Transthoracic Echocardiography

Transthoracic echocardiography (TTE) is the first line imaging test for the heart.

It uses a 2 to 5 MHz phased array probe placed on the chest wall. It produces two dimensional images, M-mode traces, spectral Doppler (pulsed wave and continuous wave), colour Doppler and tissue Doppler imaging. Where available, it adds three dimensional imaging, strain imaging and contrast enhancement (microbubbles for opacification of the left ventricle). The patient lies in the left lateral position.

The usual windows are parasternal long axis and short axis, apical four chamber, five chamber, two chamber and long axis, subcostal, and suprasternal.

The study measures chamber sizes and wall thickness, left ventricular systolic function (ejection fraction by biplane Simpson method), diastolic function, regional wall motion, valve structure and function, right heart size and pressure, pericardium, aorta, and intracardiac masses. The examination takes 30 to 45 minutes, with no radiation and no ionising contrast.

TTE is among the most frequently performed imaging tests. Heart failure affects 1 to 2% of adults and more than 10% of those over 70 years. Valvular heart disease affects around 2.5% of the population (13% of those over 75 years). Cardiomyopathy, congenital heart disease, pericardial disease and infective endocarditis are all assessed by TTE.

Left ventricular ejection fraction (LVEF) is the key measure for classification (reduced under 40%, mildly reduced 41 to 49%, preserved 50% or more) and selection of therapy. Doppler estimates of valve gradients and pulmonary pressure decide the timing of intervention.

Indications. Dyspnoea, oedema or suspected heart failure. Chest pain, myocardial infarction (wall motion, complications such as mitral regurgitation, ventricular septal rupture, free wall rupture and thrombus). Murmur, suspected valve disease and follow up of known valve disease. Suspected infective endocarditis (vegetations, abscess).

Syncope with suspicion of structural disease (aortic stenosis, hypertrophic cardiomyopathy). Atrial fibrillation (baseline). Hypertension with end organ assessment (left ventricular hypertrophy). Source of embolism. Pericardial effusion and tamponade. Suspected pulmonary embolism and pulmonary hypertension. Cardiomyopathies and screening of family members.

Congenital heart disease, adult and paediatric. Cardiotoxicity monitoring during cancer therapy. Aortic root dilatation (Marfan syndrome). Pre-operative assessment in patients with known or suspected heart disease. Intraoperative and critical care use for unexplained haemodynamic instability. Not as routine screening in asymptomatic low risk people.

Contraindications and precautions. None. Poor acoustic windows occur in obesity, chronic lung disease, chest wall deformity, and after chest surgery, and ultrasound contrast agents (a lipid or albumin shell with gas) improve endocardial definition when two or more segments are not visualised.

Contrast is used cautiously in patients with known allergy to the agent components and in those with severe pulmonary hypertension or unstable cardiopulmonary conditions. Electrocardiogram electrodes are placed for timing. Blood pressure and heart rate are recorded, as loading conditions affect results.

Preparation and technique. No fasting is needed.

The usual views are acquired in sequence:

• Parasternal long axis (left ventricle, left atrium, aortic root, aortic and mitral valves).
• Parasternal short axis at aortic, mitral and papillary muscle levels.
• Apical four chamber, five chamber, two chamber and three chamber (long axis).
• Subcostal (inferior vena cava, atrial septum, pericardium).
• Suprasternal (aortic arch).

Measurements include:

• Left ventricular internal diameter and wall thickness, LVEF by biplane Simpson method, left atrial volume index.
• Right ventricular size and function (tricuspid annular plane systolic excursion, fractional area change, S' velocity).
• Mitral inflow (E and A velocities, E/A ratio, deceleration time), tissue Doppler (e' velocity and E/e' ratio).
• Tricuspid regurgitation velocity (for pulmonary systolic pressure), inferior vena cava diameter and collapse (right atrial pressure), and aortic dimensions.

Valve gradients are calculated by the simplified Bernoulli equation (pressure gradient is 4 times the velocity squared), and valve area by the continuity equation or pressure half time.

Normal appearances. Left ventricle: end diastolic diameter 4.2 to 5.8 cm in men and 3.8 to 5.2 cm in women, wall thickness 0.6 to 1.1 cm, LVEF 55 to 70%, with uniform wall thickening and inward motion of all segments. Left atrium: volume index under 34 mL each square metre. Right ventricle: basal diameter under 4.1 cm, tricuspid annular plane systolic excursion 17 mm or more.

Aortic root 2.0 to 3.7 cm. Aortic valve: three thin leaflets opening fully, peak velocity under 2.0 m each second, valve area 3 to 4 cm2. Mitral valve: two thin leaflets, area 4 to 6 cm2, mean gradient under 5 mmHg. Trivial or mild regurgitation of the tricuspid, pulmonary and mitral valves is common and normal.

Diastolic function: E/A ratio 0.8 to 2, septal e' velocity of 7 cm each second or more, E/e' ratio under 14, tricuspid regurgitation velocity under 2.8 m each second. Inferior vena cava under 2.1 cm with over 50% collapse. Pericardium: thin and without fluid (a small physiological amount of fluid may be seen in systole).

