The diagnostic value of echocardiography pre-, intra-, and postoperatively depends on the type of cardiac disease.
Preoperatively, it is essential that echocardiography reports sequentially valvular disease etiology, specific mechanism, and valve dysfunction type and severity (eg, rheumatic disease with valvular retraction, mixed mitral valve disease with severe MR and mild MS), but also the associated ventricular and atrial alterations that may affect outcome and management.
Mitral valve diseases are now dominated by mitral regurgitation caused by degenerative diseases and functional regurgitation caused by primary LV disease; they are approached quite differently clinically.
Organic Mitral Valve Regurgitation
- Preoperative assessment: etiology and mechanism. Organic MR results from diseases affecting valve leaflets or supporting structures resulting in improper coaptation. Etiology and mechanism are important to define, as these determine reparability, which is an essential determinant of improved outcome.31 TTE can usually determine organic MR etiology (Fig. 11-4), the most frequent of which is degenerative with myxomatous mitral valve diseases with prolapse (± flail segment) or fibroelastic degeneration of the mitral leaflets, which is generally associated with primary flail leaflet or annular (± valvular) calcification.32 Distinction between the diffusely myxomatous valve and fibroelastic degeneration is not accepted by all investigators, but echocardiographic presentation is usually strikingly different with diffuse valve thickening and excess tissue (hooding) in the former, whereas the latter is characterized by a normal-appearing leaflet apart from in the flail segment. Rheumatic valves are echocardiographically characterized by thickening (with distal predominance) and valve retraction leading to shortened (sometimes absent) coaptation with limited mobility of leaflets (particularly posterior). Rheumatic lesions are difficult to distinguish from those caused by lupus, anticardiolipin syndrome, radiation, or drugs (diet pills or ergot). Endocarditis creates destructive lesions with, in addition to vegetations, ruptured chordae, or perforations. Cleft anterior leaflets are rare and easily recognized in the short axis, but smaller posterior leaflet clefts may be missed. In analyzing MR mechanisms, Carpentier's classification33 simplified description into three basic types based on leaflet motion—type 1, normal; type 2, excessive; and type 3, restricted motion—and on anatomic localization (two commissures and three segments by leaflet starting with A1 and P1 for the anterior and posterior leaflets close to the external commissure). Beyond these important and useful classifications, detailed description should be provided by echocardiography (eg, for an endocarditic etiology, mechanisms can be type 1, perforation, located on A2 for example versus mechanism type 2, ruptured chordae located on P3, for example). Complete etiology and mechanism description is usually obtained by TTE (85 to 90% in our institution) and is supported by jet direction, but may require TEE (Fig. 11-5). In operated patients, TEE is currently widely used (preoperatively or intraoperatively) so that the echo-anatomical correspondence is important to memorize. In the midesophageal position, the electronic dial 180-degree inspection arc allows complete anatomical mitral valve examination.34 Evaluation of the mitral valve with the transgastric short axis is difficult, but may confirm the location of defects. Color flow imaging, by showing where the flow convergence is located and the initial direction of the jet is useful to confirm MR mechanism. This complete etiologic and mechanistic analysis is particularly important for each surgeon to define the probability of valve repair in view of the lesions. Degenerative lesions, unless extensive annular calcification is present, are particularly prone to repair, which provides the best postoperative outcome.32
- Preoperative assessment: valve dysfunction severity. Color Doppler alerts to MR presence (Figs. 11-6 and 11-7),35 but estimation of MR severity should rely on comprehensive assessment (Fig. 11-8) based on American Society of Echocardiography criteria,8 and not just on jet extent in the LA, because jet constraints by the LA wall make this measurement unreliable.36 The signs of severe MR are classified as (Table 11-1) specific (eg, flail, large flow convergence, large vena contracta, pulmonary flow reversal), supportive (eg, dense jet, high E velocity, enlarged LV, and LA), and quantitative (regurgitant volume greater than or equal to 60 mL, effective regurgitant orifice greater than or equal to 40 mm2). It is important to note that pulmonary venous flow systolic blunting is not interchangeable with reversal; blunting can be seen in all grades of MR and has a very low predictive value for the severity of MR.37,38 The suboptimal sensitivity of PV flow reversal is another reason that highlights the importance of quantifying MR (Fig. 11-9).38 Quantitative methods derived from PISA, quantitative Doppler (Fig. 11-10), or quantitative 2D (LV volumes) have been extensively validated in mitral regurgitation.7,39,40 Although surgery is mostly reserved for patients with severe MR (Fig. 11-11), severity of the regurgitation is a continuum best quantified than categorized (Table 11-2). MR severity tends to progress by 5 and 7 mL/beat of regurgitant volume per year,41 so that patients who are not immediately operated should be regularly monitored. As indicated in the guidelines, acquiring proficiency in quantification of MR degree in an important step in developing advanced valve centers.
- Preoperative assessment: prognostic indicators. Assessment of LV is usually performed by measuring LV diameters and ejection fraction.42 End-systolic diameter greater than or equal to 40 to 45 mm43,44 and ejection fraction less than 60%45,46 are markers of poor outcome. These characteristics are considered class I indications for surgery but the postoperative outcome when these characteristics are observed45 is not optimal, so these markers should be considered as advanced signs indicating a rescue surgery. LA diameter greater than or equal to 50 mm is associated with a high risk of subsequent atrial fibrillation under medical management,47 but also after successful surgery.48 Therefore, LA dilatation should alert early for the need of surgery. Pulmonary hypertension is considered as a marker of poorly tolerated MR, although its association to subsequent prognosis is uncertain.42MR severity assessment is essential for prognosis.49 Although MR assessment may be qualitative, quantitation provides stronger prognostic information.50 In asymptomatic patients with organic, holosystolic MR,50 the risk of death under medical management increased by 18% for each 10 mm2 ERO increment. ERO was the strongest echocardiographic predictor of outcome. With ERO greater than or equal to 40 mm2 the risk of death is multiplied by 5 and that of cardiac events by 8 compared with mild MR and excess mortality is observed as compared to the general population. Importantly, surgery restores life expectancy in these asymptomatic patients. Therefore, echocardiographic data participate importantly in the indication of surgery.
- Intraoperative assessment. Before cardiopulmonary bypass TEE confirms the mitral lesions32,51 but also identifies associated conditions that may benefit from surgical therapy (eg, patent foramen ovale, appendage, or LA thrombus). Whether the valve is amenable to repair should be resolved preoperatively,32,52 and surprises are rare regarding extent or type of lesions that may lead to change in strategy. After cardiopulmonary bypass, intraoperative TEE assesses mitral repair results,53 and the need for a second pump run is based on the presence of residual MR. Timing of evaluation is crucial. Postbypass TEE performed too early with inappropriate loading conditions results in faulty assessment of residual MR. Insufficient preload and low ventricular pressure minimize regurgitant orifices with residual MR underestimation. Adequately performed postbypass TEE correlates well with predischarge assessment of residual MR.54 It is essential not to tolerate MR postbypass, unless very trivial, as residual MR initially judged acceptable often requires reoperation during follow-up.55 Thus post-CPB IO-TEE serves as a tool in deciding which patient should return to CPB for a second repair or replacement. Over time, surgical management of anterior leaflet pathology and bileaflet prolapse has evolved,56,57 and new techniques emerged that provide better results. IO-TEE still plays a pivotal role in identification of mechanisms and anatomic location of disease as well as post-CPB evaluation of results.
- After mitral valve repair, major repair failures are three-fold: insufficient correction of the mitral lesion with residual MR (eg, residual prolapse), LV outflow tract obstruction, or stenotic repair. Severe residual MR obviously is rare but requires immediate correction. Observation of milder residual MR by IO-TEE immediately after repair with “less than echo-perfect” result, leads to higher long-term reoperation risk for MR.55 IO-TEE must define mechanism and anatomic location of the defect causing residual MR to determine correction strategy and possibility of re-repair. LV outflow tract obstruction is caused by systolic anterior motion of the mitral valve with contact to the LV septum, to which contribute excess or deformed mitral tissue, small LV size, and hyperdynamic LV function.58 LV outflow tract obstruction occurs in 1 to 4% of mitral valve repairs59,60 and is diagnosed by visualization of the systolic motion combined with increased velocity through the LV outflow tract. LV outflow tract obstruction results generally in notable residual MR caused by the deformation of the mitral valve in systole, and it is essential in patients with residual MR to rule out LV outflow tract obstruction before recommending a second pump run.53 Most usually increase LV filling, reducing or discontinuing inotropic drugs, and in some cases of beta-blocker administration, resulting in elimination of LV obstruction.53 If the obstruction persists, consideration should be given to a second CPB run for sliding valvuloplasty, although the systolic anterior motion tends to improve over time,59 and most patients can be managed medically. Prevention of LV outflow tract obstruction is based on careful examination of excess tissue on pre-bypass IO-TEE to select the patients who may benefit from specific repair techniques such as sliding annuloplasty.60,61 Markedly restrictive repairs with stenosis result from combination of anatomical alterations (diseased, rigid leaflets, commissural fusion, markedly protruding mitral annular calcification) with excessive repairs (rings too small and/or large edge to edge sutures). Diagnosis is based on high transvalvular gradients greater than or equal to 8 to 10 mm Hg by Doppler. Normal postrepair gradients (3 to 6 mm Hg) may be exacerbated by high output and tachycardia with reduced diastolic filling period. It is thus prudent before a second pump run to reassess mitral gradient after cardiac output has stabilized and after administration of beta blockers to control tachycardia.
- The most common immediate complications after mitral valve replacement are periprosthetic leaks and mechanical dysfunction of the prosthesis owing to interaction of tissue remnants with the mobile elements of a prosthesis.62 In contrast to TTE, TEE has no shadowing from the mitral prosthesis, so periprosthetic MR should be carefully sought after bypass and those clinically relevant distinguished from the minor paravalvular63 or intravalvular64 leaks that are often noted. Diagnosis is accurate and should lead to prompt consideration of a second pump run, particularly if the paravalvular leak persists after protamine administration. The location and severity of the leak are critical to evaluate in multiple planes and enhance the probability of a simple repair, thus avoiding prosthesis dismounting. Mobile prosthetic elements can be impinged upon by suture or valve material, leading to obstruction or most often regurgitation, which sometimes varies beat to beat because of variable interaction. Thus it is important to examine the prosthesis for a sufficient time to ensure consistent and appropriate function.
