Cardio · imaging-noninvasive
Echocardiography: EF quantitation and diastology basics
Fellowship-level guide to core echocardiographic measures under the 2026 ESC heart failure, 2023 ESC cardiomyopathies, 2022 ESC/ERS pulmonary hypertension, 2025 ESC myocarditis and pericarditis, 2024 ESC chronic coronary syndromes and 2019 ESC pulmonary embolism guidelines, the 2022 AHA/ACC/HFSA heart failure and 2026 AHA/ACC pulmonary embolism guidelines, and the 2018 NHFA/CSANZ heart failure guideline: LVEF categories and global longitudinal strain, the HFpEF echo criteria and filling pressures, left atrial volume, RV function and TAPSE, the echocardiographic probability of pulmonary hypertension, and pericardial effusion size.
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Target exams
- EECC
- ABIM Cardiovascular Disease Certification
Red flags
- ESC 2026 HF: LVEF may be falsely high in certain situations, e.g. mitral regurgitation
- ESC/ERS 2022: echocardiography alone is insufficient to confirm pulmonary hypertension, which requires right heart catheterisation
- ESC/ERS 2022: a peak TR velocity >2.8 m/s may suggest PH, but TRV alone cannot reliably determine whether PH is present or absent
- ESC 2025: acute pericarditis patients may have a normal-appearing TTE (40%–50% of cases in first episodes), and new or worsening effusion is a diagnostic criterion
- AHA/ACC 2026: echocardiography is an inadequate test for the diagnosis of PE, though important for assessing RV function in symptomatic patients with confirmed acute PE
ESC 2026 HF calls echocardiography the cornerstone of assessment in HF, and every number on this page belongs to one body and one year.[1] The bodies do not always agree. Where they differ, the page sets them side by side rather than blending them. Treatment lives in Heart failure with reduced ejection fraction, Heart failure with preserved ejection fraction (HFpEF), Pulmonary hypertension: five groups and PAH-specific therapy and Pericardial effusion and tamponade physiology; valve areas, gradients and regurgitation grades are in Echo valve quantitation: areas, gradients, regurgitation grades.
Why echocardiography comes first
ESC 2026 HF says echocardiography is considered the first-line imaging modality in HF and remains the cornerstone of assessment.[1] It gives real-time dynamic evaluation of cardiac structures, dimensions, volumes, filling patterns, haemodynamics and function, with widespread availability and no invasion (ESC 2026 HF).[1] ESC 2023 calls it the main imaging tool in cardiomyopathy, from initial diagnosis to follow-up.[3] ESC 2025 says TTE is usually the initial imaging modality of choice for suspected inflammatory myopericardial syndrome (IMPS).[6]
Rows that call for echocardiography, by body and year
| Guideline and row | Class / COR | Level / LOE |
|---|---|---|
| ESC 2026 HF (Recommendation Table 3, diagnostic investigations in all patients with suspected HF): a transthoracic echocardiogram is recommended in patients with suspected HF to confirm the diagnosis, differentiate between HF phenotypes and aid in identifying the underlying aetiology of HF | I | C |
| AHA/ACC 2022 HF (Section 4.4, evaluation with cardiac imaging): in patients with suspected or newly diagnosed HF, TTE should be performed during initial evaluation to assess cardiac structure and function | 1 | C-LD |
| ESC 2023 cardiomyopathies (Recommendation Table 4): a comprehensive evaluation of cardiac dimensions and LV and RV systolic (global and regional) and LV diastolic function is recommended in all patients with cardiomyopathy at initial evaluation, and during follow-up, to monitor disease progression and aid risk stratification and management | I | B |
| ESC 2024 CCS (Recommendation Table 4, initial diagnostic management of suspected CCS): a resting transthoracic echocardiogram is recommended to measure LVEF, volumes and diastolic function; identify regional wall motion abnormalities; identify non-coronary cardiac disease (e.g. hypertrophy, cardiomyopathy, valve disease, pericardial effusion); and assess right ventricular function and estimate systolic pulmonary artery pressure; to refine risk stratification and guide treatment | I | B |
| ESC/ERS 2022 PH (Recommendation Table 2, diagnostic strategy): echocardiography is recommended as the first-line, non-invasive, diagnostic investigation in suspected PH | I | B |
| ESC 2025 myocarditis and pericarditis (Recommendation Table 1): complete clinical evaluation, including history, physical examination, chest X-ray, biomarkers (footnote: including hs-TnT or hs-TnI, C-reactive protein, NT-proBNP), ECG, and echocardiography, is recommended in all patients with a suspicion of myocarditis and/or pericarditis for the initial diagnostic assessment | I | C |
Among its other rows, AHA/ACC 2022 HF Section 4.4 includes three on repeat imaging and on alternative imaging when echocardiography is inadequate.[2]
- Repeat measurement (AHA/ACC 2022, COR 1, LOE C-LD): in patients with HF who have had a significant clinical change, or who have received GDMT and are being considered for invasive procedures or device therapy, repeat measurement of EF, degree of structural remodeling, and valvular function are useful to inform therapeutic interventions.[2]
