Pulmonic, and Mixed Valve Disease

Fig. 9.1

3 D TEE of a patient demonstrating impingement of the anterior leaflet of the tricuspid valve (TV) by a defibrillator lead (arrow) as viewed from the atrial aspect (A anterior, P posterior, S septal)

../images/301959_1_En_9_Chapter/301959_1_En_9_Fig2_HTML.jpg — Fig. 9.2

3 D TEE of the same patient demonstrating impingement of the anterior leaflet of the TV by a defibrillator lead (arrow) as viewed from the ventricular aspect

../images/301959_1_En_9_Chapter/301959_1_En_9_Fig3_HTML.jpg — Fig. 9.3

2D TEE image of the TV from the gastric location. A case of functional tricuspid regurgitation where non-coaptation of the leaflets is noted setting the stage for very severe TR

RV Pressure Overload. The tricuspid regurgitant jet gives key information regarding RV pressure overload both as a cause of TR and also regarding general cardiac status. Central to this evaluation is an estimate of peak RV pressure in turn allowing for estimation of systolic pulmonary artery pressure (Fig. 9.4). Using the modified Bernoulli equation, the systolic trans-tricuspid pressure gradient (Δ _p) is estimated as Δ _p = 4V ², where V is the peak trans-tricuspid flow velocity. Right ventricular pressure is estimated as RVP + RAP. Thus if the peak jet velocity is 3.58 m/s and estimated RA pressure is 15 mmHg (Fig. 9.5), RVP = 4(3.58)² + 15 = 51 + 15 or 66 mmHg. This determination helps establish whether pulmonary hypertension and its attendant etiologies are the cause of the patient’s TR, or whether there is pure volume overload either from a primary or secondary cause. While pulmonary embolism is rarely a cause of severe TR, it often causes enough TR to estimate RV pressure. The constellation of sudden dyspnea or chest pain plus the echocardiographic findings of RV dysfunction and dilatation together with pulmonary hypertension raises the clinical suspicion of pulmonary embolus. It should be noted that the pulmonary hypertension due to an initial pulmonary embolus is not severe probably because the unhypertrophied RV is capable of generating a pressure of only about 50 mmHg [6].

../images/301959_1_En_9_Chapter/301959_1_En_9_Fig4_HTML.jpg — Fig. 9.4

Continuous wave Doppler of the tricuspid regurgitation jet yields a dense image which is parabolic in contour. The density of the signal is proportional to the amount of regurgitant flow into the right atrium. The right ventricular systolic pressure is estimated using TR jet velocity, employing the modified Bernoulli equation to estimate the pressure gradient between RV and RA and adding the RA pressure estimated from inferior vena cava dilatation (see Fig. 9.5). For example, as shown above the TR maximum velocity is estimated to be 3.58 m/s. Using the modified Bernoulli equation, as follows: Pressure gradient between RV and RA during systole = 4 × (TR peak velocity)² = 4 × (3.58)² = 51 mmHg. Assuming a RA pressure of 15 mmHg, the RVSP is estimated at 66 mmHg. Pitfalls: Density of the signal is dependent on technical factors such as “gain” settings. The intensity can be increased or decreased depending on how gain is used in the display and can therefore underestimate or overestimate the peak tricuspid regurgitation velocity, thus resulting in computation of lower or higher right ventricular systolic pressures

../images/301959_1_En_9_Chapter/301959_1_En_9_Fig5_HTML.jpg — Fig. 9.5

Dilated IVC measuring at 3 cm using m-mode examination. There are respirophasic changes within the IVC. This suggests markedly elevated right atrial pressure

If an atrial septal defect is suspected but not directly visualized, agitated saline is injected intravenously producing RA and RV contrast. A left to right shunt of un-contrasted blood produces a negative contrast at the site of the shunt (Figs. 9.6 and 9.7).

