2 \200\223 V1 2 ) Gradient (mmHg) = 4(V2 lesion and V1 = velocity proximal to the lesion) (where V2 = velocity across the Both peak and mean gradients can be determined by measuring the maximal velocity and veloci ty \200\223time integral (VTI). Valve area (continuity equation) This is based on the principle that \202 ow proximal to the valve = \202 ow across the valve. The most common application is the calculation of a ortic valve area in patients with aortic stenosis, as shown below. LVOT \202 ow = LVOT ar ea \227 LVOT (VTI) by pulsed Doppler LVOT area = (cid:89) (LVOT diameter in PLAX/2)2 Aorti c valve \202 ow = Aortic valve area \227 Aortic valve VTI by CW Doppler Aortic valve \202 ow = LVOT \202 ow, Aortic valve area = (LVOT VTI/Aortic valve VTI) \227 LVOT area CHAPTER 12 Stress testing and cardiac imaging 456 The standard TTE Most laboratories employ imaging protocols incorporating acquisition of im ages from standard views in a speci \201 c sequence. Image quality is maxi- mized by avoid ing overlying lung artifacts and rib re \202 ections. Pulsed and color \202 ow Doppler i s performed following 2-D imaging in each view. Standard echo windows (and views) and the main cardiovascular struc- tures visualized are as follows: Left parasternal window \200 Long axis (PLAX): left atrium and ventricle, aortic root, mitral and aortic valves, and rig ht ventricle (see Figs. 12.6 and 12.7) Short axis (PSAX): 4 levels \200 Aortic valve/left atrial level: includes tricuspid valve (TV), right ventricular out \202 ow tract (RVOT), pulmonic valve (PV), and pulmonary artery (Pa) (see Fig. 12.6) \200 Left ventricular base/mitral valve \200 Mid-left ventricle/papillary muscle \200 Left ventr icular apex Right ventricular in \202 ow Apical window \200 4 chamber (A4C): both atria, ventricles and AV valves, inferior septal and anterolateral LV walls (Fig. 12.7). Pulmonary veins may also be seen. 5 chamber (A5C): A4C angled anteriorl y to LV out \202 ow tract (the \200\234 \201 fth chamber \200\235 in this view is the ao rtic root) 2 chamber (A2C): left atrium, anterior and inferior LV walls 3 chamber/apical lo ng axis (A3C): apical version of PLAX view with anteroseptal, posterior or inferolateral wa lls and LV out \202 ow tract \200 Suprasternal window (SS) \200 Aortic arch and head vessels \200 Proximal descending tho racic aorta Subcostal window (SC) \200 \200 4 chamber and short axis views are often imaged The inferior vena cava (IVC) and descending aorta can also be seen Right parasternal window (optional) \200 Ascending aorta and CW Doppler of aortic valve Chamber evaluation Chambers are routinely measured from M-mode tracings or, more com- monly , using digital calipers to perform assessment from 2-D images. The PLAX view is the standa rd for most chamber measurements. Area tracings provide enhanced accuracy but require adequate endo- cardial visualization for optimal accuracy. Chamber volumes are derived from 2-D measurements using geometric modeling. The most common volumetric approaches include the modi \201 ed Simpson \200\231s biplane method of disks and the area \200\223length formula. THE STANDARD TTE 457 (a) (b) Pa RVOT Rcc Ao Ncc Lcc RV Ao LV LA RA LA Figure 12.6 (a) Parasternal long axis view; (b) parasternal short axis view (aortic level). Ao, aorta; LA, left atrium; Lcc: left coronary cusp; LV, left ventricle; Ncc: noncoronary cusp; Pa, pulmonary artery; RA, right atrium; Rcc Ao: right coronary cusp of aortic valve, RVOT, right ventricular out \202 ow tract. (a) (b) RV RV LV RA IVC (c) (d) RV LV Ao Pa RA LA Figure 12.7 (a) Parasternal long axis view (RV in \202 ow); (b) parasternal short axis (mi tral valve level); (c) apical 4 chamber view; (d) suprasternal long axis view. For abbrevia tions see Figure 12.6; IVC, inferior vena cava. CHAPTER 12 Stress testing and cardiac imaging 458 3-D echo has also been validated as an accurate and reproducible method of chamber volume q uanti \201 cation and is superior to standard 2-D imaging if done properly. Most clinical labs perform measurements in real time during image acquisition, though moder n workstations allow for comprehensive off- line analysis. End-diastole is usually de \201 ned as the beginning of the QRS complex and end-systolic measurements are performed at max imum LV contraction. The American Society of Echocardiography has published guidelines for standard chamber quanti \201 cation and it is recommended that these can be applied in rou tine clinical practice. Left atrium \200 \200 Measure at ventricular end-systole. Linear (anteroposterior [AP]) measurement is made from PLAX view at aortic cusp level. Area (A4C) and volume (modi \201 ed Simpson \200\231s form ula or area \200\223length method using the A4C and A2C views) are also often quanti \201 ed. Left ventricle \200 Measure chamber diameter from PLAX at