- Inadequate echo (AHA/ACC 2022, COR 1, LOE C-LD): in patients for whom echocardiography is inadequate, alternative imaging (e.g. CMR, cardiac CT, radionuclide imaging) is recommended for assessment of LVEF.[2]
- No routine repeat (AHA/ACC 2022, COR 3: No Benefit, LOE C-EO): in patients with HF in the absence of a clinical status change, treatment interventions that might have had a significant effect on cardiac function, or candidacy for invasive procedures or device therapy, routine repeat assessment of LV function is not indicated.[2]
LV size and systolic function
Ejection fraction and the HF phenotypes
ESC 2026 HF says echocardiography evaluates systolic, diastolic and valvular function and enables the distinction between HF (stage C) phenotypes based on LVEF.[1] Its task force has eliminated the HFmrEF phenotype and reclassified HF into two phenotypes on a pathophysiological basis.[1] HFrEF is LVEF <50% with symptoms and/or signs of HF.[1] HFpEF is LVEF ≥50% with symptoms and/or signs of HF and objective evidence of cardiac structural and/or functional abnormalities consistent with the presence of LV diastolic dysfunction/raised LV filling pressures, supported by raised natriuretic peptides.[1]
The 2021 ESC HF guideline identified three phenotypes: HFrEF (LVEF ≤40%), HFmrEF (LVEF 41%–49%) and HFpEF (LVEF ≥50%).[1] That scheme is dated history here, and no mark on this page rests on it.[1]
LVEF categories by body and year
| Category | ESC 2026 HF | AHA/ACC 2022 HF (Table 4) | NHFA/CSANZ 2018 HF (Australia) |
|---|---|---|---|
| Reduced | HFrEF: LVEF <50% and symptoms and/or signs of HF | HFrEF: LVEF ≤40% | HFrEF: clinical symptoms with or without signs of heart failure and a measured LVEF of less than 50%; if LVEF is mildly reduced (41–49%), additional criteria are required (e.g. signs of heart failure; diastolic dysfunction with high filling pressure shown by invasive means, echocardiography or biomarker testing) |
| Mildly reduced | HFmrEF phenotype eliminated | HFmrEF: LVEF 41%–49% and evidence of spontaneous or provokable increased LV filling pressures (e.g. elevated natriuretic peptide, noninvasive and invasive hemodynamic measurement) | The writing committee does not recommend a separate mid-range (HFmrEF) category at this time; the 41–49% criteria above belong to the HFrEF diagnosis |
| Preserved | HFpEF: LVEF ≥50% (requires that LVEF has not previously been <50%), symptoms and/or signs of HF, and objective evidence of cardiac structural and/or functional abnormalities consistent with the presence of LV diastolic dysfunction/raised LV filling pressures, supported by raised natriuretic peptides | HFpEF: LVEF ≥50% and evidence of spontaneous or provokable increased LV filling pressures (e.g. elevated natriuretic peptide, noninvasive and invasive hemodynamic measurement) | HFpEF: clinical symptoms with or without signs of heart failure; a measured EF of at least 50%; and objective evidence of either relevant structural heart disease or diastolic dysfunction without an alternative cause (e.g. significant valvular heart disease) |
ESC 2026 HF warns that a single LVEF cut-point between HFpEF and HFrEF is somewhat arbitrary and has to be evaluated in the clinical situation, as measurement varies with both the modality and the interpreter.[1] It adds that LVEF may be falsely high in certain situations, for example mitral regurgitation.[1] LVEF is a continuous measure that may differ between methods and by sex, so ESC 2026 gives a precise value only as guidance.[1]
On improvement, ESC 2026 HF says patients with HFrEF and improved LVEF have a more favourable prognosis, but it is important to ensure they are still managed with optimal medical therapy, except for selected patients.[1] AHA/ACC 2022 says patients with HFrEF who improve their LVEF to >40% are considered to have HFimpEF and should continue HFrEF treatment.[2] For the mildly reduced range, AHA/ACC 2022 says one EF measurement at one time point may not be adequate, and the trajectory of LVEF over time and the cause are important to evaluate.[2] ESC 2026 HF likewise notes that many patients with LVEF 41%–49% may experience a deterioration in LVEF.[1]
Before symptoms, ESC 2026 HF says LV systolic dysfunction should be considered present if patients are asymptomatic and have an LVEF <50% without an alternative explanation (e.g. athlete’s heart), for both men and women and regardless of age.[1] In Australia, NHFA/CSANZ 2018 says LVEF should be measured using two-dimensional echocardiography (usually the biplane method of discs or modified Simpson’s rule) or three-dimensional echocardiography.[10] It puts the lower limit of normal for LVEF at 50–55%.[10]
ESC 2024 says patients with CCS often have preserved LVEF.[7] It calls systolic LV function the strongest predictor of long-term survival, so risk stratification by assessing it is useful in all symptomatic individuals with suspected CCS; mortality increases as LVEF declines.[7] A decreased LV function and/or regional wall motion abnormalities may increase the suspicion of ischaemic myocardial damage (ESC 2024).[7] LV dysfunction following a coronary perfusion territory is typical after a previous MI (ESC 2024).[7]
Chamber size, wall thickness and the cardiomyopathy phenotypes
