliance, the less steep the slope of the EDPVR curve, and vice versa.
ESPVR (End-Systolic Pressure-Volume Relationship) shows how maximum pressure varies with volume. The smaller the EDV, the lower the maximum generated pressure, and the smaller the stroke volume. Thus, low preload leads to low EDV, which results in lower generated pressure and ultimately smaller stroke volume.
Two-dimensional (2D) and three-dimensional (3D) echocardiography allows for the calculation of stroke volume. The drawback of stroke volume as a measure of left ventricular function is that it ignores the ability of the ventricle to generate pressure. This is evident from Figure 1, which demonstrates that stroke volume is the difference between ESV and EDV, which can be calculated without considering pressure (the y-axis). Moreover, stroke volume also ignores the ability of the ventricle to shorten. These drawbacks become clear when examining patients with dilated cardiomyopathy (DCM). These patients may have normal stroke volumes, due to their large ventricular volumes, despite severe impairment of left ventricular function.
The ability to generate pressure can be calculated by estimating stroke work (SW).
Stroke work (SW)
In physics, work is equivalent to the product of power (f) and distance (d). The work required to move an object is the product of the force needed to move the object and the distance the object is moved. With regards to the left ventricle, the object is blood, and the force is the pressure generated by the left ventricle. Stroke work is the work performed to move blood from the ventricle into the aorta.
Stroke work is represented by the area within the pressure-volume loop in Figure 1. In vivo measurement of stroke work requires continuous measurement of ventricular pressure and volume during the cardiac cycle, which is not technically feasible. However, stroke work can be approximated as the product of stroke volume and mean arterial pressure (MAP). This does, however, result in an underestimation of stroke work.
Cardiac work
Cardiac work (CW) is the product of heart rate (HR) and stroke work (SW):
CW = HR • SW (SW = SV • MAP)
Frank-Starling’s law (mechanism)
Stroke volume is greater in the supine position, as compared with an upright position. This is because venous return increases in the supine position. More blood flows back to the heart, leading to increased ventricular filling (EDV). The left ventricle responds to increased EDV by automatically increasing stroke volumes. It follows that the heart can adapt its stroke volumes to variations in left ventricular filling. This phenomenon is called Frank-Starling’s mechanism (law).
Figure 3. Frank-Starling’s mechanism.
Frank and Starling discovered that an increase in Left Ventricular End Diastolic Pressure (LVEDP) leads to stronger contractions and greater stroke volumes. This mechanism is independent of neurohumoral stimuli, although such stimuli can adjust the intensity of the mechanism. As evident in Figure 3, the Frank-Starling curve is modified by afterload and inotropy of the myocardium.
A rather simple cellular mechanism seems to explain Frank-Starling’s mechanism. When ventricular filling is increased, the myocardial fibers and their sarcomeres, are stretched. This results in troponin C becoming more sensitive to calcium (sensitivity depends on sarcomere length), which accelerates the interaction between actin and myosin, and ultimately produces more force.
The difference between contractility and contractile function
There is a discreet difference between contractility and contractile function.
Contractility describes the intrinsic ability of the myocardium to contract, regardless of preload and afterload. Contractility is the ability of individual muscle fibers to shorten. Contractility is not studied with echocardiography.
Contractile function describes the ability of the myocardium, in a given hemodynamic state (at certain preload and afterload conditions). This is synonymous with systolic function and can be estimated by echocardiography.
Preload
Preload is the force that stretches myocardial fibers during diastole. Stretching can be described by end-diastolic pressure, end-diastolic volume or end-diastolic diameter. However, neither pressure, volume, nor diameter is normalized. Therefore, preference should be given to preload adjusted for the surface area of the ventricle, which is equivalent to end-diastolic wall tension (discussed below).
Preload reserve is an important parameter. It indicates how much reserve there is in preload. A ventricle with a large preload reserve can receive a larger volume of blood (i.e. increase its LVDP). In the upright position, all healthy individuals have a large preload reserve, which becomes useful during physical activity. In the supine position, however, the preload reserve is small. This is because venous return increases so much in the supine position, that the ventricle is already stretched and operates at or close to its reserve.
Afterload
Afterload is the force that the myocardium generates during systole. Afterload can also be described in terms of wall tension, which means that the force is adjusted for surface area. Afterload depends on the thickness of the myocardium. Individuals with high blood pressure (high afterload) often develop compensatory hypertrophy, which may normalize afterload per surface area.
Wall tension
Wall tension is the force applied to the wall of the ventricle. The force should be adjusted for the ventricular surface area, resulting in wall tension per surface area (σ):
σ = (p·r)/2·t p = transmural pressure; r = ventricular radius; t = wall thickness.
Transmural pressure (p) is the pressure in the left ventricle. It can be approximated; this is done by approximating p to systolic pressure (measured as conventional blood pressure).
Chapter 4: Assessing left ventricular systolic function
Methods for assessing systolic function (contractile function)
Several echocardiographic measurements are available to assess left ventricular systolic function. These methods elucidate slightly different aspects of systolic function and their combined use allows for careful mapping of systolic function. It is important to be familiar with the advantages and disadvantages of each method. An overview of available methods follows. Each method is discussed in detail in subsequent chapters.
Stroke volume (SV)
Stroke volume is the volume of blood pumped from the left ventricle into the aorta during systole. It is easily calculated by measuring VTI (Velocity Time Integral), using pulsed wave Doppler, in the aortic valve. The stroke volume is the product of VTI and area of the LVOT, as illustrated in Figure 1.
Figure 1. Calculation of stroke volume in the LVOT, using pulsed wave Doppler and measurement of the diameter.
Cardiac output (CO)
Cardiac output is the product of stroke volume (SV) and heart rate (HR).
