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I

General Principles for Echocardiographic Assessment of LV Diastolic Function

The application of the guidelines starts with taking note of the clinical data, heart rate, blood pressure, 2D and Doppler findings with respect to LV volumes/wall thickness, ejection fraction (EF), LA volume, presence and severity of mitral valve disease as well as the underlying rhythm. The guidelines are not necessarily applicable to children or in the perioperative setting. This is an important first step because there may be recommendations that are specific to the underlying pathology. Second, the quality of the Doppler signal as well as the limitations for each parameter should be carefully examined. If a Doppler signal is suboptimal, that signal should not be used in formulating conclusions about LV diastolic function ( Figures 2 and 3 ). Third, the presence of a single measurement that falls within the normal range for a given age group does not necessarily indicate normal diastolic function (see below). Given the several hemodynamic factors that affect each signal, some measurements may fall in the normal range despite the presence of diastolic dysfunction, and none of the indices should be used in isolation. Therefore, consistency between two or more of the indices should be relied upon in an individual patient. The echocardiographic indices of diastolic function should always be interpreted in a wider context that includes clinical status and the other 2D and other Doppler parameters. Although often overlooked in reporting, the underlying pathology shown by 2D and color Doppler is critical to reaching the correct conclusions about LV diastolic function. For example, the algorithm for estimation of LV filling pressures is less likely to be helpful in a patient with normal vital signs and normal 2D and Doppler findings.

Tissue Doppler recordings of septal mitral annular velocities. In (A) , Doppler settings and sample volume location are optimal, whereas in (B) the sample volume is placed in the ventricular septum (not annulus). Doppler setting are suboptimal in (C) with low gain and in (D) with high filter.

Tissue Doppler recordings of lateral mitral annular velocities. In (A) , Doppler sample volume is located in part in LV cavity. In (B) the sample volume is in basal segment of lateral wall, in (C) the location is partly outside the heart altogether, and in (D) it is located in the left atrium above the mitral annulus.

With respect to the grading of LV diastolic dysfunction, it is the recommendation of the writing group to determine the grade of diastolic function based on the presence or absence of elevated LV filling pressures as a first step. While useful in some cases, the lower feasibility and reproducibility of flow propagation velocity (Vp) and time intervals (T _E-e′ ) led the writing group to place less emphasis on their routine acquisition and analysis. The writing group strived to recommend algorithms that are applicable to most patients with cardiac disease. Notwithstanding this effort, the algorithms are not 100% accurate. For the most successful application of the guidelines, it is incumbent on the echocardiographer to have a solid understanding of the physiologic rationale behind each variable, the situations that make any given variable less reliable, and the technical aspects and acquisition and analysis of Doppler and 2D signals.

The following sections are applicable to the general population of patients seen in an echocardiography laboratory but not in the presence of specific diseases or rhythm disorders, which are discussed separately later on in the document.

I

General Principles for Echocardiographic Assessment of LV Diastolic Function

The application of the guidelines starts with taking note of the clinical data, heart rate, blood pressure, 2D and Doppler findings with respect to LV volumes/wall thickness, ejection fraction (EF), LA volume, presence and severity of mitral valve disease as well as the underlying rhythm. The guidelines are not necessarily applicable to children or in the perioperative setting. This is an important first step because there may be recommendations that are specific to the underlying pathology. Second, the quality of the Doppler signal as well as the limitations for each parameter should be carefully examined. If a Doppler signal is suboptimal, that signal should not be used in formulating conclusions about LV diastolic function ( Figures 2 and 3 ). Third, the presence of a single measurement that falls within the normal range for a given age group does not necessarily indicate normal diastolic function (see below). Given the several hemodynamic factors that affect each signal, some measurements may fall in the normal range despite the presence of diastolic dysfunction, and none of the indices should be used in isolation. Therefore, consistency between two or more of the indices should be relied upon in an individual patient. The echocardiographic indices of diastolic function should always be interpreted in a wider context that includes clinical status and the other 2D and other Doppler parameters. Although often overlooked in reporting, the underlying pathology shown by 2D and color Doppler is critical to reaching the correct conclusions about LV diastolic function. For example, the algorithm for estimation of LV filling pressures is less likely to be helpful in a patient with normal vital signs and normal 2D and Doppler findings.

Tissue Doppler recordings of septal mitral annular velocities. In (A) , Doppler settings and sample volume location are optimal, whereas in (B) the sample volume is placed in the ventricular septum (not annulus). Doppler setting are suboptimal in (C) with low gain and in (D) with high filter.