ESC 2023 defines DCM as LV dilatation and global or regional systolic dysfunction unexplained solely by abnormal loading conditions (e.g. hypertension, valve disease, congenital heart disease) or coronary artery disease.[3] It defines HCM as increased LV wall thickness (with or without RV hypertrophy) or mass not solely explained by abnormal loading conditions.[3] In an adult, that means an LV wall thickness ≥15 mm in any myocardial segment not explained solely by loading conditions (ESC 2023).[3] Lesser thickening of 13–14 mm requires evaluation of other features, including family history, genetic findings and ECG abnormalities (ESC 2023).[3] In adult first-degree relatives of patients with unequivocal disease, ESC 2023 bases the clinical diagnosis of HCM on an LV wall thickness ≥13 mm.[3]
ESC 2023 says TTE informs on global and regional RV and LV anatomy and function, valve function, dynamic obstruction, pulmonary hypertension and pericardial effusions.[3] Three-dimensional echocardiography reliably assesses chamber volumes but needs an adequate acoustic window (ESC 2023).[3] Contrast agents can be considered for better endocardial delineation, to show hypertrabeculation, apical HCM or apical aneurysms, and to exclude thrombus (ESC 2023).[3] In its chronic coronary syndrome guideline, ESC 2024 adds that an echocardiographic contrast agent can be helpful in patients with poor acoustic windows.[7] ESC 2026 HF calls CMR the gold standard for LV volumes and mass, owing to its high spatial resolution and reproducibility.[1]
ESC 2023 Table 18: echocardiographic features that suggest specific aetiologies in HCM (all rows)
| Echocardiographic finding | Specific diseases to be considered |
|---|---|
| Increased interatrial septum thickness | Amyloidosis |
| Increased AV valve thickness | Amyloidosis; Anderson–Fabry disease |
| Increased RV free wall thickness | Amyloidosis, myocarditis, Anderson–Fabry disease, Noonan syndrome, and related disorders |
| Mild-to-moderate pericardial effusion | Amyloidosis, myocarditis/myopericarditis |
| Ground-glass appearance of ventricular myocardium on 2D echocardiography | Amyloidosis |
| Concentric LVH | Glycogen storage disease, Anderson–Fabry disease, PRKAG2 variants, Friedreich ataxia |
| Extreme concentric LVH (wall thickness ≥30 mm) | Danon disease, Pompe disease |
| Global LV hypokinesia (with or without LV dilatation) | Mitochondrial disease, TTR-related amyloidosis, PRKAG2 variants, Danon disease, myocarditis, advanced sarcomeric HCM, Anderson–Fabry disease, Friedreich ataxia |
| RVOTO | Noonan syndrome and associated disorders |
| Apical sparing pattern on longitudinal strain imaging | Amyloidosis |
Global longitudinal strain
Strain can show early systolic dysfunction before the ejection fraction falls.[1] ESC 2026 HF says global longitudinal strain (GLS) offers more sensitive measures of early systolic dysfunction even before LVEF declines, of particular value in patients undergoing chemotherapy.[1] It adds that specific strain patterns may be suggestive of amyloidosis or HCM (ESC 2026 HF).[1] ESC 2023 calls GLS a more sensitive marker than EF for subtle ventricular dysfunction, for example in genotype-positive HCM, DCM and ARVC family members.[3] It says GLS may help discriminate between aetiologies of hypertrophy, such as amyloidosis, HCM and athlete’s heart (ESC 2023).[3]
- Acute myocarditis (ESC 2025): ESC 2025 reports recent studies showing that GLS, global circumferential strain and strain rate were decreased in acute myocarditis, even with preserved EF.[6]
- Suspected CCS (ESC 2024): regional wall motion abnormalities can be hard to see; strain imaging or global myocardial work may help when LV function looks normal but CCS is suspected.[7]
- AHA/ACC 2022 Appendix 3: lists LVEF <50% and GLS <16% as suggested thresholds for ventricular systolic function.[2]
- NHFA/CSANZ 2018: GLS may be a more sensitive marker of LV contractility, but given vendor and software variability and limited routine use, the writing group recommends LVEF to categorise heart failure following diagnosis.[10]
Diastolic function and filling pressures
ESC 2026 HF says HFpEF is harder to diagnose and that the work-up should start with the assessment of pre-test probability.[1] All three criteria must be present.[1] The first two are current or prior symptoms and/or signs of HF, and an LVEF ≥50%, which requires that LVEF has not previously been <50%.[1] The third is objective evidence of cardiac structural and/or functional abnormalities consistent with the presence of LV diastolic dysfunction/raised LV filling pressures (Table 10), supported by raised natriuretic peptides.[1]
ESC 2026 HF Table 10: simplified echocardiographic criteria supporting objective evidence of HFpEF (all rows)
| Criterion | Echocardiographic threshold |
|---|---|
| LV hypertrophy | LV mass index ≥95 g/m² (female) or ≥115 g/m² (male), OR relative wall thickness >0.42 |
| LA dilatation (volume indexed by BSA) | >34 mL/m² (sinus rhythm); >40 mL/m² (AF) |
| Increased likelihood of elevated LV filling pressure | E/e′ >9 at rest (footnote: E/e′ ≥15 is more specific, but less sensitive, for the diagnosis of HFpEF) |
| Raised estimated systolic PA pressure | >35 mmHg OR TR velocity at rest >2.8 m/s |
