6 Echocardiographic Assessment of Heart Failure Resulting from Coronary Artery Disease
Acute and Chronic Ischemic Heart Failure
Basic Principles
• Heart failure (HF) is caused by coronary artery disease (CAD) in more than 65% of patients and may be acute or chronic. There are two major causes of acute post–myocardial infarction (MI) HF:
• Chronic HF results from progressive LV dilatation due to stretching of the infarct zone and expansion of the normal remote myocardium.
• LV dilatation increases wall stress that induces hypertrophy to normalize LV load and redistribute the elevated wall stress uniformly within the LV walls.
• Increased wall stress and neurohormonal activation drive the remodeling process, favoring LV dilatation and deterioration in function until a new equilibrium is reached between restraining forces exerted by the extracellular matrix and distending forces that promote LV dilatation.
• Myocardial repair involves collagen deposition and scar formation that provide an ideal substrate for re-entrant ventricular arrhythmias.
• Early diagnosis and treatment of HF is important because the prognosis of New York Heart Association (NYHA) class III/IV heart failure is poor (50% at 5 years).
• Doppler echocardiography provides a unique array of metrics for risk-stratifying patients with acute as well as chronic heart failure.
Key Points
• Knowledge of the distribution of coronary artery blood flow in the 17-segment model of the LV is important for identifying the culprit coronary artery and the likely location of the flow-limiting coronary stenosis (Figure 6-2). Subtle RWMA at rest can be amplified by exercise or pharmacologic stress.
• In ischemic cardiomyopathy with a dilated LV and an ejection fraction (EF) less than 20%, it may be difficult to rule out RWMA because endocardial excursion is severely reduced.
• Variation in the composition of the LV walls causes a heterogeneous acoustic signature from the myocardium, with increased brightness in infarcted regions due to the increased fibrosis (Figure 6-3).
• LV end-diastolic and end-systolic dimensions and volumes are both increased. The increase in end-systolic volume (ESV) is greater than the increase in end-diastolic volume (EDV), accounting for the fall in ejection fraction in acute HF.
• LV size as linear dimensions or LV volumes provides unique prognostic information for early risk stratification in HF. LV shortening and LVEF are both strong predictors of survival and adverse cardiovascular events.
• Meridional and circumferential wall stress can be calculated from echocardiographic measurements of wall thickness, cavity radius, cavity length, and LV pressure (Figure 6-4). Wall stress is a major determinant of hypertrophy and structural and functional LV remodeling. Calculation of wall stress requires that two contingencies be met—that the LV behaves uniformly without regional abnormalities (RWMAs) and that the material properties of myocardium are constant. Neither of these contingencies is met in ischemic HF. However, longitudinal, radial, and circumferential myocardial strain can be measured and used as surrogates for wall stress.
Quantification of LV Size and Function in HF
Basic Principles
Step 1
Step 2
• Paired images of the apical 4-chamber and 2-chamber views should be used to estimate LV volumes using Simpson’s rule and indexed to body surface area (BSA) or height.
• LV cavity lengths should be similar in the two apical images to avoid foreshortening of the cavity, causing spuriously small volumes.
• Quantification of LV volumes at end-diastole and at end-systole (Figure 6-5) enables calculation of LVEF:
Step 3
• LVEF is often assessed visually by experienced echocardiographers, and correlates closely with LVEF calculated from digitized biplane images.
• The correlation above breaks down in large left ventricles with EF less than 30% and distorted LV cavity shape.
• The myocardial performance index (MPI) or Tei index has been used as an indicator of LV function that is determined as:
where IVRT is the isovolumic relaxation time, IVCT is the isovolumic contraction time, and LVET is the LV ejection time.
• Regional LV function is estimated visually using the 17-segment model during rest and stress. The overall wall motion score predicts cardiac outcome.
• Regional LV function can also be evaluated using tissue Doppler imaging (TDI), in which myocardial velocities are measured. In ischemic or infarcted regions, myocardial velocities are reduced to below normal (Figure 6-6).
