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Pulmonary Arterial Hypertension: A Two-Dimensional Echocardiographic Approach from Screening to Prognosis


1 Department of Public Health and Clinical Medicine, Umea University, Sweden
*Corresponding author: Samir Kanti Saha, Department of Public Health and Clinical Medicine, Umea University, Sweden, E-mail: samirksaha@gmail.com.
Archives of Cardiovascular Imaging. 4(2): e41818 , DOI: 10.5812/acvi.41818
Article Type: Review Article; Received: Mar 31, 2016; Accepted: Apr 30, 2016; epub: May 29, 2016; collection: May 2016

Abstract


An elevated pulmonary artery pressure (PAP) from any cause is associated with increased mortality, especially in cases of primary pulmonary arterial hypertension (PAH). One of the many reasons behind a bad prognosis is the inherent difficulty in assessing right ventricular (RV) function with reproducible methods. Intensive research involving the left heart has made it relatively easy to assess left ventricular (LV) systolic and diastolic functions in many centers around the world. As for the RV, however, although increasing attention has been focused on the right-sided heart in the recent times, neither global longitudinal strain nor right ventricular ejection fraction (RVEF) has been studied well in relation to the outcome (unlike in the LV). Another issue is that the right heart functions in a circuitry involving the right atrium (RA), the RV, and the pulmonary artery. Hence, all 3 components of this circuit have important roles in unison to eject a cardiac output equivalent to the left-sided heart. In this review, we sought to discuss the ways to quantity the function of the entire circuit using both standard and advanced echocardiographic imaging modalities. As primary PAH is the classic form of pathology causing the RV to face an afterload with which it is not destined to cope, this review is mainly based on the assessment of the right heart as a circuit in idiopathic primary PAH.

Keywords: Pulmonary Arterial Hypertension; Prognosis; Idiopathic

1. Context


Pulmonary hypertension (PH) is defined as an elevated mean pulmonary artery pressure (PAPm) > 25 mmHg at rest as estimated by right-heart catheterization (RHC). There are broadly 4 classes of hemodynamically defined PH, according to the very recent guideline published in connection with the European Society of Cardiology meeting in London, United Kingdom, in 2015 (1). These are: 1) pre-capillary PH, characterized by a PAPm > 25 mmHg and a pulmonary artery wedge pressure (PAWP) < 15 mmHg (This group has 4 clinical subclasses: a) PAH, b) PH due to lung disease, c) chronic thromboembolic pulmonary hypertension (CTEPH), and d) PH with unclear and/or multifactorial mechanisms.); 2) post-capillary PH, characterized by a PAPm > 25 mmHg and a PAWP > 15 mmHg; 3) isolated post-capillary PH, characterized by a diastolic pressure gradient < 7 mmHg and a pulmonary vascular resistance (PVR) < 3 Wood units; and 4) combined pre-and post-capillary states, characterized by a diastolic pressure gradient > 7 mmHg and a PVR > 3 Wood units. The last 2 classes may have a common clinical scenario of left-heart disease and disease of unknown and/or multifactorial mechanisms (1). The last clinical classification proposed during the world symposium on pulmonary hypertension in dana point, California, in 2008 was updated in 2013 (2). Of the basic 5 classes of PH (group 1: idiopathic, group 2: due to left-heart disease, group 3: PH due to lung disease, group 4: CTEPH, and group 5: miscellaneous), Group 1 now includes under the subclasses of PAH about 12 different states, of which idiopathic PAH has been classed as 1.1. The other subclasses include portal hypertension, PAH due HIV infection, due to congenital heart disease, and due to drugs and toxins.


This chapter deals primarily with Class 1.1 type of PAH (IPAH), although the fundaments of imaging remain common to all classes of PH.


1.1. Physiology of the Pulmonary Circulation

The pulmonary circulation (a high volume, low pressure circuit) is characterized by an inflow pressure (PAP), an outflow pressure (left atrial pressure), and a pulmonary flow, which is almost equal to the systemic cardiac output. PVR, which estimates the functional state of the pulmonary circulation, is calculated through the transpulmonary gradient (PAPm-PAWP) divided by the cardiac output, usually via the catheterization of the right heart. The procedure derives left atrial pressure either by balloon-occluded pressure or PAWP, while the cardiac output is measured by thermodilution (3). Although RHC is considered the “gold standard” method for the estimation of pressures with the RV pulmonary circuit, the overestimation or underestimation of pressures particularly PAWP is not uncommon in situation where the 0 leveling at the level of the catheterization table may overestimate PAP as well as PAWP (4).