mitral lea \202 et tips at end- diastole and end-sys tole. Septal and posterior wall thickness should be measured from PLAX at mitral lea \202 et tips in end-diastole. Volumes (modi \201 ed Simpson \200\231s biplane method of disks) Derived variables \200 \200 Fractional shortening : FS = ([LVIDd \210\222 LVIDs]/LVIDs) x 100 where LVID = LV internal diameter in diastole (d) and systole (s). Ejection fraction (from 2-D- or 3-D-generated vo lumes or derived from M-mode [e.g., Teicholz formula]) Mass can be derived from M-mode meas ures (ASE-modi \201 ed Penn formula), 2-D volumetric models, or 3-D reconstruction. M-mode mass calculations tend to overquantify LV mass. Aortic root and ascending aorta \200 Linear measurements from 2-D PLAX view or M-mode at end- diastole. The root is measured at cusp level, and aorta is measured at sinotubular junction and 2 cm above this. Right atrium \200 Area, inferior/superior and lateral/medial diameter measurements from A4C view THE STANDARD TTE 459 Right ventricle \200 Irregular shape makes standardized quanti \201 cation and geometric modeling dif \201 cul t. Diameter typically is measured in A4C view at base or mid-ventricle. Qualitative compari son of size relative to left ventricle (if normal in size). \200 Pulmonary artery \200 Diameter measurement in PSAX at aortic valve level. CHAPTER 12 Stress testing and cardiac imaging 460 Assessment of wall motion Overall assessment is based on review of wall segments from multi ple standard views. In general, abnormalities of LV regional function should be apparent in more than one view. Regional wall motion is best described using the standard 16-segment model recommended by the American Society of Echocardiography: \200 Basal (6): posterior), inferior, inferoseptal Mid LV (6): Apical (4): tip of the apex is in cluded as a 17th segment.) anteroseptal, anterior, anterolateral, inferolateral (or \200 same as above anterior, lateral, inferior, and septal. (In some systems the Regional functional assessment Systolic function should be classi \201 ed as normal, globa ly hypokinetic, or demonstrating the presence of regional wall motion abnormalities. Global hypokinesis is consistent with cardiomyopathy, either ischemic or nonischemic. Some degree of regional wall motion abnormality may be present in nonischemic cardiomyopathy. The presence of distinct regional wall motion abnormalities with large areas of normal regi onal function is suggestive of underlying coronary artery disease, either areas of infarct or stunned/hibernating myocardium. Evaluation of regional wall thickening is preferable to endocardial motion, which may be in \202 uenced by tethering of adjacent segments. Unfortu nately, this is not always possible when endocardial or epicardial border de \201 nition i s suboptimal. Each regional segment is classi \201 ed as follows: 1. Normal or hyperkinetic 2. Hypokinet ic 3. Akinetic 4. Dyskinetic 5. Aneurysmal A wall motion score index can be calculated on the basis of analysis of each segment using the 16-segment model (see Fig. 12.8) and assigning a score based on the categories above: \200 \200 \200 Sum of individual wall motion scores/number wall segments visualized. A normal score is 1 ( i.e., 16/16). A higher score indicates more severe coronary disease and is predictive of fu ture cardiac events. This index may be especially useful in stress echocardiography. Identi \201 cation of hyperechogenic, thinned areas suggests the presence of scarring. ASSESSMENT OF WALL MOTION 461 Two Chamber Apical cap Apical cap Apical cap Long Axis Four Chamber Apical cap Apical cap Apical cap 1 3 2 Apical cap Apical cap Apical cap Apical Apical Apical lateral lateral lateral MidMid Mid inferolateral inferolateral inferol ateral Basal Basal inferolateral inferolateral inferolateral Apical Apical Apical inferior inferior inferior Mid MidMid inferior inferior inferior Apical Apical Apical lateral lateral Mid MidMid anterolateral anterolateral anterolateral Apical Apical Apical anterior anterior anterior MidMid Mid anterior anterior anterior Apical Apical Apical anterior anterior anterior MidMid Mid anteroseptum anteroseptum antero septum Basal Basal Basal anteroseptum anteroseptum anteroseptum Apical Apical Apical septum septum septum MidMid Mid inferoseptum inferoseptum inferoseptum Basal Basal Basal inferoseptum inferoseptum inferoseptum 4 5 6 Basal Basal Basal inferior inferior inferior Basal Basal Basal anterolateral anterolateral anterolateral Basal Basal Basal anterior anterior anterior 3 2 1 Mid Anterior Anterior Anterior Apex Base 4 6 5 Anterior Anterior Anterior Anterior Anterior Anterior Antero- Antero- Antero- lateral lateral lateral Antero- Antero- Antero- lateral lateral lateral Antero- Antero- Antero- septum septum septum Antero- Antero- Antero- septum septum septum Septal Septal Septal