Fig. 6.1 Coronary angiogram showing a normal left coronary artery.
Cardiac markers of myocardial necrosis
Cardiac volumetric imaging: magnetic resonance and computed tomography
Electrocardiographic monitoring
Cardiac catheterization is an invasive procedure during which catheters are placed within the cardiac chambers, coronary arteries, and great vessels to provide information on cardiac anatomy, pressures, disease states, function, and O2 saturations.
•Diagnosis of suspected coronary artery disease (after appropriate non-invasive assessment or if results are equivocal).
•Assessment of coronary artery disease burden and suitability for intervention, e.g. percutaneous coronary intervention (PCI), coronary artery bypass surgery, or cardiac transplantation.
•Measurement of intracardiac pressures in patients with valvular heart disease (largely superseded by non-invasive imaging).
•Detailed measurement of left and right ventricular cardiac output and pulmonary hypertension in patients considered for cardiac transplantation or with suspected congenital heart disease.
•Evaluation of O2 saturations in cardiac chambers to identify cardiac shunting.
•Myocardial biopsy in patients with cardiomyopathy of unknown cause.
•Monitoring of cardiac transplantation success/rejection.
•Pregnancy is an absolute contraindication to coronary angiography.
•Relative contraindications include:
•Severe peripheral vascular disease.
•Unstable cardiac failure or arrhythmias.
•Sensitivity to contrast agents.
The patient is fasted for 4h prior to the procedure. IV access is required, together with haemodynamic and ECG monitoring. Sedation may be used according to patient request or operator direction. It is important that the patient understands the risks of the procedure and gives informed written consent. The contrast agents used can provoke renal failure in susceptible patients. Metformin should be withdrawn for 48h prior to the procedure. In patients with renal impairment, pre-treatment with acetylcysteine is advised and a less nephrotoxic contrast agent may be considered. Contrast agent volume should be minimized.
1.The patient lies flat on a catheter laboratory table and appropriate monitoring is applied.
2.LAn is used and an aseptic technique employed. For a left heart procedure, arterial access is required. The radial artery is the most commonly employed, but the femoral artery provides an alternative route (unless significant peripheral vascular disease is present).
3.The chosen artery is cannulated using the Seldinger technique, and an access sheath inserted.
4.Fluoroscopic screening is used to monitor the passage of a guidewire and catheter to the heart.
5.Catheters are pre-shaped according to the structure being examined. Typically, a Judkins left 4 catheter is used for the left coronary artery, Judkins right 4 catheter for the right coronary artery, and an angled pigtail catheter is placed in the LV and/or aorta for examination of these structures.
6.A contrast agent is injected for image acquisition. Images of the coronary arteries are acquired in multiple planes in order to optimally identify coronary artery stenoses. Continuous pressure transducers can be used for dynamic left heart pressure monitoring, e.g. LV and aorta.
7.Evaluation of the right heart necessitates venous access. The commonest access point is the femoral vein, but the central veins, e.g. subclavian or internal jugular vein, can also be used.
8.A right heart or Swan–Ganz catheter is passed towards the right heart. Right-sided pressures, e.g. vena cavae, right atrium, right ventricle (RV), pulmonary artery (PmA), and pulmonary capillary wedge pressure (indirect left atrial (LAt) pressure), can be measured.
9.Blood samples obtained from these sites can be analysed for O2 saturation and used to identify the presence and site of cardiac shunts, e.g. atrial or ventricular septal defects. Cardiac output studies can also be performed.
Cardiac catheterization is an invasive technique, and so there are inherent risks to the procedure (1:200 patients). Full cardiopulmonary resuscitation facilities should be immediately available.
•Trauma to arterial/venous access sites, including haematoma, occlusion, aneurysm, pseudo-aneurysm, nerve damage.
•Aortic/coronary artery dissection.
•Pulmonary oedema (left main stem stenosis).
•Vasovagal response to arterial access/sheath removal.
Additionally, the patient is exposed to ionizing radiation, and so screening/image acquisition times should be reduced as much as possible. Serial studies should be avoided.
•Coronary artery anatomy and distribution of disease, to aid decisions regarding the need for revascularization (see Fig. 6.1).