CO = HR · SV
Cardiac Index (CI)
Cardiac Index (CI) is the ratio between cardiac output (CO) and body surface area (estimated by weight and height). Thus, cardiac index is cardiac output normalized to body surface area. The ultrasound system calculates body surface area using the patient’s sex, weight and height.
CI = CO / BSA BSA = Body Surface Area (m2)
Ejection fraction (EF)
Ejection fraction is the fraction of the end-diastolic volume (EDV, i.e blood volume in the ventricle at the end of diastole) that is pumped out during systole. Currently, two-dimensional (2D) echocardiography for calculation of ejection fraction is the dominant method for assessing left ventricular function (systolic function). It should be noted, however, that three-dimensional (3D) echocardiography offers greater precision in the calculation of ejection fraction, and 3D measurements will presumably replace 2D measurements in the future. Cardiac MRI (magnetic resonance imaging) is considered the gold standard for the calculation of ejection fraction.
Recommended chapter: Ejection fraction
Ejection acceleration time (EAT)
Ejection acceleration time measures the maximum systolic velocity (m/sec) in the LVOT. This parameter correlates well with left ventricular systolic function.
EAT = vmax/time
Fractional shortening (FS)
Fractional shortening (FS) is calculated by measuring the change (% reduction) in left ventricular diameter during systole. It is considered a poor measure of systolic function; it is only reliable if the left ventricle has normal geometry and no significant wall motion abnormalities. Fractional shortening can be measured in M-mode and 2D.
FS = (LVEDD – LVESD)/LVEDDLVEDD = left ventricular end-diastolic diameter; LVESD = left ventricular end-systolic diameter; The fraction is multiplied by 100 to obtain percentage (%).
| Normal FS | >25% (M-Mode) |
|---|---|
| >18% (Direct 2-D measurement) |
Tissue Doppler
Tissue Doppler records the speed and direction of myocardial motion. This is possible because myocardium also reflects ultrasound waves. In order to analyze myocardial motion, the ultrasound system must filter out all sound waves reflected by other structures, notably sound waves reflected by blood. This is achieved by filtering out signals with low amplitude and high velocity; such signals represent reflections from blood flow. Instead, the ultrasound system focuses on sound waves with high amplitude and low velocity; these waves are reflected from myocardium.
Tissue Doppler can also be used to measure the velocity of the mitral annulus, as it travels from the base to the apex during systole. Mitral annulus velocity correlates well with ejection fraction, stroke volume and is thus a measure of systolic function.
Strain and strain rate
Myocardium deforms during systole and diastole. The deformation is due to contraction and relaxation, which results in myocardium moving and deforming. Strain is the echocardiographic term for deformation. Strain and strain rate measure the extent and velocity of myocardial deformation. These parameters can be assessed using tissue Doppler or speckle tracking. The latter method is the dominating for assessing deformation.
dP/dt
In the setting of mitral regurgitation, left ventricular systolic function can be estimated by studying the acceleration of the regurgitant jet (Figure 2). The better the systolic function, the greater the increase in left ventricular systolic pressure, and, thus, the greater the acceleration in the regurgitant jet. Hence, dP/dT is a proxy for the capacity of the left ventricle to generate pressure during systole. It represents a marker of global contractile function.
dP/dT is measured by placing continuous wave Doppler in the MR jet (mitral regurgitation jet) during the isovolumetric contraction (i.e. the contraction occurring between mitral valve closure and aortic valve opening), as seen in Figure 2. Left atrial pressure is constant during this phase, which implies that the acceleration in MR jet speed is due to increase in left ventricular pressure.
Figure 2. Calculation of dP/dt.
More specifically, dP/dt is derived by measuring the time interval (s) elapsing for the MR jet to accelerate from 1 m/s to 3 m/s. Then, the constant 32 is divided by the time interval in order to approximate left ventricular pressure :
dP/dt = 32/t t=time interval (s)
dP/dt has the unit mmHg/s.
| Variable | Definition |
|---|---|
| T | Time (1 to 3 m/sec MR) (seconds, s) |
| dP/dt | dP/dt (mmHg/s) |
| Normal | ≥1200 mmHg/s |
Chapter 5: Left ventricular mass and volume (size)
Size and mass of the left ventricle
Left ventricular mass is a flawed proxy for ventricular systolic function and load. The mass is, however, an important parameter in the assessment of ventricular hypertrophy and cardiomyopathy. Numerous formulas have been developed to approximate ventricular mass. Most formulas are simple mathematical equations, included in all ultrasound systems, and assume that the geometry of the left ventricle is normal.
Figure 1. Calculation of left ventricular mass.
massLV = 1.05 (masstotal – masscavity)LV = left ventricle; 1.05 = mycoardial mass constant.
Left ventricular hypertrophy (LVH)
A diagnosis of left ventricular hypertrophy is based on total left ventricular mass, which can be calculated by obtaining the measurements shown in Figure 1. The ultrasound system automatically calculates RWT (Relative Weight Thickness), provided that the patient’s weight, height and sex are entered. RWT is a measure of the type of hypertrophy.
Generally, hypertrophy is defined as wall thickness exceeding 12 mm. Thus, wall thickness >12 mm should raise suspicion of hypertrophy.
