ejection fraction (from 2D- or 3D-generated volumes or derived from M-mode (e.g. Teicholz formula)). mass : can be derived from M-mode measures (American Society of Echocardiography (ASE)-modi \201 ed Penn formula), 2D volumetric models, or 3D reconstr uction. M-mode mass calculations tend to over-quantify LV mass. Aortic root and ascending aorta Linear measurements from 2D PLA view or M-mode. The root is measured at cuspal level, and the aorta is measured at the sinotubular junction and 2 cm a bove this. THE STANDARD TRANSTHORACIC ECHO: CONTINUED 19 Right atrium \200 Area from 2D A4Ch view. \200 Inferior/superior and lateral/medial PTP measurements. Right ventricle \200 PTP measurements are exclusively used. \200 Irregularity of chambe r con \201 guration makes standardized quantitation dif \201 cult. Pulmonary artery PTP medial \200\223lateral measurement in PSA at aortic valve level. (a) (b) RV RV LV RA IVC (c) (d) RV LV Ao RA Pa LA Fig. 1.6 (a) Parasternal long-axis view (RV in \202 ow); (b) parasternal short-axis (mitra l valve level); (c) apical 4-chamber view; (d) suprasternal long axis. Ao = aorta; IVC = in ferior vena cava; Pa = pulmonary artery. Reproduced with permission from Shanewise JS. Jour nal of the American Society Echocardiography 1999;12:884 \200\223900. 20 CHAPTER 1 Cardiac investigations Assessment of wall motion Assessment is based upon review of multiple cuts as described ear lier. In general, abnormalities of LV regional function should be apparent in more than one view. Various labeling systems have been used but the American Heart Association (AHA) Car diac Imaging Committee 17-segment model is the standard convention: \200 basal (6): anter oseptal, anterior, anterolateral, posterolateral, inferior, inferoseptal. mid LV (6): same as above. \200 apical (5): anterior, lateral inferior, septal, and true apical. See Fig. 1.7. Regional functional assessment \200 Systolic function should be classi \201 ed as \200 \230normal \200\231, \200\230globaly hypokinetic \200\231, or demonstrating the presence o f \200\230regional wall motion abnormalities \200\231. \200 Global hypokinesis is consis tent with cardiomyopathy, either ischaemic or non-ischaemic. Some degree of regional variat ion may be present in non-ischaemic cardiomyopathy. The presence of distinct regional wall motion abnormalities with large areas of normal regi onal function is suggestive of underlying coronary artery disease. Evaluation should ideally be based on the degree of regional thickening as opposed to endoc ardial motion. Unfortunately, this is not always possible. Each regional segment can be quali \201 ed as: hyperkinetic. \200 normal. \200 hypokinetic. \200 akinetic. \200 dyskinetic. Wall motion quanti \201 cation, based on similar characteristics, may be prognostically useful, but is not useful in routine evaluation. Identi \201 cation of hyper-echogenic, thinned areas suggests the presence of scarring and should be mentioned in the evaluation. Scarred segments may demonstrate endocardial motion, without wall thickening, due to tethering by peripheral segments. ASSESSMENT OF WALL MOTION 21 Ant. Ivs (ANT. IVS) Ant ANT 15 2 1 16 5 Lat (Lat) Inf. Ivs (INF. IVS) Posterior Inf 17 3 4 15 18 7 6 18 19 6 1 12 10 8 20 9 14 4 9 15 18 1 6 21 12 12 11 22 13 13 14 3 8 16 3 4 2 5 8 7 9 19 10 14 12 13 11 22 Left anterior descending coronary artery Left circumflex coronary artery and right coronary artery Right coronary artery Left circumflex coronary artery Fig. 1.7 American Heart Association 17-segment model. From Swanton H (2003) Pocket Consulta nt: Cardiology . 5th ed, Oxford: Blackwell Publishing. 22 CHAPTER 1 Cardiac investigations Assessment of LV systolic function Global functional assessment \200 Ejection fraction es timation is usually performed qualitatively. Echocardiographers need to routinely \200\230recalibrate \200\231 their assessment abiliti es by comparing qualitative readings to more accurate quantitative modalities, such as MRI, radionuclide ventriculography, 3D or even quantitative 2D ECHO (see Table 1.1 ). 