- Postoperative assessment: valvular result. Postoperative assessment is performed consistently at predischarge and yearly, as well as often 3 to 6 months postoperatively in our practice. Although the IO-TEE is quite accurate in assessing residual valve dysfunction, changes in loading conditions and remodeling may reveal valvular dysfunction. The MR recurrence rate after valve repair is 5 to 10% at 10 years55,56 and in two-thirds of cases results from new valve lesions (eg, new ruptured chordae), whereas in one-third it results from defective repair (eg, insufficiently corrected prolapse of anterior leaflet in bileaflet prolapse). TTE provides the mechanism and location of the MR and allows discussion of re-repair. It also allows assessment of MR severity. MR qualitative assessment is even more difficult after than before repair, and quantitative techniques (particularly the PISA method) are of particular importance. We rarely refer patients with moderate regurgitant volumes (30 to 60 mL/beat) for reoperation. Development of stenotic repair is rare and is observed mostly with rheumatic or rigid leaflets, sometimes after edge-to-edge repair. Standard repair represents a mild stenosis, which combined with enlarged LA may lead to new atrial fibrillation,48 and thrombus formation with possible stroke, for which TEE allows thorough examination of the LA appendage. New dysfunction of a mitral prosthesis often requires TEE examination, particularly for detection of prosthetic thrombosis or tissue degeneration.
- Left ventricular assessment. After surgical correction of MR, preload is decreased with decline of end-diastolic volume, but end-systolic indices are little changed so that ejection fraction falls by an average of 10%.44 However, this response shows large individual variation and LV reverse remodeling may affect the long-term LV function achieved. There are no definite predictors of reverse remodeling and LV end-systolic indices need to be monitored closely during the first postoperative year.43 The value of medical therapies, shown to result in reverse remodeling in patients with primary LV dysfunction (beta blockers, angiotensin-enzyme inhibitors) is not established, but early diagnosis may lead to early intervention. Irrespective, residual postoperative LV ejection fraction is an important predictor of postoperative survival and should be monitored. The result seen early after surgery is usually stable, unless marked LV dilatation results in further dysfunction or coronary disease leads to intrinsic myocardial deterioration.
Examples of morphologic examination of organic mitral regurgitation in transthoracic echocardiography. (A) The patient has a flail segment of the posterior leaflet with marked gap between anterior and posterior leaflet during systole and tip of posterior leaflet in the left atrium. (B) The simple mitral valve prolapse (or billowing mitral valve) shows posterior movement of the leaflet in the left atrium but no gap between leaflets and the tip of the posterior leaflet remains in the left ventricle in systole. Ao = Aorta; LA = left atrium; LV = left ventricle; MVP = mitral valve prolapse.
Morphologic examination of organic mitral regurgitation in transesophageal echocardiography. The patients presents with a flail posterior leaflet imaged in a long axis view. The long arrow shows the ruptured chordae of the posterior leaflet. The arrowheads show the flail segment of P2. Ao = Aorta; LA = left atrium; LV = left ventricle; RV = right ventricle.
Eccentric jet of mitral regurgitation (MR) seen a thin layer of color with aliasing appearing as a mosaic color in the left atrium (LA). The MR severity is often underestimated with this type of jet, but visualization of a large flow convergence (large arrow) in the left ventricle (LV) suggests severe MR.
Central jet of mitral regurgitation (MR) seen as a large area of mosaic flow in the left atrium (LA). The MR severity is often overestimated with this type of jet. LV = Left ventricle.
Continuous wave Doppler of mitral regurgitant (MR) jets. (A) The jet is holosystolic, but the peak velocity is reached during the first half of systole suggesting the existence of a large V wave on the left atrial pressure that leads to rapid equalization of pressure between ventricle and atrium. This type of jet is often seen in acute MR. (B) the jet is also holosystolic, but the peak velocity is reached in mid-late systole without late effacement of velocity. This type of jet is often seen in patients with chronic MR without a large V wave.
Table 11-1 Qualitative Signs of Severe Valve Regurgitation ||Download (.pdf)
Table 11-1 Qualitative Signs of Severe Valve Regurgitation
Central jets of width ≥65% of LVOT
Vena contracta >0.6 cm
Vena contracta ≥0.7 cm with large central jet or swirling eccentric jet
Large flow convergence
Systolic reversal in pulmonary veins
Flail leaflet or ruptured papillary muscle
Flail, incomplete coaptation
Central jet with area ≥10 cm2
Vena contracta >0.7 cm
Systolic reversal in hepatic veins
PHT <200 ms
Holodiastolic aortic reversal
≥Moderate LV enlargement
Dense triangular jet by CWD
Enlarged LV and LA
Dense triangular jet by CWD
Large flow convergence
Pulsed-wave Doppler of pulmonary venous flow in two cases of mitral regurgitation. (A) There a systolic flow reversal (negative flow in systole—large arrow) consistent with severe mitral regurgitation (MR) and large V wave on the left atrial pressure. (B) There is a normal forward flow (positive flow in systole—thin arrow) suggestive of the absence of V wave. The systolic pulmonary venous flow reversal is a specific sign with high positive predictive value but of low sensitivity for severe MR.
Quantitative Doppler assessment of mitral regurgitation (MR) based on stroke volume measurement using the annular diameter to calculate the annular area and its product with the pulsed wave Doppler as the stroke volume traversing the specific annular area. The left part of the figure measures the mitral stroke volume (179 mL/beat) while the right side measures the aortic stroke volume (95 mL/beat). Thus, the regurgitant volume is calculated as the difference between mitral and aortic stroke volume or 84 mL/beat.
Proximal isovelocity surface area (PISA) method of quantifying mitral regurgitation (MR). The left side of the figure shows the flow convergence zone with color baseline shift. This allows to measure the flow convergence radius (R = 0.94 cm) and using the aliasing velocity (Vr = 53 cm/s) to calculate the regurgitant flow (flow = 6.28 × R2 × Vr) at 294 mL or cc/s. The right side of the figure shows the velocity of MR measured by continuous wave Doppler. The ratio of flow by velocity is the effective regurgitant orifice, 0.53 cm2.
Table 11-2 Quantitative Thresholds for Severe Regurgitation ||Download (.pdf)
Table 11-2 Quantitative Thresholds for Severe Regurgitation
|AR||Organic MR||Functional MR||TR|
|ERO||≥0.30 cm2||≥0.40 cm2||≥0.20 cm2||≥0.40 cm2|
|RVol||≥60 mL||≥60 mL||≥30 mL||≥45 mL|
Functional Mitral Valve Regurgitation
Functional MR occurs on structurally normal valves caused by primary LV alteration (coronary disease, cardiomyopathy, myocarditis or transient LV dysfunction). Although the primary disease is myocardial, functional MR diagnosed by angiography65 or echocardiography66,67 exerts an important influence on outcome, but major controversy persists regarding the role of mitral surgery in these patients.68,69
- Preoperative assessment. Functional MR diagnosis is based on: (1) The presence of LV dysfunction (generalized most often but sometimes localized requiring a thorough regional assessment); and (2) a structurally “normal” mitral valve with normal tissue or at most minor degenerative calcifications (Fig. 11-12). It is also important to demonstrate the deformation of the mitral valve leading to functional MR. Apical and posterior displacement of papillary muscles applies traction through the inextensible chordae on both leaflets, resulting in apical displacement of the leaflet bodies, leading to altered coaptation.70,71 This deformation of normal leaflets called “tenting” directly determines functional MR severity (Fig. 11-13). The mechanism of MR is usually a central gap in coaptation, which is worse during isovolumic contraction and relaxation, when the LV exerts a low pressure on the leaflets. With ischemic LV dysfunction the MR may originate from the medial commissure in which the traction may be predominant, but apart from scars of myocardial infarction there are no specific sign of ischemic versus myopathic MR. Traction of chords on the leaflets may be inhomogeneous and predominate on one leaflet.72 In such cases an “overshoot” of the other (less tethered) leaflet behind the most tethered leaflet is observed, should not be mistaken for a prolapse and may cause unusual eccentric jets. Therefore, functional MR mechanism is not just the frequent annular dilatation but is more complex involving a combination of annular and leaflet tethering alterations (Fig. 11-14). MR severity assessment is particularly crucial in view of the notable surgical risk. MR jets that are central tend to be overestimated, and diastolic function alterations may mimic the tall E wave and low systolic venous flow, which is usually suggestive of severe MR. Thus, it is essential to quantify the MR but two essential issues need to be examined. First, functional MR is prominent during isovolumic contraction and relaxation, but as these phases involve little regurgitant driving force their contribution to the regurgitant volume is small and it is essential with the PISA method to quantify MR in midsystole. Second, the grading of MR has been established in organic MR, but recent data15,66,73 suggest that thresholds of effective regurgitant orifice (ERO) associated with poor outcome are lower in functional than organic MR. Thus, pending further confirmation patients with functional MR and ERO greater than or equal to 20 mm2 should be considered as having severe MR; and this prognostic effect comes in addition to ejection fraction and left atrial volume.74 Functional MR is dynamic. ERO often increases during exercise, which may have important functional75 and outcome15 implications, but uniformly decreases during dobutamine echocardiography, making this test useless for the assessment of functional MR. Although the role of imaging during exercise in defining the surgical indications needs further evaluation, a dynamic ERO may also decrease with interventions such as vasodilatation or beta-blockade. Not surprisingly, sedation or anesthesia necessary for TEE may minimize MR and lead to its underestimation76 compared with habitual life conditions. Preoperative assessment of functional MR should also focus on other components of the disease, namely LV remodeling, systolic dysfunction, and diastolic dysfunction because severe LV remodeling may be a marker for poor response to valve repair.77
- Intraoperative assessment. Before bypass it is essential to confirm the structurally normal mitral leaflet and to avoid in the MR assessment the pitfall of reduced loading caused by anesthesia. Thus, if the degree of MR is in doubt, assessment with increasing loading conditions similar to those of outpatient evaluation should be performed by a loading challenge, but this does not replace an appropriate outpatient evaluation. Post-bypass, IO-TEE evaluates residual MR. After repair, reduced loading conditions may lead to major underestimation of residual functional MR, emphasizing the importance of adjusting preload and afterload. Functional MR is particularly prone to recurring after surgical correction because of continued LV remodeling, continued displacement of papillary muscles and mitral valve tenting,78 despite a repair judged as adequate intraoperatively. Thus, post-bypass assessment is difficult and may be overly optimistic; therefore, a careful judgment of residual tenting and valve deformation is essential. Contrary to organic MR, the most advanced subsets of patients benefit as much from bioprosthetic replacement as they do from repair.79 Thus doubts on repair quality should be pursued aggressively to decide if a new pump run and valve replacement should be recommended.