Chapter 6: Ejection fraction (EF): Physiology, Measurement & Clinical Evaluation
Ventricular ejection fraction (EF)
For several decades, ejection fraction (EF) has been the dominating method for assessing left ventricular systolic function. Ejection fraction is simple to calculate; if the left ventricle contains 100 ml of blood at the end of diastole and 40 ml is pumped out during systole, then the ejection fraction is 40%. Thus, the ejection fraction is the stroke volume (SV) divided by the end-diastolic volume (EDV):
EF (%) = (SV/EDV)·100EF = ejection fraction
Since stroke volume (SV) is the difference between end-diastolic volume (EDV) and end-systolic volume (ESV), EF can also be calculated as:
EF (%) = [(EDV-ESV)/EDV]·100
Normal values for ejection fraction (EF)
Studies in healthy individuals suggest that the mean ejection fraction is 63% to 69%. European and American guidelines concur that the lower normal limit for ejection fraction is 55%. Reduced ejection fraction is defined as ejection fraction <55%. This implies that left ventricular pumping capacity is reduced and it is synonymous with heart failure with reduced ejection fraction (HFREF).
| Average ejection fraction | 63% to 69% |
|---|---|
| Lower normal limit | 55% |
Ejection fraction is routinely examined at rest, which does not reveal the functional (maximum) capacity of the left ventricle, as this would require measuring the ejection fraction during submaximal exercise testing. Ejection fraction reserve is the available reserve in ejection fraction that can be generated during exercise.
Effect of preload and afterload on ejection fraction
Ejection fraction is highly dependent on preload and afterload. A rapid increase in preload (e.g by increasing venous return to the heart in supine position) leads to an immediate increase in ejection fraction. Similarly, a decrease in afterload (e.g by means of decreased resistance in the systemic circulation) leads to an increase in ejection fraction. The opposites are also true; decreased preload results in reduced ejection fraction, and increased afterload results in reduced ejection fraction.
Since ejection fraction is affected by preload and afterload, it is necessary to consider loading conditions when evaluating the measured ejection fraction. Ideally, ejection fraction should be assessed during normal, with regards to the patient, loading conditions. If repeated echocardiograms yield pronounced variations in ejection fraction, then it is likely that variations in preload and afterload, rather than changes in contractile function, explains the varying ejection fraction.
Ejection fraction and left ventricular volume
Ejection fraction is also affected by left ventricular volume (size). For example, athletes have large ventricular dimensions and often lower ejection fraction, as compared with non-athletes. This is explained by the fact that the athlete’s heart produces significantly larger stroke volumes, which satisfy the body’s oxygen demand despite smaller ejection fractions.
In general, individuals with small ventricular volumes tend to have high ejection fractions. This inverse relationship appears to be a compensatory mechanism, such that small ventricular volumes are compensated with greater ejection fractions.
The significance of ventricular size becomes obvious in the setting of hypertrophic cardiomyopathy (HCM, HOCM). Individuals with hypertrophic cardiomyopathy may display normal, or supranormal ejection fraction, despite manifest heart failure and severe symptoms. These individuals exhibit pronounced hypertrophy, resulting in a reduction of ventricular volume and subsequently an increase in ejection fraction. Stroke volumes are generally reduced in hypertrophic cardiomyopathy.
Reduced ejection fraction
Numerous conditions can lead to reduced ejection fraction. Cardiomyopathy, valvular heart disease, diabetes, hypertension, renal failure, ischemic heart disease (coronary heart disease) are among the common causes. The mechanisms leading to deterioration in ejection fraction vary for these conditions. Two examples follow.
AORTIC VALVE REGURGITATION – In the setting of aortic valve regurgitation, blood regurgitates from the aorta back to the left ventricle. This results in ventricular volume overload, which the ventricle attempts to counteract by dilating and developing hypertrophy. The dilatation prevents the volume overload from causing pressure overload, and the development of hypertrophy enables the ventricle to eject larger volumes of blood. Thus, dilatation and hypertrophy mitigate the consequences of volume overload. Unfortunately, the long-term effects of dilatation and hypertrophy are remodeling of the myocardium and neurohormonal disturbances that gradually impair contractility and lead to the development of myocardial fibrosis. Ultimately, contractility of individual muscle fibers worsen and ejection fraction deteriorates.
CORONARY ARTERY DISEASE – Coronary heart disease may lead to acute myocardial infarction, which implies that some myocardium permanently ceases to contract, and overall ejection fraction is reduced.
As evident from these examples, the mechanisms leading to reduced ejection fraction may vary substantially. However, once ejection fraction has been reduced, the natural course is strikingly similar across all etiologies. Impaired ejection fraction triggers neurohormonal mechanisms (see below) that are initially beneficial, but in the long run cause deterioration of the condition. Symptoms of heart failure (eg, dyspnea, impaired performance, edema, etc.) develop sooner or later.
Neurohormonal activation in heart failure with reduced ejection fraction
Reduced ejection fraction leads to reduced cardiac output. High-pressure baroceptors in the left ventricle, aortic arch, and carotid sinus detect reductions in cardiac output and respond by increasing their afferent signaling to vasomotorcenter in the central nervous system (CNS). Activation of the vasomotorcenter results in increased activity in efferent sympathetic pathways that innervate the heart, skeletal muscle, kidney and peripheral vasculature. Activation of the vasomotorcenter also lead to increased secretion of vasopressin from the posterior pituitary gland (Figure 2).
Figure 2. Reduced ejection fraction and development of heart failure. Adapted from Hartupee et al (2017).
As evident in Figure 2, a range of neurohormonal mechanisms is triggered when ejection fraction is reduced. These mechanisms and their consequences include:
Increased sympathetic activity leads to increased heart rate and initially increased contractility, which may temporarily alleviate symptoms, but the long-term effects of sympathetic activity are devastating. Beta-blockers, which reduce the activity of sympathetic fibers, improve both cardiac function and survival dramatically in heart failure.Increased sympathetic activity leads to increased secretion of aldosterone, renin (activation of RAAS) and consequently increased concentrations of angiotensin II. This results in increased blood pressure and retention of salt and water. This subsequently results in increased cardiac preload and, in the long term, volume overload.In cardiac muscle, sympathetic activity results in desensitization of beta-adrenergic receptors, diminished norepinephrine stores, hypertrophy, fibrosis, apoptosis and increased risk of arrhythmias. Ultimately, this leads to further impairments in systolic and diastolic function.Sympathetic stimuli to peripheral vessels result in hypertension and vascular hypertrophy.When compensatory mechanisms are not sufficient to maintain normal intraventricular pressure, ventricular dilatation commences. The dilatation may initially lead to increased contractility in individual muscle fibers (refer to Frank-Starling’s law), but contractile function deteriorates gradually.