2D ECHO ejection fractions can be quanti \201 ed most ef \201 ciently on or of \202 ine by the: \200 Simpson \200\231s modi \201 ed biplane method of stacked disks : A4Ch and A2Ch LV traces are performed and the apex \200\223annulus length is divided int o a standard number of equal segments, the length of which serves as disc height. Cross-sec tional disc area is calculated from the elliptical formula ( \200 r 1 r 2 ) where r 1 and r 2 = the endocardial medial \200\223lateral dimension of each segment in the A4Ch and A2Ch views, respectively. cylinder hemi-ellipsoid model : volume is determined by measuring the LV 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 . Table 1.1 Assessment of left ventricular ejection fraction LV ejection fraction Qualitative assessment > 75 % Hyperdynamic 55 \200\22375 % Normal 40 \200\22354 % Mildy reduced 30 \200\22339 % Moderately reduced <30 % Severly reduced LV stroke volume : integration of LVOT spectra \227 LVOT area (derived from diameter in PLA view). Systemic output : LV stroke volume \227 heart rate. \200 Pulmonary stroke volume : integ ration of pulmonary artery spectral trace \227 pulmonary artery area (derived from systolic medial \200\223lateral dimension a t the level of Doppler sampling). \200 RV output : pulmonary stroke voume \227 heart rat e. \200 Pulmonic/systemic shunt ratio (Qp/Qs): pulmonary output/systemic output. Tissue Doppler of mitral and tricuspid annular motion. ASSESSMENT OF LV SYSTOLIC FUNCTION 23 Essential aspects of ECHO assessment in patients with impaired LV systolic function Anatomy \200 LV dimensions (systolic and end diastolic). \200 LV ejection fraction. \200 Reg ional wall motion abnormalities. Doppler characteristics \200 E:A ratio (grade according to Fig. 1.7 b Assessment of LV di astolic function, p. 27). \200 E deceleration time. \200 Estimate pulmonary artery (PA) systoli c (from tricuspid regurgitation (TR) jet). Estimate PA diastolic (from pulmonary regurgitation (PR) jet). \200 Estimate pulmonary ca pacitance (= stroke volume/(PAs \200\223 PAd pressures)). Implications for therapy \200 Mitral regurgitation at end diastole if AV delay too long. \200 Dys-synchrony (TDI septum/lateral annulus > 60 ms). 24 CHAPTER 1 Cardiac investigations 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, di astasis (atrioventricular pressure equilibration without LV \201 lling), and atrial systo le. These measures are generally age and heart-rate dependent, and affected by LV loading c onditions to variable degrees (see Fig. 1.8 ). 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. The following should b e taken into account when assessing these parameters: \200 E/A ratio is particularly depe ndent on sample volume placement (annulus, mitral tips, etc.) and loading conditions. E/A ratio decreases with age, and assessment must be age-normalized. An E/A ratio <1.0 is c ommon among the elderly and often represents normal aging. increasing LV \201 lling pressures (e.g. in heart failure) lead to \200\230pseudonormalization \200\231 of the ratio, which often reverts to an abnormal patt ern following maneuvers to reduce LV preload (e.g. diuresis) or Valsalva maneuver. the deceleration time correlates somewhat with invasive measures of LV stiffness, whereas o ther measures largely re \202 ect LV relaxation. Pulsed Doppler of pulmonary veins: Flow into the left atrium can be sampled. S, D, and A wa ves represent systolic and diastolic atrial \201 lling. The A wave is generated by revers e \202 ow into the pulmonary veins during atrial contraction. \200 The S/D ratio increa ses with age, as LV diastolic relaxation declines. A pulmonary vein A wave duration more th an 30 ms greater than transmitral A wave duration suggests elevated LV \201 lling pressur e. CW Doppler of LV out \202 ow/mitral in \202 ow: Isovolumic relaxation time. Tissue Doppler of medial and lateral mitral annuli (E \200\231, A \200\231) \200 This is considered the least load-dependent \201 lling variable. There is generally poor correlation between medial and lateral velocities, with the lateral annulus measurement being more reproducible. The E/E \200\231 ratio correlates roughly with LV end-diastolic pressure; a ratio > 15 is strongly suggestive of elevated \201 lling pressure, and a ratio <8 strongl y suggestive of normal \201 lling pressure. Color Doppler \202 ow propagation (CFP) slope: Rate of blood acceleration into the LV fro m the annulus to the apex. Various diastolic pro \201 les combining some of the above parameters have been suggested as indicators of degree or stage of \200\230diastolic dysfunction \200\231. (see Fig. 1.8 ). In general: \200 markers of impaired relaxation (e.g. decreased E and E \200\231 are accompanied by compensatory enhancement of A and A \200\231), reduced pulmonary venous D, a nd reduced CFP slope. ASSESSMENT OF LV DIASTOLIC FUNCTION 25 increases in LV \201 lling pressure lead to pseudonormalization of the transmitral Doppler E/A ratio, with less effect on Doppler with Valsalva maneuver and tissu e Doppler velocity ratios. as compliance decreases or a patient \200\231s position on the LV pressure \200\223 volume curve advances (operating stiffness), the transmitral DT drops below 130 ms, early D oppler \201 lling velocity is increased, and, due to elevated late diastolic LV pressures , atrial contraction and associated velocities are reduced. if E/E \200\231 ratio <8 and LA is of normal size, symptoms are unlikely to be due to diastolic heart failure. do not miss constriction (see b Constrictive pericarditis vs. restrictive myocardial disease, p. 475); look for: \200 septal \200\230bounce \200\231 and dys-schro ny. \200 inferior vena cava (IVC) dilatation. \200 hepatic vein expiratory reversal. 