- Postoperative assessment focuses on potential recurrence of MR and its mechanism if present (increased tenting versus insufficient annular restriction).68,78 Postoperative MR should also be quantified if more than mild. Beyond MR, echocardiography focuses on the assessment of LV dysfunction, its systolic and diastolic components, and its consequences on LA and pulmonary pressures. Active prevention of further LV remodeling is recommended and should be monitored by echocardiography.
Two-dimensional echocardiography showing the parasternal long-axis view of a patient with functional mitral regurgitation (MR). Note the protrusion of mitral leaflets toward the left ventricle (LV), resulting in a large tenting area (T) between leaflets and annulus (white line with x marking the mitral annulus) and in insufficient coaptation surface available on each leaflet to prevent MR. Ao = Aorta; LA = left atrium. (Reproduced with authorization of the American Heart Association.)
Two-dimensional echocardiography showing an apical view of a patient with functional mitral regurgitation (MR). The view shows the posterior papillary muscle within the left ventricle (LV), and the chordae attached to the anterior leaflet (long arrow) and to the posterior leaflet (short arrow) tethering the leaflets within the ventricle as cause to leaflet tenting. LA = Left atrium.
Schematic representation of the mechanism of functional mitral regurgitation (MR). In light gray is represented the normal position of the papillary muscle (PM) chordae (dashed lines) and mitral leaflets shown with adequate coaptation surface. With local left ventricular (LV) remodeling the papillary muscle is repositioned apically and posteriorly (dark gray) and exerts traction through the non-distensible chordae on the leaflets. Traction on the strut chords (inserted on the mid-portion of each leaflet) is most manifest, leading to deformation of the mitral leaflet, tenting, reduced coaptation, and creation of an effective regurgitant orifice (ERO). Ao = Aorta; LA = left atrium.
Mitral stenosis is currently treated preferentially by balloon valvuloplasty,80 so surgery's role is relatively limited. However, some patients may benefit from surgery rather than balloon valvuloplasty, and the role of echo in defining these subsets should be carefully examined.
- Preoperative evaluation. The classical mitral valve stenosis (MS) invariably is caused by rheumatic disease, and its features are characteristic (immobile posterior leaflet, fused commissures with reduced orifice area, and hockey stick deformation of the anterior leaflet in diastole (Fig. 11-15). Other causes of stenosis are lupus or anticardiolipin diseases (which produce very similar lesions), ergot heart disease, and other iatrogenic valve diseases (which thicken leaflets without fusing commissures), and protruding annular calcifications (which restrict the orifice without commissural fusion). Anatomical analysis is essential because balloon valvuloplasty is the most widely used procedure to treat MS and produces a commissurotomy identical to closed commissurotomy (hemi-commissurotomy in most cases). Therefore, balloon valvuloplasty is not indicated with: (1) Mitral obstructions without commissural fusion; (2) heavily calcified mitral valve; (3) MS with nodular calcification of both commissures (high risk of splitting the leaflet and not the commissures)81; and (4) MS associated with more than mild MR. In such cases, the best treatment is surgery with valve replacement. Thus, an essential component of MS echo assessment is the short-axis view to ascertain commissural fusion as well as severity and location of calcifications.81 Another decision-making component is the alteration of subvalvular apparatus.82 Very short chordae or direct insertion of papillary muscle on leaflets may lead to poor results of balloon valvuloplasty, but may allow good surgical commissurotomy, splitting commissures, and papillary muscles. MS severity is assessed using two variables, the transvalvular gradient representing the pressure overload to the LA and pulmonary circulation and the mitral valve area (MVA) (Fig. 11-16). The gradient measured is the mean gradient (Fig. 11-17), which is affected by severity of the stenosis, and increased by tachycardia and amplified transvalvular flow (anemia, pregnancy, hyperthyroidism, associated MR), and decreased by bradycardia and low cardiac output. Mild MS is associated with a resting mean diastolic Doppler (measured by continuous wave Doppler) gradient less than or equal to 5 mm Hg, moderate with a gradient 5 to 10 mm Hg, and severe with a gradient greater than or equal to 10 mm Hg. The normal MVA is 4 to 6 cm2 and guidelines for MS severity suggest thresholds of 2.0 cm2 for mild MS, 1.5 cm2 for moderate MS, and 1.0 for severe MS. However, most patients undergoing interventions for MS are in the range of 1 to 1.2 cm2 and symptomatic, so that in our institution MVA less than 1.5 cm2 are considered severe MS. MS severity assessment involves also LA enlargement and elevation of pulmonary pressure and in time may also involve right heart enlargement and failure and tricuspid regurgitation, whereas LV remains normal sized, but may show reduced ejection fraction. MVA measurement can be obtained through several methods that are combined because all methods have limitations and averaging reduces the risk of error. The pressure half-time (PHT) method is the simplest, measured from the Doppler mitral signal using the deceleration from the peak early velocity and calculates MVA using the empiric formula 220/PHT.83 However, this method may not be accurate with changes in LV or LA compliance and has a wide range of error with short diastole.84 Other methods of MVA measurement are: (1) Direct orifice planimetry in short-axis view (technically demanding); (2) continuity equation in which MVA is calculated as the ratio of flow measured on the aortic valve to mitral velocity (false if MR or AR); and (3) the PISA method, imaging the mitral inflow with color using baseline shift (requires an angle correction for the funnel shape of the mitral valve with potential for error).85,86 Important issues in MS severity assessment are: (1) The essential combination of methods of MVA assessment to minimize the potential for error; and (2) the need for exercise hemodynamic (with bike allowing continuous hemodynamic monitoring) assessment in patients who present with low gradient and doubt on the MS severity. Thus, TTE provides assessment of MS severity and in most cases the procedure most suited for treatment. Outpatient TEE is systematic in patients considered for balloon valvuloplasty to assess presence of LA thrombus and MR.
- Intraoperative assessment in patients with MS is most often that of mitral replacement, but in patients suited for open commissurotomy, provides anatomical and MR reassessment before bypass and repair assessment postoperatively. A high gradient or moderate MR may lead to consideration of a second pump run after mitral repair. Mobile element dysfunction or periprosthetic regurgitation suggests consideration for further correction after valve replacement. Although decisions with regard to repair of tricuspid regurgitation should be made preoperatively, IO-TEE allows reassessment, rarely discovery of organic tricuspid lesions, and consideration of repair of associated moderate or severe regurgitation.
- Postprocedure assessment follows the usual post-dismissal and 1-year assessment (Fig. 11-18). Mitral stenosis remains a progressive lesion even after valve repair and there is potential for recurrence of severe MS and also for progressive scarring and retraction of the mitral valve leading to MR progression. Depending on the severity of the mitral lesions, age and MR a notable proportion of patients need reoperation between 5 and 10 years after the original intervention (balloon valvuloplasty or valve repair). Patients should be carefully monitored to avoid progressive heart failure and pulmonary hypertension. After surgery, pulmonary hypertension caused by MS regress almost uniformly unless chronic pulmonary disease had developed, LV dysfunction most usually normalizes with normalization of preload unless coronary disease was present, but LA enlargement persists and patients with atrial fibrillation remain at substantial risk for stroke.
Parasternal long axis view of a patient with mitral stenosis. Note the thickening and hockey-stick deformation of the anterior leaflet of the mitral valve (mv) and the protrusion of the posterior leaflet. Note also the normal left ventricle (LV) contrasting with the enlarged left atrium (LA) and right ventricle (RV). Ao = Aorta.
Mitral valve (mv) area of a patients with mitral stenosis (MS) before (A) and after (B) commissurotomy. Note in (A) the narrow orifice and in (B) the large orifice with wide opening of the medial commissure. Note also in (A) the right ventricular (RV) enlargement with signs of pulmonary hypertension manifested by a flat septum and D-shaped left ventricle. In (B) the position of the septum and the shape of the left ventricle have normalized.
Continuous wave Doppler recording of the mitral gradient in a patient with severe mitral stenosis (MS). Note the high velocity greater than or equal to 2m/s with mean gradient greater than 13 mm Hg. Note also the flat slope of deceleration of the early diastolic velocity consistent with severe MS.
Continuous wave Doppler in the same patient as Fig. 11-16 after commissurotomy. The mean gradient is now low with rapid deceleration of early diastolic velocity consistent with mild MS.
Mixed Mitral Valve Disease
Mixed mitral valve diseases have substantial component of stenosis and regurgitation and most result from rheumatic disease, a situation now rare in western countries but prevalent in developing countries.
- Preoperative assessment recognizes the rheumatic valve lesions and the combination of stenosis and regurgitation precluding the possibility of valve repair. The major challenge is the evaluation of the severity of the mitral valve disease. Often the stenosis and regurgitation are both moderate, and criteria for severe valve diseases are difficult to establish. Transvalvular gradient higher than expected on the basis of MVA alone, reflects the severity of the combined disease.
- Intraoperative assessment shows rheumatic features and absence of postoperative complications. Tricuspid regurgitation is frequent in mixed valve disease and often requires associated repair.
- Postoperative assessment is important, not only to monitor the mitral prosthesis but also to assess LV function. LV dysfunction is a frequent complication of the MR of mixed mitral valve diseases so that aggressive detection and treatment of this complication is essential to obtain the best outcome.
Aortic valve diseases are now dominated by aortic stenosis. The aortic valve is normally formed by three cusps and is bicuspid in 1 to 2% of the population, but the physiology of the aortic valve is poorly understood irrespective of the cusp number.