ESC 2026 HF says the probability of HFpEF increases with the number of parameters in the pathological range.[1] Testing for elevated natriuretic peptides may in most patients support the diagnosis, but diagnostic thresholds for HFpEF should be critically evaluated based on patient characteristics, especially with obesity and other factors that may reduce natriuretic peptide levels.[1] ESC 2026 HF advises a pragmatic approach to give the large population of elderly patients potentially affected access to diagnosis.[1] If scoring systems are used, it says they should be interpreted with caution and used primarily to raise clinical suspicion of HFpEF rather than to establish a definitive diagnosis.[1]
When the diagnosis stays uncertain, ESC 2026 HF says CPET, exercise stress echocardiography or invasive haemodynamic assessment may be considered.[1] It calls invasive haemodynamic exercise testing the gold standard confirmatory test for HFpEF.[1] A pulmonary capillary wedge pressure ≥15 mmHg at rest or ≥25 mmHg with exercise, or an LV end-diastolic pressure ≥16 mmHg at rest, is generally considered diagnostic (ESC 2026 HF).[1] In most patients, though, ESC 2026 HF says the diagnosis of HFpEF can be made from clinical history and the Table 10 echocardiographic signs.[1] In patients with HFpEF, it describes diastolic stress testing as emerging as an important tool to unmask diastolic dysfunction that may not be apparent at rest.[1]
Same measures, different thresholds
The three heart failure guidelines do not all print the same thresholds for LV mass, LA volume or E/e′, but each uses a TR velocity above 2.8 m/s (at rest, in ESC 2026 HF).[1][2][10] AHA/ACC 2022 gives its values in Appendix 3 as suggested thresholds for structural heart disease and evidence of increased filling pressures.[2] NHFA/CSANZ 2018 counts echocardiographic evidence of high filling pressure when at least three of its four echo criteria are met.[10]
Echo thresholds for structure and filling pressure by body and year (selected rows)
| Measure | ESC 2026 HF (Table 10, supporting objective evidence of HFpEF) | AHA/ACC 2022 HF (Appendix 3) | NHFA/CSANZ 2018 HF (Section 3.3.2; echo evidence of high filling pressure needs at least three of four criteria: e′, E/e′, LA volume index, TR velocity; relevant structural heart disease is LV hypertrophy or left atrial enlargement) |
|---|---|---|---|
| LV mass and wall | LV mass index ≥95 g/m² (female) or ≥115 g/m² (male), OR relative wall thickness >0.42 | Morphology: LVMI >116/95 g/m²; RWT >0.42; LV wall thickness ≥12 mm | LV hypertrophy: increased LV wall thickness or LV mass index of more than 115 g/m² (men) or more than 95 g/m² (women) |
| LA volume index | >34 mL/m² (sinus rhythm); >40 mL/m² (AF) | Morphology: LAVI ≥29 mL/m² | Left atrial enlargement: more than 34 mL/m² |
| E/e′ | E/e′ >9 at rest (≥15 more specific, less sensitive) | Ventricular diastolic function: average E/e′ ≥15 for increased filling pressures | Average E/e′ ratio of more than 14 |
| Mitral annular e′ | Not among the Table 10 criteria | Septal e′ <7 cm/s; lateral e′ <10 cm/s | Septal e′ less than 7 cm/s or lateral e′ less than 10 cm/s |
| TR velocity and PA pressure | Estimated systolic PA pressure >35 mmHg OR TR velocity at rest >2.8 m/s | TR velocity >2.8 m/s; estimated PA systolic pressure >35 mm Hg | Tricuspid regurgitation velocity of more than 2.8 m/s |
AHA/ACC 2022 Appendix 3 also lists LVEF <50% and GLS <16% for systolic function, and BNP ≥35 pg/mL and NT-proBNP ≥125 pg/mL as biomarker thresholds.[2] Its footnote warns that these natriuretic peptide cut-offs may have lower specificity, especially in older patients or in patients with AF or CKD.[2] Where the clinical suspicion of HFpEF remains despite not meeting its criteria, NHFA/CSANZ 2018 says exercise testing may be considered.[10] In these patients, NHFA/CSANZ 2018 says the sensitivity of HFpEF diagnosis improves with measurement of filling pressure, invasively (positive if PCWP >25 mm Hg) or by echocardiography.[10] On exercise echocardiography it is positive when average E/e′ >14 or septal E/e′ >15 and peak TR velocity >2.8 m/s occur during or immediately after exercise, with septal e′ <7 cm/s at baseline (NHFA/CSANZ 2018).[10]
Diastolic findings matter outside HFpEF too.[3][7][6] ESC 2023 Table 9 links diastolic dysfunction on echocardiography to explaining symptoms and evaluating treatment efficacy in cardiomyopathy.[3] ESC 2024 says diastolic LV dysfunction has been reported as an early sign of ischaemic myocardial dysfunction and may indicate microvascular dysfunction.[7] ESC 2025 says diastolic dysfunction with preserved EF may occur in myocarditis.[6]
Left atrial volume
NHFA/CSANZ 2018 calls left atrial enlargement, a left atrial volume index of more than 34 mL/m², a consequence of high left-sided intracavity filling pressure.[10] ESC 2026 HF indexes LA volume to body surface area and, in its Table 10 criteria supporting objective evidence of HFpEF, uses >34 mL/m² in sinus rhythm and >40 mL/m² in AF.[1] AHA/ACC 2022 Appendix 3 uses LAVI ≥29 mL/m² as its morphology threshold.[2]
