|
 
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| REVIEW ARTICLE |
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| Year : 2023 | Volume
: 7
| Issue : 2 | Page : 101-108 |
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Left Ventricular Strain in Heart Failure with Preserved Ejection Fraction
Madhu Shukla, Jagdish Chander Mohan
Department of Cardiology, Institute of Heart and Vascular Diseases, Jaipur Golden Hospital, New Delhi, India
| Date of Submission | 13-Apr-2023 |
| Date of Decision | 20-Apr-2023 |
| Date of Acceptance | 21-Apr-2023 |
| Date of Web Publication | 12-Jun-2023 |
Correspondence Address:
Prof. Jagdish Chander Mohan
A51, Hauz Khas, New Delhi - 110 016
India
 Source of Support: None, Conflict of Interest: None
DOI: 10.4103/jiae.jiae_22_23
Heart failure with preserved ejection fraction (HFpEF) is a heterogeneous clinical syndrome of effort intolerance based on structural and functional abnormalities of the cardiovascular system (CVS). Its prevalence is increasing progressively in comparison to that of heart failure with reduced ejection fraction due to aging, obesity, metabolic stress, and hypertension. Multiple domains of the CVS and peripheral organs have reduced reserve capacity and increased stiffness in patients with HFpEF. This high-gain CVS exhibits increased filling pressures and reduced filling volumes under stress despite the left ventricular ejection fraction, commonly estimated parameter of contractile performance, being normal, i.e., >50%. The cost of increasing cardiac output in terms of left ventricular filling pressures is increased and their relationship shows an upward and more left-directed slope due to reduced ventricular and arterial compliance. At the tissue level, there is myocytic hypertrophy and increased extracellular matrix with capillary rarefaction. There are many phenogroups of HFpEF based on the heart's ability to secrete natriuretic peptides, degree of dysmetabolism, age, renal function, body fat, rhythm, underlying etiology, and subclinical systolic dysfunction. The left ventricle may be pressure-loaded, volume-loaded, or have equipoise with regard to remodeling. Myocardial performance estimated by parameters other than those based on distance or volume displacement may be abnormal in more than half of the patients underlying the presence of subtle systolic dysfunction. This review looks at myocardial performance and characteristics in HFpEF by deformation imaging using acoustic speckle tracking and its diagnostic and prognostic significance. Research points toward the utility of global longitudinal strain in early detection, biological characterization, and risk stratification of HFpEF. Echocardiographic speckle-tracking-based longitudinal strain analysis represents a method of relatively high value and for sensitive phenotyping of HFpEF which is yet to be utilized optimally. Other dimensions of strain, although extensively studied in HFpEF, do not add much value. The focus is on systolic deformation since there is limited utility of diastolic strain and its rate.
Keywords: Heart failure with preserved ejection fraction, left ventricular ejection fraction, longitudinal strain
How to cite this article:
Shukla M, Mohan JC. Left Ventricular Strain in Heart Failure with Preserved Ejection Fraction. J Indian Acad Echocardiogr Cardiovasc Imaging 2023;7:101-8 |
How to cite this URL:
Shukla M, Mohan JC. Left Ventricular Strain in Heart Failure with Preserved Ejection Fraction. J Indian Acad Echocardiogr Cardiovasc Imaging [serial online] 2023 [cited 2023 Sep 27];7:101-8. Available from: https://jiaecho.org/text.asp?2023/7/2/101/378417 |
| Introduction | |  |
A classic heart failure with preserved ejection fraction (HFpEF) patient has symptoms and signs of heart failure, structural alterations in the left atrium and/or the left ventricle, left ventricular ejection fraction (LVEF) >50%, and objective evidence of pulmonary and/or systemic venous congestion [Figure 1].[1] The conventional concept of HFpEF does not include heart failure with EF >50% due to pericardial or valvular causes, amyloidosis, primary right heart failure, or high-output states. However, its purer form should also exclude other confounders such as atrial fibrillation, renal dysfunction, and subclinical ischemia. Pathophysiology of HFpEF is complex and may involve diastolic dysfunction, contractile impairment, left atrial dysfunction, and pericardial restraint due to subepicardial fat, sarcopenia, endothelial dysfunction, ventriculovascular uncoupling, etc. [Figure 2].[2] Based upon diagnostic criteria, it would appear that there should be systolic–diastolic uncoupling in HFpEF. The tight relationship between systolic contraction and early diastolic recoil is a novel and load-independent parameter of systolic–diastolic coupling.