Preoperative Evaluation of Right Ventricular Function



Fig. 6.1
Pathophysiology of chronic pressure overload-induced right ventricular (RV) dysfunction and irreversible failure in patients with congestive heart failure due to primary impaired left ventricular (LV) function. CO cardiac output, LVEDP left ventricular end-diastolic pressure, PVR pulmonary vascular resistance, RV-SV right ventricular stroke volume, TR tricuspid regurgitation





6.2.2 Particularities of Primary RV and LV Failure: True Biventricular Failure


There are relevant pathophysiologic and hemodynamic differences between CHF due to primary impaired LV function and global HF due to heart muscle diseases with impaired biventricular systolic and/or diastolic function. In patients with biventricular dysfunction due to genetic or acquired myocardial alterations, the impaired LV function is usually associated with less increase in left-sided heart filling pressures (consequently also less LV and LA dilation) and induces less pulmonary intravascular congestion because of the low SV ejected by the failing RV and also because the intravascular congestion due to increased renal sodium and water retention secondary to CO reduction involves mainly the systemic circulation. Their PVR is also lower than in patients with CHF due to primary impaired LV function, and their pulmonary artery pressure (PAP) can be normal or is only moderately elevated. Clinically this may suggest a predominantly right-sided heart failure and can lead to false therapeutic decisions. In certain patients with primary biventricular failure due to severe myocardial systolic and diastolic dysfunction, the absence of relevant RV dilation due to increased myocardial stiffness, which also impedes a massive reduction of RVEF despite of the low SV of the failing RV, may suggest a predominantly LV failure. Because such a primarily damaged RV will not improve during LV support, LVAD implantation alone is useless and highly risky, especially in patients with normal PVR and low velocity of tricuspid regurgitation jets.


6.2.3 Reversibility of RV Failure by RV Afterload Reduction


Acting more as a volume pump, the RV tolerates less pressure than volume overload and has higher sensitivity to afterload changes than the LV. The distinctly load sensitivity of RV size, geometry, and performance explains its ability for reverse remodeling and functional improvement after normalization of loading conditions [6]. LVAD implantation often induces acute PVR reduction accompanied by acute changes in RV geometry with TR reduction and improvement of RV pump function [7]. In certain patients, starting of LV mechanical unloading induces acute RV dilation suggesting that the failing RV may not be able to handle the acute extra volume load induced by the LVAD-promoted increase of the CO. However, such LVAD-promoted RV volume overloading is limited because after removal of the excessive blood volume from the pulmonary vessels, the output of the LVAD into the systemic circulation will decrease correspondingly to the decrease of failing RV output. Long-term LVAD support usually further reduces the PVR facilitating RV reverse remodeling and functional recovery [3]. However, LVAD support in patients with CHF is rarely followed by complete RV recovery, and severe postoperative RVF associated with high patient mortality is more frequent than persistence of RVF after PVR reduction by lung transplantation for precapillary PH or by pulmonary endarterectomy in patients with chronic thromboembolic PH [3]. The less predictable RV improvement in CHF patients receiving an LVAD is mainly related to differences in the etiology of myocardial injury which induced the CHF, differences in duration of RVF before VAD implantation, and differences in the direct impact of the initial myocardial injury on RV myocardium and also to the impact of ventricular interdependence changes induced by LV unloading on RV geometry and function.



6.3 Main Tools for Assessment of Right Ventricular Function


Echocardiography, right heart catheterization (RHC), and cardiac magnetic resonance imaging (MRI) are the standard clinical methods for preoperative evaluation of RV function.


6.3.1 Echocardiography



Challenges and Limits in RV Echo-Assessment


There are particular challenges and limits in RV echo-assessment. RV volume and ejection fraction (EF) measurements are less reliable, and therefore, 2D echo-derived RV volume and EF calculations are not anymore recommended by the American Society of Echocardiography (ASE) for clinical use [8]. 3D echo is more useful for estimation of RV volumes and EF, but it is technically challenging and not widely available. However, the more reliable RVEF calculation by 3D echo does not change the fact that due to its afterload dependency, RVEF cannot be used as an index of myocardial contractility [8]. Nevertheless, 2D echo is still preferentially used for assessment of RV function because it allows easy measurements of RV fractional area change (FACRV) and tricuspid annulus peak systolic excursion (TAPSE), which can provide similar information to RVEF [9]. However, FACRV measurements showed high interobserver and intra-observer variability, whereas TAPSE measurements are angle dependent and influenced by both LV function and overall heart motion [9]. Recently only a poor correlation between magnetic resonance imaging (MRI)-derived RVEF and TAPSE (r = 0.45) [10] was also found. It must be also emphasized that, because of their load dependency, RVEF, FACRV, and TAPSE can change without changes in myocardial contractility. Thus, they will decrease with increasing PVR even if myocardial contractility remains unaltered. Additionally, TR can induce RVEF, FACRV, and TAPSE changes which can be misleading for assessment of RV contractile function and estimation of RV myocardial contractility.