2 6 C H A P T E R Echocardiographic classification of diastolic dysfunction 1 Stage I Impaired relaxation Stage III Reversible restrictive Stage IV Fixed restrictive Normal diastolic function Stage II Pseudonormal C a r d i a c 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 E/A>1.5 DT<140 ms E/A \2070.75 i n v e s t i g a t i o n s 2.0 s / E m , A y t i c o e V Mitral inflow l 0.0 Adur Time, ms Time, ms Time, ms Time, ms Time, ms \224E/A<0.5 \224E/A \211 0.5 \224E/A \211 0.5 \224E/A<0.5 \224E/A<0.5 2.0 s / m Mitral inflow at peak Valsalva maneuver , y t i c o e V E A l 0.0 Time, ms Time, ms Time, ms Time, ms Time, ms Fig. 1.9 ARdur>Adur +30 ms ARdur>Adur +30 ms ARdur>Adur +30 ms ARdur<Adur ARdur<Adur 2.0 s / m S D Pulmonary venous flow , y t i c o e V ARdur l 0.0 AR Time, ms Time, ms Time, ms Time, ms Time, ms Vp>45 Vp<45 Vp<45 Vp<45 A S S E S S M E N T O F 5 m c Vp , Color M-mode propagation velocity e c n a t s i D 0 Time, ms Time, ms Time, ms Time, ms Time, ms L V s / E/Ea<10 E/Ea<10 E/Ea \211 10 E/Ea \211 10 E/Ea \211 10 m Doppler tissue imaging of mitral annular motion D A S T O L C 0 , I y t i c o e V a \200 0.15 e \200 Time, ms l Time, ms Time, ms Time, ms Time, ms I F U N C T O N LV relaxation Normal Impaired Normal to \206\223 Impaired \206\223 \206\223 Impaired \206\223 \206\223 \206\223 Impaired \206\223 \206\223 \206\223 \206\223 LV compliance Normal I Atrial pressure Normal Normal \206\223 \206\223 \206\223 \206\223 \206\223 \206\223 \206\223 \206\223 \206\223 Fig. 1.8 Echocardiographic classi \201 cation of diastolic dysfunction. Reproduced with pe rmission from Journal of the American College of Cardiology, Vol 48, No.3, 2006. August 1, 2006:e1 \200\223148. Bonow et al, AHA/ACC Best Practice Guidelines. 2 7 28 CHAPTER 1 Cardiac investigations Echocardiography in aortic stenosis Etiology \200 Aortic stenosis (AS) can be congenital or, more commonly, degenerative. In late stages, severe \201 brocalci \201 cation precludes aetiologic iden ti \201 cation, even on direct intraoperative visualization. Chronic severe AS is usually accompanied by concentric LV hypertrophy, a product of pressure overload. Bicuspid aortic valve is diagnosed best on short-axis view and can display various con \201 gurations. Often a \200\230raphe \200\231 is observed, representing the undeveloped c ommisure where persistent cuspal fusion is present. Systolic cuspal \200\230doming \200 \231 is consistent with congenital AS. Degenerative AS is typically initiated in the annulus \201 brosis (most commonly in the non-coronary cusp area) and gradually proceeds to invade the cuspal bases, body, and, in later stages, the tips. Valve thickening without haemodynamic stenosis is oft en termed \200\230sclerosis \200\231. Haemodynamics \200 Stenosis is de \201 ned as a haemodynamically signi \201 cant reduct ion in valve area as indicated by a rise in transvalvular pressure gradient. Pressure gradient is dependent upon \202 ow and, in the setting of low cardiac output, may be minimally elevated despite signi \201 cant stenosis. \200 Valve a rea is generally not indexed to body size in most clinical labs, and categorization of severity may vary. One convention is as follows: \200 mild : area > 1.5 cm 2 and <2.0 cm 2 . \200 moderate : > 1.0 and <1.5 cm 2 . \200 severe : <1.0 cm 2 . \200 critical: <0.7 cm 2 . ECHO diagnosis \200 Assess cuspal separation or presence of doming. A trilea \202 et val ve with one cusp opening fully (approaching edge of the root) is probably not stenotic. CW Doppler-derived gradients are reported an instantaneous peak and/or mean. The mean gradi ent is more reliable in determining stenosis severity. Catheterization lab gradients are \200\230peak to peak \200\231, with pressure measurements that are usually not acquired simultaneously and often do not correlate with D oppler gradients. Peak transvalvular velocity > 2.5 m/s (instantaneous gradient 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 not valve area. The dimensionless obstructive index (DOI) is the ratio of LV out \202 ow tract velocity (pulsed Doppler)/transvalvular velocity (CW Doppler), and takes into account elevated \202 ow. General guidelines: \200 DOI<50 % : signi \201 cant stenosis. \200 DOI 30 \200\22350 % : moderate stenosis. \200 DOI<30 % : severe stenosis. ECHOCARDIOGRAPHY IN AORTIC STENOSIS 29 Aortic valve area is quantitated by the continuity equation. The most common errors in this assessment include: \200 under-measurement of the LVOT. \200 failure to assess LVOT Do ppler at an angle within 30 of the \202 ow vector. 