[3] By normalizing early diastolic recoil to the preceding systolic contraction, the quantum of systolic–diastolic coupling can be predicted [Figure 3]. This relationship expressed as early diastolic mitral annulus excursion to systolic mitral annular excursion ratio (which is independent of left atrial pressure) is reduced in HFpEF indicating uncoupling more than that seen as a result of normal aging. The underpin of HFpEF is obviously, by definition, disproportionate systolic–diastolic uncoupling. Normal or near normal stroke work and preload recruitable stroke work in the presence of diastolic dysfunction and elevated left ventricular (LV) filling pressures in HFpEF have been cited as an example of systolic–diastolic uncoupling.[2] This uncoupling is not universal and in a heterogeneous syndrome such as HFpEF, there may be a significant number of patients who show near normal systolic–diastolic coupling if all known parameters of systolic function such as tissue systolic velocities, longitudinal strain, strain rates, and systolic reserve are included. In fact, physiologically, it is inconceivable that systole will dissociate from diastole. Resting ejection fraction is not synonymous with systolic function and patients with HFpEF often show reduced EF reserve on exercise due to reduced recruitable preload and impaired contractility.[2] This degree of systolic dysfunction needs to be unearthed and global longitudinal strain (GLS) may be a good parameter in this regard. Echocardiography is widely used to study structure, function, and hemodynamics in heart failure and acoustic speckle tracking provides information about myocardial strain. | Figure 1: Defining heart failure with preserved ejection fraction. LAE: Left atrial enlargement, LVEF: Left ventricular ejection fraction, LVH: Left ventricular hypertrophy
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 | Figure 2: Pathogenesis of heart failure with preserved ejection fraction, LA: Left atrium, LV: Left ventricle
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 | Figure 3: The concept of systole-diastolic coupling. Typically early diastolic excursion/MPASE ratio is 0.60 which can drop to 0.40 in heart failure with preserved ejection fraction in some but significant overlap exists. MAPSE: Mitral plane annular systolic excursion
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Let us see a few examples of real-life HFpEF patients to better understand the relevance of the issue under discussion:
| Case 1 | | |
This 68-year-old female is average built and has type 2 diabetes and hypertension. She underwent coronary angioplasty of the second obtuse marginal artery in the past and is currently having grade 3 dyspnea. Her hemoglobin is 10 g%, serum creatinine 1.3 mg% (estimated glomerular filtration rate [eGFR] 45 mL/min/1.73 m2), and N-terminal pro-brain natriuretic peptide (NT-proBNP) 133 pg/mL. On echocardiographic examination, she has no segmental wall motion abnormality; her LVEF is 62% and there is no LV hypertrophy. Her early diastolic mitral inflow velocity (E) to early diastolic mitral annular velocity (e') ratio (E/e') ratio (an indirect surrogate for filling pressure) is 20 which rises to 25 on leg raising [Figure 4]. Her LV GLS is − 20% [Figure 5]. | Figure 4: Patient 1. (a) and (b) show images at rest and on leg cycling, respectively. The resting E/e' is 20 (left upper and lower panels) which increases to 25 on leg raising (right upper and lower panels). e' is 4 cm/s which increases to 5' cm/s on leg cycling. E- early diastolic mitral inflow velocity, e'- early diastolic mitral annular velocity
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 | Figure 5: Patient 1 left ventricular GLS −20% by acoustic speckle tracking. GLS: Global longitudinal strain
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The patient has LVEF of 62% and LV GLS of −20% indicating a possibly normal systolic function in the presence of significant diastolic dysfunction and elevated filling pressures (fulfilling criteria of HFpEF). However, mitral annular systolic velocity (s') (5 cm/s against e' 4 cm/s) queers the pitch pointing toward some subtle LV systolic dysfunction coupled with significant diastolic dysfunction. Is mitral annulus s' more sensitive than other parameters of systolic dysfunction or simple age-related change? Is there reduced systolic reserve on exercise?
| Case 2 | | |
This 80-year-old female who had previous hypertension and mild renal insufficiency (eGFR 54) presented with breathless on exertion of 6-month duration. Her B-type natriuretic peptide (BNP) level is 683 pg/mL. Besides other tests, her comprehensive echocardiogram is performed including measurement of LVEF, GLS, and diastolic function. Markedly increased E/e of 25 and LVEF 60% in the presence of BNP of 683 pg/mL suggests HFpEF and GLS is − 17% [Figure 6]. | Figure 6: An 80-year-old female with LVEF 60%, E/e' 25, LAVI 30 mL/m2 and LV GLS −17%. The camel-hump appearance of transmitral pulsed-wave Doppler flow is due to merging L wave. BNP: B-type natriuretic peptide, E- early diastolic mitral inflow velocity, e'- early diastolic mitral annular velocity, GLS: Global longitudinal strain, HF: Heart failure, LA: Left atrium, LAVI: Left atrial volume index, LV: Left ventricle, LVEF: Left ventricular ejection fraction
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By consensus, a GLS of −16%–−18% is considered borderline and hence this GLS of −17% may indicate subtle systolic dysfunction. Now let us look at another case.