Tissue Doppler recordings of lateral mitral annular velocities. In (A) , Doppler sample volume is located in part in LV cavity. In (B) the sample volume is in basal segment of lateral wall, in (C) the location is partly outside the heart altogether, and in (D) it is located in the left atrium above the mitral annulus.

With respect to the grading of LV diastolic dysfunction, it is the recommendation of the writing group to determine the grade of diastolic function based on the presence or absence of elevated LV filling pressures as a first step. While useful in some cases, the lower feasibility and reproducibility of flow propagation velocity (Vp) and time intervals (T _E-e′ ) led the writing group to place less emphasis on their routine acquisition and analysis. The writing group strived to recommend algorithms that are applicable to most patients with cardiac disease. Notwithstanding this effort, the algorithms are not 100% accurate. For the most successful application of the guidelines, it is incumbent on the echocardiographer to have a solid understanding of the physiologic rationale behind each variable, the situations that make any given variable less reliable, and the technical aspects and acquisition and analysis of Doppler and 2D signals.

The following sections are applicable to the general population of patients seen in an echocardiography laboratory but not in the presence of specific diseases or rhythm disorders, which are discussed separately later on in the document.

II

Diagnosis of Diastolic Dysfunction in the Presence of Normal LVEF

Differentiation between normal and abnormal diastolic function is complicated by overlap between Doppler indices values in healthy individuals and those with diastolic dysfunction. Furthermore, normal aging is associated with a number of changes in the heart and vascular system, especially slowing of LV relaxation which may lead to diastolic dysfunction. Therefore, filling patterns in the elderly resemble those observed in mild diastolic dysfunction in younger patients (40–60 years), and age should be taken into account when evaluating diastolic function variables.

The mechanisms of diastolic dysfunction in healthy sedentary elderly appear to be due in part to increased LV stiffness compared with younger individuals. Presumably there is also slowing of myocardial relaxation in the elderly, which can account for the decrease in mitral E/A ratio and in e′ velocity ( Figure 4 ), but the data on aging and relaxation are not entirely consistent across the studies. Furthermore, apparently healthy older individuals may have undetected coronary artery disease or other subclinical disorders that could lead to the wide normal ranges. Some indices, however, are less age dependent, and this includes E/e′ ratio, which is very rarely >14 in normal individuals, changes in mitral inflow velocities with Valsalva maneuver, and the difference in duration between pulmonary vein Ar velocity and mitral A velocity. The Valsalva maneuver can help distinguish normal LV filling from pseudonormal filling (and whether restrictive LV filling is reversible or not) because a decrease in E/A ratio of ≥50%, not caused by E and A velocities fusion, is highly specific for increased LV filling pressures and supports the presence of diastolic dysfunction ( Figures 5 and 6 ). The procedure should be standardized by continuously recording mitral inflow using pulsed-wave Doppler for 10 sec during the straining phase of the maneuver. Likewise, an increase in pulmonary vein Ar velocity duration versus mitral A duration (Ar-A) is consistent with increased LVEDP and diastolic dysfunction. Pulmonary artery systolic pressure (PASP), provided pulmonary vascular disease is excluded, can identify patients with increased LV filling pressures as resting values for estimated PASP are relatively age independent ( Table 3 ). In many patients, LV and LA structural changes may help differentiate between normal and abnormal diastolic function. Similar to LA enlargement in the absence of chronic atrial arrhythmia, which is often a marker of long-term or chronic elevation of LAP, pathologic LV hypertrophy is usually associated with increased LV stiffness and diastolic dysfunction. Furthermore, in patients with heart failure with preserved EF (HFpEF), LV global longitudinal function is often impaired and thus may be used to differentiate between normal and abnormal myocardial function. Although not an index of LV diastolic function, abnormal LV longitudinal systolic function can be detected by measurements of the mitral annular plane systolic excursion using M-mode, tissue Doppler–derived mitral annulus systolic velocity, and LV global longitudinal strain (GLS) by speckle-tracking. This approach has not been widely tested, but in patients with normal EFs and inconclusive data after evaluating diastolic filling, the finding of impaired GLS and reduced s′ velocity can be used as an indication of myocardial dysfunction. The reduced longitudinal strain in patients with HFpEF is consistent with several studies that have demonstrated reduced systolic mitral annular velocity in this patient population. It is also consistent with the fact that LV systolic and diastolic functions are tightly coupled.