- Preoperative assessment focuses on etiology and mechanism, although assessment is usually simplified compared with the mitral valve. Most aortic stenoses (AS) are caused by degenerative disease irrespective of the number of cusps. Recent data emphasized the atherosclerotic mechanism of AS with initial cholesterol deposition and lipid oxidization, but bicuspid valves tend to calcify more frequently than tricuspid valve for unknown reasons. Rheumatic aortic stenosis is now rare and is characterized by commissural fusion, whereas commissures are open in degenerative diseases. However, clinically the various etiologies of AS in the adult are difficult to recognize, because valves are uniformly calcified in advanced AS. Therefore, morphologically 2D echo recognizes valvular calcification associated with AS in the adult (Fig. 11-19). Absence of aortic valve calcification makes AS unlikely and makes a systolic gradient most likely to originate from subvalvular or supravalvular region. In children, calcification is inconsistent and not indispensable to AS diagnosis. Valvular calcification is difficult to analyze by echocardiography87 and is more precisely measured with high-resolution computed tomography.88 The volume or score of calcification is linked to AS severity in a nonlinear manner so that both measures are complementary in assessing AS.88 The fact that most AS are caused by valve rigidity caused by calcification and not to commissural fusion explains the lack of efficacy of balloon valvuloplasty in AS. The LV responds to pressure overload by increasing wall thickness and LV mass, but this response is variable and its absence does not rule out severe AS. LV hypertrophy regresses after aortic valve replacement, the only approved treatment of AS currently available.42 Recently developed percutaneous aortic valve replacement offer an option for inoperable patients,89 and is currently evaluated. Poststenotic aortic dilatation is frequent but rarely requires repair.
- Assessment of AS severity is the major goal of TTE. The opening of even just one aortic leaflet to the aortic wall is usually a marker for nonsevere AS, but the AS severity should be assessed quantitatively by measuring mean systolic gradient3 as marker of pressure overload and aortic valve area (AVA) to assess lesion severity.6 Normal aortic valve opening area is 2.5 to 4.5 cm2, AS is considered present with AVA less than or equal to 2 cm2 and with a pressure gradient developing across the aortic valve and AS is considered severe (Fig. 11-20) with AVA less than or equal to 1.0 cm2 (using the continuity equation) and mean gradient greater than or equal to 40 mm Hg (using the Doppler velocity).42 Other criteria of AS are peak velocity greater than or equal to 4 m/sec90,91 and velocity ratio (LV outflow tract to jet) less than or equal to 0.25.6 Indeed, in patients with LV outflow tract obstruction AVA may not be measurable and velocity may be the only available criterion to diagnose severe AS (Fig. 11-21). AS is progressive because of progressive calcium deposition, with gradient progression by 5 to 7 mm Hg per year and AVA decline by 0.1 cm2 per year.92,93 The major pitfall of gradient measurement is underestimation resulting from excessive flow-ultrasonic beam angle, so that systematic multi-window Doppler is the key to appropriate assessment of AS severity. Another pitfall is the underestimation of the LV outflow tract diameter necessary to the measurement of stroke volume and valve area. Such underestimation leads to underestimation of valve area. Thus, the triad of normal LV function, low gradient, and low AVA warrants ruling out inadequate echo measurements with comprehensive reassessment in a reference laboratory. Nevertheless, recent data suggest that severe AS with low gradient resulting from low stroke volume despite normal EF is a real entity associated with poor prognosis.94 Conversely, severe AS with low gradient is more logical in patients with reduced LV function,95–97 but the differential includes low AVA caused by insufficiently forceful ejection to overcome the inertia of a mildly stenotic valve. Diagnosis of severe AS with low gradient requires confirmation, obtained by high-resolution computed tomography measuring high calcium load88 and/or dobutamine echocardiography that increases myocardial contraction and aortic flow in patients with low EF. The classic response is an increased gradient with severe AS (Fig. 11-22) and an increased AVA with cardiomyopathy and mild AS.95,97 However, this test may not be conclusive in patients lacking contractile response96 who may benefit from AVR if the AS is severe.98
- Although classically asymptomatic severe AS was considered well tolerated, recent data demonstrated excess mortality during follow-up and noted that a large proportion of patients were never offered surgery.90 Therefore, surgery in asymptomatic patients based on echocardiographic criteria is debated. Asymptomatic patients with rapid decline in AVA and large calcification load display poor clinical outcomes under medical management87,88 and may be considered for surgery, whereas those with reduced LV function are definitely at high risk and should be offered prompt surgery if the AS is severe.99
- Intraoperative assessment examines the valve morphology, confirms the large calcification load, and can measure the orifice area by direct planimetry before institution of bypass. AVA measurement by 2D is difficult, because one has to ascertain measurement at the leaflet tip and cannot replace an appropriate Doppler hemodynamic measurement before surgery. Determination of the aortic annulus size may be helpful for early surgical sizing of allografts destined for the aortic position or homograft and may play a role in preventing patient–prosthesis mismatch, which is a cause of postoperative mortality and morbidity,100,101 and may be prevented by sizing, taking into account the patient body surface area. Another important goal of IO-TEE is examination of ascending aorta and for patients with aneurysmal dilatation, consideration of ascending aortic repair. IO-TEE in patients undergoing aortic valve replacement for severe AS may alter the planned surgical procedure in approximately 10% for unexpected severe MR, PFO, mass, or thrombus. Post-bypass, specific issues examined are lack of signs of dysfunction of prostheses and potential changes in LV function and functional MR. In patients with prominent LV hypertrophy, LV outflow tract obstruction may occur after AVR and should be detected by color imaging or Doppler and verified by simultaneous intraventricular pressure measurement. Myectomy associated with valve replacement may prevent or treat the LV outflow obstruction. Attempts at measuring prosthetic gradient using transgastric approach are of uncertain reliability and lack of patient–prosthesis mismatch cannot be ascertained by intraoperative Doppler-echo currently.
- Postoperative assessment focuses on prosthetic, LV, and aortic evaluation. Prosthetic function is not entirely predictable on the basis of patient and prosthesis size and the postoperative Doppler-echo is essential in detecting obstruction, particularly thrombosis, and after mismatch. Reoperation, considered in limited cases for mismatch,100 is the mainstay of treatment for prosthetic thrombosis or pannus formation, all manifested by prosthetic obstruction.102 In the diagnosis of prosthetic obstruction, it is important to consider the role of pressure recovery, which may lead to (usually slight) gradient overestimation by Doppler. The 2D examination rarely discriminates between causes of obstruction for which the context of occurrence is more specific. Degeneration of bioprostheses is rarely observed in elderly patients currently affected by AS, but is part of the yearly prosthetic monitoring. LV function is usually maintained after valve replacement for AS. Changes are observed in two circumstances. First, patients with LV dysfunction owing to critical AS generally display improvement in ejection fraction and sometimes normalization after AVR.103 Even small improvements have important beneficial effects on outcome, but persistence of LV dysfunction requires active medical therapy. Second, patients with associated coronary disease may display postoperatively decline in LV function owing to the coronary disease despite successful aortic valve surgery. Such patients also need active echocardiographic follow-up to ensure appropriate medical treatment.104 Ascending aortic dilatation generally stabilizes postoperatively, but the rare possibility of continued enlargement and need for repair also require regular echocardiographic follow-up. A particularly difficult group of patients for follow-up is those with postradiation heart disease,105 in whom cardiac disease is only part of postradiation lesions that affect the lungs with frequent persistence of postoperative symptoms. The valve disease is only part of the cardiac disease often involving coronary lesions, conduction abnormalities, pericardial constriction, and myocardial fibrosis. These complex lesions often lead to complex follow-up.
Two-dimensional echocardiography of a patient with aortic stenosis (AS). The aortic valve (arrows) is heavily calcified (dense nodules). Ao = Aorta; LA = left atrium; LV = left ventricle; RV = right ventricle.
Continuous wave Doppler obtained from the right parasternal window (RTP) in a patient with severe aortic stenosis (AS). The peak velocity is greater than 4 m/s and the mean gradient is 48 mm Hg.
Schematics of the measurement of aortic valve area in aortic stenosis (AS). Because blood is incompressible flow is constant through the left ventricular outflow tract (area A1) through the aortic orifice (area A2). Thus the aortic stenosis manifested itself by increased velocity (V2 > V1). Flow is equal to area multiplied by velocity aortic valve area A2 = (A1 × V1)/V2. (Reproduced by the courtesy of FA Miller.)
Measurement of aortic velocity by continuous wave Doppler in a patient with severe aortic stenosis, low ejection fraction, low output, and low gradient. The baseline (left panel) mean gradient was 21 mm Hg and increased (bottom line) with increasing doses of Dobutamine (top line). The peak dose was 7.5 μg/min and the mean gradient reached was 42 mm Hg. (Reproduced by the courtesy of D Messika-Zeitoun.)
- Preoperative assessment focuses on the etiology and mechanism in that it determines the possibility of repair.106 Most frequently aortic regurgitation in western countries is caused by degenerative diseases.107,108 Minor calcifications may be noted, but rarely with thickened myxomatous tissue. The AR is caused by annular enlargement and sometimes to valve prolapse. Bicuspid aortic valve is the second cause of AR and leads to regurgitation by mal-coaptation and sometimes prolapse of the largest cusp. Aortic root disease involves annuloaortic ectasia more often than Marfan's syndrome or aortitis (eg, syphilis). Rheumatic AR is recognized by the retraction of leaflet, leaving a central regurgitant orifice, and is rarely repairable. Endocarditis is recognized by echo when vegetations are present and may require TEE (Fig. 11-23). Repair is predictable with detection of a perforation, but is not possible with calcified or retracted leaflet. Repair is also particularly feasible with a prolapsed leaflet, especially if the valve is bicuspid or with dystrophic leaflets and moderate AR, in which resuspension of commissures may be sufficient. Therefore, morphologic assessment should be focused on clearly defining the AR mechanism.