| Case 3 | | |
This is a 37-year-old male on maintenance hemodialysis. He has significant dyspnea on routine activities despite maintaining a reasonable hemoglobin level of 11 gm%. His echocardiogram shows a normally contracting left ventricle with an ejection fraction of 52% and a GLS of −7.2% and an average E/e' of 18 [Figure 7]. | Figure 7: Patient 3. Bull's eye map shows markedly reduced global longitudinal strain with marked regional variation despite no wall motion abnormality on grey-scale imaging. LVEF is 52%. LVEF: Left ventricular ejection fraction
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There is so much mismatch between the two parameters (LVEF and GLS) of LV function in this patient of HFpEF who does not have amyloidosis and yet have characteristics of HFpEF.
| Expanding the Concept of Subtle Systolic Dysfunction in Heart Failure with Preserved Ejection Fraction | | |
Preservation of systolic endocardial motion regardless of the shortening of individual myofibers results in LV chamber contraction and normal ejection fraction. Ejection fraction denotes chamber contraction (load-dependent) and not myocardial contractility (load-independent). Shortening of muscle fibers oriented in orthogonal directions at the inner and outer surfaces of the heart causes a reduction in the transverse axis that determines ejection fraction which is disproportionate to the mid-wall myofiber shortening, a more robust parameter of contractility.[4]
Despite ejection fraction being >50%, HFpEF is often associated with mild LV systolic dysfunction and dramatic limitations in systolic reserve capacity during stress, with blunted increase in ejection fraction.[2],[4] HFpEF is usually characterized by a proportionate relationship between end-diastolic volume and stroke volume but a less linear relationship between end-diastolic and end-systolic volumes (and hence preserved ejection fraction) due to higher end-systolic elastance [Figure 8] and [Figure 9]. Indexed LV end-diastolic volume in HFpEF patients is similar to that of controls and also increases nearly normally during exercise.[4] However, end-systolic volumes are either normal or even reduced compared to matched controls at rest but do not decrease proportionately during exercise. Stroke volume index is not different from normal controls at rest but is impaired in response to exercise indicating reduced systolic function reserve [Figure 10].[5],[6],[7],[8] Impaired systolic function reserve due to reduced intrinsic contractility has been shown by exercise-invasive hemodynamic load-controlled studies.[7],[8] Atrioventricular uncoupling is also often seen in HFpEF wherein total left-sided end-systolic volume becomes higher than normal controls [Figure 11]. | Figure 8: Relationship between left ventricular end-diastolic volume and end-systolic volume in HFpEF compared to that in HFrEF due to leftward shift of the pressure-volume curve. HFpEF: Heart failure with preserved ejection fraction, HFrEF: Heart failure with reduced ejection fraction, LVESVI: Left ventricular end-systolic volume index, LVEDVI: Left ventricular end-diastolic volume index
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 | Figure 9: Relationship between LVEF and the LVESV. The steeper curve is representative of reduced distensibility and reduced reserve. HFpEF: Heart failure with preserved ejection fraction, HFrEF: Heart failure with reduced ejection fraction, LVEF: Left ventricular ejection fraction, LVESV: Left ventricular end-systolic volume
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 | Figure 10: Reduced Systolic function reserve in heart failure with preserved ejection fraction expressed by relationship of stroke volume to end-diastolic volume at rest and during exercise. LVEDV: Left ventricular end-diastolic volume
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 | Figure 11: Atrioventricular uncoupling in HFpEF as expressed by fractions of end-systolic volumes. HFpEF: Heart failure with preserved ejection fraction
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Subtle systolic dysfunction in HFpEF has been proposed for long. Petrie et al.[9] first reported reduced displacement of atrioventricular plane as a measure of systolic dysfunction in HFpEF. Mitral annular s' velocities are found to be reduced in HFpEF pari passu with decreased e'.[10] However, strain imaging is more objective, robust, and reproducible in assessing LV systolic function.[11]
| Acoustic Speckle Tracking in Heart Failure with Preserved Ejection Fraction | | |
During systole, the ventricular myocardium simultaneously shortens in the longitudinal and circumferential planes and thickens in the radial plane, with reciprocal changes in diastole. This change in size or shape is called deformation or strain. Thus, strain or deformation is the change in size or shape of a structure when a force or pressure is applied to it. It is the phenomenon of shortening, stretching, twisting, or wringing of the muscle. Hence, strain is the amount of deformation experienced by an object or structure in the direction of force applied and divided by the initial dimensions of the object or structure [Figure 12], [Figure 13], [Figure 14]. It predicts the elastic or plastic behavior of a structure and is dimensionless and relative. Such a parameter could be a better discriminator of function than the volume displacement parameters such as ejection fraction. Strain has a time domain component and hence strain rate becomes another parameter of function which may be even more discriminatory [Figure 13]. | Figure 12: The concept of myocardial strain. Stress is the force applied and strain is the deformation produced