Visual estimation of ejection fraction
Ejection fraction can be estimated visually. This means that the ejection fraction is estimated by means of eyeballing the two-dimensional video clips. This method is obviously subjective and requires a substantial amount of experience. However, studies (Gudmundsson et al) indicate that eyeballed ejection fraction correlates well with quantitative assessments of ejection fraction.
Calculation of ejection fraction with quantitative methods
Objective estimation of ejection fraction requires measurements in M-mode or two-dimensional (2D) echocardiography. Measurements in M-mode are based on two brave assumptions: (1) ventricular geometry must be perfectly normal and (2) there must not be regional differences in contractile function. These assumptions are frequently violated, such that M-mode is inferior to 2D echocardiography. Thus, 2D methods are preferred for the calculation of ejection fraction. Several methods are available, of which the best validated and most widely used is Simpson’s method.
Simpson’s biplane method for calculation of ejection fraction (EF)
Simpson’s biplane method requires making four simple measurements in order to obtain end-diastolic volume (EDV) and end-systolic volume (ESV), which are then used to calculate ejection fraction:
EF (%) = [(EDV-ESV)/EDV]·100
Simpson’s method is presumably the best 2D method for estimating left ventricular EDV and ESV, and thus ejection fraction. This method is less dependent on the geometry of the ventricle, as compared with M-mode.
Simpson’s biplane method requires tracing (i.e drawing a line along) the endocardium in apical four-chamber view (A4C) and apical two-chamber view (A2C) in diastole and systole. The entire endocardium, from mitral annulus to mitral annulus must be traced (Figure 3). The ultrasound system then divides the area into a number of equal disks and reconstructs these so that volumes can be calculated.
Figure 3. Calculation of ejection fraction (EF) with Simpson’s biplane method.
The term biplane means that the measurements are made in two planes, namely A4C and A2C. As mentioned above, the formula used to calculate ejection fraction is as follows:
EF (%) = [(EDV–ESV)]/EDV·100
Foreshortening and underestimation of ejection fraction
When visualizing the left ventricle from apical windows, small angle errors may lead to large differences in ventricular dimensions. Actually, all angle errors lead to underestimation of ventricular volumes. This is evident in Figure 4, which illustrates how angle errors lead to foreshortening.
Figure 4. Foreshortening.
References
Hartupee et al (2017): Neurohormonal activation in heart failure with reduced ejection fraction. Nature Reviews Cardiology (2017).
Gudmundsson et al: Visually Estimated Left Ventricular Ejection Fraction by Echocardiography Is Closely Correlated With Formal Quantitative Methods (2005).
Chapter 7: Fractional shortening for estimation of ejection fraction
Fractional shortening (FS) for estimating systolic function
Fractional shortening (FS) is calculated by measuring the percentage change in left ventricular diameter during systole. It is measured in parasternal long axis view (PLAX) using M-mode. The end-systolic and end-diastolic left ventricular diameters are measured. The following formula is used to calculate fractional shortening:
FS (%) = (LVEDD – LVESD / LVEDD) • 100
Figure 1. Calculation of fractional shortening.
Fractional shortening is a rather poor measure of left ventricular systolic function. This is due to the following reasons:
Left ventricular geometry must be normal.There must not be regional differences in contractile function. Otherwise, the point of measurement may not be representative.Ventricular activation must be normal. For example, in the setting of left bundle branch block (LBBB), fractional shortening is not representative of ventricular function, since the activation proceeds abnormally.
Normal value for fractional shortening (FS)
| Normal FS, M-mode | >25% |
|---|---|
| Normal FS, 2D measurement | >18% |
Advantages of fractional shortening
If ventricular geometry is normal and there are no regional wall motion abnormalities, then fractional shortening correlates strongly with ejection fraction. Similar to ejection fraction, fractional shortening is affected by preload and afterload. It possible to calculate fractional shortening using measurements in 2D.
Chapter 8: Strain, strain rate and speckle tracking: Myocardial deformation
Myocardial deformation: strain, strain rate, speckle tracking
As previously discussed, the left ventricular wall can be subdivided into three layers: the inner lining (endocardium), a thick muscle layer (myocardium) and an outer lining (epicardium). The myocardium is the thick muscle layer, in which the muscle fibers are organized into several sheets wrapping around the ventricle with varying orientation. This organization allows the left ventricle to contract in a highly sophisticated and effective way (Figure 1).
Myocardial fibers adjacent to the endocardium are longitudinally oriented (from base to apex) and yield a longitudinal shortening (Figure 1A), which means that the base is pulled towards the apex.
Myocardial fibers in the middle layer (mid-wall) are oriented circularly around the short-axis. Contraction in this layer results in radial shortening, meaning that the diameter of the ventricular cavity decreases (Figure 1B).
The muscle fibers adjacent to the epicardium are oriented approximately 60° in relation to the fibers of the mid-wall. Contraction in this layer results in a twisting (rotating) motion of the entire left ventricle. Basal segments rotate clockwise, and the apex rotates counterclockwise. This rotating, or twisting, contraction is called circumferential shortening (Figure 1C).
Left ventricular function depends on a complex interaction between the muscle fibers in these layers, which collectively produces a highly efficient pumping mechanism.
Figure 1A-2C. The orientation of myocardial muscle fibers results in longitudinal, radial and circumferential shortening (contraction).