Interpretation.

• Systolic heart failure: LVEF under 40% (reduced), dilated left ventricle, global hypokinesis (dilated cardiomyopathy) or regional wall motion abnormality (ischaemic), functional mitral regurgitation, and left ventricular thrombus (echogenic mass at the apex of an akinetic segment).
• Heart failure with preserved ejection fraction: LVEF 50% or more, left atrial enlargement (volume index over 34), increased wall thickness, diastolic dysfunction (E/e' over 14, septal e' under 7, tricuspid regurgitation velocity over 2.8 m each second), and raised pulmonary pressure.
• Diastolic dysfunction grades 1 (impaired relaxation) to 3 (restrictive filling).
• Regional wall motion abnormality: hypokinetic, akinetic or dyskinetic segments in a coronary artery territory (left anterior descending, circumflex, right coronary).
• Complications of myocardial infarction include aneurysm, pseudoaneurysm, papillary muscle rupture, ventricular septal rupture, pericardial effusion and right ventricular infarction.
• Cardiomyopathies:
  • Hypertrophic: asymmetrical septal thickness over 15 mm, systolic anterior motion of the mitral valve, left ventricular outflow gradient over 30 mmHg at rest or with provocation.
  • Restrictive and infiltrative (amyloid): increased wall thickness with speckled "sparkling" myocardium, biatrial enlargement, reduced global longitudinal strain with apical sparing, small pericardial effusion.
  • Takotsubo (apical ballooning).
  • Arrhythmogenic right ventricular cardiomyopathy (dilated right ventricle with regional dyskinesia).
  • Non-compaction (trabeculated left ventricle).
  • Chagas disease (apical aneurysm).
• Aortic stenosis: thickened, calcified, restricted leaflets.
• Severe aortic stenosis: peak velocity 4.0 m each second or more, mean gradient 40 mmHg or more, valve area under 1.0 cm2 (indexed under 0.6 cm2 each square metre), or dimensionless index under 0.25. Low flow, low gradient stenosis is seen with reduced stroke volume.
• Aortic regurgitation: diastolic jet in the left ventricular outflow tract, vena contracta width over 6 mm, pressure half time under 200 ms for severe regurgitation, holodiastolic flow reversal in the descending aorta, and a dilated left ventricle.
• Mitral stenosis (rheumatic): thickened leaflets with commissural fusion and "hockey stick" doming, mean gradient over 10 mmHg and valve area 1.5 cm2 or less (severe 1.0 cm2 or less), enlarged left atrium, and spontaneous contrast or thrombus.
• Mitral regurgitation: primary (prolapse, flail leaflet, rheumatic) or secondary (functional).
• Severe mitral regurgitation: vena contracta 7 mm or more, effective regurgitant orifice area 0.4 cm2 or more, regurgitant volume 60 mL or more, systolic flow reversal in pulmonary veins, and a dilated left atrium and ventricle.
• Right heart: right ventricular dilatation and dysfunction, tricuspid regurgitation, and dilated inferior vena cava without collapse (raised right atrial pressure).
  • Pulmonary embolism: McConnell sign of akinetic mid free wall with preserved apex.
  • Pulmonary hypertension: septal flattening, "D-shaped" left ventricle, pulmonary systolic pressure estimated by 4 times tricuspid regurgitation velocity squared plus right atrial pressure, over 35 to 40 mmHg abnormal.
• Infective endocarditis: oscillating mobile mass on a valve (vegetation), valve perforation, flail leaflet, paravalvular abscess (thickened aortic root, echolucent cavity), and new regurgitation.
• TTE sensitivity is about 60 to 70%, so transoesophageal echocardiography is performed if suspicion remains.
• Pericardial disease:
  • Pericardial effusion (small under 10 mm, moderate 10 to 20 mm, large over 20 mm).
  • Tamponade (right atrial and right ventricular diastolic collapse, plethoric inferior vena cava, exaggerated respiratory variation of mitral and tricuspid inflow over 25% and 40% respectively).
  • Constrictive pericarditis (thickened pericardium, septal bounce, respiratory ventricular interdependence, preserved or raised e' velocity, hepatic vein expiratory flow reversal).
• Congenital heart disease: atrial septal defect (right heart dilatation, shunt on colour Doppler), ventricular septal defect, patent ductus arteriosus, coarctation of the aorta, bicuspid aortic valve, tetralogy of Fallot, transposition of the great arteries, and Ebstein anomaly.
• Aorta: aortic root dilatation (over 4.0 cm), ascending aortic aneurysm, dissection (intimal flap in the root or arch), and coarctation.
• Intracardiac masses: thrombus (left atrial appendage better seen by transoesophageal echocardiography; left ventricular apical thrombus), myxoma (pedunculated mass in the left atrium attached to the septum), papillary fibroelastoma, and metastases or lymphoma.
• Prosthetic valves: gradient and effective orifice area against expected values for valve type and size, dehiscence, paravalvular leak, obstruction by thrombus or pannus.
• Strain imaging: global longitudinal strain weaker than -18% suggests early myocardial dysfunction, including cardiotoxicity (a fall of over 15% from baseline or an LVEF fall of over 10 points to under 50%).