30 CHAPTER 1 Cardiac investigations Transoesophageal echocardiography Clinical indications Transoesophageal echocardiography (T OE) is a semi-invasive test that has advantages over transthoracic ECHO (TTE). The TOE tran sducer is closer to the heart and has a higher frequency (5 MHz), thus giving better resolu tion than TTE (2.5 MHz). The oesophageal approach means that an unobstructed ECHO window is possible in those patients with poor trans thoracic windows, and it also allows the use of TOE in the intra- operative setting without interfering with the operative \201 eld. Vir tually all TOE probes have multiplane scanning capability. See Fig. 1.9. Patient preparation The procedure is performed using local anesthesia and, if required, int ra- venous (IV) sedation. Prior to procedure \200 The patient is fasted for 4 hours. \200 Any dentures are remove d and the back of the throat is sprayed with lidocaine (Xylocaine ), taking care not to exceed the maximum dose because absorption of the local anesthetic can cause systemic effec ts (nausea, drowsiness, and ataxia). IV midazolam (dose 2 \200\2236 mg) can be given for sedation, but in the majority of patients, local anesthesia will suf \201 ce. Flumazenil may be required to reverse the effect of midazolam. Procedure \200 Oxygen and wall suction should be available. A nurse should be available to assist in monitoring during and after the procedure. A bite guard is used. The patient is placed in the left lateral position with the neck \202 exed. Oxygen saturation and the ECG are monitored. The sheathed TOE probe is lubricated with gel and introduced gently to the pharynx. Once th e patient swallows, the probe is advanced into the esophagus. The patient should be told th at the initial gag feeling will ease with the passage of the probe from the pharynx into th e esophagus. Undue force must be avoided. Post-procedure \200 The patient should be \200\230nil by mouth \200\231 for 1 h post-pro cedure, for the effect of the local anesthetic to wear off. Some patients such as pediatric or adolescent patients with complex congenital heart disease will require general anesthes ia. Pitfalls \200 Serious complications are rare (0.2 % ) and the mortality rate is less than 0.01 % . Serious complications include oesophageal rupture, laryngospasm, ventricular arrh ythmia, and severe hypoxia. TRANSOESOPHAGEAL ECHOCARDIOGRAPHY 31 The proximal aortic arch and the upper portion of the ascending aorta is a \200\230blind s pot \200\231 because of the interposition of the trachea and right bronchus between the hea rt and esophagus, and dissection could be missed. Due to the resolution of TOE, certain nor mal structures e.g. Chiari network, aortic valve strands, prosthetic valve sutures, might b e inadvertently mistaken as pathology. Indications for transoesophageal echocardiography \200 Valve disease: mitral valve prolapse, assess mitral stenosis for mitral valvuloplasty. aortic regurgitation, adjunct to assess aortic stenosis. \200 Prosthetic valve dysfunctio n. Bacterial endocarditis. \200 Cardiac source of embolism, including patent foramen ovale ( PFO). \200 Aortic pathology: acute aortic dissection, aortic rupture and aortic aneurysm, atheroma. Prior to DC cardioversion. \200 Cardiac masses. \200 Pericardial disease and masses. \200 Congenital heart defects. \200 Intraoperative monitoring of valve procedures, LV an d RV function. \200 Intensive therapy unit (ITU) setting to determine cause of haemodynamic collapse. Guiding interventional procedure \200\224 atrial septal defect (ASD) closure, mitral valvuloplasty. Poor transthoracic window. 3 2 C H A P T E R 1 C a r d i a c (a) ME four chamber (b) ME two chamber (c) ME LAX (d) TG mid SAX i n v e s t i g a t i o n s (e) TG two chamber (f) TG basal SAX (g) ME mitral commissural (h) ME ME AV SAX (i) ME AV LEX (j) TG LAX (k) Deep TG LAX (l) ME bicaval Fig. 1.10 (m) ME RV inflow-outflow (n) TG RV inflow (o) ME asc aortic SAX (p) ME asc aortic LAX T R A N S O E S O P H A G E A L (q) Desc aortic SAX (s) UE aortic arch LAX (r) Desc aortic LAX (t) UE aortic arch SAX E C H O C A R D O G R A P H Y Fig. 1.9 Standard TOE views: AV, aortic valve; LAX, long axis; ME, mid oesophageal; RV, rig ht ventricular. SAX, short axis; TG, transgastric. Reproduced with permission from Shanewis e JS. Journal of the American Society Echocardiography 1999;12 : 884 \200\223900. I 3 3 34 CHAPTER 1 Cardiac investigations TOE 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 TTE. Once a TTE has excluded major causes such as mitral valve disease, a TOE