Lateral Lateral Infero- Infero- Infero- septum septum septum Infero- Infero- Infero- septum septum septum Infero- Infero- Infero- lateral lateral lateral Infero- Infero- Infero- lateral lateral Inferior Inferior Inferior Inferior Inferior Inferior Inferior Inferior Inferior 1 2 3 Two Chamber Long Axis Four Chamber Base Mid Apex 4 5 6 RCA or CX LAD or CX RCA or LAD RCA LAD CX Figure 12.8 A 17-segment wall segment model (top). Coronary perfusion territories (bottom). Reprinted with permission from Lang et al. (2005). J Am Soc Echo 18:1440 \200\2231463. CHAPTER 12 Stress testing and cardiac imaging 462 Assessment of LV systolic function Global functional assessment \200 Ejection fraction (E F) estimation (see Table 12.1). 2-D echo ejection fractions of \202 ine by means of the fo llowing methods: \200 is usually performed qualitatively can be quanti \201 ed most ef \201 ciently on or Simpson \200\231s modi \201 ed biplane method of disks : A4C and A2C LV traces are obtaine d and the apex \200\223annulus length is divided into a standard number of equal segments, the length of which serves as disc height. Cross-sectional disc area is calculated from the elliptical formula ((cid:89) r1r2), where r1 and r2 are the endocardial medial \200\223lat eral dimension of each segment in the A4C and A2C views, respectively. Area Length method: endocardial area (A) on the PSA view at the papillary muscle level and the longest apex \200\223annulus length (L) in any apical view. Volume = 5/6 AL. Volume is determined by measuring the LV LV stroke volume: PLAX view). Systemic cardiac output: Pulmonary stroke volume: systolic me dial \200\223lateral dimension at level of Doppler sampling). RV output: Pulmonary stroke v olume \227 heart rate. Pulmonic/systemic shunt ratio (Qp/Qs): systemic cardiac output, aid s in describing the degree of intracardiac shunting, e.g., in atrial septal defects. LVOT VTI \227 LVOT area (derived from diameter in \200 LV stroke volume \227 heart rate. RVOT VTI \227 RVOT area (derived from \200 pulmonary cardiac output/ Stress echocardiography This is performed in conjunction with exercise (usually treadmill) or after administration of a pharmacological stress agent (i.e., dobutamine). Standard view s are PLAX, PSAX mid-ventricle, A4C, and A2C. Images are acquired at rest and immediately post-stress following exer- cise or at rest, lo w-dose, peak-dose, and post-dobutamine infusion. Images are displayed in quad screen format for direct comparison of rest and stress images. Sensitivity and speci \201 city are 75% \200\22385% and 80% \200\22390%, respectively, and are comparable to SPECT perfusion imaging. In patients with coronary Table 12.1 Assessment of LV ejection fraction LV ejection fraction Qualitative assessment >75% Hyperdynamic 55% \200\22375% Normal 40% \200\22354% Mildly reduced 30% \200\22339% Moderately reduced <30% Severely reduced ASSESSMENT OF LV SYSTOLIC FUNCTION 463 artery disease, sensitivity for detection of \202 ow-limiting stenosis increases with the number of coronary arteries involved. A wall motion score index (WMSI), as described previously, can be calculated at rest and fo llowing stress to determine the extent of scarring and/or ischemia. An exercise WMSI above 2 predicts a high risk (>5%/ year) of future cardiac events (see Table 12.2). A normal exercise echocardiogram is associated with a very low rate of future cardiac events (<1%/year). Contrast can be administered to improve endocardial border de \201 nition. Common applications \200 Diagnosis of coronary disease in patients with chest pain or angina (or equivalent) Determi ne physiological signi \201 cance of a coronary stenosis prior to revascularization Risk s trati \201 cation following myocardial infarction (MI) Viability testing using dobutamine stress \200 \200 Biphasic response to dobutamine suggests hibernating myocardium and predicts functional rec overy and improved outcome following revascularization. Preoperative risk strati \201 cation in selected patients at increased risk for postoperat ive cardiac complications following noncardiac surgery, especially those with intermediate or major clinical predictors of increased risk and poor baseline functional status Follow-u p of patients after coronary revascularization, especially if symptomatic Assess physiologi cal signi \201 cance of valvular lesions, particularly mitral stenosis and mitral regurgit ation Differentiate true aortic stenosis from \200\234pseudo- \200\235aortic stenosis in p atients with low transvalvular gradient due to low cardiac output Findings of high risk \200 \200 Decreased LVEF or increase LV end-systolic volume during stress Extensive ischemia (multipl e dysfunctional segments with stress) suggesting multivessel disease Ischemia at low worklo ad Resting LVEF <40% Resting wall motion abnormalities with