Traditional methods for investigating left ventricular function — e.g ejection fraction (EF), fractional sorting (FS), etc — do not elucidate regional variations in contractile function, or the effectiveness of longitudinal, radial, and circumferential contraction. Thus, methods such as ejection fraction may provide easily obtained parameters, but fail to provide important insights into left ventricular mechanics.
Regional differences in contractile function are of utmost importance, particularly in the setting of (confirmed or suspected) myocardial ischemia. As a clear example, consider a patient with ischemic heart disease, who has normal ejection fraction but impaired contractile function in the inferior wall. This finding is referred to as inferior wall motion abnormality and it may evidence of myocardial infarction, which would have implications for the management of this patient, regardless of the ejection fraction. Hence, it is important to detect and characterize wall motion abnormalities.
Methods have been developed for the quantification of regional myocardial function. These methods analyze the motion and deformation (change in shape) of the myocardium during systole and diastole. Deformation imaging has been implemented in clinical practice and is now widely recommended. This chapter discusses the theoretical and practical aspects of deformation (strain, strain rate) and myocardial motion.
Myocardial motion
Myocardial motion concerns the movement of myocardium from one point to another. During the motion, all myocardium within a particular region displays the same velocity. The motion is characterized by two variables: distance and velocity. Distance denotes the distance the myocardium travels, and velocity denotes the speed of the motion.
Myocardial motion and velocity can be measured with pulsed tissue Doppler (see Pulsed Wave Doppler). Tissue Doppler allows for sampling of specific regions or structures. This is done by placing the sample volume (SV) in the region of interest. This is routinely done to measure the velocity of the mitral annulus, which during systole travels towards the apex, and then recoils to its starting position. Mitral annulus velocity is used to study longitudinal contraction; during systole, the base, and thus the mitral annulus, moves towards the apex and during diastole, the opposite motion occurs. The mitral annulus velocity is an important measure of global longitudinal systolic function. Figure 2 demonstrates the measurement of mitral annulus velocity with pulsed tissue Doppler.
Figure 2. Pulsed tissue Doppler analyzing motions of the mitral annulus.
Color tissue Doppler can also be used to study regional velocities. It has the advantage of studying larger areas of myocardium simultaneously, which does, however, come at the expense of lower temporal resolution.
Disadvantages of using motion as a marker of function
The major disadvantage of using motion as a measure of regional contractile function is that all myocardium is interconnected. Motion in one area is directly affected by motion in adjacent areas. This allows even necrotic myocardium (e.g due to myocardial infarction) to move during systole and diastole (viable and contracting myocardium surrounding the necrotic zone will pull and push the dead myocardium, such that it displays a motion). It follows that measurement of motion in a single point can be highly misleading since the motion in one point depends on the motions of the surrounding myocardium.
The solution is to use deformation as a measure of function. The rationale for measuring deformation is that dead myocardium will not deform (change shape) during systole and diastole, regardless of motions in surrounding myocardium. Measuring deformation has proven to be superior to measuring motion.
Strain and strain rate: Measures of deformation
Strain is defined as shortening or lengthening of myocardium. Shortening occurs when myocardium contracts, and lengthening occurs when myocardium relaxes (stretches out). These two deformations can be studied by means of echocardiography. The main objective is to determine whether myocardial motion is normal by measuring the degree of deformation (strain) and the speed at which it occurs (strain rate).
Strain and strain rate should be relatively similar throughout the myocardium since all regions should deform approximately equally during the cardiac cycle. Examination of strain and strain rate can identify regional differences in deformation, which indicates pathology. Moreover, it can elucidate the overall myocardial deformation, which is an indicator o global function.
Strain: The degree of deformation
Strain is the degree of deformation, i.e. how much the myocardium is deformed. It is calculated by measuring the extent of shortening or lengthening during the cardiac cycle. The formula for strain is as follows:
Strain = (L–L0)/L0·100L0 = initial myocardial length; L = final length.The constant 100 transforms strain into percent (%).
If the initial length of the area measured is 10 mm and the final length is 12 mm, then strain will be +20% (positive strain). If the initial length is 10 mm and the final length is 7 mm, then strain will be –30% (negative strain). Contraction (shortening) gives negative strain and relaxation (lengthening) gives positive strain (Figure 3).
Figure 3. Myocardial strain.
Strain can be measured in all directions of deformation; it is possible to study longitudinal, radial and circumferential strain.
Strain rate: the speed of deformation
Strain rate is the speed of deformation, i.e. deformation per unit time (seconds). It can be mathematically proven that deformation per unit time is equivalent to the difference in velocity within an area divided by the length of the area, as follows:
Strain rate = (V1 – V2) / d
According to the above formula, strain rate can be obtained by measuring the velocity (using pulsed tissue Doppler) in two points of myocardium, and the distance between the points (Figure 4).
Figure 4. Strain rate. Velocity is measured in two points along the ultrasound beam (V1, V2). The difference in velocity (V1–V2) is divided by the distance (d) between them, which provides the strain rate.
Strain rate is a measure of the velocity of deformation between two measurement points. As for strain, a negative value indicates contraction, and a positive value indicates relaxation.
By mapping strain rate in many parts of the myocardium simultaneously, it is possible to determine if strain and strain rate is equal in all parts, which is expected. Pulsed tissue Doppler computes both strain and strain rate simultaneously.