Step 4
• Regional myocardial ischemia can be located by measuring regional strain using speckle tracking. Myocardial strain (S) is defined as the change in length (ΔL) at end systole as a function of resting length (L0) and strain rate is the rate of change of strain with time:
• Strain can be measured from the apex to base as longitudinal strain. The echo-derived values for myocardial strain have been validated against magnetic resonance imaging and have correlated closely both in healthy normal subjects and in a number of disease entities. Ischemic or infarcted myocardial segments in HF associated with CAD can be identified by the depressed regional and global longitudinal strain values and by the different times to peak strain from the various myocardial regions in the infarcted/ischemic versus normal segments (Figure 6-7).
Echocardiographic Detection of Thrombus in HF
Basic Principles
• Thrombus usually occurs at the LV apex or adjacent to a region of LV wall that is severely hypokinetic or dyskinetic. The amplitude of endocardial motion in the infarct zone is low, such that there is slow adjacent intracavitary blood flow velocity that looks like “smoke” and is a precursor of thrombus formation.
• Left atrial (LA) dilatation is common in HF due to high filling pressures. LA thrombus is especially frequent in the LA and the LA appendage in patients with atrial fibrillation and atrial flutter. Thrombus in the left heart chambers has the potential for cardioembolism, causing stroke or loss of organ function. Detection of LV thrombus is of paramount importance because appropriate anticoagulation can be instituted immediately.
Key Points
Step 1
• Thrombus appears as a homogeneous mass with no discernible architecture and a different acoustic signature from the myocardium. Thrombus is most frequently located at the LV apex, adherent to an infarct zone or in the LA (Figure 6-9).
Step 2
• The morphology of the thrombus determines its likelihood for embolization. The features of thrombus associated with embolism are large size, convexity toward the LV cavity, and excessive mobility.
• The LV apex should be examined in all three standard apical views as it may be difficult to differentiate thrombus from LV trabeculations at the apex. This may be facilitated by using a high-frequency short-focus transducer to acquire “off-axis” images, apical long axis and tomographic transaxial images to include the LV apex (see Figure 6-8).
Step 3
• If there is still doubt as to the presence of LV thrombus, enhancing endocardial definition with intravenous contrast presents the thrombus as a filling defect within the contrast-filled LV cavity (Figure 6-10). Transesophageal echocardiography can be used to confirm or rule out intracardiac thrombus.
Postinfarction Ventricular Septal Defect
Basic Principles
• Persistent refractory acute HF or new-onset intractable HF several days post-MI should suggest severe LV volume overload due to MR (Figure 6-11) or rupture of the interventricular septum into the right ventricle (VSD) (Figure 6-12).
• Distinguishing the two mechanical lesions purely on the auscultatory features of a harsh holosystolic murmur is unreliable despite claims to the contrary.
• Doppler echocardiography removes the clinical doubt because color flow Doppler technology enables unequivocal localization of the VSD and at the same time can rule out MR (see Figure 6-12).
• The size of the defect in the ventricular septum can often be visualized directly and semiquantified by the maximal width of the color flow Doppler jet.
Key Points
Step 1
• When an infarct-related VSD is suspected as the cause of new-onset refractory HF post-MI, it is important to obtain a complete assessment of the hemodynamics noninvasively.
Step 2
• The location of the VSD can be determined using color flow Doppler velocity mapping. Post-MI VSDs usually occur in the anterior apical septum following a left anterior descending coronary artery (LAD) occlusion. Inferoposterior VSDs result from a right coronary artery occlusion or a dominant left circumflex artery occlusion.
• Color flow mapping should be used to direct the continuous wave Doppler beam to achieve an angle of incidence between the direction of trans-septal flow and the insonating Doppler beam close to 0 degrees. This is frequently difficult with inferior VSDs that follow a serpiginous course through the posterior septum. The entrance of the jet in the septum and its exit are separated sometimes by several centimeters, which makes orientation of the Doppler beam difficult if not impossible.