Once the diagnosis of PAH has been established by RHC, the pathophysiological consequences rely on the identification of the prognostic marker(s) using imaging techniques, of which standard and advanced 2D echocardiographic techniques remain the modalities of the primary and universal choice. Since the RV and the RA are components of the RV–pulmonary circulation circuit, the most important victim of the elevated afterload resulting from a dysfunctional pulmonary circulation is indeed the RV even though RA remodeling eventually plays a part in the progression of the disease, which is fatal. According to REVEAL (Registry to evaluate early and long-term pah disease management) registry, the 3-year mortality rate can be as high as 60% (5).


Echocardiographic assessment in suspected cases of PAH should involve the RV, the RA, and the pulmonary vasculature. The dysfunction of all 3 components of the RA–RV–pulmonary vasculature circuitry has been linked to death in PAH. Therefore, it is extremely important to study the circuit in its entirety, as discussed below.


1.2. Echocardiographic Assessment of the Right Heart/Pulmonary Circuit in Idiopathic Pulmonary Arterial Hypertension
1.2.1. Right Ventricle

The RV undergoes significant structural and functional impairment as a result of the increased afterload due to an elevated PAP (6). This adverse remodeling and maladaptation leads to decreased RV strain and inevitably to end-stage heart failure and eventually to death (7, 8). It is, therefore, extremely important to study RV structural and functional parameters in any case with suspected PH of any cause, especially IPAH. RV apical views should be acquired as per the guidelines of the American Society of Echocardiography (9).


Because of the complex geometry of the RV, there are multitudes of measures necessary to accurately quantify RV systolic function. What can provide some telltale signs of the underlying pathology is a careful visual assessment of RV size with the measurement of the dimensions (any value > 38 - 40 mm measured at end diastole is considered abnormal) from multiple planes, thickness (> 5 - 6 mm is considered abnormal; preferred view in that case is the subcostal window), altered septal curvature in diastole (volume overload, as in shunts), and altered septal curvature in diastole and systole (pressure overload). Thereafter, a combination of the following measures is often necessary to arrive at a conclusive decision vis-a-vis the functional status of the RV as regards the systolic function and the degree of pressure overloading caused by the dysfunctional pulmonary vasculature.


1.3. Tricuspid Annular Plane Systolic Excursion

Tricuspid annular plane systolic excursion (TAPSE) is one of the most common measures of RV systolic function obtained using M-mode echocardiography and is recommended by the American society of echocardiography’s guideline for the routine evaluation of RV function. Although TAPSE measures the longitudinal motion of the RV, it has a good correlation with global systolic markers such as 2D RVEF, radionuclide-derived RVEF, and 2D-derived fractional area change (FAC [%]) (9). An excursion < 16 mm is considered abnormal in the absence of previous thoracic surgery for valvular, coronary, aortic, or congenital lesions or in the absence of atrial fibrillation. In a mixed cohort of IPAH and CTEPH, a TAPSE < 15 mm was one of the independent predictors of all-cause mortality in a 3-year follow-up study (10). In a Swedish observational study (11) involving a small cohort of cases from northern Sweden, however, TAPSE had no correlation with RHC-obtained PVR. Fine et al. (8) showed that TAPSE was inferior to RV strain in predicting cardiopulmonary and all-cause mortality. One of the major limitations of TAPSE is that the value can be falsely elevated in a failing RV (10). Also, in severe tricuspid regurgitation, TAPSE could be falsely elevated because of volume-driven, hyperdynamic state perhaps providing a supraphysiological stroke output. The differential diagnosis of lower TAPSE values, nevertheless, must include chronic LV systolic failure (12) and heart failure with a preserved LV systolic function (13), clinical states in which pulmonary artery systolic pressure (PASP) is also elevated (clinical class 2 PH or hemodynamically defined post-capillary PH). Personal experience from this author suggests that TAPSE is also probably unreliable in the transplanted heart to detect RV systolic dysfunction. This is probably because of the fact that TAPSE measures longitudinal motion and does not take into account the radial contribution for ejection, unlike fractional area change (RVAC [%]), discussed below. It should be mentioned here that in the background of an elevated afterload, RV remodeling does take place in the form of hypertrophy (and dilatation, eventually) whereby radial fibers play an important role in ejection.