Figure 5. Examination of strain (longitudinal strain) with tissue Doppler. Septal strain is examined. Y-axis depicts strain (% deformation) and x-axis depicts time. Source
Figure 6. Measurement of longitudinal strain rate with Doppler. The Y-axis shows strain rate (1/s) and the x-axis shows time. Negative values are observed during systole (contraction). Source
Figure 7. Parameters on strain and strain rate diagrams. Both panels show the same myocardial area, i.e basal septum. Source
To calculate strain and strain rate using tissue Doppler, a frame rate of 100 FPS is used. The advantage of tissue Doppler is that the temporal resolution is very high and the method is adequate for measuring longitudinal strain. Unfortunately, tissue Doppler is angle dependent (incorrect angle of insonation leads to an underestimation of strain rate) and, moreover, radial and circumferential strain cannot be investigated. These shortcomings have been overcome by means of speckle tracking, which is discussed next.
Speckle tracking
Speckle is the term for the structures that the myocardium displays on the ultrasound image. If you carefully examine Figure 7, you can see that the myocardium does not produce a homogeneous signal, but a pattern of variations in the echo signal is seen. These structures are called speckles and they arise due to the interactions of ultrasonic waves (reflections, proliferation, interference) with the tissue.
Figure 8. (A) The myocardium is encircled within the dashed lines. As seen here, the myocardium is not homogeneous on the ultrasound image. It appears structured, in varying shades of gray. These structures are called speckles (B) The same image with speckles highlighted.
Speckle tracking
Speckles move during systole and diastole and it is possible to analyze the velocity and distance of their motions. This is called speckle tracking and this method has largely replaced tissue Doppler to measure strain and strain rate. Figure 9 illustrates how speckles are tracked in the two-dimensional plane. Strain is defined as the change in the distance between two speckle-points, divided by the initial distance:
S = (L1−L0) / L0L0 = initial distance between the points.L1 = new distance between the points.
Figure 9. Speckle tracking.
Speckle tracking is entirely based on the ultrasound image, and no Doppler measurements are required. This makes speckle tracking more reliable since it is not sensitive to the angle of insonation. However, speckle tracking offers a lower temporal resolution, which makes the method poorer in the setting of tachycardia (precision is reduced at high heart rate) and when studying speckles located remotely (from the transducer). Moreover, speckle tracking is inferior for lateral motions, which is due to the fact that ultrasound has a lower lateral resolution, as compared with axial resolution.
Speckle tracking uses 40 to 80 FPS (frames per second) and up to 100 FPS may be needed during tachycardia. Speckle tracking can be used for all four chambers, although measurements in the right atrium and right ventricle are generally less precise due to difficulties identifying speckles.
Global and regional strain
Modern ultrasound systems calculate both regional and global strain. Regional strain is the strain calculated in each segment. Global strain is the average of all individual segments.
Figure 10. Left ventricle in short-axis view (PSAX) at the papillary muscle level. Circumferential strain is calculated. Upper left panel: the left ventricle is divided into 6 segments, which are analyzed separately. Upper right panel: a line is drawn for each segment. The maximum values for each segment are printed in the lower right panel (automatically calculated values). The lower middle panel shows circumferential and radial strain and strain rate. Lower left panel shows a color-coded M-mode image of the selected parameters. Source
Figure 11. Apical four-chamber view (A4C) with analysis of longitudinal strain. The patient has heart failure with asynchronous activation of the left ventricle (ventricular myocardium is not activated synchronously). As can be seen here, septal parts (yellow arrow and yellow-marked myocardium) are activated before the lateral ones (red arrow and red marked myocardium). Source
With speckle tracking, strain and strain rate can be calculated for movements in longitudinal, radial and circumferential directions. In apical four-chamber view (A4C), the longitudinal strain is most important. Longitudinal strain is a robust marker of cardiac function and correlates well with, for example, ejection fraction (EF). The longitudinal deformation depends primarily on subendocardial muscle fibers since these are oriented in the longitudinal direction. Circumferential deformation (best analyzed in PSAX) primarily reflects epicardial fibers. Longitudinal strain decreases in diseases such as hypertension, diabetes, and cardiomyopathy.
Chapter 9: Left Ventricular Segments for Echocardiography and Cardiac Imaging
Standardized myocardial segmentation for echocardiography and cardiac imaging
Cardiovascular imaging modalities have developed rapidly in the past few decades. The repertoire of available methods includes echocardiography, cardiovascular magnetic resonance (CMR), cardiac computed tomography (CT), single-photon emission computed tomography (SPECT), positron emission computed tomography (PET) and coronary angiography. These modalities aim to image the myocardium, assess wall motions and myocardial perfusion. However, due to varying strengths, limitations and clinical applications of these modalities, the definitions of cardiac planes, ventricular segments, and coronary arterial territories evolved differently. This resulted in difficulties when comparing examinations in clinical practice and research. Therefore, the American Heart Association (AHA) and the European Society for Cardiology (ESC) have established a standardization for ventricular segmentation, nomenclature and assignment of coronary arterial territory (Cerqueira et al).
The purpose of standardizing ventricular segmentation, arterial territories and nomenclature is to develop consistency across examinations. This is of utmost importance when assessing myocardial structure, perfusion and wall motion.
Cardiac planes
All imaging modalities define, orient and display the heart using the long axis of the left ventricle and selected planes oriented at 90° angles relative to the long axis. With regards to echocardiography, this implies that the following planes are used: short axis, vertical long axis, and horizontal long axis. These three planes correspond to the parasternal short-axis view (PSAX), apical two-chamber view (A2C), and apical four-chamber view (A4C), respectively (Table 1).
Table 1. Cardiac Planes in Echocardiography
| Plane | Echocardiographic view |
|---|---|
| Short axis | Parasternal short-axis view (PSAX) |
| Vertical long axis | Apical two-chamber view (A2C) |
| Horizontal long axis | Apical four-chamber view (A4C) |
Segments of the left ventricle
Based on anatomical landmarks and autopsy studies (Edwards et al), the left ventricle is divided into three equal parts along the long axis of the ventricle. This creates three circular sections of the left ventricle named basal, mid-cavity, and apical. These three parts are divided into a total of 17 segments (Figure 1). Six basal segments, constituting 35% of myocardial mass; six mid-cavity segments, constituting 35% of myocardial mass and 5 apical segments, constituting 30% of myocardial mass. The 17-segment model provides the best agreement with anatomic data, as compared with other segmentation models.