remote ischemia \200 \200 Table 12.2 Interpretation of stress echocardiogram Resting wall motion Stress wall motion Interpretation Normal Hyperdynamic Normal Normal Abnormal Ischemia Abnormal Unchanged Scar Abnormal Improved Nontransmural scar without ischemia Abnormal Worse Ischemia CHAPTER 12 Stress testing and cardiac imaging 464 Assessment of LV diastolic function Evaluation of LV diastolic function includes measuremen t of the various phases of diastole, including isovolumic relaxation, early \201 lling, d iastasis (atrioventricular [AV] pressure equilibration without LV \201 lling), and atrial systole. The characteristics of these \201 lling phases are generally age and heart-rate dependent and affected by LV loading conditions to variable degrees (see Fig. 12.9). Pulsed Doppler mitral in \202 ow: E wave (peak early diastolic velocity), A wave (peak atr ial systolic velocity), E/A ratio, and transmitral deceleration time (DT, time interval fro m peak E wave to its return to baseline). The following should be taken into account when assessing these parameters: \200 The E/A ratio is particularly dependent on sample-volume placement (annulus, mitral tips, e tc.) and loading conditions. E/A ratio decreases with age and assessment must be age-normal ized. An E/A ratio <1.0 is common among the elderly (age >65 years) and often represents no rmal aging. Increasing LV \201 lling pressures (e.g., in heart failure) lead to pseudonor malization of the E/A ratio, which often reverts to an abnormal pattern following maneuvers to reduce LV preload (e.g., diuresis, nitroglycerin, or Valsalva maneuver). The DT correla tes with invasive measures of LV stiffness, whereas other measures largely re \202 ect LV relaxation. Pulsed Doppler of pulmonary veins: Assessment of LA \201 lling, which is affected by the diastolic properties of the LV. Usually the right upper pulmonary vein is sampled in the A4 C view and guided by color \202 ow Doppler, though optimal visualization is often dif \201 cult. S, D, and A waves represent systolic and diastolic atrial \201 lling. The A wa ve is generated by reverse \202 ow into the pulmonary veins during atrial contraction. \200 \200 The S/D ratio increases with age as LV diastolic relaxation declines. A pulmonary vein A wa ve duration >30 ms greater than transmitral A wave durations suggests elevated LV \201 ll ing pressure. CW Doppler of LV out \202 ow/mitral in \202 ow: Isovolumic relaxation time (IVRT) is the interval between aortic valve closure and mitral valve open- ing. Changes in IVRT tend to p arallel those seen in DT with increasing diastolic dysfunction. Tissue Doppler of septal and lateral mitral annuli (E \200\231, A \200\231) \200 \200 \200 This is less dependent on loading conditions. The septal mitral annular velocity is the pre ferred measurement. The E/E \200\231 ratio correlates with LV end-diastolic pressure and a ratio >15 is strongly suggestive of elevated \201 lling pressure, with a ratio <8 strongl y suggestive of normal \201 lling pressure. Color Doppler M-mode: Rate of blood \202 ow into the LV from annulus to apex is determine d by measuring the slope of the line along the edge of the color Doppler M-mode tracing. No rmal propagation velocity (Vp) is >45 \200\22350 cm/sec. Ratio of E/Vp >2 correlates with e levated LA pressure. ASSESSMENT OF LV DIASTOLIC FUNCTION 465 These parameters are used to determine the severity of diastolic dysfunc- tion (see Fig.12. 9). In general: \200 Markers of impaired relaxation (e.g., decreased E and E \200\231 are accompanied by compens atory enhancement of A and A \200\231), reduced pulmonary venous D, and reduced Vp. Increas es in LV \201 lling pressure lead to pseudonormalization of the transmitral Doppler E/A r atio, reversal of the pulmonary vein S/D ratio, and increased E/E \200\231 ratio. As compli ance decreases, the transmitral DT drops below 130 ms, early Doppler \201 lling velocity is increased and, because of elevated late diastolic LV pressures, atrial contraction and a ssociated velocities are reduced. If E/E \200\231 ratio <8 and LA is of normal size, sympto ms are unlikely to be due to diastolic heart failure. Do not miss constriction. Look for the following: \200 \200 \200 \200 \200 Septal \200\234bounce \200\235 and dyssynchrony IVC dilatation Hepatic vein expiratory rev ersal Excessive mitral in \202 ow respiratory variation Restrictive \201 lling pattern o n mitral in \202 ow Doppler with normal tissue Doppler mitral annular velocities 4 6 6 C H A P T E R 1 2 Echocardiographic classification of diastolic dysfunction S t r e s s Stage III Reversible restrictive Stage I Impaired relaxation Stage IV Fixed restrictive Stage II Pseudonormal Normal diastolic function t e s t i n g a n d E/A \211 0.75 E/A>1.5 DT<140 ms 0.75<E/A<1.5 DT>140 ms E/A>1.5 DT<140 ms 0.75<E/A<1.5 DT>140 