1.4. Right Ventricular Fraction Area Change

2D echocardiography-obtained RVFAC (%) is acquired from RV-focused view (slight tilting of the probe to exclude part of the lateral LV cavity in order that the RV apex as well as its free wall is clearly viewed both during systole and during diastole). Then RV inner area is traced during systole (RVAs) and during diastole (RVAd). RVFAC (%) is then calculated by subtracting the areas divided by RVAd and is expressed in percentages. RVFAC (%) provides an estimate of RV systolic function. A value < 35% is considered abnormal. In a group of patients with PAH, Sachdev et al. (7) reported a mean RVFAC value = 27%. In the VALIENT ECHO study (14), an RVFAC < 35% was incrementally associated with the cardiovascular composite outcome in a group of multinational patients post myocardial infarction, once again indicating that primary LV dysfunction must be ruled out in the clinical situations of an elevated RV afterload. RVFAC (%) is perhaps superior to TAPSE for the evaluation of RV systolic function, for reasons discussed above.


1.5. Right Ventricular Index of Myocardial Performance

Also known as (RV) Tei index, the right ventricular index of myocardial performance (RIMP) provides an index of the global systolic function. RIMP can be estimated using standard (conventional spectral) pulsed-wave Doppler (global and volumetric or “blood pool” index), color tissue Doppler imaging (TDI), or non-Doppler speckle-tracking echocardiography (STE) (regional and mechanical index). The spectral Doppler recordings of the tricuspid inflow and the pulmonary artery flow (RV ejection) are utilized to calculate RIMP. This “blood pool” method requires 2 consecutive cycles of the tricuspid inflow Doppler envelope (E and A waves for each cycle). The advantage of the advanced imaging (pulsed-wave TDI/color TDI) is that it provides a superior temporal resolution with a high signal-to-noise ratio. For color TDI, however, a frame rate > 100 Hz is recommended. Whichever method is used, RIMP is calculated through dividing the sum of the isovolumic contraction and relaxation times by the ejection time. Any value > 0.40 - 0.50 is considered a depressed RV systolic function. In a study involving 93 human subjects with CTEPH (pre-capillary PH), Blanchard et al. (15) found that not only pulsed-wave TDI-obtained RIMP correlated with hemodynamically obtained PVR, but also the index was abnormally high in the study subjects and decreased after pulmonary thromboendarterectomy. Interestingly, the close correlation between the index and PVR persisted after surgery, indicating the value of RIMP in PAH. One of the major strengths of RIMP is that it is independent of RV geometry, as the values are traditionally derived using the blood pool pulsed-wave Doppler.


1.6. Spectral Doppler-Derived Right Ventricular dp/dt Max

Ventricular dp/dt max stands for the rate of pressure development during the phase of isovolumic contraction and has been traditionally measured by cardiac catheterization. It has been long known that catheterization-obtained LV dp/dt correlates well with that obtained by standard Doppler echocardiography, using the mitral regurgitation velocity envelope. LV contractility (dp/dt) can be estimated by using the time interval between 1 and 3 m/sec on the mitral regurgitation velocity continuous-wave spectrum. The rate of the Doppler-derived velocity increase is converted to a rate of pressure increase by using the modified Bernoulli equation (4 × MV2). It means that the difference in pressure is always 32 mmHg between the spatial change of velocity during the interval of 1 m/s and 3 m/s. In the final calculation to derive dp/dt , 32 (mmHg) is divided by the time it takes to increase regurgitant velocity from 1 m/s to 3 m/s. A faster time is in tandem with a stronger contractility (16). In a similar manner, RV dp/dt max is estimated using the tricuspid regurgitation velocity envelope. In a series of patients with PAH, the concept of dp/dt max has been used in which the investigators have found that not only an RV dp/dt < 410 mmHg/s was a predictor of 3-year mortality, compared with the clinical markers of prognosis such as New York Heart Association class and 6-minute walk distance, RV dp/dt max had an equivalent receiver operating characteristic accuracy and an equally significant hazard ratio (10).