In pulmonary hypertension, ESC/ERS 2022 says LA size and signs of LV hypertrophy should always be measured, to separate group 2 PH from other forms and to assess the likelihood of LV diastolic dysfunction.[4] It says PH associated with left heart disease is likely with known cardiac disease, multiple cardiovascular comorbidities or risk factors, AF at diagnosis, and LV hypertrophy, increased LA size and reduced LA strain on imaging.[4] ESC 2023 Table 9 links LA size on echocardiography to SCD risk prediction in HCM and to systematic AF screening when the LA is enlarged.[3]
ESC/ERS 2022 Table 23, patient phenotyping and likelihood of left heart disease as the cause of PH (echocardiography row only)
| Feature | PH-LHD unlikely | Intermediate probability | PH-LHD likely |
|---|---|---|---|
| Echocardiography | No LA dilation; E/e′ <13 | No LA dilation; grade <2 mitral flow | LA dilation (LAVI >34 mL/m²); LVH; grade >2 mitral flow |
RV function and TAPSE
ESC/ERS 2022 says echocardiographic measures of RV function include TAPSE, RV fractional area change, RV free-wall strain and the tissue Doppler tricuspid annulus velocity (S′ wave), and potentially RV ejection fraction from 3D echocardiography.[4] It says the TAPSE/sPAP ratio, a non-invasive measure of RV–PA coupling, may aid in diagnosing PH.[4] A TAPSE/sPAP ratio <0.55 mm/mmHg is one of the Table 10 ventricular signs (ESC/ERS 2022).[4]
Both acute PE guidelines print a cut-off for TAPSE.[9][8] AHA/ACC 2026 calls echocardiography an inadequate test for the diagnosis of PE, but important for assessing RV function in symptomatic patients with confirmed acute PE.[9] In its diagnostic-testing rows, AHA/ACC 2026 says that in acute PE with TTE, RV dysfunction should be assessed and reported by named parameters to assist with risk stratification (COR 1, LOE B-NR).[9] The parameters are RV/LV end-diastolic ratio, RV end-diastolic diameter, TAPSE, estimated RV systolic pressure, RV free wall hypokinesis with sparing of the apex (McConnell’s sign), tricuspid systolic velocity, paradoxical septal motion and IVC respirophasic collapse.[9]
AHA/ACC 2026 PE Table 4: optimal methods of RV dysfunction assessment on echocardiogram (all rows)
| Parameter | Recommended technique | Definition of parameter |
|---|---|---|
| RV dimension | 1) End-diastole from an RV-focused parasternal long view; 2) apical RV-focused view with the RV free wall visualised throughout the cardiac cycle | 1) EDD ≥30 mm; 2) RV basal EDD ≥41 mm |
| RV/LV | End-diastolic ratio (apical or subcostal view) | RV/LV >0.9 |
| TAPSE | Distance of systolic excursion of the RV free wall: M-mode cursor on the lateral tricuspid annulus from the RV-focused view, parallel to annular motion (base to apex) | TAPSE ≤1.7 cm is abnormal |
| TDI S′ velocity | From the RV-focused view, pulsed-wave Doppler cursor on the lateral tricuspid annulus | TDI S′ ≤9.5 cm/s is abnormal |
| TR velocity | Continuous-wave Doppler from multiple windows; the highest velocity is used to calculate RV systolic pressure | ≥2.9 m/s suggests pulmonary hypertension |
AHA/ACC 2026 says sensitivity and specificity increase if more than one parameter of RV dysfunction is present.[9] ESC 2019 PE says decreased TAPSE may be present in PE.[8] Of the echocardiographic parameters used to stratify the early risk of patients with PE, an RV/LV diameter ratio ≥1.0 and a TAPSE <16 mm are the findings for which an association with unfavourable prognosis has most frequently been reported (ESC 2019 PE).[8] It says evidence of RV dysfunction on echocardiography is found in ≥25% of unselected patients with acute PE.[8] In acute PE the two bodies print different cut-offs: TAPSE ≤1.7 cm as abnormal (AHA/ACC 2026), and TAPSE <16 mm as one of the two findings most frequently reported with an unfavourable prognosis (ESC 2019).[9][8]
Echocardiographic probability of pulmonary hypertension
ESC/ERS 2022 defines PH as a mean pulmonary arterial pressure >20 mmHg at rest.[4] PH leads to RV pressure overload and dysfunction, whatever the cause, and echocardiography can detect it (ESC/ERS 2022).[4] Yet echocardiography alone is insufficient to confirm PH, which requires right heart catheterisation (ESC/ERS 2022).[4] No single echocardiographic parameter reliably informs about PH status and aetiology, given the heterogeneity of PH and the geometry of the RV (ESC/ERS 2022).[4]
The systolic PA pressure estimate rests on the peak TR velocity and the TRV-derived pressure gradient, after excluding pulmonary stenosis, taking into account a non-invasive estimate of RA pressure (ESC/ERS 2022).[4] Because RA pressure estimates are inaccurate and derived variables amplify error, ESC/ERS 2022 recommends using the peak TR velocity, not the estimated sPAP, as the key variable for assigning the echocardiographic probability of PH.[4] A peak TRV >2.8 m/s may suggest PH, but TRV alone cannot reliably determine whether PH is present or absent (ESC/ERS 2022).[4] TR velocity may underestimate the gradient, for example in severe TR, or overestimate it, for example with high cardiac output in liver disease or sickle cell disease (ESC/ERS 2022).[4]
ESC/ERS 2022 Recommendation Table 2 (diagnostic strategy): the five rows under its Echocardiography heading
| ESC/ERS 2022 row | Class | Level |
|---|---|---|
| Echocardiography is recommended as the first-line, non-invasive, diagnostic investigation in suspected PH | I | B |
| It is recommended to assign an echocardiographic probability of PH, based on an abnormal TRV and the presence of other echocardiographic signs suggestive of PH (see Table 10) | I | B |