- AR results in both volume and pressure overload of the LV, which adapts by both concentric and eccentric remodeling until a point of afterload mismatch when LV systolic function fails. Assessment of LV size and systolic function by echo is essential. The recommended approach is M-mode 2D-guided, but with increasing frequency LV volumes are calculated, particularly with use of contrast injection. Moderate LV dysfunction defined as EF less than or equal to 50% and severe LV dysfunction (EF ≤35%) justify rescue surgery, but result in decreased postoperative survival.108 No lower limit of EF contraindicates firmly surgery. Even patients with EF less than or equal to 35% may benefit from valve replacement. EF less than 55% is associated with reduced survival under medical treatment and should be strong consideration for surgery before LV dysfunction affects postoperative survival. Marked LV enlargement is another indication for surgery and is uncovered by LV dimensions greater than or equal to 75 mm (end-diastolic) or greater than or equal to 55 mm (end-systolic)109 or better greater than or equal to 25 mm/m2 (end-systolic adjusted to body surface area)107 as women with smaller body sizes almost never reach absolute LV sizes comparable to men.110 These differences lead to worse postoperative outcomes in women, emphasizing adjustment of LV measures to body size.110 Exercise changes in LV function may be helpful, but monitoring of complex variables such as wall stress limit applicability.111
- Assessment of AR severity is vital to the surgical indication and should be based on comprehensive integration of all signs.8 Among qualitative approaches, color Doppler (Fig. 11-24) detects the presence of aortic regurgitation and provides simple measures of AR severity (Fig. 11-25). Vena contracta greater than or equal to 0.6 cm and ratio of jet width/left ventricular outflow tract width greater than or equal to 65% in parasternal long axis view suggest severe AR (Fig. 11-26), but jet length does not correlate with AR severity.112 Color Doppler has many limitations when assessing AR severity and is used as a gross estimation. Eccentric jet direction leads to underestimation of AR and jets arising from the entire coaptation line of bicuspid valves may be overestimated. Holodiastolic flow reversal in the abdominal or descending thoracic aorta is consistent with severe AR (Fig. 11-27). Maximum AR velocity (measured by CW Doppler) deceleration suggest severe AR with fast pressure half-time (<200 ms, Fig. 11-28). However, AR velocity deceleration is also influenced by LV compliance and reflects elevated LV end-diastolic pressure. Quantitative AR assessment is essential for patients with moderate or severe AR.8 Regurgitant volume and ERO can be calculated by PISA,113 quantitative Doppler (mitral and aortic stroke volumes) or LV volumetric method.40 Although regurgitant volume greater than or equal to 60 mL/beat, similarly to MR is consistent with severe regurgitation, smaller ERO (≥30 mm2) than in MR is consistent with severe AR because the longer diastolic than systolic time allows larger volume overload for smaller orifice size.8 Quantitative methods are not as consistently applicable in AR than in MR, but have relatively few limitations and should be used in clinical practice similarly to MR.113
- Intraoperative assessment. Pre-bypass, IO-TEE verifies the aortic valve lesions and the extent of aortic aneurysmal dilatation. Aortic valve repair is a safe alternative to valve replacement in selected patients with AR and requires detailed assessment of the AR mechanism.106 Assessment of the AR mechanism by IO-TEE is accurate and reliable compared with surgical findings. Rarely, IO-TEE notes aortic dissection or wall hematoma not previously diagnosed, and IO-TEE can assist in identifying patients likely to benefit from aortic valve repair.114 AR quantitation is challenging by TEE, and although deep transgastric views may show the AR flow convergence, imaging is usually poor using this view. A broad jet width on color-flow in central AR is suggestive of severe regurgitation but a simple and more reliable method is measurement of the vena contracta width by TEE, a surrogate measure of the ERO.115 Vena contracta assessment by TEE is feasible and has been validated for AR.
- Post-bypass IO-TEE verifies the functional result anatomically and for residual AR. This early assessment is important because aortic valve repair is a technique in progress, and results that appear mediocre should lead to consideration of a second pump run. Mismatch is unusual after valve replacement for AR because the annulus is generally dilated with AR and often allows insertion of a sufficiently sized prosthesis. Residual periprosthetic regurgitation is a notable problem in patients with endocarditis, particularly when recent, and these patients should be actively evaluated with appropriate loading conditions.
- Postoperative assessment focuses on prosthetic or repair function. In patients with allograft replacement of the aortic valve and homograft replacement of the pulmonary valve, calcification of the pulmonary homograft may develop and requires a systematic examination of the pulmonary outflow tract. Valve repair failure most often involves recurrent prolapse, and timely diagnosis requires regular echo follow-up.106,116 Patients with AR are younger than those with AS, and bioprosthetic or homograft aortic valve replacement are associated with notable rates of primary failure depending on age. In patients with dystrophic aortic valves, late aortic dissection may develop and requires careful examination of the aorta and progressive aortic dilatation should lead to consider TEE or computed tomography. LV function is of particular concern if patients were operated with EF less than 50%.108 In general, because of the high preoperative wall stress, aortic valve replacement is associated with improvement in LV function, but the effect is usually modest and the need for vasoactive treatment aimed at improving LV function and clinical outcome should be assessed postoperatively.
Imaging of the aortic valve in a patient with endocarditic aortic regurgitation (AR). The long arrow denotes vegetation, whereas the arrowhead denotes a perforation of the noncoronary cusp. Ao = Aorta; LA = left atrium; LV = left ventricle.
Parasternal view of aortic regurgitation (AR) using color flow imaging. The flow convergence (thin arrow) and jet (thick arrow) are well seen. Note the limited expansion of the jet resulting from its eccentricity.
Quantitation of aortic regurgitation (AR) using the proximal isovelocity surface area (PISA) method. Note that the color baseline is shifted upward. On the left panel analysis of the flow convergence allows measurement of the regurgitant flow and on the left panel, AR velocity is measured using continuous wave Doppler to calculate the regurgitant volume (RVol) as flow multiplied by the ratio of regurgitant time velocity integral (RTVI) to regurgitant velocity (RVel).
Parasternal view of aortic regurgitant flow used to delineate and measure the vena contracta (narrow neck) of the aortic regurgitation.
Recording of pulsed-wave Doppler in the high descending aorta in a patient with severe aortic regurgitation. Note a holodiastolic reversal of flow with high velocity (arrow) during diastole.
Continuous wave Doppler recording in a patient with endocarditic aortic regurgitation (AR). The rapid deceleration of AR velocity in diastole is quite different from that noted in Fig. 11-25 and is consistent with acute and severe AR revealing low end-diastolic gradient between the low aortic diastolic pressure and the high left ventricular end-diastolic pressure. The pressure half-time of 154 ms is shorter than the 200 threshold for severe AR.
Mixed Aortic Valve Disease
Mixed aortic valve disease is often rheumatic or associated with aortic valve calcifications precluding valve repair. The essential step in preoperative evaluation is severity assessment of the valve disease. A composite of moderate AS (with valve area >1.0 cm2) and moderate AR (with regurgitant volume <60 mL) may represent severe valve disease and is diagnosed by a higher mean gradient than the AS severity would justify. IO-TEE and postoperative monitoring are similar to those of AS and AR.
Tricuspid valve diseases are dominated by functional tricuspid regurgitation. However, the numerous etiologies that may result in notable tricuspid disease and the frequency with which these lesions may be ignored are salient issues.
Tricuspid valve stenosis is mostly rheumatic, associated with mitral stenosis, and rarely pure. It is difficult to diagnose as there are no absolute morphologic criteria. The essential diagnostic step is to perform a continuous wave Doppler examination of the tricuspid valve when the morphology is unusual. Mean gradients greater than or equal to 5 mm Hg are significant for the tricuspid valve, and the degree of inferior vena cava dilatation reflects the hemodynamic consequences of the stenosis. IO-TEE can also examine the obstruction of tricuspid valve if the preoperative hemodynamic assessment was insufficient. Tricuspid valve replacement is usually required and postoperative echo focuses on the appropriate function of the prosthesis. Other causes of organic tricuspid valve disease, such as carcinoid heart disease, produce in general mixed tricuspid valve disease with dominant regurgitation.
Tricuspid Valve Regurgitation
- Preoperative assessment. Tricuspid regurgitation (TR) is called functional when the valve is structurally normal and regurgitation ensues from incomplete coaptation. Functional TR is the usual consequence of right ventricular dilatation owing to pulmonary hypertension of left-sided heart disease or pulmonary disease, but can also be caused by primary right ventricular dysfunction or primary atrial and annular dilatation seen in chronic atrial fibrillation. Organic causes of TR include myxomatous valve degeneration with or without ruptured chordae.117 TR caused by excessive valve movement can also result from endocarditis with destructive lesions, blunt chest trauma with chordal or papillary muscle rupture, and iatrogenic trauma postmyocardial biopsy. Echocardiography establishes the mechanism more definitely than the etiology of these types of TRs, but is essential in planning valve repair, which is often highly successful.117 Organic TR with restricted valve motion includes serotoninergic lesions such as carcinoid heart disease, diet drug valve diseases, ergot valve disease, postradiation valve disease rarely, or more frequently leaflet impingement (or perforation) by pacemaker or defibrillator leads.118 The degree of valve thickening or rigidity is an essential guide in predicting repair versus replacement. Congenital causes such as Ebstein's anomaly are uncommonly diagnosed in adulthood but may cause severe TR and may be easily missed by a cursory echocardiography.
- There is growing appreciation of tricuspid valve regurgitation as an independent predictor of long-term outcome irrespective of the original cause of this heterogeneous valve disease.117,119 The important consequence of this recognition is that surgery for isolated TR is more common, that in left-sided valve disease the coexistence of TR should not be ignored because simultaneous correction is often required and that high-quality echocardiographic assessment of TR severity is warranted as the clinical signs of TR are often ignored. Assessment of TR severity uses mainly: (1) The size of the jet in the right atrium (larger is more severe), but with the usual limitation of jets (underestimated with eccentricity and overestimated with high ventricular pressure); (2) vena contracta width greater than or equal to 7 mm as a sign of severe TR,120 useful but limited by lateral resolution issues; (3) the presence of systolic flow reversal in hepatic veins, specific for severe TR but not sensitive; and (4) quantitation of TR by the PISA method.121,122 For TR quantitation, as right- versus left-sided circulatory system is a lower pressure system, thresholds for severe TR compared with MR are similar for ERO (≥0.40 cm2), but lower for regurgitant volume (≥45 mL/beat).122 Severe TR can lead to right-sided volume overload with right ventricular and right atrial enlargement, and right ventricular systolic dysfunction.117 There are no quantitative criteria to assess these changes yet, but qualitative assessment provides useful information. With right ventricular volume overload, the septum may display paradoxic motion and affect LV function and ultimately exercise capacity. With advanced cases, inferior vena cava and hepatic veins dilatation reflect elevated right atrial pressure.