../images/301959_1_En_9_Chapter/301959_1_En_9_Fig6_HTML.jpg — Fig. 9.6

A TEE image of a small atrial septal defect (arrow) is shown in the bicaval view

../images/301959_1_En_9_Chapter/301959_1_En_9_Fig7_HTML.jpg — Fig. 9.7

A TEE image of agitated saline contrast bubbles crossing the shunt into the LA

Assessment of TR severity. Assessment of TR severity is made from the size and penetration of the TR jet, the width of the vena contracta, the morphology of Doppler wave forms and reversal of flow in systemic veins. Figure 9.8 demonstrates measurement of the TR vena contracta, the size of the jet as it exits the regurgitant orifice. In general, the larger the orifice, the greater is the magnitude of TR. The morphology of the Doppler wave form provides additional information about TR severity (Fig. 9.9). In the case demonstrated a large regurgitant orifice produces severe TR despite low flow velocity. Indeed the orifice can be so wide as to produce laminar instead of turbulent flow (Fig. 9.10) and the jet velocity is low but dense in contour (Fig. 9.11).

../images/301959_1_En_9_Chapter/301959_1_En_9_Fig8_HTML.jpg — Fig. 9.8

Severe TR is demonstrated by color Doppler . The *vena contracta* measures 8 mm (arrows). Note the severely dilated right atrium. A vena contracta width greater than 7 mm signifies severe tricuspid regurgitation. The Nyquist limit (red circle) should be set between 50 and 70 cm/s. In this case the severe TR was caused by impingement of a defibrillator lead on the anterior leaflet of the tricuspid valve with severe restriction of leaflet movement. Pitfall: Strict vigilance is needed during imaging to optimize the color gain. One can increase or decrease the jet area by suboptimal color gain settings

../images/301959_1_En_9_Chapter/301959_1_En_9_Fig9_HTML.jpg — Fig. 9.9

Low velocity severe TR. Note the triangulated waveform of the TR jet (arrows) in the same patient shown in Fig. 9.8. Compare the density of the TR jet with the TV inflow which is of the same spectral density suggesting significant regurgitant flow. However, the jet velocity is low (<2 m/s). This suggests ventricularization of the RA pressure. In such instances, it is not possible to estimate RVSP. The TV inflow demonstrates an E velocity greater than 1 m/s (open arrow), which is another semiquantitative measure of severe TR

../images/301959_1_En_9_Chapter/301959_1_En_9_Fig10_HTML.jpg — Fig. 9.10

Color Doppler examination of the tricuspid valve from an RV focused view in the mid-esophageal location. Notice the absence of any turbulent flow and that the regurgitant jet appears as laminar flow (arrow) which can sometimes be an interpreted as mild TR if a high degree of diagnostic suspicion for severe TR is not entertained

../images/301959_1_En_9_Chapter/301959_1_En_9_Fig11_HTML.jpg — Fig. 9.11

Very low velocity but severe TR. A corresponding continuous wave Doppler examination from the patient shown in Fig. 9.10 demonstrates very low velocity but dense and triangulated envelope (arrow) consistent with very severe TR

Reversal of flow into the great veins gives further evidence of severe TR (Figs. 9.12 and 9.13). While more quantitative measures such as PISA (proximal isovelocity surface area ) may be employed, they have not gained the same acceptance as they have for mitral regurgitation. In accordance with the suspicion of severe TR, the RA and RV also should be enlarged. Although examination of the jugular venous pulse provides an accurate estimate of central venous pressure (CVP) in experienced hands, the pulsations may be difficult to see in some patients. In such cases echocardiographic findings of a dilated inferior vena cava indicates that CVP is elevated (Fig. 9.5).

../images/301959_1_En_9_Chapter/301959_1_En_9_Fig12_HTML.jpg — Fig. 9.12

Hepatic systolic flow reversal . In the same patient, there is systolic reversal in the hepatic veins on pulsed Doppler examination (solid downward arrows). Upward arrows indicate atrial systolic reversal which is normal. There is forward diastolic predominant flow following the reversed systolic flow

../images/301959_1_En_9_Chapter/301959_1_En_9_Fig13_HTML.jpg — Fig. 9.13

Systolic flow reversal in the Superior Vena Cava . In the same patient, there is systolic reversal in the SVC on pulsed Doppler examination (solid downward arrows). Upward arrows indicate atrial systolic reversal which is normal. There is forward diastolic predominant flow following the reversed systolic flow

Cardiac Catheterization

Echocardiography is clearly the main modality for diagnosing TR. However if the clinical presentation is such that catheterization is planned to resolve other clinical issues, right heart catheterization can add hemodynamic information supportive of the diagnosis of severe TR. Right atrial pressure is elevated and the tracing demonstrates a large v wave. In very severe cases, the atrial pressure becomes ventricularized, whereby the right atrial tracing appears more like an RV tracing as RA and RV nearly become one continuous chamber. It should be noted that thermodilution determination of cardiac output is unreliable in the face of severe TR.