The figure shows the three independent determinants of e′, which are LV relaxation, restoring forces, and lengthening load. Rate of relaxation reflects decay of active fiber force. Restoring forces which account for diastolic suction, are illustrated by an elastic spring which is compressed to a dimension ( L _min ) less than its resting length ( L ₀ ) and recoils back to resting length when the compression is released. Lengthening load is the pressure in the left atrium at mitral valve opening, which “pushes” blood into the left ventricle and thereby lengthens the ventricle. The figure is based on data from Opdahl et al .

Valsalva maneuver in a patient with grade II diastolic dysfunction. At baseline, E/A ratio is 1.3 ( left ) and decreases to 0.6 (impaired relaxation pattern) with Valsalva.

Continuous recording of mitral inflow during standardized Valsalva maneuver for 10 sec showing the decrease in E/A ratio with straining, which is consistent with elevated LV filling pressures.

In summary, the following four variables should be evaluated when determining whether LV diastolic function is normal ( Figure 7 ) or abnormal. The presence of several abnormal findings as well as cutoff values with high specificity for myocardial disease is recommended to decrease false positive diagnoses of diastolic dysfunction. The four recommended variables and their abnormal cutoff values are annular e′ velocity (septal e′ < 7 cm/sec, lateral e′ < 10 cm/sec), average E/e′ ratio > 14, LA maximum volume index > 34 mL/m ² , and peak TR velocity > 2.8 m/sec. On the basis of the writing group’s collective expert opinion, average E/e′ ratio is recommended for simplification. Although E/e′ ratio may be obtained at septal or lateral annulus, and different values exist because of the normally higher lateral annular velocities, an average E/e′ ratio > 14 is used throughout this document and is consistent with recent studies in normal subjects. It is recognized that at times only the lateral e′ or septal e′ velocity is available and clinically valid and in these circumstances a lateral E/e′ ratio > 13 or a septal E/e′ > 15 is considered abnormal. The latter sentence applies to laboratories that acquire only septal or lateral velocities. The above are general guidelines for annular velocities and ratios. Age appropriate cutoff values, when available, should be considered when evaluating older individuals. LA maximum volume index is recommended and not LA anteroposterior diameter by M-mode, as LA enlargement can occur in the medial-lateral and superior-inferior directions only, resulting in an increased LA volume while the chamber anteroposterior diameter is still within the normal range.

Example of normal findings from a young subject. Left shows normal LV size in parasternal long-axis view, with a normal mitral inflow pattern and E/A ratio > 1 in middle panel . Lateral e′ velocity is normal at 12 cm/sec ( left ).

LV diastolic function is normal if more than half of the available variables do not meet the cutoff values for identifying abnormal function. LV diastolic dysfunction is present if more than half of the available parameters meet these cutoff values. The study is inconclusive if half of the parameters do not meet the cutoff values ( Figure 8 A). For example, a 60-year-old patient with a septal e′ velocity of 6 cm/sec, septal E/e′ ratio of 10, LA maximum volume index of 30 mL/m ² , but no recorded TR signal has normal diastolic function.

(A) Algorithm for diagnosis of LV diastolic dysfunction in subjects with normal LVEF. (B) Algorithm for estimation of LV filling pressures and grading LV diastolic function in patients with depressed LVEFs and patients with myocardial disease and normal LVEF after consideration of clinical and other 2D data.

III

Echocardiographic Assessment of LV Filling Pressures and Diastolic Dysfunction Grade

The key variables recommended for assessment of LV diastolic function grade include mitral flow velocities, mitral annular e′ velocity, E/e′ ratio, peak velocity of TR jet, and LA maximum volume index ( Figure 8 B). Supplementary methods are pulmonary vein velocities and as a means to identify mild reduction in systolic function, LV GLS by speckle-tracking echocardiography (STE). Because patients with reduced LVEFs also have impaired diastolic function (examples shown in Figures 9–11 for heart failure with reduced EF [HFrEF]), the evaluation has a different focus than in patients with normal LVEF (≥50%) (examples shown in Figures 12–15 for HFpEF). The main reason for evaluating diastolic function in patients with reduced EFs is to estimate LV filling pressure. As in several other patient groups, it is important to look for consistency between the different parameters. When using such an integrated approach, a reliable estimate of LV filling pressure can be achieved in most patients. Given the presence of situations in which LAP and LVEDP are different and because LAP is the pressure that relates better with mean PCWP and thus pulmonary congestion symptoms at the time of the echocardiographic examination, the algorithm is presented with the premise of estimating mean LAP. The approach starts with mitral inflow velocities and is applied in the absence of atrial fibrillation (AF), significant mitral valve disease (at least moderate mitral annular calcification [MAC], any mitral stenosis or mitral regurgitation [MR] of more than moderate severity, mitral valve repair or prosthetic mitral valve), LV assist devices, left bundle branch block, and ventricular paced rhythm.