- Intraoperative assessment. TR is often overlooked and should be assessed without sedation in the outpatient setting.123 IO-TEE before initiation of bypass requires restoration of preload conditions to assess TR. Quantitative assessment of TR by TEE has limitations and cannot replace preoperative assessment. Annular enlargement is important to assess because it is associated with recurrence of TR,124 or even development of severe TR in patients with no or mild TR preoperatively.124 Annulus diameter greater than 70 mm has been considered as markedly enlarged,124 but there is no consensus on specific annular diameters (absolute or adjusted for body size) that should indicate tricuspid repair. After bypass it is important to assess residual TR, although its absence is not invariably synonymous with operative success. Persistent right ventricular enlargement and dysfunction tend to improve later. IO-TEE in patients in whom tricuspid surgery is considered results in alteration of surgical plan in approximately 10% of cases. Rarely is surgery converted to tricuspid replacement as is considered a predictor of worse survival.
- Postoperative assessment focuses mostly on relatively frequent recurrent TR. TR recurrence depends on surgical techniques used, such as lack of ring annuloplasty,125 lesions (leaflet tethering or thickening),126 severe TR at baseline,125,126 IO residual TR, and persistence of pulmonary hypertension of left-sided disease. Right ventricular enlargement and dysfunction improve but often incompletely, particularly if pressure or volume overload persists.
Pulmonary valve diseases are mostly congenital but can also be acquired, owing to carcinoid heart disease (now exceptionally rheumatic heart disease) and endocarditis.
- Preoperative assessment requires the proactive examination of the pulmonary valve as the usual examination tends to record few views of the valve and TEE may be particularly helpful. Knowledge of a disease susceptible to affect the pulmonary valve is essential in focusing attention to this valve.127 The valve morphology is difficult to analyze and requires unusual views, elongating the subvalvular, valvular, and supravalvular region. Thickening can be observed and more rarely prolapse, retraction, or vegetation. Morphologically, pulmonary annulus can be constricted in carcinoid disease in association to intrinsic valve thickening.128 Dilatation of pulmonary artery is important to assess and may require TEE. Hemodynamic assessment is somewhat simpler. Continuous wave Doppler assesses appropriately pulmonary stenosis. Mild pulmonary regurgitation is frequent in normal individuals. Severe pulmonary regurgitation is rare, detected by color Doppler, but ascertaining severe regurgitation is difficult because the jet may be of limited extent and duration owing to equalization of pulmonary and right ventricular pressure. In such cases, rapid deceleration of regurgitant jet is suggestive of severe regurgitation.
- IO assessment. As pulmonary stenosis is most usually treated by balloon valvuloplasty, operative treatment is reserved for regurgitant or mixed lesions. Measurement of pulmonary annulus and assessment of subvalvular or supravalvular stenosis is important to operative management. Postoperative assessment of pulmonary regurgitation intends to avoid more than moderate residual regurgitation but is more difficult than outpatient evaluation as restoration of normal hemodynamic condition is inconsistent. Careful examination of color and continuous wave Doppler is important in that regard.
- Postoperative assessment focuses on assessing function of native repaired or prosthetic pulmonary valve. Degeneration, stenosis, and regurgitation may develop over time and should be diagnosed early with a combination of color and continuous wave Doppler. Right ventricular dilatation and dysfunction may persist after surgery or recur with dysfunction of the treated pulmonary valve.129
The incidence of bacterial endocarditis has remained unchanged despite the decline in rheumatic valve disease, and effective antibiotics continue to carry considerable mortality and morbidity. As the risk associated with endocarditis drops precipitously with therapy, prompt diagnosis and treatment are essential to improve diagnosis.
- Preoperative assessment is centered on diagnosis and assessment of complications. Echocardiography aids in the rapid diagnosis of endocarditis provides one of two major Duke diagnostic criteria by demonstrating presence of typical vegetations.130 Less typical but suspicious lesions represent a minor diagnostic criterion. Vegetations vary in size or shape and are mobile masses attached to endocardium or implanted material and frequently showing high-frequency oscillations. Vegetations are made of fibrin and are of low density when recent, but there are no definitive criteria to differentiate them from thrombi, particularly on foreign material, or from Lamb's excrescences when small.131 Therefore, diagnosis of vegetation implies contextual interpretation. TEE is superior to TTE in detecting vegetations (sensitivity 95% versus 65 to 80%, respectively), especially in prosthetic valve endocarditis, in which TTE may miss vegetations because of shadowing. Right-sided vegetations are usually bigger than left-sided and TEE does not improve diagnostic accuracy.
- Apart from diagnosis, TTE and TEE evaluate the presence and severity of endocarditic lesions. Endocarditis is destructive to valves and cardiac tissue, and may lead to abscess formation. Valve lesions are perforations or ruptures of supportive structures. Perforations are voids that are often difficult to visualize directly by TTE or TEE, but color observation of regurgitating flow with flow convergence in the center of a valve leaflet is strongly supportive of a perforation.58 Ruptures of chordae have nonspecific features unless a vegetation is attached to their tip. Aortic valve prolapse may result from destruction of the central coaptation zone or supporting commissural area. Abscesses may involve any region of the myocardium, but often involve the fibrosa between mitral and aortic annulus. Expansion of annular abscesses may lead to conduction abnormalities or cavity (aneurysm) formation when the abscess ruptures in a cardiac cavity, most often the LV, with sometimes secondary rupture and fistula formation. These complex lesions are better identified by TEE than TTE.132 Of note, abscess cavities are rarely seen around the mitral and tricuspid annuli and abscesses are more prone to be present in patients with prosthetic valve endocarditis. Nevertheless, in all cases of endocarditis comprehensive assessment of all possible abscesses and fistulous tracts is indispensable. Assessment of severity of valve lesions is particularly difficult, because regurgitations resulting from destructive valve lesions form and progress acutely by sudden tissue loss. Thus, clinical signs of regurgitation, particularly murmur intensity and color flow jets, may not be impressive because of rapid equalization of pressure (eg, in acute endocarditic AR, LV diastolic pressure is markedly elevated and early in diastole equalizes the aortic pressure so that murmur and jet are brief and of low energy). This acuteness makes quantitation of regurgitation, particularly measure of effective regurgitant orifice, essential in assessing regurgitation severity.8 Also heart failure may rapidly progress because of valve regurgitation, particularly in patients with acute endocarditic AR, and surgery may be urgently indicated. In patients with MR or TR, heart failure may be controllable with medical treatment and may offer some opportunity for sufficient antibiotic therapy.133 Nevertheless, even in clinically stable endocarditis it is essential to monitor lesions and valvular regurgitation severity by regular echocardiography. Rarely, vegetations can be complicated by accumulation and valvular obstruction, and more frequently by embolism. Characteristics of vegetations, such as size (>10 mm) and marked mobility, are predictors of the risk of embolism,134 which led to the controversy regarding intervention for ablation of vegetations. Although this controversy is unresolved, the precipitous decline in vegetation size with antibiotic treatment and the risk of embolism associated with surgery should be taken into account in this discussion.134 Over time endocarditic lesions become chronic and vegetations heal, leaving fibrotic lesions offering more solid suturing possibilities.
- Intraoperative assessment confirms the lesions, assesses the possibility of silent progression and an unexpected abscess cavity or fistulous tract, and reassesses regurgitations that may have appeared moderate on preoperative assessment. Careful examination is particularly important in moderate lesions that may require interventional treatment simultaneously with severe lesions.
- Post-bypass, it is essential to examine the surgical correction of complex abscesses and fistulous tracts. Also, examination of all reparative procedures and seating of prosthetic valves is particularly important, because recently infected valvular and annular tissue may not offer a solid basis for suturing.
- Postoperative assessment usually demonstrates that acute LV dysfunction is reversible. Recurrence of endocarditis is rare with appropriate antibiotic treatment, and development of echocardiographic signs may be delayed, in contrast to fever and positive blood cultures. A possible complication is the occurrence of aseptic perivalvular regurgitation developing with some delay after the intervention. Low-intensity murmurs may contrast with symptoms, and early detection is paramount by systematic TTE and sometimes TEE in order to provide appropriate care. Repeated prosthetic dehiscence owing to tissue friability is not uncommon and makes such situations difficult to manage.
Prosthetic valves require specific approaches, and comparison with early postoperative assessment is essential to detect dysfunction.
Echocardiography of Prosthetic Valves
Although valve repair is generally preferred, valve replacement remains the leading way to correct severe valvular disease. Echocardiography is currently the best approach to evaluate prosthetic valves, but has limitations for appropriate interpretation. All prostheses are responsible for acoustic shadowing behind them, so examination of all aspects of a prosthesis often requires both TTE and TEE. Morphologically, specific characteristics influence the imaging of mechanical prostheses. For example, in a ball-cage prosthesis, the ball transmits ultrasound slower than blood, so its distal limit appears beyond the prosthetic seating. In bileaflet prostheses, leaflets may be placed with an angle to the thoracic wall, thereby preventing visualization. Struts of bioprostheses may prevent imaging of leaflets. With Doppler, the presence of a restrictive orifice may create pressure recovery, so gradients may be somewhat overestimated, particularly with small aortas. In prostheses that have no clinical signs of dysfunction, it is important to obtain early and serial hemodynamic assessment to serving as a reference if the clinical issue of dysfunction arises. Each prosthesis is characterized by its gradient, effective orifice area, and physiologic regurgitation. The gradient is measured by continuous wave Doppler, from apical views for mitral and tricuspid prostheses and multiple views for aortic prostheses. Mean and peak gradient are measured using the same 4V2 formula used in native valves. Each type and size of prosthesis has a range of expected gradient that should be used as a guide to assessment of normal function. Effective orifice area (EOA) is measurable for aortic prostheses, similarly to the valve area of AS, as the ratio of stroke volume (LV outflow tract) to time velocity integral of prosthetic jet velocity. For mitral and tricuspid prostheses measuring orifice area relies on aortic stroke volume, which is not adequate if AR or prosthetic regurgitation is present. Lack of mitral or tricuspid prosthetic stenosis beyond the normal range is defined by a rapidly declining velocity (and gradient) in early diastole. Physiologic regurgitation of prostheses is common and constant in appearance in mechanical prostheses but rare in bioprostheses. It is readily visible for aortic prostheses, but more difficult to detect with TTE for mitral or tricuspid prostheses because of prosthetic shadowing, and may be only observable by color with TEE. However, physiologic regurgitation is detectable by continuous wave Doppler and is usually brief, faint, and central. TEE is not necessary in normally functioning prostheses clinically and by TTE unless other lesions (eg, aortic dilatation or aneurysm) are suspected.