Step 3
• Assessment of the magnitude of the shunt flow across the VSD should be achieved by quantifying blood flow in the pulmonary circulation (Qp) and the systemic circulation (Qs) using the Doppler principle that volume flow can be calculated as the product of the velocity-time integral (VTI) and the cross-sectional area (CSA) of the flow stream.
• The main pulmonary artery is visualized in its long axis either from the left parasternal view of the short axis of the aortic valve (Figure 6-13) or from the corresponding view from the subcostal window to measure the diameter (d) of the main pulmonary artery. The pulmonary artery is assumed to be circular in CSA and equals 2π(d/2)2. The velocity signal in the main pulmonary artery is recorded from exactly the same location as the diameter is measured, so that pulmonary flow (Qp) is calculated as:
Postinfarction MR
Basic Principles
• MR occurs in almost two thirds of patients with acute and chronic HF, and results in an increase in LV load that often escalates the deterioration in an already dysfunctional LV, worsening the risk for HF and death from complex ventricular arrhythmias.
• The mechanism of MR in chronic HF is usually progressive increase in LV chamber size and secondary mitral annular dilatation. The latter perturbs the geometry of the mitral subvalve apparatus, increases the tenting area, and prevents normal leaflet coaptation, causing MR (Figure 6-14).
• In acute HF, the mechanism of MR is different from that in chronic heart failure. Acute HF is most frequently due to ischemia that damages the papillary muscles, occasionally causing papillary muscle rupture and severe MR (Figure 6-15). More commonly, ischemia disrupts the temporal coordination of the mitral valve (MV) and subvalve apparatus during valve closure.
• Color flow Doppler velocity mapping is exquisitely sensitive to MR such that even mild MR is easily detected as a turbulent regurgitant jet in the LA during systole.
• Since the onset of MR may have dire hemodynamic consequences and necessitate surgical repair of the MV in already high-risk patients, it is important to be able to quantify the severity of MR accurately and determine whether the valve is repairable.
• There are methods for quantifying the severity of MR that involve making a single measurement, and more labor-intensive methods that necessitate multiple measurements. In general, the more measurements made, the greater the likelihood of inclusion errors.
Mitral Regurgitant Volume
Basic Principles
• Any difference between total antegrade blood flow across the MV and antegrade blood flow across the aortic valves (AVs) represents the mitral regurgitant volume (MRV) flow, or backward flow into the LA during systole. Blood volume flow is computed as the product of the VTI and the CSA of the flow stream:
• When this method is used, whether with 2D or three-dimensional (3D) echo, several key points are important (Figure 6-16).
Key Points
• Calculation of volume flow by this method requires attention to detail because volume computation is dependent upon accurate measurement of diameter of the LV inflow and outflow tracts for calculation of CSA. Even small errors in measurement of diameter are amplified by a square-power function and thus have a major effect on blood volume flow determination.
• The blood flow velocity signals across the LV inflow and outflow tracts must be recorded at the exact same site at which the diameter measurements are made.
• Doppler signals must be high quality and continuous. Of equal importance, they must be digitized very carefully in order to generate an accurate and meaningful VTI. This is particularly relevant with the LV inflow tract signal, and this is best achieved by ensuring that the baseline is down-shifted to provide the velocity signal as a full-scale deflection. This large velocity signal enables accurate digitization and a more fiducial VTI.
Measurement of the Width of the Vena Contracta
Basic Principles
• The vena contracta (VC) demonstrated by color flow Doppler is the narrowest region of the mitral regurgitant jet that resides between the proximal zone of flow convergence, where the jet velocity increases as the blood flow approaches the regurgitant orifice, and the zone of jet expansion within the LA (Figure 6-17).
Proximal Isovelocity Surface Area (PISA)
Basic Principles
• As a laminar flow stream approaches a finite regurgitant orifice, it accelerates, and in doing so creates a series of hemispheres (Figure 6-18) that are seen by color flow Doppler as alternating bands of blue and red, the surface areas of which share fixed flow velocity—known as isovelocity surface areas (see Figure 6-18).
• The color bands alternate each time the flow velocity exceeds the Doppler Nyquist limit, and each subsequent surface area has a progressively greater isovelocity surface with a progressively smaller surface area.