should be performed to examine the following: Key views \200 Left atrial clot or spontaneous contrast (0 ME (mid-oesophageal) four chamber, 90 ME bicaval). Left atrial appendage for clot (90 ME two chamber). \200 Patent foramen ovale (90 M E bicaval). \200 Atrial septal aneurysm (90 ME bicaval). \200 Atrial myxoma (0 ME four chamber, 90 ME two chamber, 90 ME bicaval). LV cavity for left ventricular thrombus, including apex (120 TG long axis (LAX)). Aortic atheroma ( > 4 to 5 mm, mobile and ulcerated aortic plaques have the highest risk of embolization) in the ascending arch and descending aorta. Aortic and mitral valves for vegetations. Diagnosis of patent foramen ovale \200 10 ml of saline is agitated by injecting between t wo syringes connected by a three-way tap. Some operators report better opaci \201 cation w ith colloid (e.g. Haemaccel ) rather than saline. Position the TOE probe at either 0 or 180 at mid-esophagus level to visualize the right atrium. Inject agitated saline. \200 Repeat with Valsalva maneuver induced by asking the patient to cough, or try to blow out the plunger from a 2 ml syringe. The presence of bubbles in the left heart chamber \200\231s three cardiac cycles after opaci \201 cation of the right atrium is required for a diagnosis of PFO. Sensitivity of detection of R \200\223L shunt can be improved by injecting into the femoral vein rather than an antecubital vein, but this is not routinely done. Diagnosis of atrial septal aneurysm \200 The base of the aneurysm should measure at least 1.5 cm. \200 The excursion of the membrane should be at least 1.5 cm in the direction of either atrium. TOE IN AORTIC DISSECTION 35 TOE in aortic dissection TOE can demonstrate the presence of an intimal \202 ap in the ao rta with great accuracy (sensitivity of 99 % , speci \201 city 98 % ). TOE should examine the following: Key views \200 Presence of intimal \202 ap in: ascending aorta (120 ME aortic valve (AV) LAX, 0 ME ascending aortic short axis (SAX)). descending aorta (0 descending aortic SAX, 90 descending aortic LAX). aortic arch (0 UE aortic arch LAX, 90 UE aortic arch SAX). Coronary artery involvement (0 ME AV SAX). \200 Aortic valve for regurgitation, annula r diameter, cusp (120 ME AV LAX). Site of intimal rupture, color \202 ow mapping to determine true and false lumen. Aortic rupture with collection around the aorta and pericardial effusion. \200 Thrombus o r spontaneous contrast in false lumen. Blood pressure control should be initiated prior to TOE, and sedation should generally be given to avoid undue hypertension. Pitfalls \200 Blind spots in the proximal arch. \200 Aortic artifacts are especially co mmon in dilated aorta \200\224 artifacts are characterized by their position parallel to t he aortic wall, blood \202 ow velocities similar on either side of the artifact, and supe rimposition of the color \202 ow map over the artifact. An equivocal TOE examination should prompt the use of another imaging modality such as CT or MRI. Aortic intramural haematoma (AIH) This appears as an area of wall thickness > 7 mm with or without the presence of an echolucent space in the aortic wall. It may be dif \201 cult to distinguish this entity from an atherosclerotic plaque or penetrating aortic ulcer, and ot her imaging modalities may be required. Diagnosis of AIH \200 (cid:2) 7 mm crescent or circular thickening of the aortic wall. \200 Extending 1 \200\22320 cm longitudinal. \200 No intimal \202 ap or Doppler \202 ow in thickened aortic wall. 36 CHAPTER 1 Cardiac investigations TOE in endocarditis TOE is more sensitive (sensitivity > 90 % ) than TTE for the detection of vegetations (sens itivity <60 % ) in infective endocarditis (IE), especially if the vegetations are <5 mm in size. TOE is the investigation of choice in: \200 patients with poor TTE window. \200 prosthe tic valve endocarditis. \200 high or intermediate suspicion of IE with negative TTE. \200 detection of IE-related complications. Some authorities feel that all patients with I E should have TOE for early detection of complications such as aortic abscess formation, an d for Staphyloccocus aureus IE, where the risk of complications is high. Note that negative TTE and TOE has a negative predictive value of 95 % . If clinical suspicion remains high, TOE should be repeated in 7 \200\22310 days . Echocardiographic criteria for diagnosis of IE according to Duke classi \201 cation \200 Vegetations. \200 Abscess formation: most commonly occurs in the aortic root followed by the ventricular septum, mitral valve, and papillary muscle. TOE has a sensitivity of 80 % compared to TTE, which is 30 % . Prosthetic valve dehiscence. OR \200 New valvular regurgitation. Other complications incl ude: lea \202 et