Mechanical Prosthesis Dysfunction
There is no primary failure of mechanical prostheses components because the ball variance of Starr-Edwards prostheses and strut ruptures of Bjork-Shiley prostheses have been eliminated. The mechanism of failure of mechanical prostheses is rarely by tissue interposition or more frequently by obstruction owing to thrombosis or its chronic equivalent, pannus formation, or periprosthetic regurgitation. Tissue interposition is usually detected early and characterized mostly by regurgitation because of lack of closure of the mobile element, but can have a component of stenosis. Incomplete movement of the mobile element can be detected by TTE, TEE, or fluoroscopy with angle of movement measurement. Hemodynamic dysfunction is detected by Doppler. Increased flow velocities beyond normal range (and beyond previous measurement) suggest increased pressure gradients and prosthetic obstruction. However, with increased flow (pregnancy, anemia, hyperthyroidism, sepsis) gradients may increase so that stenosis should be characterized if possible by measuring the effective orifice area using continuity equations.135 A ratio of valvular to subvalvular velocity greater than or equal to 3 suggests aortic prosthesis stenosis, whereas a slow decline in diastolic velocity suggests mitral or tricuspid prosthesis stenosis.136 A stenotic prosthesis should rule out patient–prosthesis mismatch by confrontation with prosthetic size and previous measurements.101 Sudden obstruction suggests acute thrombosis, whereas progressive obstruction suggests pannus formation, but the mechanism of obstruction is rarely directly defined by echocardiography, although a thrombus may be seen by TEE in acute thrombosis. Thrombus size affects the potential efficacy of thrombolysis.137 If thrombolysis is elected as a treatment because the prosthesis is in a tricuspid location or reoperation is high risk, monitoring of the prolonged thrombolysis administration requires daily echocardiography with subsequent frequent measurements because recurrence is common, affecting approximately half of successfully treated patients.138 Pannus obstruction is organized and not affected by thrombolysis.102 Postoperatively recurrence of prosthetic thrombosis should be monitored by Doppler. If large enough, periprosthetic regurgitation is usually associated with hemolysis and heart failure or progression of symptoms, but inconsistently with a murmur. TTE detects easily the regurgitant jet on aortic prostheses and jet origin determination requires complete prosthesis scanning to observe periannular flow (Fig. 11-29). Shadowing often prevents TTE from recording the color jet for mitral and tricuspid prostheses, but detection of periprosthetic regurgitation is possible by continuous wave Doppler, leading to TEE for assessing regurgitation severity (Fig. 11-30).
Transesophageal imaging of severe periprosthetic regurgitation (arrowheads) around the sewing ring (SR) of a mitral prosthesis (MP). LA = Left atrium; LV = left ventricle.
Physiologic regurgitation (arrows) on a St. Jude mitral prosthesis (MP).
Biological Prosthesis Dysfunction
Although thrombus (exceedingly rare) and periprosthetic regurgitation (rare) may occur on bioprostheses, primary tissue failure is the most frequent failure mode.139 The specific mechanism can be early, because of tears, which are often close to struts, or late, because of calcification or rupture of cups. The diagnosis of valve stenosis caused by calcification is based on standard Doppler criteria of excessive gradient, decreased effective orifice area, persistence of end-diastolic high velocity in mitral and tricuspid prostheses, and direct visualization of calcifications by TTE or TEE if necessary. The diagnosis of tissue failure with regurgitation is suspected by murmur and confirmed by color imaging, but severity is often difficult to confirm because of eccentric jets (even by TEE). In this circumstance, observations of a severe lesion such as a torn cusp and a large flow convergence proximal to the intraprosthetic regurgitant orifice are important clues to a severe regurgitation. With primary tissue failure it is important to exclude prosthetic endocarditis by blood cultures and searching for vegetations by TEE.
Coronary artery disease is the most frequent indication for cardiac surgery. Echocardiography does not allow direct observation of coronary lesions unless intravascular ultrasound is used for proximal coronary segments, but observes consequences of coronary disease. Echocardiography is pivotal to suspect coronary disease on the basis of stress-induced ischemia, assess myocardial viability, and diagnose myocardial infarction and its complications requiring surgical intervention.13
Diagnosis of Coronary Diseases
Echocardiography uses multiple tomographic planes to assess regional wall motion.13 The American Society of Echocar-diography recommends 16-segment analysis of LV for regional wall motion evaluation. Wall thickness increase in systole greater than or equal to 40% characterizes normal LV contractility, whereas reduced contractility (hypokinetic) is less than 30% and absent (akinetic) is less than 10%. Myocardial segment outward motion during systole (dyskinesis) is usually associated with thinning, whereas aneurysm is permanent wall outward bulging with or without dyskinesis. LV segments are scored from 1 to 5—with 1, normal; 2, hypokinetic; 3, akinetic; 4, dyskinetic; 5, aneurysmal—and the wall motion score index is the sum of scores divided by the number of segments visualized.13 A wall motion score index of 1 is normal and greater than or equal to 2 is associated with poor outcome after myocardial infarction. Resting scar (wall akinetic, dyskinetic, or aneurysmal and dense with thinning) is a resting abnormality diagnostic of myocardial infarction and coronary disease (wall motion abnormalities without scar are seen in cardiomyopathies). Stress echo can identify coronary disease by inducing new regional wall motion abnormalities.14 There are many stress modalities, including exercise treadmill or bicycle, pharmacologic with dobutamine, adenosine, or dipyridamole, and rarely TEE atrial pacing.140 Pharmacologic or pacing stress testing is reserved for patients who are unable to exercise enough to reach maximum effort. With stress, normal LV response is hyperdynamic with increased ejection fraction and decreased LV end-systolic dimension. Resting regional wall motion abnormalities unchanged with stress are consistent with coronary disease (previous myocardial infarction) but without ischemia. Increased LV end-systolic dimension or decreased ejection fraction with stress suggest severe coronary artery disease. The diagnostic value of stress echo is imperfect, with acceptable sensitivity but mediocre specificity similar to other stress modalities. The indication of stress echo for diagnosing coronary disease should be weighed according to the pretest probability of disease and is most contributive in the intermediate probability range. The prognostic value of stress echo is considerable in patients presenting with chest pain, justifying its widespread use.141 In evaluating chest pain, echo may reveal resting regional wall motion abnormalities consistent with acute coronary syndrome, but is usually associated with a good prognosis if normal. Stress echo is safe in patients with no sign of myocardial infarction or ischemia and normal baseline echo. In overt acute coronary syndromes, a wall motion score index greater than or equal to 1.7 suggests a large area at risk. Postoperatively, stress echo is most useful when chest pain is moderate or atypical to weigh the indication of repeat coronary angiogram. The localizing value of regional abnormalities for a specific coronary bed is mediocre and cannot imply that a specific graft may be dysfunctioning.
Myocardial contraction declines when greater than or equal to 20% of myocardial wall is ischemic or infracted. Resting hypokinesis or akinesis does not rule out viability (myocardial hibernation) and may improve with revascularization. Dobutamine stress echo is the preferred stress method to assess viability in patients with LV dysfunction (with or without regional abnormalities).142 With increasing infusion rates of dobutamine, initial improved contractility of an akinetic segment at low dose suggests viability, and worsening with higher doses (biphasic response) suggests ischemia. This biphasic pattern suggests viable myocardium and improvement potential with revascularization. Functional recovery after revascularization is frequent when sustained improvement with dobutamine (monophasic response) is observed, but is rare with scarred or unresponsive myocardium. Strain rate imaging with low-dose dobutamine may be useful to detect viability.
Complications of Coronary Diseases
Heart failure with cardiogenic shock complicating acute myocardial infarction is the leading cause of hospital death caused by myocardial infarction and may be caused by various mechanisms demanding specific interventions. Echocardiography identifies mechanisms of circulatory failure and also high-risk patients with LV dysfunction, particularly with markedly reduced ejection fraction or MR greater than or equal to moderate.143
Free wall rupture is an important cause of death. There are no predictive echocardiographic features defining a high risk of rupture, but echocardiography provides early and rapid diagnosis in patients with this fatal complication. In hemodynamically unstable patients, free wall rupture should be suspected with pericardial effusion, particularly a gelatinous-appearing pericardial clot and with thin-walled myocardium.144 An incomplete free wall rupture results in a “subepicardial aneurysm” contained by the epicardial layer. The pericardial effusion, even if compressive and with signs of tamponade, should not be taped for evacuation because this may precipitate catastrophic rupture, but minimal echo-guided tap to confirm blood presence may help the surgical decision. Rarely, color Doppler detects flow in the pericardial cavity, but absence of such flow does not rule out rupture. Intramyocardial hematoma is consistent with impending rupture. A pseudoaneurysm is a contained rupture bordered by an organized clot, and is diagnosed on the basis of a narrow neck with to and fro flow and carries a considerable risk of delayed rupture. Detection of early free wall rupture allows surgical repair. Postoperatively, as the infarct is often limited in size, excellent long-term result can be obtained.