ms 2.0 c e s / E c a r d i a c m Mitral inflow A , y t i c o e V l 0.0 i Adur m a g i n g Time, ms Time, ms Time, ms Time, ms Time, ms \210\206E/A \211 0.5 \210\206E/A \211 0.5 \210\206E/A<0.5 \210\206E/A<0.5 \210\206E/A<0.5 2.0 c e s / Mitral inflow at peak Valsalva maneuvre m E , y t i c o e A l 0.0V Time, ms Time, ms Time, ms Time, ms Time, ms ARdur>Adur +30 ms ARdur>Adur +30 ms ARdur<Adur ARdur<Adur ARdur>Adur +30 ms 2.0 c e s / m Pulmonary venous flow S D , y t i c o e V ARdur l 0.0 AR ms Time, ms Time, ms Time, ms Time, ms Time, >45 <45 <45 <45 Vp Vp Vp Vp 5 m c Vp , Color M-Mode propagation velocity e c n a t s i D A S S E S S M E N T O F 0 Time, ms Time, ms Time, ms Time, ms Time, ms E/Ea<10 E/Ea<10 E/Ea \211 10 E/Ea \211 10 E/Ea \211 10 c e s / Doppler tissue imaging of mitral annular motion m L V , y t i c o e V a \200\231 D A S T O L C e \200\231 Time, I ms Time, ms Time, ms Time, ms Time, ms l Normal Normal LV relaxation LV compliance Atrial pressure Impaired Normal to \206\223 Normal Impaired \206\223 \206\223 \206\221 \206\221 Impaired \206\223 \206\223 \206\223 \206\221 \206\221 \206\221 Impaired \206\223 \206\223 \206\223 \206\223 \206\221 \206\221 \206\221 \206\221 I F U N C T O N Normal Figure 12.9 Echocardiographic classi \201 cation of diastolic dysfunction. I 4 6 7 CHAPTER 12 Stress testing and cardiac imaging 468 Echocardiography in aortic stenosis Etiology Aortic stenosis (AS) can be congenital (i.e., unicuspid or bicuspid valve) or, more commonly, degenerative. In late stages, severe \201 brocalci \201 cation pre- cludes etiologic identi \201 cation even on direct intraoperat ive visualization. Chronic severe AS is usually accompanied by concentric LV hypertrophy du e to pressure overload. Bicuspid aortic valve is diagnosed best on short axis view and can display various con \201 gurations. Often a \200\234raphe \200\235 is observed representing the undeveloped co mmissure where persistent cuspal fusion is present. Systolic cuspal \200\234doming \200 \235 is consistent with congenital AS, as is best seen in the PLAX view. Degenerative AS typically starts in the annulus \201 brosis (most com- monly in the nonco ronary cusp area) and gradually proceeds to invade the cusp bases, body, and, in later stag es, the tips. Valve thickening without hemodynamic stenosis is termed sclerosis, and is a c ommon cause of mur- mur in asymptomatic adults. Hemodynamics Stenosis is de \201 ned as a hemodynamically signi \201 cant reduction in va lve area as indicated by a rise in transvalvular pressure gradient. Pressure gradient is dependent on \202 ow and, in the setting of low cardiac output, may be minimally elevated despite signi \201 cant stenosis (i.e., low- gradient aortic stenosi s). Aortic stenosis severity is categorized according to the valve area, trans- valvular velocity, and mean pressure gradient (see Table 12.3). ECHO diagnosis \200 Assess cusp separation or presence of doming. A trilea \202 et valve with one cusp opening fully (approaching edge of the root) is probably not signi \201 cantly stenotic. CW Doppl er-derived gradients are reported as instantaneous peak and/or mean. The mean gradient is m ore reliable in determining stenosis severity. Cath lab gradients are \200\234peak to peak \200\235 with pressure measurements that are usually not acquired simultaneously and often do not correlate with the peak gradient by Doppler, which re \202 ects the maximal instan taneous pressure. The mean gradients obtained by ECHO and catheterization are comparable. Table 12.3 2006 ACC/AHA classi \201 cation of AS severity Measurement Normal Mild Moderate Severe Jet velocity (m/sec) <2.0 2.0 \200\2233.0 3.0 \200\2234.0 >4.0 Mean gradient (mmHg) <10 10 \200\22325 25 \200\22340 >40 Valve area (cm2) 3 \200\2234 1.5 \200\2232.0 1.0 \200\2231.5 <1.0 ECHOCARDIOGRAPHY IN AORTIC STENOSIS 469 CW Doppler can underestimate the transvalvular gradient if the ultrasound beam is not paral lel to the direction of \202 ow. Peak transvalvular velocity >2.5 m/sec (instantaneous gr adient of 25 mmHg) suggests some degree of stenosis. Elevated cardiac output or signi \201 cant aortic regurgitation will increase transvalvular \202 ow and gradient but should no t affect calculations of valve area. The dimensionless index (DI) is the ratio of LVOT velo city or VTI (pulsed Doppler)/transvalvular velocity or VTI (CW Doppler) and essentially cor rects for abnormal cardiac output. General guidelines are as follows: \200 \200 \200 DI <0.5: signi \201 cant stenosis DI 0.25 \200\2230.5: moderate stenosis DI <0.25: severe stenosis Aortic valve area is calculated using the following continuity equation: Aortic valve area = (LVOT VTI/Aortic valve VTI) \227 LVOT area Measuring wall thickness for LVH, assessing LV systolic function, and look- ing for coexist ent mitral regurgitation are other