Critical values and findings needing immediate action.

• Cardiac tamponade (large effusion with chamber collapse, plethoric inferior vena cava, shock): urgent pericardiocentesis or surgical drainage.
• Aortic dissection involving the root or arch (flap, aortic regurgitation, effusion): emergency CT angiography or transoesophageal echocardiography and cardiac surgery.
• Mechanical complications of myocardial infarction (papillary muscle rupture, ventricular septal rupture, free wall rupture): emergency surgical referral and stabilisation.
• Massive pulmonary embolism with right ventricular strain and shock: thrombolysis or embolectomy.
• Mobile left heart mass or vegetation with embolic events, heart failure, or abscess: urgent cardiology and cardiac surgery review.
• Severe symptomatic aortic stenosis, severe acute mitral or aortic regurgitation with haemodynamic compromise: urgent valve intervention.
• Severely reduced LVEF (under 20 to 30%) with cardiogenic shock: intensive care and mechanical support evaluation.
• Left ventricular thrombus after infarction: anticoagulation.
• Prosthetic valve thrombosis or obstruction: urgent thrombolysis or surgery.
• Severe left ventricular outflow obstruction or hypertrophic cardiomyopathy with syncope: specialist care and avoidance of vasodilators and dehydration.
• Large pericardial effusion without tamponade: close monitoring and elective drainage depending on cause.

Limitations and artefacts.

• Image quality depends on the acoustic window; in 10 to 20% of patients (obesity, emphysema, ventilated patients, chest wall deformity) endocardial definition is poor, and contrast, a different window, or alternative imaging (cardiac MR, transoesophageal echocardiography) is needed.
• LVEF has inter-observer variability of 5 to 10 points and underestimates volume (foreshortening of the left ventricle, poor endocardial border detection); 3D echocardiography and contrast reduce this.
• Doppler gradients depend on the angle (underestimation if the beam is not parallel to flow), on loading conditions and on heart rate.
• Bernoulli overestimates gradients in the presence of pressure recovery or high proximal velocity. In low flow states, severe aortic stenosis can have a low gradient.
• Valve regurgitation severity is hard to measure, uses an integrated approach with several parameters, and varies with blood pressure and loading.
• Pulmonary pressure estimation requires a measurable tricuspid regurgitant jet and an estimate of right atrial pressure; it can be inaccurate by 10 mmHg or more compared with catheterisation, and is not diagnostic of pulmonary hypertension alone.
• Right ventricular assessment is difficult because of its complex shape.
• Small structures (vegetation under 3 mm, left atrial appendage thrombus, small shunts, coronary anomalies) are missed; transoesophageal echocardiography or other tests are used.
• Normal values vary with age, sex, body size and ethnicity; indexing to body surface area is needed.
• The study is operator dependent, and an incomplete study should be stated.
• Echocardiography at rest does not exclude coronary artery disease.
• Foetal and paediatric study needs a specialist.

Special groups.

• Pregnancy: safe; physiological changes include mild increase in chamber size, increased cardiac output, and trivial regurgitation; used for peripartum cardiomyopathy, rheumatic mitral stenosis and congenital disease.
• Athletes: physiological hypertrophy (wall thickness up to 13 mm, left ventricular diameter up to 6 cm) must be separated from cardiomyopathy.
• Older adults: aortic sclerosis and mitral annular calcification are common; degenerative aortic stenosis and amyloid.
• Children: normal values are scaled to body size (Z-scores), and congenital lesions are the main indication.
• Critically ill and ventilated patients: limited windows, focused studies, and fluid responsiveness assessment.
• Patients with cancer: serial studies for cardiotoxicity (anthracyclines, trastuzumab, immune checkpoint inhibitors).
• Patients with HIV: pericardial effusion, pulmonary hypertension and cardiomyopathy.
• Regions: rheumatic heart disease is a major cause of heart failure and valve disease in young people (screening by handheld echocardiography detects latent disease).
• Other major causes in such regions are dilated cardiomyopathy, peripartum cardiomyopathy, hypertensive heart disease, tuberculous pericarditis (large effusion, constriction), endomyocardial fibrosis (obliterated apex with restrictive filling), Chagas disease, and congenital disease.
• Echocardiography is often the only cardiac test available.

Follow up tests.

• Electrocardiogram, chest radiograph, natriuretic peptides (B-type natriuretic peptide, N-terminal pro-B-type natriuretic peptide), troponin.
• Transoesophageal echocardiography (endocarditis, left atrial appendage thrombus, prosthetic valve, aortic dissection, mitral valve assessment).
• Stress echocardiography or stress imaging (ischaemia and low flow aortic stenosis).
• Cardiac MR (cardiomyopathy, myocarditis, infiltration, viability, congenital disease).
• CT coronary angiography and calcium scoring, invasive coronary angiography and right heart catheterisation.
• Ambulatory rhythm monitoring, blood cultures (endocarditis), pericardial fluid analysis.
• Genetic testing and family screening.
• Repeat echocardiography at set intervals for valve disease (annually in severe, every 1 to 2 years in moderate).
• Referral to cardiology or cardiac surgery.