Ventricular Septal Rupture
Ventricular septal rupture complicating myocardial infarction occurs in the first weeks of infarction. Echo shows the ventricular septal defect, but it is important to use multiple views to identify it, as those associated with inferior infarction may be elusive. The defect borders are ragged, different from those of congenital defect and fall of myocardial eschars tend to increase the defect size progressively. Color Doppler is critical to diagnosis by demonstrating directly left-to-right shunt at the ventricular level, and TEE is rarely needed. Surgery is preferable before hemodynamic compromise is intractable but shunt may recur postsurgery because of progressive septal necrosis, which should be monitored. Closure by endovascular devices is possible but entails the possibility of a recurrent shunt postprocedure.
MR associated with acute myocardial infarction may be functional or organic because of papillary muscle rupture, but both are often silent, so MR is frequently revealed by echo, which is indicated by hemodynamic compromise or pulmonary edema. Rupture of papillary muscle may be incomplete (one head partially separated but remaining attached to papillary muscle) or complete (head detachment from papillary muscle resulting in a flail leaflet). The morphologic abnormality is diagnosed by TTE, but TEE may be necessary.145 Color flow imaging detects MR, but may underestimate MR because of rapid and severe increase in LA pressure. Confirmation by echo of papillary muscle rupture leads to prompt surgical correction. Repair is often feasible with IO-TEE monitoring and MR rarely recurs postoperatively.
Right Ventricular Myocardial Infarction
Right ventricular myocardial infarction is typically associated with an inferior infarct, but rarely is isolated. Patients present with elevated jugular venous pressure contrasting with clear lungs, or may present with hypotension or shock. TTE provides rapid diagnosis, showing an enlarged and hypokinetic right ventricle, commonly associated with LV inferior wall motion abnormalities. Color Doppler reveals TR with normal pulmonary pressure and low peak velocity. High right atrial pressure may lead to right-to-left shunting via a patent foramen ovale, clinically manifest as hypoxemia and diagnosed by agitated saline contrast injection showing the shunt as contrast passing from right to left atrium. TEE is useful for diagnosing shunt and supporting closure of patent foramen ovale percutaneously and resulting in marked clinical improvement. The right ventricular function almost universally improves over time, but residual TR may be observed and may require surgical correction.
Pericardial, Endocardial, and Myocardial Diseases
Pericardial effusion was the first clinical application of echocardiography and remains, with other pericardial diseases, one of the most important indications of the test.
Pericardial effusion is an echo-free space around the heart after anatomical landmarks of the pericardium, covering both ventricles and most of the right atrium, whereas a small portion of the LA wall is surrounded by pericardium. Pericardial effusion should be differentiated from left pleural effusion, an echo-free space extending posteriorly to the descending aorta and from increased pericardial fat content, of typical granular appearance that does not deserve medical attention. Pericardial effusion is often compressive if large (with a swinging heart within the effusion), but tamponade may occur in small acute effusions. Diagnosis of tamponade relies on inferior vena cava dilatation, invagination of right atrial wall in diastole, expiratory collapse of right ventricle, and marked respiratory variability (of opposite timing) of mitral and tricuspid inflows.146 Although classically large effusions required surgical drainage, an echo-directed pericardial tap with prolonged catheter drainage is now the mainstay and is particularly useful in postoperative effusions. Approaches are most often para-apical and rarely subcostal. Effusions of aortic dissection or myocardial infarction should not be drained percutaneously because full rupture may ensue. Other indications of surgical drainage are purulent effusions, pericardial thrombi, and loculated effusions that cannot be safely reached. Postoperatively echo monitors recurrence of effusions and possible occurrence of constriction.147
These can occur while fluid remains in the pericardium, but are mostly caused by a thickened rigid pericardium.148 Classical tuberculosis pericarditis is now rare and most constrictive pericarditis is idiopathic, postoperative, and rarely results from hemopericardium, purulent pericarditis, radiation, or inflammatory disease of the pericardium. The diagnosis should be suspected when heart failure with dilatation of inferior vena cava is associated with normal LV function. Echo-Doppler signs specific of pericardial constriction are increased pericardial thickness (which is difficult to measure), ventricular interaction indicating fixed intrapericardial space diagnosed by leftward septal shift, decreased mitral inflow and pulmonary venous flow, and increased tricuspid inflow during inspiration, atrial interaction with diastolic hepatic venous flow reversal with expiration,149 and isolation from thoracic pressure changes with stable superior vena caval flow with respiration. Pericardial constriction should be differentiated from restrictive cardiomyopathy, which is not associated with ventricular interaction and displays reduced myocardial velocity by tissue Doppler (which is normal in pericardial constriction). Pericardial constriction and chronic obstructive pulmonary disease share the respiratory variation of flow, but subtle differences allow diagnosis. Thus, Doppler is the mainstay of preoperative diagnosis of constriction. IO-TEE shows the thickened pericardium and monitors the sudden hemodynamic changes post-pericardectomy. Postoperatively echo monitors the persistence of constrictive signs that may result from severe epicarditis or insufficient pericardectomy.
Endomyocardial fibrosis starts as endomyocarditis with thrombosis, which becomes organized and fibrotic, resulting in elevated filling pressures. Images show the apical obliterative thrombosis early, which invades the region below the posterior mitral leaflet and encases it. Eosinophilia is generally observed. Fibrosis ensues and results in mitral and tricuspid regurgitation. IO-TEE allows monitoring of potential aggravation of valve regurgitations during endomyocardectomy. Postoperative persistence of signs of elevated pressures is common.
Cardiomyopathies are usually easily diagnosed when presenting with congestion owing to LV dysfunction. Regional wall motion abnormalities may be present and are not synonymous with coronary diseases. It is not possible to rule out myocarditis by echo. IO-TEE during cardiac transplantation excludes dysfunction of the donor heart and monitors tolerance of frequent residual pulmonary hypertension. Posttransplantation assessment notes atrial enlargement, a feature of the atrial connection, with dual atrial activity. Over time, myocardial biopsy may result in severing of tricuspid chordae and flail tricuspid valve and require tricuspid repair. Restrictive cardiomyopathy is exemplified by amyloidosis, which characteristically displays wall thickening of LV and RV, mild valvular regurgitation, pericardial effusion, and restrictive LV filling. Occurrence of LV systolic dysfunction or irreversible diastolic dysfunction is associated with poor prognosis. Rarely these patients undergo cardiac transplantation. Hypertrophic cardiomyopathy may be mostly basal and obstructive. LV outflow tract obstruction results from the characteristic septal bulge with systolic anterior motion of the mitral valve and is diagnosed by late peaking systolic acceleration by Doppler. These patients benefit from myectomy guided by measures of depth and thickness of the septal bulge to be removed by IO-TEE.150 Elimination of the obstruction and MR are the IO measures of success as well as absence of iatrogenic ventricular septal defect. Midventricular and apical hypertrophic cardiomyopathy can be easily missed and have complex intracardiac flows but rarely require surgery.
The entire thoracic aorta can be visualized by combined TTE and TEE,151 but TEE provides complete and detailed imaging of the aorta and should be preferred if a disease of the aorta is suspected.
Aortic dissection can be diagnosed by TTE, despite limited view, which may be sufficient to direct patients to the operating room where TEE is performed, but TEE should be performed when the diagnosis is uncertain. TTE has limited sensitivity (79%) compared with TEE (99%) in diagnosing aortic dissection, and a negative TTE should be followed by TEE when aortic dissection is suspected.152 Aortic dissection is seen as an undulating intimal flap and should be distinguished from artifacts often seen in the aorta, particularly using color flow imaging. Proximally, the extent of the dissection, dislocation of the Valsalva sinuses intima, prolapse or aortic cusp, and presence and severity of AR should be defined, but should not delay surgery in type A dissection. Involvement of coronary ostia (particularly right) may cause myocardial infarction but is not easily defined, even by TEE. Pericardial effusion may cause tamponade, is particularly concerning for imminent aortic rupture and should lead to prompt surgery. IO-TEE helps define extent of residual dissection of thoracic aorta and presence of pleural effusion. Postoperatively, TEE evaluates residual AR if the aortic valve has been preserved, and LV function if myocardial infarction is suspected and there is progression of residual aortic dissection.
Aortic Hematoma and Rupture
Intramural hematoma precedes aortic dissection in 15 to 20% of cases.151,153 It results from blood collection between intima and adventitia and appears as increased echo density along the aortic wall visible by TEE but usually not by TTE. Aortic perforation can be caused by aortic ulcers complicating atherosclerosis. Diagnosis is raised in older patients with upper chest (and back) pain but is difficult even using TEE. Aortic rupture complicates deceleration injury and can be diagnosed by TEE. Despite the trauma, TEE is feasible in most patients, rarely complicated, and sensitive to detect isthmic rupture. Pseudoaneurysm resulting from containment of rupture by surrounding tissue can be differentiated from true aneurysm by sharply demarcated rupture site and narrow communication between aorta and pseudoaneurysm.
Aortic aneurysms are visualized and measurable by TTE and TEE, but complete extent is determined better by TEE (Fig. 11-31). Rupture rates increase with aneurysm size, considerable if greater than or equal to 6 cm but are also notable between 5.5 and 6 cm. Smaller aneurysms can be followed serially with echo. Patients with Marfan's syndrome and those with bicuspid aortic valve are at risk of aortic dilatation and potentially dissection. Sinus of Valsalva aneurysm is best assessed from parasternal long and short axis views and may cause compression of adjacent structures or may rupture into the cardiac chambers, most commonly the right atrium or right ventricle.154
Annulo-aortic ectasia associated with aortic regurgitation diagnosed by transthoracic echocardiography. Ao = Aorta; LV = left ventricle.
Aortic atherosclerosis causes plaques and debris within the aorta, particularly in older people. Plaques of higher thickness, irregular surface (ulceration), and with mobile components have higher embolic potential.155 Intraoperatively, the presence of severe aortic plaques is of particular importance when an intra-aortic balloon pump is considered. The role of cholesterol embolism in postoperative strokes and decline in renal function is uncertain.
Aortic coarctation can be diagnosed by TTE with suprasternal imaging and Doppler gradient measured at rest and with exercise. TEE shows the narrowed descending thoracic aorta and both the frequently associated bicuspid aortic valve. Postoperatively echo follows the residual stenosis and the progression of aortic valve dysfunction and of ascending aortic enlargement.