•Left ventricular size and function.
•Aortic and mitral valve integrity.
•Right ventricular size and function.
•Tricuspid and pulmonary valve integrity.
•Congenital abnormalities, e.g. shunts.
•Myocardial histopathology where biopsy is taken.
Invasive coronary angiography has high resolution for the evaluation of coronary artery disease and is the current gold standard imaging technique for this application. However, CT coronary angiography is rapidly becoming an accurate alternative means of depicting coronary artery atheroma, particularly in the proximal vessels. Advances in echocardiography and cardiovascular MR (CMR) have reduced the need for right heart catheterization, but the latter is still the only means with which to obtain direct histopathological information from myocardial structures.
The procedure is invasive and the risks involved are not insignificant. Whilst coronary angiography is the gold standard for the demonstration of anatomical coronary arterial lesions, it provides little information regarding their physiological significance on the myocardium. The information should therefore be used in conjunction with imaging techniques that can assess the adequacy of myocardial perfusion, e.g. stress nuclear imaging, stress echocardiography, or CMR.
Further reading
Callan P, Clark AL. Right heart catheterisation: indications and interpretation. Heart 2016; 102: 1–11.
Fihn SD, Blankenship JC, Alexander KP, et al. 2014 ACC/AHA/AATS/PCNA/SCAI/STS Focused update of the guideline for the diagnosis and management of patients with stable ischemic heart disease. J Am Coll Cardiol 2014; 64: 1929–49.
When cardiac muscle is damaged, certain substances, e.g. troponins I (TnI) and T (TnT), myoglobin, and creatine kinase, are released into the bloodstream and can be measured by biochemical assays. Such assays can be helpful in making the diagnosis of ACS or myocardial contusion. Myoglobin and creatine kinase (CK and CK-MB) are relatively non-specific cardiac markers of myocardial necrosis (CK is also released by skeletal muscle) that are elevated within 2–4h of myocyte damage. Troponins (TnT and TnI) are cardiac muscle proteins that are released into the peripheral circulation more slowly and are highly specific for myocardial injury. High-sensitivity troponin assays (hsTnT and hsTnI) detect troponins at much lower concentrations than the standard troponin assays available previously, allowing more rapid diagnosis in ACS. Using a high-sensitivity assay, an initial elevation of circulating troponin levels is detectable within 3h of the event, peaking at around 24h (see Fig. 6.2).
Patients presenting with unstable ischaemic cardiac pain are initially labelled as having an ACS and are categorized on the basis of their initial 12-lead ECG into ST-segment elevation ACS (which requires urgent reperfusion via primary PCI or thrombolysis) or non-ST-segment elevation ACS (which requires appropriate antiplatelet and antithrombotic therapy, followed by coronary revascularization as appropriate). MI is confirmed later if there is a rise in markers of myocardial necrosis, most commonly troponins. When these markers are raised, those presenting with an ST-segment elevation ACS are classified as ST-elevation myocardial infarction (STEMI) and those with non-ST-elevation ACS are classified as non-ST-elevation MI (NSTEMI).
•In conjunction with the clinical history and 12-lead ECG to diagnose and categorize suspected ACS.
•To ascertain the extent of any myocardial injury following coronary revascularization procedures.
•To identify myocardial contusion following thoracic trauma.
A 10mL venous blood sample is sufficient. For hsTnT or hsTnI testing, this sample is ideally taken 3–6h after the patient’s most severe symptoms. Repeat sampling is necessary to demonstrate a rise in cardiac markers.
In patients who have had thrombolysis for acute MI, bleeding or haematoma formation may occur spontaneously at venepuncture sites.
Within the normal population, 99% of individuals will have a hsTnT <14ng/L. In the appropriate clinical setting of chest pain typical of acute MI ± ECG changes:
•An elevated troponin (hsTnT >30ng/L) is consistent with a diagnosis of MI.
•Acute MI (STEMI and NSTEMI) can be confidently excluded if a high-sensitivity troponin result is within normal limits 6h after the onset of symptoms.
