Echocardiography is increasingly used for the diagnosis and management of congenital and acquired cardiac diseases. While a number of different echocardiographic formats are used in clinical practice, each involves reflection of ultrasound from cardiovascular tissues, specialised processing of returned (echoed) signals, and the ultimate display of this information in some recognisable visual or auditory format. Echocardiography has become increasingly sophisticated, and the combined modalities have largely replaced cardiac catheterisation and angiocardiography for diagnosis and assessment of cardiac lesions. Although the newest technologies are expensive and limited to referral hospitals and clinics, many practising veterinarians use, or will soon acquire, echocardiographs. Furthermore, veterinarians who are not yet performing echocardiographic studies, often find referral for echocardiography helpful or even essential for establishing a cardiac diagnosis, assessing ventricular function, determining a prognosis, and guiding medical or surgical therapy.
The echocardiographic examination must be placed within a proper clinical perspective (Table 1). Most importantly, echocardiography is not a substitute for a careful clinical examination and routine diagnostic studies such as measurement of arterial blood pressure, determination of serum thyroxine, measurement of the PCV, and thoracic radiography. Cardiac auscultation is still a useful and expedient method for identifying serious heart diseases; however, it should be appreciated that a significant percentage of cats with cardiomyopathy do not have an auscultable murmur or gallop. Furthermore, in up to 25% of cats examined with heart murmurs in our practice, we are unable to demonstrate significant morphologic lesions by 2D ECHO or unambiguous flow disturbances by Doppler studies.
Table 1.
Echocardiographical modalities
| Study | Morphological detail | Assessment of chamber size and haemodynamic burden a | Measurements of ventricular function | Abnormal blood flow | Valvular function |
|---|---|---|---|---|---|
| M-mode | Limited | Indirect estimates from detection of chamber enlargement, hypertrophy, abnormal valve movements or altered ventricular septal motion | Left ventricular shortening fraction; velocity of circumferential fibre shortening; systolic time intervals; mitral valve E-point to septal separation b | Does not detect | Poor Indirect assessment from imaging and valve motion |
| 2D | Excellent | As per M-mode echo; dilatation of the great vessels can also be detected readily | Ventricular ejection fraction c from volume estimates or shorten areas from short axis tomograms | Does not detect | Limited Indirect assessment from imaging and valve motion |
| Contrast Echo | Limited to imaging of the blood pool | Indirect—inferred from abnormal blood flow patterns | None | Sensitive, especially for right to left shunting | Limited unless performed during cardiac catheterisation |
| Pulsed-wave Doppler | None | Indirect—inferred from abnormal blood flow patterns Limited by inability to quantify high velocity signals c | Systolic estimates include aortic and pulmonary artery maximal velocity velocity time integral and acceleration time; diastolic estimates are based on analysis and measurements of mitral valve inflow velocity profiles and analysis of flow in pulmonary veins | Sensitive | Sensitive measure of valvular stenosis or insufficiency |
| Colour-coded Doppler | Limited to colour coding of the blood pool | Indirect—inferred from abnormal blood flow patterns Quantitation by analysis of the flow convergence region | Tissue Doppler imaging can be used to assess diastolic ventricular function | Sensitive | Sensitive measure of valvular insufficiency; stenosis can be detected but must be verified by other modalities |
| Continuous wave Doppler | None | Indirect—inferred from abnormal blood flow patterns Quantitation through calculation of pressure gradients across lesions | Similar to pulsed-wave Doppler | Sensitive | Sensitive measure of valvular stenosis or insufficiency |
Haemodynamic load refers to the increase in volume pumped or pressure generated by the ventricle during each cardiac cycle. In general, the more severe the cardiac lesion, the greater the haemodynamic burden.
For M-mode indices of ventricular function, left ventricular shortening fraction = (ventricular diastolic dimension—ventricular systolic dimension)/diastolic dimension; velocity of circumferential fibre shortening = shortening fraction/ejection time; systolic time intervals include pre-ejection period (onset of QRS to aortic opening) and ejection time; mitral valve E-point to septal separation = distance in cm from from mitral valve opening to the ventricular septum.
Ejection fraction = ventricular stroke volume/ventricular end-diastolic volume. A special form of pulsed-wave Doppler—high pulsed repetition frequency Doppler—can measure high velocity flow signals; this is a hybrid of pulsed and continuous wave Doppler.
Echocardiography should be performed and echocardiograms are best interpreted by clinicians who are knowledgeable of feline heart disease. One must understand the pertinent issues and questions during the examination. Moreover, the clinical assessment and treatment plan prescribed should be directed by an individual capable of integrating information from all sources, including the history, physical examination, radiography and laboratory tests. Therapeutic decisions should not be abdicated to a consultant unless that individual has a complete understanding of the clinical situation and has examined the patient and medical records. The echocardiographer must appreciate ultrasound physics and instrumentation so that artifacts are not overinterpreted and important information is not suppressed. Echocardiographic studies are very repeatable in experienced hands, but results can be highly operator and equipment dependent.