Also Doppler-derived indices of RV function, such as the myocardial performance index (MPI) and the TR-derived rate of RV pressure rise (dp/dt), which are unaffected by RV geometry, are increasingly used for RV echo-assessment. The clinical value of RV dp/dt ratio is limited by the angle and load dependency of measurements [810]. RV dp/dt measurements are also less accurate in severe TR [6]. Afterload dependence and unreliability of measurements in patients with elevated RA (including severe TR) limit the diagnostic value of MPI, and the ASE does not recommend MPI as the sole quantitative method for evaluation of RV function [8]. The time interval between onset and cessation of TR flow corrected for heart rate (TRDc), a surrogate for early systolic equalization of RV and RA pressure, appeared also useful for evaluation of RV function. A decreased TRDc in CHF patients before LVAD implantation was identified as a risk factor for postoperative RVF [11].

RV wall motion assessment by TDI-derived velocity measurements is also useful because velocity appeared less load dependent than displacement. A major limitation of TDI is the angle dependency of measurements. Nevertheless, especially the tricuspid lateral annulus peak systolic wall motion velocity (TAPS’), which correlates with TAPSE but is less load dependent, the RV isovolumic contraction peak velocity (IVCV) and the RV isovolumic acceleration (IVA) appeared suited for evaluation of RV contractile function [12].

Strain imaging is also useful for RV evaluation because myocardial strain (deformation) is not affected by the movement of the entire heart, and deformation analysis (strain and strain rate imaging) allows discrimination between active and passive myocardial tissue movement. Angle-independent speckle-tracking-derived strain imaging parameters like the RV longitudinal peak systolic strain (PSSL) and strain rate (PSSrL) appeared particularly useful for assessment of RV contractile function [13]. Main limitations of speckle-tracking strain imaging are dependency on image quality plus relatively low temporal resolution and segmental reproducibility of measurements (especially for 3D speckle tracking), as well as the influence of RV loading conditions especially on myocardial strain values [13].

Pressure overload-induced RVF in CHF due to primary impaired LV function is finally the result of both systolic and diastolic RV dysfunctions. However, only RV systolic dysfunction was identified as a predictor of mortality in CHF [8]. Echo assessment of RV diastolic function is also challenging because it cannot be described by a single parameter, and the influence of respiration, heart rate, and preload changes on trans-tricuspid velocities can induce misleading diastolic parameter changes [8].


RV Echo Evaluation in Relation with Its Loading Conditions


Distinctly load dependency of RV size, geometry, and function indicates the necessity for RV evaluation in relation with its loading conditions, especially in patients with CHF due to primary impaired LV function where RVF is induced by pathological loading conditions, which are potentially reversible during LVAD support. The usefulness of integrative approaches for RV evaluation, using combinations of parameters which include RV afterload, was increasingly investigated during the last years [314]. Very promising appeared to be the RV stroke work index (SWIRV) because its calculation from RHC-derived data (i.e., SWIRV = { [mean PAP – mean RAP] · SV }/body surface area) appeared more useful than any echo variable used individually for evaluation of RV function in end-stage CHF [15]. However, because echo-estimations of right atrial (RA) and mean PAP are less reliable than their direct measurements during RHC, the poor correlation between echo-derived and RHC-derived SWIRV calculations is not surprising and therefore echo-derived SWIRV is rarely used for assessment of RV function. However, recently, two simplified composite echo-derived variables which incorporate either TAPSE and load or SV and load were identified as more easy calculable surrogates for the SWIRV [16]. One of them is the “simplified RV contraction-pressure index” (sRVCPI), which incorporates TAPSE and load, and is derived as sRVCPI = TAPSE · ΔP RV–RA, where ΔP RV–RA is the pressure gradient between RV and RA [17]. sRVCPI showed a close correlation with RHC-derived SWIRV (r = 0.68; p < 0.001) [15]. The other is the “RV stroke work” (RVSW), which incorporates SV and load RVSW = (pulmonary valve-area · VTIPV) · (4 · peak TR velocity) [2], where VTIPV is the velocity-time integral of the systolic trans-pulmonary jet, which also showed a close correlation with the RHC-derived SWIRV (r = 0.74; p < 0.0001) [16].