CK may be elevated in skeletal muscle injury, as well as with MI. Direct estimation of CK-MB, the isoenzyme that is more specific for cardiac muscle, may be helpful. Troponins are more specific for cardiac injury but may also be elevated in cardiac failure, arrhythmias, renal failure, or PE, and so the clinical context should always be taken into account. Timing of blood samples is critical since values may be normal if blood is taken too soon after symptom onset. Troponins may remain elevated for up to 14 days following a cardiac event, and so the diagnosis of re-infarction using troponins alone may be unreliable.
Further reading
Shah ASV, Anand A, Sandoval Y, et al. High-sensitivity cardiac troponin I at presentation in patients with suspected acute coronary syndrome: a cohort study. Lancet 2015; 386: 2481–8.
Sherwood MW, Newby LK. High-sensitivity troponin assays: evidence, indications, and reasonable use. J Am Heart Assoc 2014; 3: e000403.
Thygesen K, Alpert JS, Jaffe AS, et al. Third universal definition of myocardial infarction. J Am Coll Cardiol 2012; 60: 1581–98.
Cardiac volumetric imaging is now established as a powerful tool to visualize the anatomy, size, and function of cardiac structures, i.e. valves, chambers, myocardium, pericardium, and great vessels. Advanced technology MR imagers and multislice CT scanners are increasingly available to clinicians. These techniques provide information regarding the aetiology and severity of most congenital and acquired cardiac abnormalities.
The indications for CMR and CT are shown in Table 6.1. CMR is especially useful in patients with IHD where a comprehensive assessment of left ventricular function, reversible myocardial ischaemia, and myocardial viability can be made. Cardiac CT is of particular value in screening for coronary artery disease and for assessment of the great vessels and coronary arteries.
Table 6.1 Indications for CMR and CT
| Condition | MRI | CT |
| Congenital heart disease | +++ | ++ |
| Anatomy, size, or mass of cardiac chambers (left atrium, LV, right atrium, RV) | ++++ | +++ |
| Global and regional left ventricular function | ++++ | +++ |
| Screening (cardiomyopathy, including arrhythmogenic right heart) | ++++ | + |
| Valvular heart disease (aortic, mitral, tricuspid, and pulmonary) | +++ | + |
| Prosthetic heart valves | +++ | + |
| Cardiac masses | +++ | ++ |
| Pericardial disease | +++ | ++ |
| Aortic disease | +++ | ++++ |
| Coronary artery anatomy and patency | ++ | ++++ |
| Screening for coronary artery disease | + | ++++ |
| Myocardial perfusion | +++ | – |
| Stress study in IHD | ++++ | – |
| Myocardial viability | ++++ | + |
•Presence of any ferrous metal, e.g. intracranial clips, intra-ocular foreign bodies, shrapnel (MRI).
•Temporary or permanent pacing systems (MRI), unless MRI-conditional.
•Internal cardioverter–defibrillator (ICD) systems (MRI), unless MRI-conditional.
•Clinically dehiscing Starr–Edwards valve prostheses manufactured between 1960 and 1964 (MRI).
•Severe claustrophobia (more of an issue with MRI).
•Allergy to non-ionic contrast agents (CT).
•Pregnancy is a relative contraindication to MRI, but an absolute contraindication to CT.
A patient questionnaire is performed to exclude contraindications. Patients should be relaxed and have the procedure explained, so that they are able to co-operate effectively. Breath-holding techniques should be practised prior to the scan to achieve optimal image quality. Height and weight are required for indexing cardiac measurements. Where stressors are to be used, a 12-lead ECG should be obtained. IV access is required for contrast agent administration.
The patient is positioned on the imaging couch. Electrodes are attached to allow image acquisition to be gated to the ECG. For CMR, a cardiac coil is selected and earplugs supplied. Images are then acquired in order to evaluate the clinical problem.
These are used for anatomical assessment and contribute, with optional contrast agent enhancement, towards tissue characterization.
Cine sequences are used for anatomical assessment and particularly for cardiac function. Repetitive short-axis slices from the cardiac base to the apex are summated to calculate left ventricular function. This is an extremely accurate method, since it avoids geometrical assumptions created by regional wall abnormalities. It is therefore a gold standard method for the calculation of left ventricular ejection fraction (EF), mass, and other cardiac volumes. The technique can be used in conjunction with pharmaceutical stress (e.g. dobutamine) in a manner analogous to stress echocardiography to identify regional reversible myocardial ischaemia.