• The flow rate at every isovelocity shell surface area is the same as that at the regurgitant orifice in accordance with the law of conservation of mass.
• Assuming the isovelocity surface area to be hemispherical, flow rate equals the surface area of the hemisphere (2πr 2) × the aliasing velocity, where r is the radius of the first aliased hemisphere (Figure 6-19). This flow rate is the regurgitant flow rate across the MV, from which the mitral regurgitant orifice area (ROA), regurgitant volume (RV), and regurgitant fraction (RF) can be calculated:
Key Points
• It is important to reduce the aliasing velocity to between 30 and 40 cm/s by shifting the baseline because this enhances the aliasing signal.
• The angle between the insonating Doppler beam and the direction of blood flow must be as close to 0 degrees as possible in the apical 4-chamber and the apical 2-chamber imaging planes.
• The MV plane must be identified unequivocally because the radius to be measured is from the MV plane to the first aliasing isovelocity surface area.
• The accuracy of PISA is compromised when the flow field is incomplete or hemi-ellipsoidal rather than hemispherical.
• The continuous wave Doppler velocity signal must be of the highest quality so it can be confidently traced throughout systole to obtain the mitral regurgitant VTI (Figure 6-20).
Flow Reversal
Basic Principles
• Blunting or reversal of the blood flow velocity in the pulmonary veins during systole is a qualitative means of assessing the severity of MR. The flow velocity signal shows either systolic blunting or reversal of flow (Figure 6-21).
Key Points
Pericardial Effusion
Basic Principles
• Pericardial effusions occasionally complicate acute HF (Figure 6-22), usually resulting from an ST-segment elevation MI (STEMI), and in so doing may compromise the already unfavorable and unstable hemodynamics.
• Pericardial tamponade rarely intervenes in acute HF, and only occasionally does the increased pericardial pressure necessitate percutaneous pericardiocentesis.
• Patients with cardiac rupture and rapid onset of tamponade, whether in the hospital or in the field, do not survive unless there is “contained rupture” due to prior fusion of the parietal and visceral pericardium from pericarditis.
• Contained rupture—also known as LV pseudo-aneurysm—is uncommon, usually arising from the inferobasal LV wall (Figure 6-23).
• Pseudo-aneurysm can be differentiated from true LV aneurysm by echocardiography by the relatively narrow neck that represents the rupture site via which blood gains access to the pericardial space (see Figure 6-23). Blood flow into the pericardium can usually be demonstrated by color flow Doppler velocity mapping.
• By contrast, a true ventricular aneurysm has a wide neck, and there is no breach of the LV wall (Figure 6-24). There is either akinesis or dyskinesis with wall thinning that appears highly echo-reflective because of the formation of a fibrous scar post–MI repair.
Key Points
• In patients with acute HF associated with an anterior STEMI and marked cardiomegaly, pericardial effusion should be excluded by transthoracic echocardiography. If the pericardial effusion is circumferential, it must be distinguished from a left pleural effusion since the latter is a frequent finding in HF.
Step 1
• A pericardial effusion must be identified early. This can be achieved from the left parasternal view, in which a pericardial effusion is anterior to the descending thoracic aorta and does not extend behind the LA because the posterior pericardium is reflected at the atrioventricular sulcus onto the inferior pulmonary veins in the vast majority of patients.
RV Infarction
Basic Principles
• HF due to RV infarction may occur from right coronary artery occlusion as an isolated RV event or, more commonly, in association with inferior or inferoposterior LV infarction.
• Recognition of RV infarction is important because the treatment of MI involving the LV presenting with HF is aimed at reducing intravascular volume. Appropriate volume repletion is the optimal treatment strategy in RV infarction. Intravenous diuretics following RV infarction may induce severe hypotension and shock.
Key Points
• RV infarction can be diagnosed unequivocally by echocardiography as new RV RWMAs involving the RV free wall, RV dilatation, and severe global contractile dysfunction (Figure 6-25) usually measured as percent change in cavity area (A) from diastole (DA) to systole (SA) because there is no accepted algorithm for computing RV volumes:
• RV longitudinal shortening results in reduction in tricuspid annular plane systolic excursion (TAPSE) that is often accompanied by abnormal septal motion.