Assessing RV Function. Unlike for mitral and aortic regurgitation, there are no well-recognized benchmarks signifying that RV dysfunction is developing that might in turn trigger therapeutic intervention. The difficult geometry of the RV further complicates estimation of RV volume and function and RV ejection fraction is not routinely reported. A common estimation of RV function is made by measuring tricuspid annular plane systolic excursion (TAPSE) [7] although its role in assessing RV function in the presence of TR is uncertain. The premise of TAPSE is that it measures RV long axis shortening and thus measures contraction in that plane. Right ventricular strain has also been employed to assess RV systolic function [8]. However both TAPSE and strain are load dependent and thus affected by TR alterations in both preload and afterload. Correction of primary severe TR is recommended when there is “progressive deterioration in RV function or progressive RV dilatation” but specific numeric cutoffs for when these conditions exist are not uniformly agreed upon. Accurate assessment of changes in RV volume and function over time is accurately made with cardiac MRI.

Therapy

For most cases of secondary TR, standard therapy is treatment of the left heart or lung disease responsible for causing the TR. Thus the treatment of left heart failure reduces LV filling pressure, in turn reducing pulmonary artery pressure, reducing RV size, and improving TR. Likewise improving lung function and oxygenation in a patient with lung disease reduces pulmonary vascular resistance, in turn reducing pulmonary artery and RV pressure, thus reducing RV size, improving secondary TR. In the case of pulmonary vascular hypertension, pulmonary vasodilators may reduce pulmonary hypertension, thereby reducing RV volume, partially restoring tricuspid competence.

Secondary TR and Left-Sided Valvular Heart Disease

An exception to the strategy for treating secondary TR by treating its primary cause is when TR is caused by the consequences of severe left-sided valvular heart disease (VHD), especially mitral regurgitation. While it is reasonable to expect that mechanical correction of left-sided VHD (valvotomy, valve repair or valve replacement) would improve secondary TR, such improvement does not always occur and is difficult to predict [9–11]. In cases where TR does not improve or even worsens following successful mitral or aortic valve surgery, the patient may then suffer from right heart failure due to TR, raising the prospect of a second heart operation to address the TR. In small reported series, such operations have led to unexpectedly-high mortality [12, 13]. While percutaneous methods are being developed to address this problem [14–16], long-term assessment of those solutions is not yet available. In most cases, severe TR, whether primary or secondary, will be addressed with tricuspid valve repair, usually employing a ring annuloplasty, at the time of left-sided valve surgery. More difficult is the decision to operate on mild or moderate secondary TR because it is uncertain whether tricuspid repair is beneficial or not.

Impact of Secondary TR on Outcome

Nath et al. have demonstrated that the presence of TR negatively affects prognosis (Figs. 9.14 and 9.15) even in patients with normal pulmonary artery pressure and normal LV ejection fraction (EF) [17], supporting TR intervention at the time of left-sided valve surgery. As noted above, it is often hoped that correction of left-sided lesions will reduce LV filling pressure, simultaneously decreasing pulmonary artery pressure, thereby relieving TR without direct TR surgery. Unfortunately existing data are confusing and lead to no definitive course of management. Yilmaz et al. found that in nearly 700 mitral repairs of primary mitral regurgitation (MR), TR untreated at the time of surgery rarely progressed and only 1 patient required re-operation at follow-up [18]. Thus they have encouraged a conservative approach to treating TR during mitral surgery. At the other end of the spectrum, Dreyfus and colleagues have espoused tricuspid annuloplasty during mitral surgery even in the absence of TR if tricuspid annular dimension exceeded 70 mm [19] (at surgery) while Mahesh et al. have suggested the same strategy for an annular dimension >21 mm/m² at preoperative echocardiography [20]. This aggressive approach is supported by Kwak et al. who found that 27% of patients with no TR at the time of left-sided surgery developed moderate or severe TR within 5 years following operation, especially if atrial fibrillation occurred [10]. Several other authors also found progression or the new occurrence of TR in 14–50% of patients with untreated tricuspid valves at the time of mitral surgery [21–23].