perforation, \201 stula, and chordal rupture. Key views \200 Aortic root abscess seen (60 ME AV SAX). \200 Mitral valve views (see b TOE for mitral regurgitation, p. 38). \200 Tricuspid valve (0 ME four chamber, 120 TG LAX). \200 Pulmonary valve (90 ME RV in \202 ow \200\223out \202 ow). TOE is u seful prior to surgery to exclude infection on other valves and to look for abscess formati on that will require additional procedures. Pitfalls Valve strands (Lambl \200\231s excrescences), chordal structures from myxoma- tous degeneration, and non-speci \201 c valvular thickening may be mistaken as vegetations, le ading to a false-positive TOE result. TOE IN ENDOCARDITIS 37 Echocardiographic features requiring surgical referral \200 Acute aortic or mitral regurg itation causing left ventricular failure. There may be associated valve destruction such as perforation or chordal rupture. Prosthetic valve dehiscence causing haemodynamic compromise. \200 Large abscess formation or extension of abscess despite antibiotics. \200 Vegetations \200\224 recurrent emboli zation. \200 High risk of embolic events for mitral valve vegetation > 10 mm. \200 Incr ease in vegetation size after 4 weeks of antibiotics. 38 CHAPTER 1 Cardiac investigations TOE for mitral regurgitation (MR) \200 Morphological assessment of mitral valve to determ ine mechanism of regurgitation: \200 elongation or rupture of chordae. \200 retraction of chord. \200 prolapse or restriction of lea \202 ets. \200 subvalvular apparatus. \200 annular diam eter, degree of calci \201 cation. \200 LV size and regional wall abnormalities. Key views (see Fig. 1.10 ) \200 Lea \202 et prolapse or restriction (0 ME four chambe r, 45 ME mitral commissural, 90 ME two chamber, 120 ME LAX). Annular diameter (120 ME LAX). \200 Lea \202 et prolapse (0 TG basal SAX). \200 Subvalvular apparatus (90 TG two chamber). How to assess severity of MR using TOE \200 Length of regurgitant jet. \200 Timing of M R: early systolic vs. holosystolic by color M-mode. \200 Direction of jet: eccentric wall hugging or central. \200 Pulmonary venous \202 ow (see Table 1.2). \200 Other featur es of severe MR: regurgitant jet width at its origin, (cid:2) 0.5 cm in 120 o view, so-called \200\230vena contracta \200\231. active volume-loaded LV. \200 Peak E-wave velocity > 1.5 m/s. Table 1.2 Assessment of severity of MR using pulmonary venous \202 ow Grade Length (MR jet/LA size) Timing Direction Pulmonary venous \202 ow I 1/3 Early Central Normal 2 2/3 <Pansystolic Central Normal 3 2/3 Pansystolic Eccentric Normal or reversed 4 3/3 Pansystolic Eccentric or central Reversed TOE FOR MITRAL REGURGITATION (MR) 39 P2 P2 AM P3 AM P1 AM 90 120 45 TG 0 P2 P3 AM P1 AM AM P2 0 P1 P2 P3 Fig. 1.10 Assessment of the mitral valve by TOE. Reproduced with permission from Shanewise JS. Journal of the American Society Echocardiography 1999; 12 : 884 \200\223900. 40 CHAPTER 1 Cardiac investigations TOE for mitral valve prolapse Mitral valve prolapse (MVP) causes eccentric mitral regurgita tion, hence prolapse of the posterior lea \202 et produces anteriorly directed jet and vis e versa. Note that when the MR jet hugs the wall of the left atrium, the reported severity should be upgraded. The left and right pulmonary veins should be sampled with pulse wave to check for systolic \202 ow reversal. Classical MVP \200 At least 2 mm displacement of the mitral lea \202 et beyond the mitra l annular plane in any view. \200 Mitral valve thickness > 5 mm. Non-classical MVP \200 The prolapsing lea \202 ets are not thickened (<5 mm) and are una ffected by myxomatous degeneration. Such patients are not at increased risk of complications such as severe MR, infective endoc arditis, and sudden death as compared to the classical form of MVP. TOE FOR MITRAL VALVE REPAIR 41 TOE for mitral valve repair \200 Mapping of the prolapsing mitral valve segments can be p erformed to aid surgical planning. Two-thirds of cases of MVP involve the middle scallop of the posterior lea \202 et, and 70 % of these cases can be successfully repaired. \200 Ruptured chordae and \202 ail mitral valve lea \202 ets should be noted. \200 The mitral annulus diame ter is also measured (upper limit normal is 35 mm), and the presence of annular calci \201 cation noted. 