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 | Figure 13: The concept of strain rate as a more discriminatory parameter of function
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 | Figure 14: Vectors of myocardial strain. (a) Longitudinal strain, (b) Radial and circumferential strain, (c) Subendocardial versus subepicardial myocardium
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Strain can be easily measured using echocardiography and cardiac magnetic resonance (CMR). While echocardiography is a convenient, widely available cost-effective technique, it is limited by acoustic windows and operator reliance. CMR, on the other hand, can serve as a gold standard for morphological structure and function assessment even though it is expensive, time-consuming, and has several other caveats. Common domains of the LV strain and strain rate studied by acoustic speckle tracking are longitudinal, radial, and circumferential although area strain has also been evaluated in many clinical situations.[11]
LV global strain is an accurate and sensitive measure of myocardial deformation, allowing for angle-independent quantification of myocardial function in multiple dimensions based on the LV active shortening in the longitudinal, circumferential, directions, and thickening in radial direction.[11] It is more reproducible than EF and does not rely on geometrical assumptions. Wall stress is greater in the subendocardial layer and this region sustains higher deformational change than the subepicardium during systole, leading to higher strain values and higher susceptibility to injury.[11] Impaired LV GLS is common in HFpEF because of possible subclinical LV systolic dysfunction.[12],[13],[14],[15],[16] Less is known regarding the combined analysis of strains in longitudinal, circumferential, and radial axis in HFpEF, and GLS is the only strain parameter which has been extensively studied. In the Prospective comparison of ARNI with ARB on Management Of heart failUre with preserved ejectioN fracTion (PARAMOUNT) trial which studied the impact of angiotensin-neprilysin inhibitor on functional parameters of HFpEF, a substantial number of patients was characterized by reduced LV longitudinal and circumferential strains compared to normal controls with similar LVEF.[15] Both types of strain had modest correlation with LVEF which was >45% in every case by inclusion criteria.[15] Circumferential strain was consistently higher than the longitudinal strain. Abnormal longitudinal and circumferential strains were present in 67% and 40% of cases of HFpEF, respectively (below two standard deviations). The worse longitudinal strain was associated with lower ejection fraction, stroke volume, and tissue s' velocity. In the Treatment of Preserved Cardiac Function Heart Failure With an Aldosterone Antagonist (TOPCAT) study which employed therapy with spironolactone in HFpEF patients, 52% of patients had reduced longitudinal strain and the median value in all was −15.8% and this value was unrelated to the mitral E/e' ratio.[14] In the Phosphodiesterase-5 Inhibition to Improve Clinical Status and Exercise Capacity in Heart Failure with Preserved Ejection Fraction (RELAX) trial, 65% of HFpEF patients had reduced GLS.[11] In acute heart failure, GLS was abnormal in 76% of patients with HFpEF.[16] In a meta-analysis of 22 studies involving 2284 patients with HFpEF, the mean GLS of the LV was −15.7% compared to −19.9% in normal controls.[17] This mean figure is typical of most HFpEF patients [Figure 15]. | Figure 15: A 70-year-old female with heart failure with preserved ejection fraction. Left ventricular global longitudinal strain is -16% (a) and ejection fraction is 53% (b); (c) dilated inferior cava, and (d) restrictive transmitral flow pattern with prominent L wave
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| Left Ventricle Global Longitudinal Strain in Diagnostic Criteria of Heart Failure with Preserved Ejection Fraction | | |
The normal GLS value has been reported to range from − 15.9% to −22.1% in a large meta-analysis.[18] The lower limit corresponding to two-fold standard deviations below the mean in normal 880 Indian adults is reported to be-15.25%.[19] Using 16% as cutoff, the patients can be classified as having impaired (GLS <16%, ignoring the minus sign for easy comprehension) or normal (GLS ≥16%) GLS. Values are somewhat vendor-dependent, but GLS <16% represents the reduction in LV systolic function and GLS between 16% and 18% represents borderline values. A large meta-analysis of 22 studies has shown that reduced GLS is found in ~50%–60% of HFpEF cases [Figure 16].[17] In conclusion, it is obvious that patients with HFpEF have significantly lower LV longitudinal systolic function. | Figure 16: Schematic diagram showing the proportion of HFpEF patients with reduced left ventricular global longitudinal strain. Reduced GLS is reported in 52%–76% of all. GLS: Global longitudinal strain, HFpEF: Heart failure with preserved ejection fraction
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Diagnostic criteria such as the H2FPEF score or the HFA-PEFF score have been proposed in HFpEF.[20],[21] Only in HFA-PEFF, the use of GLS <16% as one of the minor criteria is included. Incorporation of GLS into the diagnosis of HF may be a reasonable approach that needs validation by invasive hemodynamic studies. It cannot be ascertained that the reduction in the GLS is due to HFpEF and not as a result of associated comorbidities.