The veterinarian should appreciate the advantages and limitations of an echocardiographic study. A complete echocardiographic study should: (1) reveal the pertinent congenital or acquired anatomic lesions (morphologic diagnosis); (2) estimate haemodynamic burden through quantitation of cardiac chamber size (dilatation and hypertrophy); (3) quantify ventricular systolic function: (4) estimate ventricular diastolic function; (5) evaluate valvular function; and (6) refine haemodynamics with pressures estimates. Properly gathered and interpreted, this information should lead to a definitive cardiac diagnosis and illustrate the haemodynamic consequences of structural and functional cardiac lesions. Such detailed information can be obtained through complementary echocardiographic modalities; however, limited echo studies can also be useful in selected situations, as with rapid screening for pericardial effusion or when an expedient estimate of left ventricular ejection fraction is needed.
The routine feline echocardiographic study should include images obtained from the right and often the left hemithorax. Short axis images from the papillary muscle, mitral, and aortic/left atrial levels are obtained. The papillary muscles and left ventricular walls should be assessed for hypertrophy and the left auricle examined for thrombus. The right ventricular outlet can be examined and interrogated by Doppler studies. Long axis images optimised for the left ventricular inlet (left atrium, mitral valve) and left ventricular outlet (outflow tract, aortic valve, aorta) are essential. Diastolic measurements of at least four wall segments should be taken using these 2D ECHO imaging planes. Diastolic wall measures of 6 mm or greater are considered indicative of hypertrophy. The routine M-mode echo is also recorded to measure left ventricular wall and chamber dimensions, but placing the cursor across the papillary muscles will lead to significant measurement error. Furthermore, the M-mode may fail to identify regional hypertrophy. The maximal left atrial systolic diameter should be measured by 2D studies. In most normal cats, this measure will be <16 mm. Volume depletion (including zealous diuresis) can lead to misleading results inasmuch as chamber dimensions are reduced and ventricular ‘pseudohypertrophy’ may be induced. Global ventricular function should be estimated. Dynamic obstruction should be sought using 2D imaging, M-mode interrogation of the valve and Doppler studies. Mitral regurgitation is common in cats with cardiomyopathy, and this systolic event can be identified by Doppler studies. The left hemithorax is examined when Doppler methods are available. Mitral regurgitation and dynamic outlet obstruction can be identified from an apical window. Transmitral flow patterns, isovolumetric relaxation time, and pulmonary venous flow patterns are recorded and measured to identify diastolic dysfunction. Tissue Doppler imaging may be employed to evaluate wall motion. The interior of the left auricle is scrutinised for thrombus using 2D ECHO from a craniodorsal transducer position whenever that chamber is enlarged.
Echocardiography is clearly useful in the assessment of cats with heart diseases, especially with acquired disorder of the myocardium. There are also indications for performing echocardiography in cats with congenital heart diseases. Salient features of these clinical conditions are summarised in Tables 2 and 3.
Table 2.
Usual echocardiographical findings in feline congenital heart diseases
| Cardiac disorder | 2D echocardiography | M-mode echocardiography | Doppler studies |
|---|---|---|---|
| Atrial septal defect | ‘Drop out’ of atrial septal echoes (ASD); dilatation of the RA, RV, PA, ±LA | Paradoxical ventricular septal motion and right ventricular volume overload | Low velocity shunt across the defect |
| Ventricular septal defect | ‘Drop out’ of ventricular septal echoes (VSD); dilatation of the LA, LV, ±RV, ±PA; ± evidence of RV outlet obstruction; rarely prolapse of aortic valve into VSD | Evidence of volume overload; Normal LV shortening fraction | Turbulent, high velocity systolic jet crossing the defect; possibly aortic regurgitation a |
| Patent doctus arteriosus | Dilation of the LA, LV, Ao, PA; can generally image ductal ampulla; often evidence of pulmonary hypertension and RV hypertrophy | Normal to reduced shortening fraction | Continuous, high velocity, turbulent flow traversing the ductus and entering the pulmonary artery a,b |
| Tetralogy of fallot | Large subaortic ventricular septal defect; RV hypertrophy; RA dilation; right ventricular outflow obstruction; aortic malalignment (override); contrast echocardiography demonstrates right to left shunting | RV hypertrophy; malalignment of the aorta; flat ventricular septal motion; relatively small left heart chambers | Turbulent, high velocity systolic signal in the RV outlet and pulmonary artery; low velocity shunt from right to left across the VSD |
| Mitral valve dysplasia (congenital mitral regurgitation) | Valve thickening, abnormal chordae tendineae or papillary muscles, possible leaflet fusion; dilated LA and LV; may have left ventricular outflow tract obstruction as well | Thick mitral valve; abnormal valve motion; dilated LA and LV; increased LV shortening fraction | Turbulent, high velocity, systolic signal of mitral regurgitation in the LA; possible increase in diastolic mitral valve velocities b,c |
| Tricuspid valve dysplasia (congenital tricuspid regurgitation) | Valve thickening, abnormal chordae tendineae or papillary muscles, possible leaflet fusion; dilated RA and RV | Thick tricuspid valve; abnormal valve motion; dilated RA and RV; paradoxical ventricular septal motion | Turbulent, high velocity systolic signal in the RA; possible increase in diastolic tricuspid valve velocities c,d |
Major points are emphasised; this table is not comprehensive. LA, left atrium; RA, right atrium; LV, left ventricle; RV, right ventricle; Ao, aorta; PA, pulmonary artery; PDA, patent ductus arteriosus; VSD, ventricular septal defect; ASD, atrial septal defect.