Figure 1. Standardized myocardial segmentation and nomenclature for echocardiography. The left ventricle is divided into 17 segments for 2D echocardiography. One can identify these segments in multiple views.
The basal part is divided into six segments of 60° each. The segments along the circumference are basal anterior, basal anteroseptal, basal inferoseptal, basal inferior, basal inferolateral, and basal anterolateral. The mid-cavity part is also divided into six 60° segments (mid anterior, mid anteroseptal, mid inferoseptal, mid inferior, mid inferolateral, and mid anterolateral). The apical part is divided into four 90° segments (apical anterior, apical septal, apical inferior, and apical lateral) and the apex (Table 2).
Table 2. The 17 segments of the left ventricle
Basal Segments Mid-cavity Segments Apical Segments1.basal anterior7.mid anterior13.apical anterior2.basal anteroseptal8.mid anteroseptal14.apical septal3.basal inferoseptal9.mid inferoseptal15.apical inferior4.basal inferior10.mid inferior16.apical lateral5.basal inferolateral11.mid inferolateral17.apex6.basal anterolateral12.mid anterolateral
These 17 segments can be arranged as a polar (bull’s-eye) plot with the apex in the center, the four apical segments as the first ring, the six mid-cavity segments as the second ring, and the six basal segments as the outer ring (Figure 2).
Figure 2. Circumferential polar plot of the 17 myocardial segments and the recommended nomenclature for tomographic imaging of the heart.
The attachment of the right ventricular wall to the left ventricle is used to identify and separate the septum from the left ventricular anterior and inferior free walls.
Figure 3. Assignment of the 17 myocardial segments to the territories of the left anterior descending (LAD), right coronary artery (RCA), and the left circumflex coronary artery (LCX).
References
Cerqueira et al: Standardized Myocardial Segmentation and Nomenclature for Tomographic Imaging of the Heart A Statement for Healthcare Professionals From the Cardiac Imaging Committee of the Council on Clinical Cardiology of the American Heart Association (2002).
Edwards et al: Standardized nomenclature and anatomic basis for regional tomographic analysis of the heart. Mayo Clin Proc. 1981;56:479–497.
Chapter 10: The Coronary Arteries
Coronary arteries and arterial territories
The two main coronary arteries emanate from the aortic bulb (Figure 1):
The right coronary artery (RCA) originates on the right aspect of the aortic bulb.The left main coronary artery (LMCA) originates from the left anterior aspect of the aortic bulb. The LMCA is short and branches into the two arteries supplying the anterior and left side of the heart, as follows: The left anterior descending coronary artery (LAD).The left circumflex coronary artery (LCX).
Figure 1 shows the coronary arteries and their relation to the ECG leads. Note that Figure 1 is a right-dominant system (i.e PDA is supplied from RCA).
Figure 1. The coronary arteries and their relation to the ECG leads. Localization of myocardial infarction / ischemia is done by using ECG changes to determine the affected area and subsequently the occluded coronary artery (culprit).
Figure 2 shows the coronary arterial territories in relation to the 17 segments of the left ventricle.
Figure 2. Assignment of the 17 myocardial segments to the territories of the left anterior descending (LAD), right coronary artery (RCA), and the left circumflex coronary artery (LCX).
Coronary artery dominance: left dominance vs. right dominance
The coronary artery that supplies the PDA (posterior descending coronary artery), which supplies the inferior wall of the left ventricle, determines the coronary artery dominance (Figure 1). A right-dominant system implies that the PDA is supplied by the right coronary artery (RCA). A left-dominant system implies that the PDA is supplied by the left circumflex coronary artery (LCX). The right-dominant system is by far the most common anatomy, occurring in 90% of all individuals.
Right coronary artery (RCA)
The right coronary artery supplies the entire right ventricle via the right marginal artery (r. marginalis dx).In 90% of individuals, the right coronary artery gives off the posterior descending artery (PDA) which supplies the inferior wall of the left ventricle. When the RCA gives off PDA, the anatomy is referred to as a right-dominant system (if the LCX gives off PDA, it is referred to as a left-dominant system).In patients with right-dominance the RCA supplies the atrioventricular (AV) node.In 60% of individuals, the right coronary artery gives off branches to the sinoatrial (SA) node.The posterior third of the interventricular septum is supplied by the right coronary artery.Arteries to the posterior wall (these arteries branch of after the right marginal artery) may be given off by the RCA (and otherwise the LCx).
Left anterior descending coronary artery (LAD)
The LAD supplies the anterior two-thirds of the interventricular septum (this area is referred to as anteroseptal area).The LAD supplies the large anteriosuperior wall (often referred to as the anterior wall) and the apical part of the lateral wall.The LAD may stretch all the way to the inferior wall and supply its most apical area (this area is referred to as the inferoapical area). Occasionally the LAD is very long and supplies a significant portion of the inferior wall; this type of LAD is called wrap-around LAD (because it wraps around the apex).
Left circumflex coronary artery (LCX)
In 90% of individuals, the coronary circulation is right-dominant, meaning that the PDA is given off by the RCA. In these individuals, the LCx only supplies the basal and mid parts of the posterolateral wall. As discussed previously, this part of the left ventricle is difficult to capture with the conventional leads in the 12-lead ECG.In 10% of individuals, the coronary circulation is left-dominant, meaning that the PDA is given off by the LCx. Thus the LCx supplies the inferior wall in 10% of all individuals.The LCx supplies the AV-node in 10% of all individuals.