Also recently, composite echo variables which incorporate either longitudinal displacement and load (i.e., TAPSE/systolic PAP and TAPSE/PVR) or velocity of myocardial shortening and load (i.e., afterload-corrected peak systolic longitudinal strain rate) were also found suited for assessment of RV contractile function [14, 18, 19]. The TAPSE/systolic PAP ratio is a simplified approach to assess RV contraction by plotting fiber longitudinal shortening versus the force generated for overcoming the imposed load [18]. This allows estimations of RV performance status which in turn might facilitate the decision-making process and prognosis assessments in clinical praxis. The limitations of this index are related to the well-known limitations of TAPSE and systolic PAP echo measurements. Nevertheless, in a larger study, this index appeared as a strong and independent predictor of mortality in patients with HF due to primary impaired LV function [11]. Because PVR is a critical determinant of RV systolic function, its inclusion into echo-derived composite variables can also be beneficial for RV assessment. Echo-derived RV ejection efficiency (RVEe), defined as RVEe = TAPSE/PVR, is such a composite variable which reflects that relationship in a simplified manner [19]. However, there is controversy on the reliability of echo-derived PVR estimations in patients with PVR >6 Wood units [819]. Future studies are necessary to determine if echo-derived RVEe is indeed able to predict patient outcome.

The afterload-corrected peak systolic longitudinal strain rate, a reproducibly and easy obtainable combined variable for assessment of RV adaptability to load, defined as PSSrL · ΔPRV-RA, where PSSrL is the peak global systolic longitudinal strain rate and ΔP RV-RA the pressure gradient between RV and RA, is based on the relationship between RV myocardial shortening velocity and RV load [16]. Because myocardial shortening velocity is load dependent, RV systolic pressure increase reduces the PSSrL. Nevertheless, as long as RV contractile function remains unchanged, due to the ΔP RV-RA increase, the RV load-corrected PSSrL will remain relatively stable. However, if RV afterload increase overwhelms RV ability to adapt its contractile function correspondingly, in addition to PSSrL reduction, there will be also a ΔP RV-RA reduction due to the increase of RA pressure, even before the RV systolic pressure finally also becomes lower due to progressive impairment of RV contractility. The load-corrected PSSrL will be therefore more useful for the evaluation of RV adaptability to loading conditions than the PSSrL alone.

A distinctly different approach for assessment of RV contractile function is provided by the recently introduced “RV load-adaptation index” (LAIRV). The LAIRV, a composite echo-derived variable based on the relationship between RV load and RV dilation, also taking the RA pressure into account, is reflected by the ratio between the systolic mean pressure gradient between the RV and RA (ΔPRV-RA) and RV end-diastolic volume per long-axis length (EDV/L ED):



$$ \begin{array}{c} LA{I}_{RV}=\frac{\varDelta {P}_{RV- RA}}{ ED V/{L}_{ED}}\approx \frac{VT{I}_{TR}}{A_{ED}/{L}_{ED}}\\ {}=\frac{VT{I}_{TR}\left( c m\right)\cdot {L}_{ED}\left( c m\right)}{A_{ED}\left( c{m}^2\right)}\end{array} $$

Thus, using the TR velocity-time integral (VTITR) instead of ΔP RV-RA and the easily measurable RV end-diastolic area (A ED) instead of the RV end-diastolic volume (EDV), a dimensionless index of similar value for RV evaluation can be obtained (◘ Fig. 6.1) [3, 6, 14]. Because ΔP RV-RA is calculated from the mean velocity of the TR jet, the use of VTITR instead of ΔPRV-RA is unrestricted possible and has the advantage to include also the duration of systolic loading. The use of A ED instead of EDV is justified by the good correlation between the echo-derived RV-A ED and the MRI-derived RV-EDV [20]. Thus, a small RV area relative to long-axis length (size and geometry unaltered) in a patient with high VTITR (i.e., high RV systolic pressure and relatively low RA pressure) yields a high LAIRV which indicates good adaptation to load (RV ability to increase systolic pressure without relevant RV dilation and without RA pressure increases suggesting good RV contractile function) and the potential of RV to improve its performance after reduction of loading conditions. A large area relative to long-axis length (spherical dilation) despite a relatively low VTITR yields a low LAIRV indicating poor adaptation to load (excessive RV dilation despite low RV pressure-load indicating impaired RV systolic function) suggesting a reduced myocardial contractility. LAIRV values <15 indicate low RV adaptability to load which is insufficient to prevent RVF even at normal PVR [36]. Thus, RV evaluation in relation to its actual loading conditions can be helpful in proper decision making especially before VAD implantation (◘ Fig. 6.2).