| It is recommended to maintain the current threshold for TRV (>2.8 m/s) for echocardiographic probability of PH according to the updated haemodynamic definition | I | C |
| Based on the probability of PH by echocardiography, further testing should be considered in the clinical context (i.e. symptoms and risk factors or associated conditions for PAH/CTEPH) | IIa | B |
| In symptomatic patients with intermediate echocardiographic probability of PH, CPET may be considered to further determine the likelihood of PH | IIb | C |
ESC/ERS 2022 Table 10: additional echocardiographic signs suggestive of PH (all rows)
| A: The ventricles | B: Pulmonary artery | C: Inferior vena cava and RA |
|---|---|---|
| RV/LV basal diameter/area ratio >1.0 | RVOT AT <105 ms and/or mid-systolic notching | IVC diameter >21 mm with decreased inspiratory collapse (<50% with a sniff or <20% with quiet inspiration) |
| Flattening of the interventricular septum (LVEI >1.1 in systole and/or diastole) | Early diastolic pulmonary regurgitation velocity >2.2 m/s | RA area (end-systole) >18 cm² |
| TAPSE/sPAP ratio <0.55 mm/mmHg | PA diameter >AR diameter; PA diameter >25 mm | — |
Signs from at least two of the three categories (A/B/C) must be present to alter the level of echocardiographic probability of PH (ESC/ERS 2022 Table 10 footnote).[4] The probability may then be determined as low, intermediate or high and, interpreted in clinical context, can be used to decide the need for further investigation, including cardiac catheterisation in individual patients (ESC/ERS 2022, Figure 5).[4] The Figure 5 legend adds that the 2.8 m/s TRV threshold was not changed with the updated haemodynamic definition of PH.[4] Figure 5 itself is a drawn chart and is not reproduced here.[4]
[5] [4]After this step, ESC/ERS 2022 says patients with another cause identified and/or a low probability of PH should be managed accordingly.[4] Referral to a PH centre follows when an intermediate or high probability of PH is established, or with risk factors for PAH or a history of PE (ESC/ERS 2022).[4] A mid-systolic notching pattern of RV outflow tract flow may suggest pre-capillary PH (ESC/ERS 2022).[4] ESC/ERS 2022 adds that exercise echocardiography, proposed to uncover HFpEF, is unable to diagnose or classify PH in this context.[4] Classification and treatment of PH are in Pulmonary hypertension: five groups and PAH-specific therapy.
Pericardial effusion
ESC 2025 calls echocardiography the primary diagnostic tool for diagnosis, sizing, assessment of haemodynamic effects and follow-up of pericardial effusion.[6] TTE can detect effusion and assess its haemodynamic importance, as well as constrictive pathophysiology (ESC 2025).[6] ESC 2025 says acute pericarditis may show a normal-appearing TTE in 40%–50% of first episodes, but new or worsening effusion is a diagnostic criterion for pericarditis.[6]
Measure in end-diastole.[6] ESC 2025 assesses effusion size by the end-diastolic distance of the echo-free space between the epicardium and the parietal pericardium.[6] It recommends that images include the extent and location of each effusion measurement, as this allows follow-up studies.[6]
ESC 2025 Table 10: classification of pericardial effusion (all rows)
| Feature | Category |
|---|---|
| Onset | Acute (≤4 weeks); subacute (>4 weeks to ≤3 months); chronic (>3 months) |
| Size (maximal end-diastolic diameter) | Mild: <10 mm; moderate: 10–20 mm; large: >20 mm |
| Distribution | Circumferential/loculated |
| Composition | Transudate/exudate |
In acute pericarditis, a large effusion (>20 mm on echocardiography; HR 2.15) is one of the major high-risk features in ESC 2025 Table 16.[6] Asymptomatic patients with mild idiopathic effusions do not generally require specific monitoring (ESC 2025).[6] With at least moderate effusions in asymptomatic patients, ESC 2025 calls follow-up every 6 months reasonable, ideally in specialised centres.[6]
ESC 2025 says TTE enables the recognition of cardiac tamponade and of constriction.[6] Tamponade is a clinical diagnosis, based on a suggestive history, symptoms and signs with imaging confirmation by echocardiography (ESC 2025).[6]
ESC 2025 Table 17: echocardiographic signs of cardiac tamponade (all rows; n.a., not available)
| Echocardiographic feature | Sensitivity | Specificity |
|---|---|---|
| Large pericardial effusion with swinging heart | n.a. | n.a. |
| Diastolic collapse of the RA | 50%–100% | 33%–100% |
| Duration of diastolic collapse of the RA as a ratio of the cardiac cycle length >0.34 | >90% | 100% |
| Diastolic collapse of the RV | 48%–100% | 72%–100% |
| Respiratory changes of the mitral E velocity >25%–30%, tricuspid E velocity >40%–60% | n.a. | n.a. |
| Inferior vena cava plethora (dilatation >20 mm and <50% reduction of diameter with respiratory phases), as well as hepatic vein dilatation | 97% | 40% |
ESC 2025 Recommendation Table 12 recommends pericardiocentesis (echocardiography-, CT- or fluoroscopy-guided) for cardiac tamponade, suspected bacterial or neoplastic pericarditis, or symptomatic moderate to large pericardial effusion despite medical therapy (Class I, Level C).[6] Tamponade physiology and drainage are in Pericardial effusion and tamponade physiology.