1.7. Tissue Doppler Imaging-Derived Tricuspid Lateral Annular Systolic Velocity

Originally designed to quantify LV function, the modality has been applied successfully to quantify RV systolic function. A typical velocity profile contains peak systole and early and late diastolic waves, expressed in cm/s. In the acquisition of a reliable velocity profile, care should be taken to avoid angulation errors. This can be done by correctly aligning the Doppler cursor with the basal RV segment (17). In a healthy RV, the peak systolic velocity (S') should be > 10 cm/s, measured at the basal segment of the RV. Although 1D-TDI is now out of fashion principally because of its angle-dependency and low signal-to-noise ratio, the S' value should be reported in daily practice. Under normal conditions, the S' wave should instantaneously lead to the early diastolic velocity without any detectable isovolumic relaxation period. If the isovolumic relaxation is detected in a measureable manner, this should provide indirect evidence of an elevated PASP. Therefore, in daily practice, TDI is highly recommended. Tissue Doppler velocity has been very scarcely applied in PAH. In a series of human subjects with suspected PH undergoing RHC and TDI of the RV, the investigators found a decreased value of S' in subjects with a low RV stroke volume indexed to the body surface area (RVSVi). RVSVi increased after an epoprostenol injection, and so did TDI-obtained peak systolic velocity, strain, and strain rate (18). The data indicate the clinical value of S' obtained by the TDI-based longitudinal velocity estimation of the lateral tricuspid annulus.


1.8. Two-Dimensional Speckle-Tracking Echocardiography

2DSTE is an angle-dependent modality that uses a non-Doppler-based algorithm to quantify the strain by taking advantage of the motion of the ultrasound beam-derived “speckles” embedded in the myocardium. 2DSTE has now practically replaced 1DTDI because of its far superior reproducibility and very nigh signal-to-noise ratio. According to the 2015 ASE’s recommendation on chamber quantification, the accumulated information (albeit heavily weighted by a single vendor) denotes that a global longitudinal RV free wall strain rate > -20% (i.e., < 20% in absolute value) is probably abnormal (17). In the 1st ever study to use 2DSTE along with TDI, the investigators showed that not only were all STE and tissue Doppler echocardiography variables significantly lower in patients with PAH than in healthy controls, the baseline echocardiographic variables improved significantly after vasodilator therapy. Additionally, the baseline echo variables also correlated with 6-minute walk distance. The Association was, nonetheless, weaker with tissue Doppler echocardiography than with STE (19). Rajagopal et al. (20) cleverly utilized the currently available LV-based STE software to compute RV global longitudinal strain from multiple 2D views (similar to LV global longitudinal strain, using triplane imaging). Hopefully in the near future, new RV-dedicated software will be available to reproduce RV global longitudinal strain using the existing software dedicated for the LV (Figure 1).


Figure 1.
Dedicated Software to Evaluate Right Ventricular Volume and Function

1.9. Pulmonary Vasculature
1.9.1. Pulmonary Acceleration Time

The pulmonary artery acceleration time (PAT) should be obtained by placing the pulsed-wave Doppler sample volume 1 cm distal to the pulmonary valve leaflets in the parasternal short-axis view at the aortic root level. PAT is measured from the onset of ejection to peak ejection using the calipers online. A normal PAT should exceed 100 ms. In a study involving 29 subjects with combined IPAH and PH (of other causes), PAT was non-linearly but inversely associated with RHC-obtained PASP and PAPm. The authors demonstrated that a PAT cutoff = 90 mmHg had the best sensitivity and specificity to detect a PASP > 38 mmHg (21).


In a group of 98 patients undergoing cardiac surgery, where intraoperative transesophageal echocardiography was used while a pulmonary artery catheter was placed as part of routine care (22), the authors found that a PAT < 107 ms indicated a relatively linear relationship that could be described by the equation PAPm (mmHg) = 77 - (0.49 × PAT). The morphology of the pulsed-wave Doppler envelope is important. If the envelope has a mid-systolic notch, it generally provides indirect evidence of an elevated PASP (23).