LV and RV pressure recordings along with mitral inflow and tricuspid inflow obtained from a patient with dilated cardiomyopathy. LV pressure recordings are shown to the left with red arrows denoting LV pre-A pressure and LVEDP. Both are increased with LV pre-A pressure at 19 mm Hg and LVEDP at 30 mm Hg. Mitral inflow ( top ) shows restrictive filling pattern. In comparison, RV pressure recordings ( right ) show RV pre-A pressure at 8 mm Hg and RV end-diastolic pressure (RVEDP) at 12 mm Hg. The corresponding tricuspid inflow pattern ( bottom ) shows an impaired relaxation pattern. In the presence of normal LV and RV filling pressures and myocardial dysfunction, both tricuspid inflow and mitral inflow reveal an impaired relaxation pattern. Thus, the presence in this case of an impaired relaxation pattern for tricuspid inflow and a restrictive filling pattern for mitral inflow supports the conclusion that LV filling pressures are elevated. Abbreviations as in other figures.

Mitral inflow ( left ) and pulmonary venous flow ( right ) from a patient with HFrEF. Notice the increased E/A ratio >2 and reduced S/D ratio in pulmonary venous flow. Both findings are consistent with increased LAP in this patient population.

Septal tissue Doppler velocities from a patient with HFrEF and ventricular dyssynchrony. Mitral annular e′ (early diastolic annular velocity) should be distinguished from the biphasic velocity during isovolumic relaxation (IVR) period. Mitral annular late diastolic velocity (a′) follows the “P” wave. Isovolumic contraction velocity (IVC) is biphasic. Systolic ejection velocity (s′) follows IVC velocity and precedes IVR velocity.

( Left ) Mitral inflow from a patient with HFpEF. Mitral inflow pattern is consistent with elevated LV filling pressures. Notice the abbreviated mitral A velocity with short duration. DT of mitral E velocity (Mdt) measured at 200 msec. This is seen in patients with markedly delayed LV relaxation such that LV diastolic pressure continues to decline after mitral valve opening. ( Right ) Pulmonary venous flow from the same patient. Notice the decreased S/D ratio and the increased amplitude and velocity of Ar signal consistent with increased LVEDP. Abbreviations as in other figures.

Mitral inflow from a patient with hypertensive heart disease with normal EF. Patient has LV hypertrophy and a moderately enlarged left atrium. Mitral inflow shows pseudonormal LV filling pattern consistent with elevated LV filling pressures and grade II diastolic dysfunction.

Mitral inflow ( left ) and IVRT ( right ) from another patient with HFpEF and heart rate 60 beats/min. E velocity was 96 cm/sec with A velocity of 65 cm/sec. Mid-diastolic flow (L velocity) is present because of the slow and impaired LV relaxation and the increased LAP. The arrows in the right panel point to IVRT between aortic valve closure and mitral valve opening. IVRT was short at 48 msec consistent with increased LAP.

L velocity from a patient in sinus rhythm and increased LAP. Notice the presence of L velocity in mitral inflow and septal tissue Doppler signals ( arrows ).

The proposed algorithm is based on expert consensus and has not been validated. Because diastolic dysfunction is a result of underlying myocardial disease in patients with reduced or preserved LVEF, a rather similar approach can be considered in these populations. When the mitral inflow pattern shows an E/A ratio ≤ 0.8 along with a peak E velocity of ≤50 cm/sec, then mean LAP is either normal or low. The corresponding grade of diastolic dysfunction is grade I. When the mitral inflow pattern shows an E/A ratio ≥2, LA mean pressure is elevated and grade III diastolic dysfunction is present. DT is usually short in these patients (<160 msec) but in some patients it can exceed 160 msec in the presence of an E velocity > 120 cm/sec as it takes a longer time for a higher E velocity to decelerate. In this situation, the writing group recommends using only the E/A ratio in the classification scheme. On the other hand, mitral DT should be used for assessment of LV diastolic function in patients with recent cardioversion to sinus rhythm who can have a markedly reduced mitral A velocity because of LA stunning at the time of the echocardiographic examination, thus leading to an E/A ratio ≥ 2 despite the absence of elevated LV filling pressures ( Figure 16 ). Of note, in young individuals (<40 years of age), E/A ratios > 2 may be a normal finding, and therefore in this age group other signs of diastolic dysfunction should be sought. Importantly, normal subjects have normal annular e′ velocity which can be used to verify the presence of normal diastolic function.