../images/301959_1_En_9_Chapter/301959_1_En_9_Fig14_HTML.png — Fig. 9.14

Progressively worse TR negatively impacts prognosis both in patients with pulmonary hypertension (panel a) and without (panel b) pulmonary hypertension. From Nath J, et al. [17]. Reprinted with permission from Elsevier

../images/301959_1_En_9_Chapter/301959_1_En_9_Fig15_HTML.png — Fig. 9.15

Progressively worse TR negatively impacts prognosis both in patients with low left ventricular ejection (LVEF) (panel a) and with normal LVEF (panel b). From Nath J, et al. [17]. Reprinted with permission from Elsevier

When left unattended, existing TR often improves initially after left-sided surgery but then worsens over time (Fig. 9.16) [9]. Virtually all studies are concordant in demonstrating reduced TR when the tricuspid valve is repaired at the time of left-sided surgery [13, 24–29]. Most also found improved RV remodeling post tricuspid repair [26–29]. In addition, tricuspid surgery has reduced the incidence of heart failure or improved functional capacity in some studies [27, 29]. No study has demonstrated that correction of mild-to-moderate TR during mitral or aortic surgery prolongs life, indeed most found no change in survival with tricuspid repair [13, 25–27] although mortality adjusted for comorbidities was improved in at least one study [24]. Most recently David et al. found that TR was relatively rare at the time of mitral surgery [30]. While TR was associated with a worse survival outcome, poor prognosis was due more to cofactors associated with TR (age, atrial fibrillation, poor LV function, etc.), than the TR itself. Probably because of these comorbidities, treatment of TR at the time of mitral surgery did not ameliorate the negative impact of preoperative TR on outcome [30].

../images/301959_1_En_9_Chapter/301959_1_En_9_Fig16_HTML.jpg — Fig. 9.16

The course of moderate TR after left-sided surgery is shown over time, color coded by grade (left) and by numerical grade (right). After initial improvement, many patients suffer gradual worsening. Kusajima K, et al. [9]. Reprinted with permission from Oxford University Press

In summary, virtually all studies demonstrate that tricuspid repair reduces the risk of TR progression following surgery. Some reports also demonstrate objective clinical improvement with less heart failure, faster return of RV function toward normal and better exercise capacity when tricuspid repair accompanied left-sided valve surgery. Whether treating TR at the time of left-sided surgery improves survival is uncertain. Because repeat heart surgery to correct residual symptomatic severe TR carries substantial risk, most surgeons prefer to address more than mild TR with tricuspid repair during left-sided valve surgery and thus surgical tricuspid interventions have increased in frequency over the past decade [31]. Several studies of TR progression are summarized in Table 9.1.

Table 9.1

Studies of functional tricuspid regurgitation

Ref #	N	Background	Intervention	Result
[9]	96	MVS	None	Initial TR DEC then INC
[10]	335	MVS, AVS	None	26% with no I-TR developed 2–4+ TR in 5 years
[11]	165	MVS	None	88% vs. 46% 5 year survival 0,1+ TR vs. ≥2+ TR
[18]	699	MVS	None	Initial TR DEC then INC 1 pt needed TR Surg
[19]	311	MVS	None vs. TVR	Mortality same but NYHA better with TVR
[22]	174	MVS	None	16% with 1 = 2+ ITR became severe in 8 years
[24]	110	MVS	No TVR vs. TVR	Adjusted survival 45% no TVR vs. 75% TVR
[25]	225	MVS	No TVR vs. TVR	93% <2+ TR in TVR vs. 61% for no TVR at 4 years
[26]	645	MVS	No TVR vs. TVR	TVR predicted recovery of RV function
[27]	624	MVS	No TVR vs. TVR	TVR decreased TR and HF but not mortality
[28]	44	MVS	R_nd no TVR vs. TVR	2–4+ TR in 28% vs. 0% no TVR vs. TVR

AVS Aortic Valve Surgery, DEC Decrease, HF Heart Failure, I Initial, INC Increase, MVS Mitral Valve Surgery, R _nd Randomized Trial, TR Tricuspid Regurgitation, TVR Tricuspid Valve Repair

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Tags: Valvular Heart Disease

Apr 23, 2020 | Posted by admin in CARDIOLOGY | Comments Off

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