1.10. Estimation of Pulmonary Artery Systolic Pressure

PASP should be estimated routinely irrespective of the referral reasons if there is a detectable tricuspid regurgitation. In PAH, suspicion of the diagnosis often starts with the documentation of an elevated PASP. It is estimated using the max tricuspid regurgitation velocity from all 3 views, namely RV inflow and the parasternal short-axis and apical 4-chamber views. (The maximum transtricuspid gradient should be taken using the modified Bernoulli equation.) This peak gradient is then added up with the estimated central venous (RA) pressure. RA pressure by standard echocardiography is estimated through the diameter of the inferior vena cava (IVC) and its respiratory collapsibility. The American Society of Echocardiography (9) states that simplicity and uniformity of reporting requires that specific values of RA pressure, rather than ranges, be employed to determine PASP. In addition, an IVC diameter < 2.1 cm collapsing > 50% with a sniff denotes a normal RA pressure = 3 mmHg (range = 0 - 5 mmHg), while an IVC diameter > 2.1 cm collapsing < 50% with a sniff indicates a high RA pressure = 15 mmHg (range = 10 - 20 mmHg). In scenarios where the IVC diameter and collapse fail to fit this paradigm, an intermediate value = 8 mmHg (range = 5 - 10 mmHg) may be drawn upon. This author suggests adding > 20 mm (RA pressure) to the peak transtricuspid gradient if the hepatic veins are dilated with the systolic reversal of the flow by pulsed-wave Doppler in addition to IVC dilatation and reduced respiratory responsiveness. A note of caution though is that the numbers should match each other generally in all cases. For example, it is expected that the RA would be dilated in case the pressure is reaching 30 mmHg, except in acute pulmonary embolism. The correlation between RHC-obtained and echo-Doppler-obtained PASP is usually very good, if estimated as per the guideline (11, 24).


1.11. Estimation of Pulmonary Vascular Resistance

An elevated PVR is the hallmark of PAH. Using RHC, PVR is estimated through dividing the transpulmonary pressure gradient (PAPm-PAWP) by the cardiac output. As the usual practice is to screen suspected patients with PAH using echocardiography before RHC, investigators have used different ways of noninvasive estimations of PVR. One of the most commonly cited formula was proposed by Abbas et al. (25). The formula states that PVR = TRV/VTI RVOT × 10 + 0.16, where TRV is the tricuspid regurgitation velocity and VTI RVOT is the velocity time integral of the RV outflow continuous wave envelope. One of the major drawbacks of the equation is that it does not take into account the wedge pressure, which is essential to estimate the transpulmonary gradient. However, using the equation, Ling and Marwick (26) showed how 4 different clinical scenarios, as shown in the Table 1, could be resolved bedsides differentiating RV/pulmonary vascular dysfunction due to different background diseases. The 4th scenario is most probably due to intrinsic RV dysfunction.


Table 1.
Four Possible Clinical Scenarios of Dysfunctional Right Ventricular and Pulmonary Vasculature

1.12. Right Atrium: A “Forgotten Chamber”

The RA has 3 principal functions: a reservoir function, during which the chamber receives blood from the vena cavae during ventricular systole (closed tricuspid valve); a passive conduit function during early diastole; and a booster pump function during atrial contraction during late diastole. Although generally not suitable for the echocardiographic estimation of the biplane volume (unlike in the left atrium), it is possible to quantify albeit in a single plane the minimum/maximum volumes, conduit volume, active and passive emptying fraction, expansion index, and ejection fraction. This requires a time-consuming process and it is dependent on an ECG signal of high resolution with a distinct P wave. To circumvent this time-consuming calculations, investigators have studied STE-obtained RA mechanics (reservoir strain) in PH due to left-heart failure (12) as well as in IPAH (11). Both RA strain and RA strain rate (Figures 2 and 3) have been used in the Swedish cohort and have been shown to have a good association with both PVR (reservoir strain) and PASP (booster strain) with the excellent reproducibility of the strain measures. More data are needed to adapt the STE of the RA in PAH. One disadvantage with this is the fact that to date no dedicated software algorithm has been available to study RA mechanics. However, RA area (normal < 18 cm2) and volume should be estimated as these have important diagnostic and prognostic values in PAH, regardless of etiology (Table 2).


Figure 2.
Right Atrial Strain (%) Imaging, Showing Three Mechanical Phases in a Normal Subject

Figure 3.
Right Atrial Strain Rate Imaging, Showing Three Mechanical Phases in a Normal Subject

Table 2.
Echocardiographic Markers That May Suggest Pulmonary Arterial Hypertension

2. Conclusions


PAH is a devastating disease with very high mortality. Echocardiography plays a central role in the screening and follow-up as well as in assessing the prognosis and risk stratification. Grapsa et al. (27) recently showed that moderate-to-severe tricuspid regurgitation had the greatest odds of mortality 7 years upfront. No other RHC measures actually demonstrated such a high hazard ratio! On the other hand, the study on the Stanford (USA) cohort by Haddad et al. (28) showed that a “simple heart score” consisting of RV systolic dysfunction, enlarged RA, and systolic blood pressure < 110 mmHg could be very useful for predicting the outcome in PAH. The authors also reported that this score was almost similar to the NIH (Natational Institutes of Health) and REVEAL scores, indicating the validity of the data obtained in the study.