Myocardial perfusion is assessed by imaging the first pass of a T1-shortening contrast agent (gadolinium). The contrast agent passes through the right heart and lungs to the left heart. It is carried into the myocardium by the coronary circulation, giving rise to a rapid ↑ in myocardial signal intensity. Myocardial areas with reduced blood flow have slower and reduced signal change. The effect is enhanced by use of pharmaceutical coronary artery vasodilators, e.g. adenosine, and can be used for the identification of MI and reversible ischaemia. In contrast to nuclear perfusion imaging, high spatial resolution allows detection of subendocardial, as well as transmural, ischaemia.
Gadolinium is an interstitial contrast agent, and it accumulates within 10min after administration in tissue where extracellular membranes are damaged. This is a powerful tool to delineate between myocardial scar tissue (↑ signal intensity) and viable or hibernating myocardium (no change in signal intensity on delayed imaging).
Velocities can be encoded into grey scale to measure the motion of cardiac structures and the flow within great vessels. This has similar applications to echocardiographic Doppler imaging and can be used to quantify valvular disease, e.g. stenosis or regurgitant volumes, and congenital heart disease, e.g. cardiac shunts.
A volume (3D) image acquisition is performed after a bolus of gadolinium reaches an area of interest within the great vessels. This technique is useful for evaluating aortic disease, congenital heart disease, and the presence of RAS.
An infusion of iodinated contrast agent is given, and a volume image acquisition is attained during a 15–20s breath-hold. Where coronary arteries are the area of interest, a coronary artery calcification score is performed initially, and these data can then be used to guide further imaging. A β-blocker may be required to lower the heart rate to optimize the image resolution. Images are then post-processed to reconstruct them to attain clinical information according to scan indication.
If appropriate screening is carried out to exclude patients with contraindications, then MRI carries minimal risk. Patients who are haemodynamically unstable, e.g. acute aortic dissection, should undergo an alternative form of imaging. CT exposes the patient to ionizing radiation, and so this should limit its application.
Figures 6.3–6.9 show the types of images that can be acquired by CMR imaging.
Volumetric imaging is non-invasive and facilitates excellent temporal and spatial definition of soft tissues. It overcomes difficulties of echocardiography where acoustic window availability limits the scan. CMR uses no ionizing radiation and so is ideal for serial imaging. A very comprehensive examination can be performed and allows dynamic assessment of the heart and great vessels at a single visit. Multislice CT provides very accurate information regarding coronary artery disease and is a non-invasive alternative to traditional coronary angiography.
CMR image quality may be impaired by artefact in some patients, especially if metal is present, e.g. non-ferrous surgical clips, spinal rods, or prosthetic valves. Rapid heart rates degrade the image quality in multislice CT.
Fig. 6.3 Examples of volumetric imaging techniques—MRI black blood sequence illustrating aortic coarctation bypass.
Fig. 6.5 MRI cine sequence demonstrating huge inferoposterior left ventricular aneurysm containing a thrombus.
Fig. 6.6 MRI delayed enhancement study delineating subendocardial scar tissue in the anteroseptal wall following MI.
Fig. 6.7 MRI first-pass perfusion: (i) prior to contrast injection; (ii) contrast agent appears in the RV and (iii) LV; (iv, arrow) contrast opacifies normally perfused myocardium, (v, arrow) but identifies an inferoseptal subendocardial perfusion deficit.
Myerson SG, Francis J, Neubauer S.Cardiovascular Magnetic Resonance. Oxford: Oxford University Press, 2010.
Nicol E, Stirrup J, Kelion AD, Padley SPG.Cardiovascular Computed Tomography. Oxford: Oxford University Press, 2011.
Echocardiography is the use of US to visualize the anatomy, size, and function of cardiac structures, i.e. valves, chambers, myocardium, pericardium, and great vessels. The technique provides information regarding the aetiology and severity of most congenital and acquired cardiac abnormalities.