A334653_1_En_6_Fig2_HTML.gif


Fig. 6.2
Right ventricular (RV) load adaptation index (LAI) and load-corrected global peak systolic longitudinal strain rate (PSSrL) in two patients with end-stage congestive heart failure due to primary impaired left ventricular function. In patient A, the more dilated RV (A1) with a lower pressure gradient between RV and right atrium (A2) and a lower velocity of RV myocardial shortening (A3) yield a 33.5% and 39.4% lower LAI and load-corrected PSSrL, respectively, in comparison with patient B (B1, B2, B3). The low LAI and load-corrected PSSrL in patient A indicate a high risk for RV failure after LVAD implantation (need for temporary or even permanent mechanical support also for the RV). The relatively high LAI in patient B indicates RV ability to improve during LVAD support. TR tricuspid regurgitation, VTI TR TR velocity-time integral, V max maximum (peak) velocity, ΔP RV-RA pressure gradient between RV and right atrium

Recently, also 3D echo data were used for assessment of the relationship between RV remodeling and afterload. Regression analysis between 3D echo-derived RV end-systolic volume-index and systolic PAP appeared able to distinguish between adapted, adapted-remodeled, and adverse-remodeled RV [21].


6.3.2 Right Heart Catheterization


RHC which provides valuable direct hemodynamic data, also allowing calculations of PVR and certain composite variables which allow RV assessment in relation to loading conditions, is another cornerstone for RV evaluation.

Invasive measurements of certain hemodynamic variables like CVP (central venous pressure), PCWP (pulmonary capillary wedge pressure), PAP, and CI (cardiac index) are essential for preoperative RV evaluation because high CVP and CVP/PCWP ratio and low CI and mean PAP decrease were often identified as risk factors for RVF after LVAD implantation [3, 6, 22]. However, CVP, PAP, PCWP, and CI measured before LVAD implantation were not found in all studies significantly different in patients with and without postoperative RVF, and alone none of them appeared able to predict RVF or freedom from RVF after LVAD implantation [3]. For certain hemodynamic variables like CI and PCWP, this might be in part also due to the lower accuracy of measurements. Particularly concerning for RVF after LVAD implantation is high CVP in the setting of low PAP [36]. The ratio of RA pressure and PCWP can help to differentiate patients with relevant intrinsic RV dysfunction from those with a congested right-sided heart (without altered RV contractility) due to elevated left-sided filling pressures. A high CVP/PCWP ratio (>0.63) reflects inherent RV dysfunction, whereas a low CVP/PCWP ratio reflects right-sided congestion as a result of high left-sided filling pressures.

Among the RHC-derived composite variables for RV evaluation, the SWIRV, which allows RV assessment in relation to its afterload, can be particularly suited for preoperative decision making between LVAD and BVAD implantation because SWIRV appeared more reliable than any echo variable used individually for evaluation of RV function in end-stage CHF [15]. SWIRV values <300 mmHg/mL/m2 usually reflect significant RV dysfunction, and patients with the need for RVAD support after LVAD implantation showed preoperatively significantly lower SWIRV values than those without post-LVAD RVF [22]. A weakness of the SWIRV is its less precise calculation in patients with higher degree of TR or in those with low CI because of the less reliable CO measurements by the thermodilution method in such patients.

Composite variables derived from both RHC and echo measurements can also be useful for RV evaluation before VAD implantation. Thus, composite variables which incorporate longitudinal displacement and load like TAPSE/systolic PAP and TAPSE/PVR or velocity of myocardial shortening and load (afterload-corrected PSSrL) already appeared suited for assessment of RV contractile function even if their calculation was exclusively based on echo measurements, although echo-derived estimation of PAP and especially that of PVR is not very accurate [14, 18, 19]. However, those composite variables might become more reliable by a combined use of echo-derived TAPSE or PSSrL measurements and RHC-derived PAP measurements or PVR calculations, respectively.

Analysis of RV function by pressure-volume loops, possible with conductance catheters, allows quantification of various parameters like ∆P/∆t, stroke work, elasticity, and compliance which can be helpful for preoperative decision making before VAD implantation. However, RV conductance measurements by pressure-volume loops are more challenging than LV conductance measurements (difficulties in obtaining reliable ventricular volumes), and to date the clinical usefulness of these measurements for preoperative prediction of RV function after LVAD implantation is not established.