LA stunning after cardioversion. On the day of the cardioversion, LA stunning leads to markedly reduced mitral A velocity of 19 cm/sec and an apparent “restrictive LV filling” on the basis of mitral E/A ratio. Three days later, LA function improves with increased A velocity and a decreased E/A ratio consistent with impaired LV relaxation but normal LV filling pressures.

When mitral inflow shows an E/A ≤ 0.8 and the peak E velocity is >50 cm/sec, or if the E/A ratio is >0.8 but <2, other signals are necessary for accurate evaluation. We recommend the following parameters: peak velocity of TR jet by CW Doppler obtained from multiple views, E/e′ ratio and LA maximum volume index. A TR jet peak velocity > 2.8 m/sec supports the presence of elevated LV filling pressures, and the same conclusion can be reached when E/e′ ratio is elevated. In patients in whom one of the three main criteria is not available, the ratio of pulmonary vein peak systolic to peak diastolic velocity or systolic time-velocity integral to diastolic time-velocity integral < 1 supports the presence of elevated LV filling pressures. In healthy young people (<40 years of age), pulmonary venous S/D ratio can be <1, but the normality of findings including mitral annular e′ velocity and LA maximum volume index should rarely cause confusion. Importantly, among the above mentioned parameters, the peak velocity of TR jet by CW Doppler provides a direct estimate of PASP when combined with right atrial pressure. Because it is uncommon to have primary pulmonary arterial disease coexisting with HFrEF, an elevated PASP supports the presence of elevated LAP.

If all three parameters are available for interpretation and only one of three meets the cutoff value, then LAP is normal and there is grade I diastolic dysfunction. If two of three or all three available parameters meet the corresponding cutoff values then LAP is elevated and there is grade II diastolic dysfunction. If only one parameter is available, LAP and grade of diastolic dysfunction should not be reported and likewise if there is discrepancy between the only two available parameters. The assessment of LV filling pressures is important in patients with HFrEF as it can successfully guide medical treatment.

In patients with preserved EFs, the same initial evaluation of clinical presentation and 2D and color Doppler echocardiographic findings such as LVEF, regional wall motion abnormalities, LV hypertrophy, LA maximum volume index and significant mitral valve disease is performed to aid the assessment of LV diastolic function. Cardiac structural as well as functional information should be used when assessing diastolic function in patients with preserved EFs. In particular an enlarged LA that is clearly larger than the right atrium in the optimally aligned apical four-chamber view is strongly suggestive of chronically elevated LV filling pressure, provided conditions such as anemia, atrial arrhythmias and mitral valve disease can be excluded. Athletes may also have enlarged atria without increased LV filling pressures. However, a normal LA volume index does not exclude the presence of diastolic dysfunction when other findings are consistent with its presence. In particular, a normal LA volume is often noted in patients in the earliest stage of diastolic dysfunction and in situations with an acute increase in LV filling pressures. For LV hypertrophy (most reliably confirmed by LV mass that exceeds gender-specific normal range ), the finding of pathologic LV hypertrophy is consistent with diastolic dysfunction. Elevated PASP calculated from the TR jet ( Figure 17 ) is strongly suggestive of elevated LV filling pressure unless pulmonary parenchymal or vascular disease is known to be present.

TR velocity (3.3 m/sec) by CW Doppler ( left ) and hepatic venous flow ( right ) from a patient with HFpEF. RV–to–right atrial pressure gradient was 43 mm Hg and hepatic venous flow showed predominant forward flow during diastole (D), consistent with elevated right atrial pressure (10–15 mm Hg). Thus, PASP was estimated at 53 to 58 mm Hg. In normal elderly subjects without cardiac disease, predominant forward flow in hepatic veins occurs during systole. As right atrial mean pressure increases, flow pattern shifts so most flow occurs during diastole. Furthermore, the atrial reversal signal (Ar) that occurs because of right atrial contraction generating a positive pressure gradient between the right atrium and the hepatic veins increases in amplitude and duration with increasing RA pressure as seen in this recording.