| Global Longitudinal Strain versus Left Ventricular Ejection Fraction | | |
GLS and LVEF both denote different aspects of LV systolic function. There is a reasonably good correlation between LVEF and GLS.[22] However, the ejection fraction represents the contractile ability of circumferential fibers while the GLS represents the longitudinal contraction of vulnerable subendocardial muscle fibers. Longitudinal fibers have a greater susceptibility to injury, ischemia, and hypoxia and are the first to get affected. GLS is not only an early marker of systolic dysfunction but also is more reproducible.[23] The impact on circumferential strain on the other hand is controversial with variable results.[14],[24] It must be noted that in healthy controls, LV GLS and LVEF will find a good correlation but not in diseased states as the GLS is disproportionately decreased.
| Global Longitudinal Strain as a Prognostic Marker in Heart Failure with Preserved Ejection Fraction | | |
In a substudy from the TOPCAT trial, impaired GLS was common (52%) and the strongest echocardiographic predictor of the primary outcome (cardiovascular death, heart failure hospitalization, or aborted cardiac arrest) with an adjusted hazard ratio of 1.14 (confidence interval: 1.04–1.24) per 1% decrease on multivariable analysis.[14] Combined data from multiple studies have also suggested that GLS <16% in HFpEF patients is associated with twice greater cardiovascular mortality compared to those whose GLS is >16%. Reduced GLS has been found to correlate with symptoms and reduced exercise capacity by some.[25] However, there is disagreement about the role of GLS in impacting 6-min walk time, quality of life, or peak oxygen consumption.[13] In the study of acute heart failure admissions due to HFpEF, in-hospital and 30-day adverse events were better predicted by GLS but 1-year mortality or rehospitalization was unaffected.[16] There is a modest correlation between GLS and NT-Pro BNP levels.[12] GLS by CMR modestly correlates with extracellular volume by T1 mapping and is associated with adverse cardiovascular events.[26]
| Current Status | | |
GLS has been proposed as the test of choice for the detection of early LV systolic dysfunction. It has the potential to improve risk stratification in HFpEF, redefine criteria for disease classification, and determine treatment in asymptomatic systolic dysfunction resulting from a variety of etiologies that contribute to HFpEF. There is a strong case for the incorporation of GLS into clinical decision-making. According to the recent consensus document from the European Association of Cardiovascular Imaging, GLS should be measured routinely in addition to EF, in patients who are being evaluated for potential HFpEF.[27] In principle, mitral annular motion by M-mode or systolic mitral annular velocities by tissue Doppler provides similar diagnostic information. The evidence supporting GLS, however, is stronger and the other two methods extrapolate local information as an indicator of global LV function. There are specific phenotypes where GLS measurement provides information about the substrate of HFpEF.
| Conclusion | | |
The longitudinal systolic function of the left ventricle as reflected by GLS is reduced in a high proportion of patients with HFpEF. The reduced GLS is difficult to predict based on clinical and other imaging features. Reduced GLS in HFpEF is associated with worse prognosis. Should it become an important diagnostic or prognostic criterion in routine practice remains to be answered.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
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[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8], [Figure 9], [Figure 10], [Figure 11], [Figure 12], [Figure 13], [Figure 14], [Figure 15], [Figure 16]
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