6.3.3 Cardiac Computed Tomography and Magnetic Resonance Imaging


Both cardiac computed tomography (CCT) and MRI allow reliable and reproducible assessment of RV size, geometry, SV, and EF without geometric assumptions about the RV. Multi-slice spiral CCT and MRI measurements of RV volumes, mass, SV, and EF also show high correlations (r ≥ 0.91) [23]. Major limitations like nephrotoxicity, ionizing radiation, low temporal resolution, and especially the difficulties in the examination of patients with inotropic-dependent end-stage CHF make CCT less useful than echocardiography for preoperative RV evaluation in VAD candidates. However, after LVAD implantation, when RV assessment by transthoracic echocardiography becomes more difficult, especially due to device-related artifacts, CCT can be considered as a useful imaging modality for RV evaluation.

Although MRI is increasingly used for RV evaluation because it is particularly suited for assessing RV volume and for calculation of SV, RVEF, and tricuspid valve regurgitant volumes and, in combination with RHC-derived hemodynamic data, also able to assess independently RV function, remodeling, afterload, and contractile properties, there are yet no published data on its usefulness and safety for preoperative RV evaluation in MCS candidates. The main limitation for the use of MRI to evaluate RV function before final decision making between LVAD and BVAD implantation is the restriction of MRI use only to hemodynamic stable patients without implanted defibrillators and/or devices for biventricular pacing. In addition, MRI cannot be used postoperatively for RV assessment because the method is contraindicated in the presence of an LVAD.


6.4 Prediction of RV Improvement and Anticipation of RV Failure After LVAD Implantation


Like LV performance, RV performance is a reflection of contractility, preload, and afterload, also being influenced by valvular function, heart rhythm, synchrony of ventricular contraction, and ventricular interdependence. Nevertheless, in comparison with the LV, size, geometry, and performance of the RV are definitely more sensitive to changes in loading conditions, especially to afterload changes. This explains RV ability to improve during its afterload reduction inducible by mechanical LV support.

However, RV reverse remodeling with TR reduction and improvement of myocardial function after LVAD implantation depend not only on the reversibility of myocardial alterations by reduction of RV loading conditions but also on the reversibility of pathologic circulatory and metabolic changes induced by both imbalanced neurohumoral and inflammatory reactions to the low CO- and CHF-related end-organ failure (especially the kidney and liver). Additionally, changes of interventricular interactions induced by sudden LV unloading and potential intraoperative and early postoperative complications can impair the initial ability of the RV to improve after LVAD implantation. Prediction of RV improvement during LVAD support is therefore a highly complex and challenging issue.


6.4.1 Risk Factors for Postoperative RV Failure


RVF with and without the necessity of additional RVAD support complicates 10–40% of LVAD implants. Patients with different post-LVAD course of RV function show already preoperatively significant differences in certain laboratory data reflecting relevant pathophysiological consequences of severe CHF (especially hepatic and renal dysfunction), echo variables (especially those for RV assessment), and invasively obtained hemodynamic parameters [7, 11, 2224]. RV end-diastolic S/L axis ratio > 0.57, TR > 2nd degree, FACRV < 31%, ΔP RV-RA < 35 mmHg, RV/LV diameter ratio ≥ 0.75, TAPS’ < 8 cm/s, PSSL < −9.6%, PSSrL<0.6/s, LA volume index <38 mL/m2, CVP >15 mmHg, elevated serum bilirubin, creatinine and lactic dehydrogenase (LDH) levels, plus elevated markers of inflammation were identified by univariate analysis as the most relevant risk factors [6, 11, 19, 22, 2534]. TR ≥ moderate to severe, CVP/PCWP ratio >0.63, CVP > 15 mmHg, RV/LV diameter ratio ≥ 0.75, blood urea nitrogen >39 mg/dL, and ventilatory support were revealed as risk factors for postoperative RVF also by multivariate analysis (◘ Tables 6.1 and 6.2) [6, 11, 22, 24, 27, 31, 34]. However, these variables were not identified in all studies as significant risk factors for RVF. This might be mainly due to the differences between centers with regard to defining RVF and their selection criteria for VAD support. With only few exceptions, the numerous risk factors for RVF after LVAD implantation appeared alone unable to predict reliably RVF or freedom from RVF.


Table 6.1
Univariate logistic regression data on the relevance of selected generally accepted preoperative risk factors for RV failure after LVAD implantation


























Selected risk factors for RHF

Odds RVF

95% CI

P value

High serum creatinine [22, 29]

1.68

1.30–2.18

< 0.01

1.42

0.66–3.10

0.36

High blood urea nitrogen [11, 22]

1.03

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Nov 3, 2017 | Posted by in CARDIOLOGY | Comments Off on Preoperative Evaluation of Right Ventricular Function

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