Chronic Heart Failure
Basic Principles
• Chronic HF resulting from CAD can be caused by a discrete clinically recognized acute MI or, less commonly, be the cumulative effect of recurrent episodes of myocardial ischemia associated with recurrent minor myocardial damage that remains clinically unrecognized.
• LV dilatation may be global or regional, resulting in ischemic dilated cardiomyopathy (Figure 6-26) or discrete LV aneurysm formation, respectively (Figure 6-27). LV aneurysms are most common in the antero-apical region from occlusion of the proximal to mid-LAD (see Figure 6-26). Inferior LV aneurysms are less common and result from occlusion of either the right coronary artery or a dominant left circumflex coronary artery (Figure 6-28). Aneurysms must be carefully examined by 2D or 3D echocardiography for retained thrombus as described above.
• LV remodeling results in asymmetric mural hypertrophy induced by regional disparities in stress distribution.
• As the LV enlarges, it assumes an abnormal shape, transitioning from an ellipsoidal to a spherical shape that can be quantified echocardiographically as the LV short- and long-axis ratio (see Figure 6-14). Distortion of LV shape post-MI predicts poor clinical outcome over and above that of LV size.
• The LV dilatation and distortion also disrupts the MV apparatus and annular geometry, causing MR. It is important to ascertain the severity of MR and determine whether MV repair can be achieved safely in HF patients with already compromised LV function. Assessment of MR in chronic HF is the same as in acute HF as described above.
• Chronic HF that develops post-MI begins the process known as LV remodeling, which may continue for months to several years. LV remodeling has been fully characterized by Doppler echocardiography as a progressive increase in LV volume with a decrease in the LV mass/volume ratio because LV hypertrophy can no longer normalize wall stress. Increased wall stress stretch-activates a portfolio of neurohormones and local tropic factors that further drive the remodeling process to ischemic dilated cardiomyopathy and terminal HF (see Figure 6-26).
• Simultaneous with the structural and functional remodeling, there is the development of prolongation of the QRS duration in 35% to 50% of HF patients that is associated with inter- and intraventricular dyssynchrony. Doppler echocardiography can readily detect LV dyssynchrony, its impact on LV architecture and function, and MR and its reversal with cardiac resynchronization therapy.
Figure 6-28 Examples of an antero-apical LV aneurysm (upper panels) and an inferior basal LV aneurysm (lower panels).
Key Points
• Myocardial velocities by TDI in the normal heart vary in magnitude from the LV apex to the base of the heart, and this consistent gradient is maintained. However, the time to peak velocity during LV ejection in the normal heart is similar from all regions of the myocardium, demonstrating the exquisite temporal coordination during contraction. This temporal coordination is typically lost and the magnitudes of the peak velocities are lower and vary by myocardial region, being lowest in areas of infarction, in HF of ischemic etiology. In ischemic HF, some regions attain peak myocardial velocities early while other regions peak late (see Figure 6-6). If the difference between the time to peak for two opposing LV walls is greater than 65 ms, dyssynchrony is present.
• Measuring a time interval between peak septal excursion and peak posterior LV wall excursion by M-mode echocardiography in HF patients of greater than 135 ms is consistent with dyssynchrony.
• It is important to ensure that the sample volumes track the myocardium throughout the cardiac cycle, because tracking from within the cavity or from outside the epicardium results in spuriously low myocardial velocities.
• Speckle tracking enables fiducial tracking of the myocardium so that regional displacement and regional strain can be measured accurately.
• The time to peak displacement (Figure 6-29) and time to peak strain (Figure 6-30) can be compared by region, which in the normal heart is closely coordinated in time. By contrast, in ischemic HF some regions attain peak values early while in some regions the peak velocities are considerably delayed c/w dyssynchrony.
• LV dyssynchrony is associated with an incrementally worse prognosis after adjustment for LV size and function.
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