Chapter 11: Regional Myocardial Contractile Function: Wall Motion Abnormalities
Echocardiographic assessment of regional contractile function
Systolic ventricular function is one of the strongest predictors of total and cardiovascular mortality. Previous chapters have discussed several methods for assessment of global and regional ventricular function. Assessment of regional wall motion is an integral aspect of virtually every echocardiographic examination. Wall motion is assessed in each segment of the left ventricle (Figure 1; refer to Segments of the Left Ventricle). Regional wall motion abnormalities are defined as regional abnormalities in contractile function. Ischemic heart disease is the most common cause of wall motion abnormalities. Assessment of wall motion abnormalities is particularly important in the setting of chronic or acute coronary artery disease.
All types of ischemia–chronic, acute, or subacute–lead to regional abnormalities in contractile function. The abnormalities affect the myocardial area supplied by the arteries distal to the occlusion or stenosis. If the ischemia persists for 20 minutes, myocardial infarction ensues, resulting in permanent wall motion abnormalities.
Figure 1. Standardized myocardial segmentation and nomenclature for echocardiography. The left ventricle is divided into 17 segments for 2D echocardiography. One can identify these segments in multiple views.
Note that the terms ischemic heart disease (IHD), coronary heart disease (CHD), and coronary artery disease (CAD) are used interchangeably throughout this text.
Wall motion abnormalities in ischemic heart disease
In the setting of stable ischemic heart disease, an atherosclerotic plaque causes ischemia when myocardial oxygen demand exceeds the oxygen supply. The most characteristic manifestation of ischemic heart disease is angina pectoris developing during physical activity; myocardial oxygen demand increases during physical activity, but an atherosclerotic plaque may prevent oxygen supply from increasing in parallel with oxygen demands. Depending on several factors–including the severity of the stenosis/occlusion, microvascular function, myocardial oxygen extraction, presence of collateral circulation, etc–ischemia may also develop during resting conditions. Indeed, in patients with ischemic heart disease, the majority of all ischemic episodes are asymptomatic (refer to The Ischemic Cascade). Acute coronary syndromes occur when atherosclerotic plaques rupture or erode, leading to atherothrombosis and occlusion. This causes severe ischemia and the vast majority of patients experience angina pectoris.
Myocardial ischemia: Supply-demand imbalance vs. lack of supply
In clinical practice, ischemia is often described as a consequence of an imbalance between oxygen demand and supply. According to this theory, ischemia occurs when the oxygen demand exceeds the oxygen supply. However, experimental and clinical studies have shown that myocardial metabolism, and thus contractility, is tightly coupled to oxygen supply. The myocardium is capable of upregulating or downregulating metabolism (i.e contractility) according to oxygen supplies. Consequently, reduced oxygen supply would not result in ischemia, since the myocardium adapts and downregulates metabolism to avoid developing ischemia. According to this theory, ischemia occurs only if there is an absolute lack of oxygen (Heusch et al).
Ischemic myocardium exhibits wall motion abnormalities
In the setting of ischemia, myocardial contractility is downregulated or completely ceased. The ischemic area will immediately display wall motion abnormalities. This is useful in emergency medicine since the presence of wall motion abnormalities in a patient with chest pain strongly suggests myocardial ischemia as the underlying cause of the symptoms.
The degree and extent of wall motion abnormalities correlate well with the severity and extent of ischemia. In the setting of moderate ischemia, the myocardium becomes hypokinetic, meaning that the ischemic segments contract less than the surrounding segments. During pronounced ischemia, the myocardium becomes akinetic (contractions have ceased). Akinetic myocardium is also called stunned myocardium. Myocardial stunning may normalize completely if the ischemia is alleviated before infarction ensues.
Echocardiography for assessment of wall mobility
Regional wall motion can be assessed with a scoring system developed by the American Society for Echocardiography (ASE). The left ventricle is divided into 17 segments (Figure 1) and each segment should be assessed for contractility (motion) using the following scoring system:
| Points | Abnormality |
|---|---|
| 1 | Normal motion |
| 2 | Hypokinesia |
| 3 | Akinesia |
| 4 | Dyskinesia |
Wall Motion Score Index (WMSI)
The Wall Motion Score Index (WMSI) is calculated by dividing the number of points by 17. If all segments move normally, the ratio is 1 (17 divided by 17). WMSI >1.7 is typically associated with heart failure.
The most frequent cause of regional wall motion abnormality is ischemic heart disease. Myocardial infarction may cause regional hypokinesia, akinesia or dyskinesia. The distribution of wall motion abnormalities should match the territory of a coronary artery.
Unfortunately, echocardiography can not determine whether wall motion abnormalities are new or old. This implies that echocardiography can not differentiate acute ischemia and old infarctions. However, the morphology of the myocardium may provide guidance. Scar tissue (i.e myocardial infarction) becomes thinner and appears brighter (echogenicity is higher) in the ultrasound image. Thus, wall motion abnormalities affecting thinner and brighter myocardium suggests infarction as the underlying cause.
Other causes of regional wall motion abnormalities
Although myocardial ischemia is the most common cause of wall motion abnormalities, there are numerous other causes, listed in Table 1. The most common among these is left bundle branch block (LBBB).
| Table 1. Differential diagnoses for regional wall motion abnormalities |
|---|
| Left bundle branch block (LBBB) |
| Pacemaker |
| Pre-excitation |
| Premature ventricular beats |
| Constrictive pericarditis |
| Right ventricular strain |
| Non-ischemic dilated cardiomyopathy (DCM) |
| Takotsubo syndrome |
| Sarcoidosis |
| Hemochromatosis |
If wall motion abnormalities involve more than one arterial territory, non-ischemic causes should be suspected (Table 1). Furthermore, normal thickening of the myocardium also suggests non-ischemic causes.