Mild increases in diastolic mitral (PDA, VSD) and systolic aortic velocities (PDA) will usually be recorded owing to increased volume flow.
The velocity depends on the relative pressure between the systemic and pulmonary circulations; generally the velocity is directly related to pressure differences and inversely related to the diameter of the defect.
Mild increases in diastolic tricuspid and systolic pulmonary artery velocities will usually be recorded owing to increased transvalvular flow.
Congenital atrioventricular valve stenosis is relatively rare, but would be associated with other findings including a narrowed valve orifice or tethered valve leaflets, dilated atrium, increased transvalvular diastolic velocities (E and A waves), prolonged pressure half-time, and often concurrent valvular regurgitation.
Table 3.
Usual echocardiographical findings in feline acquired heart diseases
| Cardiac disorder | 2D echocardiography | M-mode echocardiography | Doppler studies |
|---|---|---|---|
| Pericardial effusion | Fluid-filled, sonolucent or mixed-echoic pericardial space; possible cardiac or heart base tumour (usually lymphoma); collapse of the RA and RV in cardiac tamponade; may observed pleural effusion as well | Sonolucent pericardial space evident; abnormal cardiac motion; RA and RV collapse if tamponade | Exaggerated respiratory variation in the transvalvular tricuspid and pulmonary artery velocity signals |
| Feline hypertrophic cardiomyopathy | LA dilatation; LV hypertrophy; hypertrophy may be symmetric and involving the entire ventricle, asymmetric with hypertrophy of the septum or free wall, or focal hypertrophy of the ventricle | Normal to decreased LV dimensions; LV hypertrophy; LA dilation; normal to increased shortening fraction; possible systolic anterior motion of the septal mitral valve leaflet | Turbulent, high velocity systolic signal of mitral regurgitation often recorded in the LA; turbulent, high velocity systolic signal recorded in the left ventricular outlet in cats with obstructive form of hypertrophic cardiomyopathy; ± abnormal isovolumetric relaxation time |
| Feline restrictive (intermediate) cardiomyopathy | LA dilatation, RA dilatation, ±RV dilatation; mild LV dilatation with variable hypertrophy; hyperechoic subendocardium; regional ventricular wall dysfunction is possible | Normal to mildly decreased LV shortening fraction; LA dilatation; possible regional wall motion abnormalities | Variable; turbulent high velocity systolic signals of mitral or tricuspid regurgitation may be recorded |
| Dilated cardiomyopathy | LA and LV or generalised cardiac dilatation; global ventricular hypokinesis or marked depression of systolic ventricular free wall contraction and thickening | Ventricular and atrial dilatation; decreased LV shortening fraction is required to establish the diagnosis; increases E-Point to Septal separation, ± delayed mitral valve closure (B-shoulder) indicates elevated atrial and ventricular diastolic pressures | Turbulent, high velocity systolic signals of mitral and tricuspid regurgitation are common; decreased aortic velocity and acceleration time; abnormal indices of diastolic ventricular function |
| Feline hyperthyroidism | Mild to moderate LA and LV dilatation; LV hypertrophy; variable RA and RV dilatation; if heart failure, all chambers dilated and pleural effusion | LV hypertrophy; mild to moderate LV and LA dilatation; increased LV shortening fraction in most cases; normal to decreased shortening fraction if heart failure | Variable: may observe turbulent jets of mitral regurgitation or tricuspid regurgitation; increased aortic velocity may be recorded |
| Bacterial endocarditis | Valvular thickening—irregular often oscillating echodensities on aortic or mitral valves; longstanding cases may appear calcified; dilation of the left atrium and left ventricle if volume overload is severe | Highly thickened valve; echodense material moves in association with the cardiac cycle; cardiomegaly due to volume or pressure overload; premature closure of the mitral valve in peracute, severe aortic regurgitation | Evidence of valvular regurgitation and increased transvalvular flow velocities across the affected heart valve; in cases of chronic endocarditis the valve may become stenotic with Doppler evidence of aortic or mitral valve stenosis |
| Heartworm disease | Dilated PA, RV, RA; may observe echogenic densities (double, parallel lines) in the main or branch PA; filaria may be evident in the right ventricle and right atrium | If severe, RV dilatation and flat or paradoxical ventricular septal motion | Possible a high velocity diastolic signal of pulmonary insufficiency in the RV outlet; possibly high velocity tricuspid regurgitation |
For abbreviations, see Table 2.