Several imaging modalities are available, including 2-dimensional (2D), 3D, motion-mode (M-mode), Doppler, and contrast agent enhancement (see Figs 6.10–6.15).
Fig. 6.12 Colour Doppler of eccentric jet of severe mitral regurgitation 2° to mitral valve prolapse. (
Colour plate 1.)
Fig. 6.14 Laminar pulsed-wave Doppler flow in a patient with mitral stenosis. ( Colour plate 2.)
Fig. 6.15 Continuous-wave Doppler of tricuspid regurgitation, with PmA systolic pressure calculated as 54mmHg (plus right atrial pressure). ( Colour plate 3.)
2D echocardiography allows real-time visualization of cardiac anatomy, abnormalities of cardiac structures, and their motion. Image quality is enhanced by use of harmonic imaging and contrast opacification. With some systems, 3D imaging is also possible.
3D echocardiography is now widely available and used in both TTE and TOE. The modality is particularly useful for the assessment of left ventricular size and function, of congenital heart disease (morphology and function), and in the guidance of interventional procedures (e.g. percutaneous atrial septal defect closure).
M-mode imaging samples movement of cardiac structures along a single scan line, creating a graph of the motion of sampled structures against time. It is useful for accurate timing of cardiac events and measurement of cardiac dimensions.
Doppler is the comparison of transmitted US beam frequency with received US frequency reflected from moving structures, e.g. soft tissues (Doppler tissue imaging) or blood cells. The direction of motion and its velocity can be assessed. When blood cells reflect US as they move towards the transducer, they compress the US wavelength, whereas if they are moving away, the US wavelength lengthens. The change in frequency between the transmitted and reflected wavelengths is the Doppler shift frequency.
Continuous-wave (CW) Doppler acquires velocity data along the US beam’s entire path. Blood flow of varying strengths and velocities is demonstrated in blood vessels and through the cardiac valves. The signal is represented graphically on a spectral display. Flow away from the transducer is reflected below the zero line; flow towards the transducer is +ve in deflection. Signal density and shape give an indication of the severity of any abnormalities.
CW Doppler velocity data can be used to measure the pressure gradients between the cardiac chambers according to the Bernoulli equation. The data thus obtained can be used to calculate the severity of valvular stenosis, expressed in terms of mean and peak pressure gradients, and effective orifice area. The pressure half-time can be used to estimate the severity of diastolic valvular lesions, i.e. mitral stenosis and aortic regurgitation. It is defined as the time taken for the peak gradient to fall to half of its original value. It is inversely related to the effective orifice area.
The velocity of blood is sampled within a small area. Since this involves only a small sample volume, it localizes blood flow. It is particularly useful for evaluating low velocity flow such as cardiac inflow and outflow tract velocities. At higher velocities, it is limited by the problem of aliasing.
Colour Doppler colour-codes the direction and velocity of blood flow through cardiac structures. Blood flow in the direction away from the US probe is depicted as blue, whereas blood flowing towards the probe is red. ↑ blood flow velocity is reflected by colour mixing or turbulence. This is a useful screening tool for abnormal jets of blood and can be used to estimate the severity of some abnormalities.
Microbubbles, consisting of a gas core encapsulated by a protein shell, can be used as contrast agents to improve image quality. Typically, they are used in conjunction with harmonic imaging to allow opacification of the left ventricular volume and thereby assess wall motion. Research is continuing into their use to assess myocardial perfusion.
TTE, where the US beam is directed to the heart from outside the chest wall, is the most commonly performed examination. In certain clinical situations, more information is obtained by directing the US beam towards the heart from the oesophagus, and this is termed TOE. This allows image acquisition without interference of the chest wall, i.e. ribs, soft tissues, and lungs. US beam attenuation is small and a high-frequency transducer can be used, giving rise to higher spatial resolution than with TTE. This facilitates improved definition of the posterior cardiac structures, i.e. valves, atria, and aorta. Relatively small structures, such as cardiac vegetations, may be visualized with greater accuracy.
Indications for TTE and TOE are shown in Table 6.2.