42 CHAPTER 1 Cardiac investigations TOE in chronic ischaemic MR \200 Typically, the mitral valve is structurally normal and t herefore MR is termed \200\230functional \200\231. Remodeling of the LV displaces the papillary muscle towards the apex, and traction on the m itral lea \202 ets causes incomplete lea \202 et closure. \200 The zone of coaptation i s displaced towards the apex, and \200\230systolic tenting \200\231 of the mitral valve is seen. LV remodeling and dilatation appears to be necessary for severe MR to develop. Isolated seg mental wall motion abnormalities without LV dilatation are not generally associated with se vere MR. Annular dilatation will exacerbate incomplete lea \202 et coaptation but does not, in isolation, cause MR. In the presence of an inferior or posterior infarct, the posterobasal wall (site of the pos teromedial papillary) of the LV may become aneurysmal. This can exert asymmetrical traction on the chordae, resulting in retraction of the posterior lea \202 et. There is abnormal a pposition, and an eccentric, anteriorly directed, jet of MR results. Key views \200 Restriction of lea \202 et, systolic tenting of MV (0 ME four chamber, 45 ME mitral commissural, 90 ME two chamber, 120 ME LAX) Annulus size (120 ME LAX). \200 LV assessment, especially the posterobasal wall (90 ME two chamber, 0 TG mid SAX). TOE FOR MITRAL STENOSIS 43 TOE for mitral stenosis Assessment for suitability for percutaneous balloon mitral valvulop lasty (PBMV see b Mitral regurgitation, p. 158): \200 LA and left atrial appendage (LAA) thrombus \200\224 relative contraindication. grade 2 MR \200\224 relative contraindication. \200 mitral valve anatomy: mobility. \200 thickening. \200 calci \201 cation. \200 subvalvular thickening. 44 CHAPTER 1 Cardiac investigations TOE for assessment of cardiac masses \200 Normal anatomy that should not be mistaken for pathology : Chiari network, eustachian valve near the inferior vena cava, trebeculations in the left atrial ap pendage, ridge separating the left pulmonary vein and left atrial appendage. Myxomas are the most common primary cardiac tumor (50 % of all tumors), and speci \201 c features can be delineated on TOE: \200 attached by a stalk to the interatrial septum near the fossa ovalis in 90 % of cases. 75 % are in the LA. \200 may have a speckled, cystic appearance with frond-like projectio ns. \200 may be multiple. If they occur elsewhere, they may be mistaken for thrombus (ten d to be homogeneous in appearance) or other tumors. may cause valve obstruction. Fibroelastomas are benign tumors that attach to valve apparatus. They have a frond-like app earance and may mimic vegetations or myxoma. \200 Primary malignant cardiac tumors and se condary metastatic disease can in \201 ltrate the epicardium, myocardium, or endocardium, or present as intracavity m ass. Pericardial involvement in malignant disease frequently causes pericardial effusion. This page intentionally left blank 46 CHAPTER 1 Cardiac investigations TOE assessment of mitral valve prosthesis TOE is especially sensitive in detecting MR in as sociation with a prosthetic valve, because the left atrium is imaged in the foreground and is therefore devoid of the artifacts generated by the metal elements of the prosthetic valv e. Paraprosthetic mitral leak The sewing ring of the mechanical prosthetic valve appears as a bright ring attached to the mitral annulus. If a signi \201 cant circumference of the sewi ng ring has come away (e.g. from endocarditis), a rocking movement of the valve will be evi dent \200\224 this \200\230rocking prosthetic valve \200\231 is characteristic of a parti al dehiscence of the valve. Key views The mitral valve sewing ring should be identi \201 ed in and interrogated with c olor \202 ow and CW Doppler: \200 0 ME four chamber. \200 90 ME two chamber. \200 120 ME LAX views of the mitral valve. The motion of the prosthetic valve mechanism (e.g. tilting disc) should be assessed to ensure the disks or occluder are moving freely i n 120 ME LAX view. The presence of \202 ow outside the sewing ring (i.e. paraprosthetic) is not normal, alth ough small or mild jets may be seen early after valve implanta- tion. This represents failu re of the sutures attaching the valve ring to the annulus, either from technical failure or from the effect of endocarditis. Paraprosthetic leaks are more likely in the presence of a calci \201 ed mitral annulus. Transprosthetic mitral leak Mechanical prosthetic valves have regurgitation during closure of the valve, which arises within the sewing ring (i.e. intraprosthetic). These \200\230cl osing jets \200\231 are a normal feature and should not be mistaken as pathological. In gen eral they can be easily distinguished from pathological regurgitation (see Table 1.3 ). Cau ses for abnormal intraprosthetic leak include pannus or thrombus preventing the occluder fr om functioning properly. Tissue mitral prosthesis This should be assessed in the same way as a mechanical prosthesis . The prosthetic valve lea \202 et should be assessed for: \200 prolapsing lea \202 et. \200 \202 ail lea \202 et. \200 thickened cusps ( > 3 mm \200\224 higher risk of d ysfunction). \200 the Doppler signal