(Nagueh SF, Kopelen HA, Zoghbi WA. Relation of mean right atrial pressure to echocardiographic and Doppler parameters of right atrial and right ventricular function. Circulation 1996;93:1160–9; Rudski LG, Lai WW, Afilalo J, et al. Guidelines for the echocardiographic assessment of the right heart in adults: a report from the American Society of Echocardiography endorsed by the European Association of Echocardiography, a registered branch of the European Society of Cardiology, and the Canadian Society of Echocardiography. J Am Soc Echocardiogr 2010;23:685–713).

Similar to patients with depressed EFs, LAP is likely normal in the presence of an E/A ratio ≤ 0.8 along with a peak E velocity of ≤50 cm/sec in patients with structural heart disease and normal EF. The corresponding grade of diastolic dysfunction is grade I. In patients with an E/A ≤ 0.8 along with a peak E velocity of >50 cm/sec, or an E/A ratio > 0.8 but < 2, additional parameters should be examined. As in patients with depressed LVEFs, these include LA maximum volume index, peak velocity of TR jet and average E/e′ ratio. Importantly, all three indices have been shown to be of value in identifying patients with HFpEF. Cutoff values for elevated LAP are average E/e′ > 14, LA maximum volume index > 34 mL/m ² and TR jet > 2.8 m/sec. Because the pulmonary venous S/D ratio often is <1 in healthy young individuals, this index is of little value in patients with normal LVEF.

When two of three or all three variables meet the cutoff threshold, mean LAP is elevated and there is grade II diastolic dysfunction. Conversely, if two of three or all three variables do not meet the cutoff threshold, then LAP is normal and grade I diastolic dysfunction is present. If one of two available parameters gives opposite information to the other signal, or if there is only one parameter with satisfactory quality for analysis, neither LAP nor diastolic grade should be reported. In the presence of an E/A ratio ≥ 2, grade III diastolic dysfunction is present. Table 4 presents a summary of the expected findings for the different grades of diastolic dysfunction.

IV

Conclusions on Diastolic Function in the Clinical Report

Although several invasive parameters of LV diastolic function such as the time constant of LV relaxation (τ) or LV chamber stiffness may be inferred or derived from Doppler echocardiographic findings, the association between invasive and noninvasive parameters is not perfect. Furthermore to date, there is no specific targeted treatment for these abnormalities that has proved useful in clinical trials. In comparison, specific comments on the status of LV filling pressures are more helpful to the referring physician in terms of narrowing a differential diagnosis. The conclusion could be one of three options: normal, elevated or cannot be determined ( Table 5 shows examples from several laboratories on reporting findings about LV diastolic function). The writing group believes it is important to include this conclusion when feasible, particularly in patients referred with symptoms of dyspnea or diagnosis of “heart failure.” In addition, the grade of LV diastolic dysfunction should be included in the reports along with the estimated LV filling pressures. The rationale for this recommendation comes from several single center and epidemiologic studies showing the independent and incremental prognostic information provided by LV diastolic dysfunction grade in several settings including HFrEF, HFpEF and acute myocardial infarction. Finally, when feasible, comparison with previous studies and comments about changes in diastolic dysfunction grade or lack thereof, should be added as this can inform treatment decisions and predict future events of admissions for heart failure and total mortality. Consideration may be given to diastolic stress testing in borderline cases (see section on diastolic stress test). Furthermore, right heart catheterization may be needed in difficult cases to determine if PCWP is elevated or if there is a discrepancy between right ventricular (RV) and LV filling pressures indicating the presence of pulmonary vascular disease.

V

Estimation of LV Filling Pressures in Specific Cardiovascular Diseases

The following sections discuss the pathophysiology of disorders with abnormal cardiac structure, valve disease and atrial arrhythmias, which modify the relationship between indices of diastolic function and LV filling pressure ( Table 6 ). In some of the disorders the algorithm outlined above has significant limitations. PASP estimated from the TR jet, however, is a valid index of LAP in all conditions mentioned, provided there is no evidence of pulmonary vascular or parenchymal disease. In the absence of AF or atrial flutter, mitral valve disease or heart transplantation, an increased LA volume with a normal appearing right atrial size is a robust indicator of elevated LAP. One significant limitation to this marker is if heart failure therapy has resulted in normalization of pressures with persistent LA dilatation. In this setting, the presence of increased TR velocity > 2.8 m/sec is suggestive of elevated LAP.