essential aspects to the echocardiographic evaluation of aortic stenosis. CHAPTER 12 Stress testing and cardiac imaging 470 Transesophageal echocardiography (TEE) TEE is a minimally invasive test that has advantages over TTE due to the higher ultrasonic frequency (5 \200\2237 MHz) and improved spatial res olution, particularly for structures located in proximity to the esophagus (i.e., atria, va lves; see Fig. 12.10) (see Box 12.4 for common indications). The transesophageal approach also allows for an unobstructed echo- cardiographic window in those patients with poor transthoracic acoustic windows. It is also valuable in the intraop erative setting without interfering with the operative \201 eld. Virtually all TEE probes have multiplane scanning capability. Patient preparation The procedure is performed using topical anesthesia and IV conscious se dation. Prior to procedure \200 \200 The patient is NPO for 4 \200\2236 hours prior to the procedure. Obtain patient history to determine if there are contraindications or risk factors for complications from the procedu re and/or sedation (i.e., known esophageal pathology or dysphagia, pulmonary disease such a s COPD or sleep apnea). Perform physical exam with particular attention to oropharynx/airwa y. Any dentures are removed and the back of the throat may be sprayed with lidocaine (Xyloc aine ) or benzocaine (note that these agents can have adverse side effects that are dose- dependent). Viscous lidocaine can also be gargled and swallowed for local anesthesia. Short -acting IV benzodiazepenes (i.e., midazolam) and opiate analgesics (i.e., fentanyl) may be administered for sedation. Continuous pulse- oximetry, BP, and HR monitoring is required. R eversal agents (i.e., Narcan, \202 umazenil) should be readily available. Perform under g eneral anesthesia if conscious sedation is not possible or if deemed unsafe. \200 \200 Procedure \200 Oxygen and wall suction should be available. A nurse should assist in monitoring during and after the procedure. A bite guard is used. The patient is placed in the supine or left lat eral position with the neck \202 exed. The TEE probe is lubricated with gel and introduce d gently to the pharynx. Once the patient swallows, the probe is advanced into the esophagu s. Excessive force should be avoided, especially if resistance is felt during intubation. Post-procedure The patient should be NPO for 1 \200\2232 hours post-procedure to allow reco v- ery of the gag re \202 ex. (b) ME two chamber (c) ME LAX (d) TG mid SAX (a) ME four chamber T R A N S E S O P H A G E A L (f) TG basal SAX (g) ME mitral commissural (h) ME ME AV SAX (e) TG two chamber E C H O C A R D O G R A P H Y I (j) TG LAX (k) deep TG LAX (l) ME bicaval (i) ME AV LEX Figure 12.10 Standard TEE views: ME, mid-esophageal; LAX, long axis; TG, trans-gastric; SAX , short axis; AV, aortic valve; RV, right ventricular; UE, upper esophageal. Reprinted with permission from Shanewise JS, Cheung AT, Arouson S, et al. (1999). J Am Soc Echocardiogr 1 2(10):884 \200\223900. ( T E E ) (continued) 4 7 1 4 7 2 C H A P T E R 1 2 S t r e s s t e s t i n g (m) ME RV inflow \200\223outflow (n) TG RV inflow (o) ME asc aortic SAX (p) ME asc aortic LAX a n d c a r d i a c i m a g i n g (q) desc aortic SAX (r) desc aortic LAX (s) UE aortic arch LAX (t) UE aortic arch SAX Figure 12.10 (Contd.) TRANSESOPHAGEAL ECHOCARDIOGRAPHY (TEE) 473 Box 12.4 Common indications for TEE \200 Valvular disease, especially prior to surgery (i.e., MVP with severe MR) and prosthetic val ve dysfunction Infective endocarditis Cardiac source of embolism, including patent foramen ovale (PFO) Aortic pathology (aortic, rupture, aneurysm, atheroma) Atrial \201 brillation prior to DC cardioversion Cardiac masses Pericardial disease Congenital heart defects Intr aoperative monitoring during cardiac surgery Guiding interventional procedures \200\224ASD/ PFO closure, mitral valvuloplasty Poor transthoracic windows \200 \200 \200 \200 \200 \200 \200 \200 Pitfalls Serious complications are rare (0.2%) and include esophageal perfora- tion, bronch ospasm/laryngospasm, arrhythmias, and severe hypoxia due to aspiration or respiratory depre ssion from sedation. Mild pharyngeal dis- comfort is common and self-limited. Mortality rat e is <0.01%. The proximal aortic arch and the upper portion of the ascending aorta is a blind spot becau se of the interposition of the trachea and right bronchus between the heart and esophagus, and dissection limited to this area could be missed (though this is rare). Given the resolu tion of TEE, certain nor- mal structures (e.g., Chiari network, aortic valve strands, prost hetic valve sutures) might be inadvertently mistaken as pathological. CHAPTER 12 Stress testing and cardiac imaging 474 TEE for a cardiac source of embolism Patients who have suffered a cerebral embolic