for a \202 ail cusp shows a characteristic striate d \200\230zebra-stripe pattern \200\231. TOE ASSESSMENT OF MITRAL VALVE PROSTHESIS 47 Obstruction of the prosthetic mitral valve This may be due to thrombus or pannus formation. The diagnosis is made by \201 nding: \200 limited movement of the occluder or disc. \200 haemodynamic con \201 rmation by \201 nding a high peak pressure gradient across t he mitral valve( > 2.5 m/s) or a prolonged pressure half-time ( t > 200 ms). Features of normal closing jets \200 Short jets <3 cm length. \200 Narrow base <5 mm. \200 Early systolic rather than pansystolic leak. Table 1.3 Upper limit of pressure half-time (ms) for commonly used valves Maximum t (ms) Valve type Starr \200\223Edwards 170 St Jude 131 CarboMedics 117 Carpentier \200\223Edwards 171 Native valve 60 48 CHAPTER 1 Cardiac investigations TOE for aortic valve prosthesis \200 The orientation of the aortic valve means that the s ewing ring will obstruct the view of the ori \201 ce of the valve for mechanical and stented tissue aortic valves. Thus, assessment of aortic paraprosthetic leak on 2D imaging is limited compared t o mitral valve assessment. CW interrogation is not possible because the LVOT is orientated perpendicular to the ultras ound beam, when the aortic valve is assessed from the standard ME views. A combined TTE and TOE approach is required, because TTE is ideally suited to Doppler interrogation of the aortic valve. Deep transgastric view A deep transgastric TOE allows imaging of the aortic valve in the fo re- ground, and allows proper alignment of the Doppler signal from the aortic valve (0 d eep TG LAX and 120 TG LAX views). This view is useful to assess: \200 movement of the aortic prosthetic valve mechanism. \200 color \202 ow Doppler interrogation for aortic regurgitation. \200 CW assessment of aortic regurgitation. \200 CW measurement of the a ortic valve gradient. The use of the deep transgastric TOE view is especially useful for as sess- ment of aortic prosthetic valve function when a mechanical mitral prosthesis is also present. This is because acoustic shadowing from the mitral valve obscures the LVOT in all ME TOE views of the aortic valve. However, this view is not possible in all patients. Regurgitation is most commonly transprosthetic in aortic tissue valves. The following may b e visible on TOE: cusp thickening ( > 3 mm predicts risk of valve failure), cusp tear, cusp prolapse, and \202 ail cusp. Rocking of the aortic prosthesis is due to dehiscence of th e valve (40 % circumfer- ence affected) and best seen in the 0 ME AV SAX and 120 ME A V LAX views. Key views The aortic valve prosthesis is assessed in: \200 0 ME AV SAX. \200 120 ME AV LAX. \200 0 deep TG LAX. \200 120 TG LAX. TOE FOR AORTIC VALVE PROSTHESIS 49 TOE assessment of normal and dysfunctional aortic prosthetic valves Normal peak gradient across mechanical aortic valve prosthesis \200 St Jude Medical. \200 Medtronic Hall. Signi \201 cant stenosis or obstruction likely in mechanical aort ic valve \200 Peak velocity of > 4 m/s or mean velocity of 3 m/s are suggestive of 24 7 mmHg. \200 21 7 mmHg. obstruction. Tissue aortic valves \200 Aortic valve area by continuity equation <1 cm 2 . \200 Mean gradient > 26 mmHg. \200 Ratio of LVOT to peak velocity across aortic valve <0.2. Stentless aortic valves \200 (Freestyle or Toronto valve) or aortic homograft s do not have the disadvantage of a sewing ring casting an acoustic shadow on the aortic va lve ori \201 ce, and TEE gives excellent views of valve cusps. Some of these valves are in distinguishable from native valves on TOE. 50 CHAPTER 1 Cardiac investigations Intraoperative TOE Indications AHA class I indications \200 Cardiac valve repair. \200 Haemodynamic compromise where LV function is unknown. \200 Complex endocarditis surgery w here perivalvular extension is suspected. Complex valve replacement such as homograft valve replacement with coronary reimplantation. Ascending aortic dissection with aortic valve involvement. \200 Posterior or loculated pe ricardial effusion. \200 Congenital heart surgery. \200 Hypertrophic obstructive cardio myopathy (HOCM surgery). AHA class II indications \200 Heart valve replacement. \200 Ca rdiac tumor removal. \200 Coronary surgery including \200\230off pump bypass \200\231. \200 Cardiac aneurysm repair. \200 LV or RV assist device implantation. \200 Ascending aortic dissection without aortic valve involvement. \200 Cardiac trauma. \200 Intracar diac thrombectomy or pulmonary embolectomy. \200 Heart and/or lung transplantation to ass ess anastomotic sites. Key views (see Fig. 1.11 ) LV assessment is made on these views: 0 ME four chamber. \200 90 ME two chamber. \200 120 ME LAX. \200 0 TG mid SAX.