A

Hypertrophic Cardiomyopathy

A comprehensive approach is recommended for assessment of LV diastolic function and filling pressures in patients with hypertrophic cardiomyopathy (HCM) (example shown in Figure 18 ). This includes E/e′ ratio, LA volume index, pulmonary vein atrial reversal velocity, and peak velocity of TR jet by CW Doppler. In general, individual variables when used alone, have modest correlations with LV filling pressures in patients with HCM, likely related to variability in phenotype, muscle mass, amount of myocardial fiber disarray, and obstructive versus nonobstructive physiology. This leads to different combinations of altered relaxation and compliance and resultant variations of mitral inflow patterns. Aside from assessment of LV filling, 2D and Doppler indices of LV diastolic function provide incremental prognostic information in this population. In children with HCM, septal E/e′ ratio predicted adverse outcomes including death, cardiac arrest and ventricular tachycardia. There are similar results in adults with HCM, showing worse outcomes in patients with an enlarged left atrium, abnormal diastolic function detected by E/e′ ratio, or restrictive LV filling.

(A) Two-dimensional imaging of a patient with HCM ( left top ) in the parasternal long-axis view sowing systolic anterior motion of the mitral valve ( arrow ). Mitral inflow shows an E/A ratio > 1 ( right top ). Septal ( bottom left ) and lateral ( bottom right ) tissue Doppler early (e′) and late (a′) diastolic velocities are markedly reduced consistent with severely impaired LV relaxation. Average E/e′ ratio is >14, consistent with elevated mean LAP. Abbreviations as in other figures. (B) Peak TR velocity (3.42 m/sec) by CW Doppler from the same patient in (A) . Peak RV–to–right atrial systolic pressure gradient is 47 mm Hg. Thus, PASP is ≥47 mm Hg.

More recently, studies using STE have reported the association between LV systolic and diastolic strain, LA strain and LV diastolic function. Furthermore, they have provided mechanistic insights linking LV function, including torsion and untwisting, to exercise tolerance. There is growing interest in studying the relation between early diastolic vortices and LV filling in HCM. While promising, additional studies and technical developments are needed before they can be endorsed as routine measurements in patients with HCM.

• 1.
  

  Variables recommended for evaluation of diastolic function in patients with HCM are average E/e′ ratio (>14), LA volume index (>34 mL/m ² ), pulmonary vein atrial reversal velocity (Ar-A duration ≥ 30 msec), and peak velocity of TR jet by CW Doppler (>2.8 m/sec). The parameters can be applied irrespective of the presence or absence of dynamic obstruction and MR, except for patients with more than moderate MR, in whom only Ar-A duration and peak velocity of TR jet are still valid.

  
  
• 2.
  

  If more than half of the variables (total available variables three or four) meet the cutoff values, then LAP is elevated and grade II diastolic dysfunction is present. If <50% of the variables (total available variables three or four) meet the cutoff values, then LAP is normal and grade I diastolic dysfunction is present. In case of 50% discordance with two or four available variables, findings are inconclusive to estimate LAP. Estimation of LAP is not recommended if there is only parameter with a satisfactory signal.

  
  
• 3.
  

  Grade III diastolic dysfunction is present in the presence of a restrictive filling pattern and abnormally reduced mitral annular e′ velocity (septal <7 cm/sec, lateral <10 cm/sec).

Key Points

B

Restrictive Cardiomyopathy

Restrictive cardiomyopathies are composed of a heterogeneous group of heart muscle diseases including idiopathic restrictive cardiomyopathy, cardiac amyloidosis, and sarcoidosis. In the earlier stages of cardiac amyloidosis, diastolic function can vary from grade 1 diastolic dysfunction with impaired relaxation and normal LV filling pressures to grade 2 (pseudonormalization). In later stages, grade 3 diastolic dysfunction occurs when LV relaxation is impaired along with markedly elevated LV filling pressures. There has been a gradual evolution of the diastolic function techniques applied in studying these patients, initially using mitral inflow and pulmonary vein flow, to tissue Doppler and now STE, which can be used to measure strain and strain rate. The advanced stages of restrictive cardiomyopathy, are characterized by typical restrictive physiology with a dip and plateau pattern for early diastolic LV pressure changes with time, mitral inflow E/A ratio > 2.5, DT of E velocity < 150 msec, isovolumic relaxation time (IVRT) < 50 msec, decreased septal and lateral e′ velocities (3–4 cm/sec), but with a higher lateral e′ compared with septal e′ velocity (unlike constrictive pericarditis, in which septal e′ is often higher, or annulus reversus), E/e′ ratio > 14, as well as a markedly increased LA volume index (>50 mL/m ² ) . Figure 19 shows a validated algorithm from the Mayo Clinic comparing constrictive pericarditis with restrictive cardiomyopathy. The presence of a normal annular e′ velocity in a patient referred with heart failure diagnosis should raise suspicion of pericardial constriction.