Pitfalls
Special populations
- Children (ESC 2023): correct cardiac dimensions and wall thickness for body size using z-scores, defined as the number of standard deviations from the population mean.[3]
- Older adults (ESC 2026 HF): a pragmatic approach to HFpEF diagnosis is advised to give the large population of elderly patients potentially affected access to diagnosis.[1]
- Atrial fibrillation (ESC 2026 HF): in Table 10, the simplified echocardiographic criteria supporting objective evidence of HFpEF, the LA dilatation threshold is >40 mL/m² in AF, against >34 mL/m² in sinus rhythm.[1]
- Obesity (ESC 2026 HF): testing for elevated natriuretic peptides may in most patients support the diagnosis of HFpEF, but diagnostic thresholds for HFpEF should be critically evaluated based on patient characteristics, especially with obesity and other factors that may reduce natriuretic peptide levels.[1]
- Chemotherapy (ESC 2026 HF): GLS offers more sensitive measures of early systolic dysfunction even before LVEF declines, of particular value in patients undergoing chemotherapy.[1]
- Athletes: ESC 2026 HF says LV systolic dysfunction should be considered present with an asymptomatic LVEF <50% in the absence of alternative explanations, such as athlete’s heart, and ESC 2023 says GLS may help discriminate HCM from athlete’s heart.[1][3]
- Poor acoustic windows: in its chronic coronary syndrome guideline, ESC 2024 says an echocardiographic contrast agent can be helpful in patients with poor acoustic windows; AHA/ACC 2022 recommends alternative imaging for LVEF when echocardiography is inadequate (COR 1, LOE C-LD).[7][2]
Evidence, guidelines and regional differences
ESC
Europe
- ESC 2026 HF: HFrEF is LVEF <50% with symptoms and/or signs of HF; the HFmrEF phenotype is eliminated
- ESC 2026 HF Table 10 (simplified echocardiographic criteria supporting objective evidence of HFpEF) includes E/e′ >9 at rest and LA volume index >34 mL/m² (sinus rhythm) or >40 mL/m² (AF)
- ESC/ERS 2022: maintaining the current TRV threshold (>2.8 m/s) for the echocardiographic probability of PH under the updated haemodynamic definition is recommended, Class I, Level C
AHA/ACC
United States
- AHA/ACC 2022 HF: HFrEF LVEF ≤40%; HFmrEF 41%–49% and HFpEF ≥50%, both requiring evidence of spontaneous or provokable increased LV filling pressures; HFimpEF previous LVEF ≤40% then >40%
- AHA/ACC 2022 Appendix 3 includes average E/e′ ≥15 and LAVI ≥29 mL/m²
- AHA/ACC 2026 PE Table 4 includes TAPSE ≤1.7 cm as abnormal and TR velocity ≥2.9 m/s as suggesting pulmonary hypertension
NHFA/CSANZ
Australia and New Zealand
- NHFA/CSANZ 2018: HFrEF is clinical symptoms with or without signs of HF and a measured LVEF of less than 50%; if LVEF is mildly reduced (41–49%), additional criteria are required (e.g. signs of HF; diastolic dysfunction with high filling pressure shown by invasive means, echocardiography or biomarker testing); the writing committee does not recommend a separate mid-range category at this time
- NHFA/CSANZ 2018: echocardiographic high filling pressure needs at least three of septal e′ less than 7 cm/s or lateral e′ less than 10 cm/s, average E/e′ more than 14, LA volume index more than 34 mL/m² and TR velocity more than 2.8 m/s
In Australia and New Zealand
NHFA/CSANZ 2018 chose a 50% LVEF cut-off between HFrEF and HFpEF mainly for therapeutic reasons.[10] Its writing committee did not recommend a separate mid-range EF (HFmrEF) category at that time.[10] The 2024 CSANZ position statement calls TTE the most widely available and utilised imaging modality for screening, diagnosis and serial monitoring of abnormalities of cardiac structure or function.[11] Its abstract says it covers TTE assessment of the left and right ventricles, valve disease, pericardial disease, pulmonary hypertension and other areas.[11]
Guidelines checked for this topic
Rows on this page come from ESC 2026 HF, ESC 2023 cardiomyopathies, ESC/ERS 2022 PH, ESC 2025 myocarditis and pericarditis, ESC 2024 CCS and ESC 2019 PE.[1][3][5][6][7][8] AHA/ACC rows come from the 2022 HF and 2026 PE guidelines, and ANZ statements from NHFA/CSANZ 2018 HF and the CSANZ 2024 TTE position statement abstract.[2][9][10][11] Each is the newest of its body in its area among the guidelines checked for this topic (census 2026-10-09). The 2021 ESC HF phenotypes appear only as dated history.[1] The not-held list follows.