event, e specially at a young age (<50 years), may have a cardiac source of emboli that is not evide nt on transthoracic echocardiogram (TTE). Once a TTE has excluded major causes such as mitr al valve disease, a TEE should be performed to examine the following areas. Key views \200 Left atrial thrombus or spontaneous contrast (0 mid-esophageal [ME] four chamber, 90 ME bicaval, two chamber and long axis [LAX]) Left atrial appendage for thrombus (90 ME two chamber) Patent foramen ovale (PFO) (90 ME bicaval) Atrial septal aneurysm (90 ME bicav al) Atrial myxoma (0 ME four chamber, 90 ME two chamber, 90 ME bicaval) LV cavity for left ventricular thrombus, including apex (120 TG LAX) Aortic atheroma (>4 mm, mobile an d ulcerated aortic plaques have the highest risk of embolization) in ascending arch and des cending aorta Aortic and mitral valves for vegetations and \201 broelastomas \200 \200 \200 \200 Diagnosis of patent foramen ovale \200 Color Doppler imaging to detect right-to-left shunt. Bubble study \200 10 mL of saline is agitated by injecting between 2 syringes connected by a three-way stop-c ock. Position the TEE probe at either 0 or 180 right atrium. Inject agitated saline. Repeat with Valsalva maneuver, if necessary. The presence of bubbles in the left heart chambers t hree cardiac cycles after opaci \201 cation of the right atrium is consistent with the dia gnosis of PFO. Sensitivity of detection of R \200\223L shunt can be improved by injecting i nto the femoral vein rather than an antecubital vein, but this is not routinely done. at ME level to visualize the \200 \200 Diagnosis of atrial septal aneurysm \200 \200 The base of the aneurysm should measure at least 1.5 cm. The excursion of the membrane shou ld be at least 1.5 cm in the direction of either atria. M-mode can be useful to accurately measure the excursion of the aneurysm. The existence of an atrial septal aneurysm in conjun ction with PFO (but not in isolation) has been shown to increase stroke risk. TEE IN AORTIC DISSECTION 475 TEE in aortic dissection TEE can demonstrate the presence of an intimal \202 ap in the ao rta with great accuracy (sensitivity of 99%, speci \201 city of 98%). Key views \200 Presence of intimal \202 ap in the following: \200 \200 \200 Coronary artery involv ement (30 \200\22345 ME AV SAX) Aortic valve for regurgitation, annular dilation, cusp in volvement (120 ME AV LAX) Site of intimal rupture, color Doppler to determine true and fa lse lumen Aortic rupture with collection around aorta Pericardial effusion Thrombus or spon taneous contrast in false lumen Ascending aorta Descending aorta Aortic arch (120 ME AV LAX, 30 ME ascending aortic SAX) (0 desc aortic SAX, 90 descending aorti c LAX) (0 UE aortic arch LAX, 90 UE aortic arch SAX) \200 \200 \200 Blood pressure control (i.e., B-blockers) should be initiated prior to TEE an d adequate sedation should be given to avoid hypertension during esophageal intubation. Pitfalls There are blind spots in the proximal arch. Aortic artifacts (imaging artifacts that mimic dissection) \200 Artifacts have parallel position to the aortic wall and are motion dependent on true struct ures. Blood \202 ow velocities are similar on either side of the artifact. Use superposit ioning of color Doppler over the artifact without mosaic pattern to indicate turbulence and \202 ow that does not follow an anatomical structure. \200 An equivocal TEE examination should prompt the use of another imaging modality such as CT o r MRI. Aortic intramural hematoma (AIH) This appears as an area of wall thickness >7 mm with or wi thout the pres- ence of an echolucent space in the aortic wall. It may be dif \201 cult to dif- ferentiate from an atherosclerotic plaque or penetrating aortic ulcer, and other imag ing modalities such as CT or MRI may be required. Diagnosis of AIH (cid:116) \200 7 mm crescent or circular thickening of aortic wall \200 \200 Extending 1 \200\22320 cm longitudinal No intimal \202 ap or Doppler \202 ow in thicken ed aortic wall CHAPTER 12 Stress testing and cardiac imaging 476 TEE in endocarditis Box 12.5 TEE is more sensitive (sensitivity >90%) than TTE for the detection of vegetations (sensiti vity <60%) in infective endocarditis (IE), especially if the vegetations are <5 mm in size. TEE is the preferred diagnostic test \200 \200 \200 \200 Patients with poor TTE windows Prosthetic valve endocarditis Intermediate or high clinical suspicion for IE with negative TTE IE with complications (i.e., abscess, hemodynamically si gni \201 cant valvular insuf \201 ciency) Some authorities feel that all patients with clinical IE should have TEE for early detectio n of complications such as perivalvular abscess formation, and for Staphyloccocus aureus IE , where the risk of complications is high. This approach is also cost-effective. A negative TTE and