Algorithm comparing constrictive pericarditis and restrictive cardiomyopathy. Note restriction is associated with elevated E/A ratio, short DT and decreased mitral annular velocity (<6 cm/sec). The figure is based on data from Welch TD, Ling LH, Espinosa RE, et al. Echocardiographic diagnosis of constrictive pericarditis: Mayo Clinic criteria. Circ Cardiovasc Imaging 2014;7:526–34.

Grade 3 diastolic dysfunction is associated with a poor outcome in patients with restrictive cardiomyopathy. It is important to make the distinction between restrictive LV filling, which can occur with other diseases such as coronary artery disease, dilated cardiomyopathy and HCM, and restrictive cardiomyopathy. STE of LV myocardium in patients with cardiac amyloidosis has shown a distinctive phenotype of apical sparing ( Figure 20 ) using a polar plot of LV longitudinal strain compared with hypertensive heart disease, HCM, and aortic stenosis. Similar to tissue Doppler imaging, the ratio of LV free wall strain to LV septal strain by STE is about 1 in patients with restrictive cardiomyopathy, whereas it is usually <1 in patients with constriction because of less deformation of the LV anterolateral wall compared with the LV septum.

• 1.
  

  Patients with early disease usually have grade I diastolic dysfunction that progresses to grade II as the severity of the disease advances.

  
  
• 2.
  

  In patients with advanced disease, grade III diastolic dysfunction is present and is characterized by mitral inflow E/A ratio > 2.5, DT of E velocity < 150 msec, IVRT < 50 msec, and decreased septal and lateral e′ velocities (3–4 cm/sec).

  
  
• 3.
  

  Patients with constrictive pericarditis usually have septal e′ velocity higher than lateral e′ velocity, or annulus reversus, and E/e′ ratio should not be used to estimate LV filling pressures in patients with constrictive pericarditis.

Key Points

Restrictive physiology in advanced cardiac amyloidosis showing ( left upper ) elevated E/A ratio and short DT, decreased mitral annular septal velocities ( left lower ) and lateral velocities ( right lower ) and apical sparing on deformation imaging ( right upper ).

C

Valvular Heart Disease

i

Mitral Stenosis

In this condition, transmitral blood flow velocities and mitral annular dynamics are largely determined by the degree of valvular disease and therefore of limited value as indicators of LV disease. Typically, patients with mitral stenosis have normal or reduced LV diastolic pressures, except for the rare occurrence of coexisting myocardial disease. The same hemodynamic findings are present in patients with other etiologies of LV inflow obstruction, such as prosthetic mitral valve, large LA tumor, cor triatriatum sinustrum, and congenital mitral valve stenosis. Nevertheless, a semiquantitative estimation of instantaneous LAP can be provided in early and late diastole by Doppler variables. The shorter the IVRT (corresponds to time interval between second heart sound and mitral valve opening snap) and the higher the peak E-wave velocity, the higher the early diastolic LAP. LAP is significantly elevated at end-diastole if the mitral A velocity remains >1.5 m/sec at this point.

The time interval between onset of mitral E velocity and annular e′ velocity can be applied to estimate LV filling pressures in patients with mitral valve disease. In the presence of impaired LV relaxation, the e′ velocity is not only reduced but also delayed such that it occurs at the LA-LV pressure crossover point. In comparison, mitral E velocity occurs earlier with elevated LAP. Thus the time interval between the onset of mitral E velocity and annular e′ velocity is prolonged and can correct for the effect of LV relaxation on IVRT. IVRT/T _E–e′ ratio correlates well with mean PCWP and LAP in patients with mitral stenosis ( Figure 21 ). However, the E/e′ ratio is not useful.

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