As PVR is the ultimate hallmark of PAH, newer mathematical models should be constructed and use for example, RA reservoir strain because the Abbas formula (25) does not take into account the PAWP. This is probably the reason why the Abbas formula had a poor correlation with the RH-obtained data in the Uppsala cohort (21).


Finally, the basics of the qualitative and quantitative assessment of the right-sided heart using the existing 2D and standard echocardiography to accurately estimate PASP, RA, RV remodeling, RV systolic function alone or in combination with TAPSE, FAC (%), and TDI-derived S' are the key elements that should be meticulously obtained, recorded, and reported. The STE assessment of RA mechanics is optional at this stage but should be encouraged, even though dedicated 2D-based right-sided software is not yet available. Despite 2 recently published wonderful studies using 3DSTE in PAH (29, 30) the modality is not available except for research purposes as of today. When more widely available and normative data are published, 3DSTE should be used as a complement to the long established 2D and standard Doppler echocardiography. Modern-day echocardiography should also be used as a strong prognostic tool (7, 8, 28) beyond the conventional use as a screening tool in PAH. Only in very selective cases such as to study the delayed enhancement of the RV and the contrast enhancement of the pulmonary artery (angiography) could cardiac magnetic resonance imaging be considered for diagnostic and prognostic purposes (31). The ejection fraction of the RV has not been studied or validated extensively. Whenever needed, such as before transplantation, RVEF could be drawn upon via the uniplane Simpson method using 2D echocardiography or radionuclide methods. Isotope-independent cardiac magnetic resonance and 3D echocardiography may also provide RVEF quite accurately as the radionuclide method. Unpublished data have shown the great potential of a 3D algorithm that can generate RVEF, TAPSE, FAC (%), and RV global strain from a full volume data set, showing an excellent correlation between 3D and cardiac magnetic resonance-obtained RVEF. Its value in PAH has yet to be investigated.

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Table 1.

Four Possible Clinical Scenarios of Dysfunctional Right Ventricular and Pulmonary Vasculature

Scenarios Description
1 Right ventricular dysfunction with an increased pulmonary artery systolic pressure and pulmonary vascular resistance (pulmonary arterial hypertension )
2 Preserved right ventricular systolic function with an increased pulmonary artery systolic pressure and a normal pulmonary vascular resistance (left ventricular disease)
3 Right ventricular dysfunction with a normal pulmonary artery systolic pressure and an increased pulmonary vascular resistance (low stroke output)
4 Right ventricular dysfunction with a normal pulmonary artery systolic pressure and pulmonary vascular resistance (e.g., intrinsic right ventricular disease)

Table 2.

Echocardiographic Markers That May Suggest Pulmonary Arterial Hypertension

Simple Echocardiographic Signs That May Indicate Referral For Right-Heart Catheterization to Rule Out Idiopathic Pulmonary Arterial Hypertension (After Ruling Out Left Ventricular Disease or Shunts) in Patients With Unexplained Dyspnea
1 Peak tricuspid regurgitation velocity > 3.5 m/s, irrespective of the inferior vena cava diameter with the alteration of the septal curvature and an estimated pulmonary artery systolic pressure > 50 mm Hg
2 Dilated right ventricle (from any 2 levels) with fractional area change < 35%
3 Significant pulmonary regurgitation
4 Pulmonary artery acceleration time < 90 - 00 ms with mid-systolic notching of the PA ejection envelope
5 E/E´ ratio (E´ = the average of septal and lateral E´) < 8 - 10

Figure 1.

Dedicated Software to Evaluate Right Ventricular Volume and Function

Figure 2.

Right Atrial Strain (%) Imaging, Showing Three Mechanical Phases in a Normal Subject

Figure 3.

Right Atrial Strain Rate Imaging, Showing Three Mechanical Phases in a Normal Subject