- Not held as text, so not checked for this topic and not used: the ASE/EACVI 2015 chamber quantification recommendations (PMID 25559473), the ASE 2025 diastolic function recommendations (PMID 40617625), the ASE 2025 right heart guideline (PMID 40044341), the full text of the CSANZ 2024 TTE position statement (PMID 38749800) and the 2022 ESC cardio-oncology guidelines (PMID 36017568).
Exam pearls
- ESC 2026 HF: HFrEF is LVEF <50% with symptoms and/or signs of HF; HFmrEF is gone; improved LVEF is a rise of at least 10% (absolute) to at least above 40%.[1]
- AHA/ACC 2022: HFrEF ≤40%; HFmrEF 41%–49% and HFpEF ≥50%, both requiring evidence of spontaneous or provokable increased LV filling pressures; HFimpEF previous ≤40% then >40%.[2]
- ESC 2026 HF Table 10 (simplified echocardiographic criteria supporting objective evidence of HFpEF): LV mass index ≥95/≥115 g/m² (female/male) or RWT >0.42; LA volume indexed by BSA >34 (sinus rhythm) or >40 (AF) mL/m²; E/e′ >9 at rest (E/e′ ≥15 is more specific, but less sensitive, for the diagnosis of HFpEF); estimated sPAP >35 mmHg or TRV at rest >2.8 m/s. The other ESC 2026 HFpEF criteria are current or prior symptoms and/or signs of HF and an LVEF ≥50% that has not previously been <50%, and the objective evidence must be supported by raised natriuretic peptides.[1]
- ESC 2023: adult HCM is LV wall thickness ≥15 mm in any segment not explained solely by loading conditions; 13–14 mm needs evaluation of other features; in adult first-degree relatives of patients with unequivocal disease, the threshold is ≥13 mm.[3]
- ESC/ERS 2022: peak TRV is the key variable, threshold >2.8 m/s; signs from at least two of categories A/B/C change the probability level.[4][5]
- AHA/ACC 2026 PE Table 4 includes TAPSE ≤1.7 cm and TDI S′ ≤9.5 cm/s as abnormal, and its RV/LV definition is >0.9.[9]
- ESC 2025: effusion mild <10 mm, moderate 10–20 mm, large >20 mm, measured as the maximal end-diastolic diameter.[6]
- ESC 2025 Table 17: RA diastolic collapse lasting >0.34 of the cardiac cycle has >90% sensitivity and 100% specificity for tamponade.[6]
References11ShowHide
- [1]Køber L, et al. 2026 ESC Guidelines for the management of heart failure. Eur Heart J, 2026.PMID 42661420
- [2]Heidenreich PA, et al. 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. J Am Coll Cardiol, 2022.PMID 35379503
- [3]Arbelo E, et al. 2023 ESC Guidelines for the management of cardiomyopathies. Eur Heart J, 2023.PMID 37622657
- [4]Humbert M, et al. 2022 ESC/ERS Guidelines for the diagnosis and treatment of pulmonary hypertension. Eur Heart J, 2022.PMID 36017548
- [5]Humbert M, et al. 2022 ESC/ERS Guidelines for the diagnosis and treatment of pulmonary hypertension. Eur Respir J, 2023.PMID 36028254
- [6]Schulz-Menger J, et al. 2025 ESC Guidelines for the management of myocarditis and pericarditis. Eur Heart J, 2025.PMID 40878297
- [7]Vrints C, et al. 2024 ESC Guidelines for the management of chronic coronary syndromes. Eur Heart J, 2024.PMID 39210710
- [8]Konstantinides SV, et al. 2019 ESC Guidelines for the diagnosis and management of acute pulmonary embolism developed in collaboration with the European Respiratory Society (ERS). Eur Heart J, 2020.PMID 31504429
- [9]Creager MA, et al. 2026 AHA/ACC/ACCP/ACEP/CHEST/SCAI/SHM/SIR/SVM/SVN Guideline for the Evaluation and Management of Acute Pulmonary Embolism in Adults: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. J Am Coll Cardiol, 2026.PMID 41712898
- [10]Atherton JJ, et al. National Heart Foundation of Australia and Cardiac Society of Australia and New Zealand: Guidelines for the Prevention, Detection, and Management of Heart Failure in Australia 2018. Heart Lung Circ, 2018.PMID 30077227
- [11]Chong A, et al. 2024 CSANZ Position Statement on Indications, Assessment and Monitoring of Structural and Valvular Heart Disease With Transthoracic Echocardiography in Adults. Heart Lung Circ, 2024.PMID 38749800