TEE has a negative predictive value of 95%. If clinical suspicion remain s high, however, TEE should be repeated in 7 \200\22310 days, as small vegetations (<2 mm) may be missed on the initial study. Echocardiographic criteria for diagnosis of IE according to Duke classi \201 cation \200 Vegetations: irregular mobile echodensities usually seen along lines of valve closures down stream from regurgitant \202 ow. These are typically located on the atrial side of the mi tral valve (anterior lea \202 et more common) and the ventricular side of the aortic valve . Myocardial abscess by ventricular septum, mitral valve, and papillary muscle. TEE has a s ensitivity of 80%, compared to 30% for TTE. Prosthetic valve dehiscence. New valvular regur gitation. most commonly occurs in the aortic root followed \200 Other complications that can be diagnosed by echocardiography include lea \202 et perforat ion, \201 stula, and chordal rupture. Key views \200 \200 \200 \200 Aortic valve, aortic root (30 \200\22345 ME AV SAX, 120 ME LAX) Mitral valve views (see p. 37) Tricuspid valve (0 ME four chamber, 120 TG LAX) Pulmonary valve (90 ME RV in \202 ow \200\223out \202 ow) TEE is useful prior to surgery to exclude involvement of other valves and to look for an ab scess or other complication that may require additional surgical procedures (see Box 12.6). Sensitivity of TEE and of TTE are com- parable for the detection of right-sided vegetation s. TEE IN ENDOCARDITIS 477 Pitfalls Valve strands (Lambl \200\231s excrescences), chordal structures from myxoma- tous degeneration, and nonspeci \201 c valvular thickening may be mistaken as vegetations, lea ding to a false-positive result. Box 12.6 Echocardiographic features requiring surgical referral \200 Acute severe aortic or mitral regurgitation causing LV failure or hemodynamic compromise Pr osthetic valve dehiscence, especially if hemodynamic compromise Myocardial abscess Vegetati ons with recurrent embolization despite antibiotics Mitral valve vegetation >10 mm due to a ssociated increased risk of embolism Increase in vegetation size after 2 \200\2234 weeks of antibiotics \200 \200 \200 CHAPTER 12 Stress testing and cardiac imaging 478 TTE/TEE in mitral regurgitation (MR) Assessment of mitral valve (MV) morphology is required to determine the mechanism of regurgitation and associated structural abnormalities: \200 \200 \200 \200 \200 \200 \200 \200 \200 \200 Elongation or rupture of chords Papillary muscle rupture Retraction of chords Prolapse or t ethering of lea \202 ets Subvalvular apparatus thickening or calci \201 cation Annular di lation Annular calci \201 cation LV size and function LA size Regional wall motion abnorma lities may suggest ischemic MR. Key TEE views (see Fig. 12.11) \200 Lea \202 et prolapse or restriction (0 ME four chamber, 45 ME mitral commissural, 90 ME two chamber, 120 ME LAX) Annular diameter (120 ME LAX) Lea \202 et prolapse (0 T G basal SAX) Subvalvular apparatus (90 TG two chamber) Anterior and posterior lea \202 e ts are each divided into three segments to describe location of pathology. \200 \200 \200 Assessment of MR severity (by TEE or TTE) \200 \200 \200 \200 Length/area of regurgitant jet Density of spectral Doppler tracing Timing of MR: early syst olic vs. holosystolic by color M-mode Direction of jet: eccentric or central \200 Coanda effect Doppler may underestimate severity of regurgitation Pulmonary venous systolic \202 ow reversal (see Table 12.4) Calculation of regurgitant volume (RV) and effective r egurgitant ori \201 ce area (EROA) using PISA or volumetric method Other features of sever e MR: \200 \200 : size of eccentric wall-hugging regurgitant jet on color \200 Regurgitant jet width at its origin (vena contracta) >0.7 cm Peak E-wave velocity >1.5 m/se c Proximal isovelocity surface area (PISA) \200 Identify isovelocity hemispheric shells on ventricular aspect of valve in apical view using color Doppler with adjusted aliasing velocity. Measure radius of isovelocity shell (r) and aliasing velocity. Measure MR peak velocity and VTI from spectral tracing. \200 \200 \200 (cm2) = 2(cid:83)r2 x aliasing velocity/MR peak velocity EROA RV (mL) = EROA x MR VTI Volumetric method \200 RV (mL) = Total stroke volume (SV) \200\223 Forward stroke volume \200 \200 \200 Reg urgitant fraction (RF%) Total SV = Mitral in \202 ow volume (in absence of signi \201 cant AR) MV in \202 ow vol ume = MV VTI (from PW Doppler) Forward SV = LVOT VTI x MV area ((cid:83)r2) x LVOT area = RV/Total stroke volume x 100 TTE/TEE IN MITRAL REGURGITATION (MR) 479 90 45 120 TG 0 AM P2 P3 P1 AM AM P2 P1 0 P2 P3 Figure 12.11 Assessment of the mitral valve by TEE. Reprinted with permission from Shanewis e JS, Cheung AT, Arouson S, et al. (1999). J Am Soc Echocardiogr 12(10):884 \200\223900. Table 12.4 Assessment of MR severity Parameter Mild