Table 6.2 Indications for TTE and TOE
| Condition | TTE | TOE |
| Congenital heart disease | ++ | +++ |
| Suitability for percutaneous closure of atrial septal defect | − | ++++ |
| Anatomy, size, and function of the cardiac chambers (left atrium, LV, right atrium, RV) | +++ | ++++ |
| Global and regional left ventricular function | +++ | +++ |
| Valvular heart disease (aortic, mitral, tricuspid, and pulmonary) | +++ | ++++ |
| Assessment for mitral valvuloplasty | + | ++++ |
| Prosthetic heart valves | ++ | ++++ |
| Infective endocarditis (and its complications) | ++ | ++++ |
| Guide to safe cardioversion (AF) | − | +++ |
| Intra-operative assessment of valve disease/repair/replacement | − | +++ |
| Pulmonary hypertension | ++ | +++ |
| Unexplained pulmonary hypertension/right-sided dilatation | + | ++++ |
| Cardiac source of embolus in TIA/CVA/peripheral embolism | + | +++ |
| Cardiac masses | ++ | +++ |
| Pericardial disease | +++ | ++ |
| Aortic disease | + | +++ |
| Screening (cardiomyopathy) | +++ | ++ |
TTE is a very safe imaging technique with no known side effects. Contraindications to TOE include:
•Cervical spine instability, e.g. RhA, ankylosing spondylitis.
•Oesophageal disease, e.g. stricture, carcinoma, oesophageal varices.
•Haemodynamically unstable patients, including significant hypoxia.
For both procedures, the patient is made comfortable on an imaging couch in the left lateral position with the head end raised to at least 60°. Cardiac electrodes should be applied to obtain an ECG trace. Aqueous gel is used on the probe to aid US beam conduction. For TOE, the patient should be nil by mouth for at least 6h prior to the procedure and IV access sited. Any loose teeth or dentures should be removed. The throat should be sprayed with an LAn, e.g. lidocaine, and a bite guard inserted prior to intubation. The patient may be sedated according to the clinical situation, patient preference, or operator recommendation. Antibiotic prophylaxis is not required.
For TTE, the probe is applied to the chest in standard imaging positions (parasternal, apical, subcostal, and suprasternal), and the following imaging planes (see Fig. 6.16) are acquired with use of all available modalities:
•Parasternal (long axis and short axis).
•Apical (2-, 3-, 4-, 5-chamber).
For TOE, the probe is passed gently over the tongue towards the cricopharyngeal muscles. Gentle continuous pressure is applied, and the patient is encouraged to swallow until the probe lies within the oesophagus. Views of the cardiac structures are acquired from varying levels within the oesophagus, gastro-oesophageal junction, and stomach.
Fig. 6.16 Transthoracic imaging planes: (a) parasternal long axis, (b) parasternal short axis at level of aortic valve, (c) mitral valve, (d) papillary muscles, (e) suprasternal notch, (f–i) apical 5-, 4-, 3-, and 2-chamber views, (j) subcostal plane. LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle; Ao, aorta; PA, pulmonary artery; AV, aortic valve; MV, mitral valve; DAo, descending aorta.
TTE is extremely safe. TOE is a semi-invasive procedure, and so informed written consent should be obtained. Intubation of the oesophagus carries a risk of ~1 per 2000 of oesophageal trauma. There is a small risk of laryngospasm and cardiac arrhythmia (usually supraventricular). This usually resolves spontaneously on probe withdrawal. Neither technique should be performed on a haemodynamically compromised patient where an interventional procedure is delayed by inappropriate image acquisition, e.g. aortic dissection, cardiac tamponade.
TTE is cheap and non-invasive and requires no ionizing radiation, ensuring that serial examinations are without risk. It is portable and can easily be used at the bedside. The technique provides a comprehensive assessment of cardiac anatomy, function, and blood flow. TOE has similar advantages to TTE, with the difference that it is a semi-invasive technique but offers superior spatial resolution, particularly of structures in close proximity to the probe (e.g. left atrium, mitral valve). It is a powerful tool for intra-operative use and in patients with limited transthoracic windows.
Transthoracic image quality may be limited by inadequate acoustic windows in patients with obesity, lung disease, and chest wall deformities, and those undergoing artificial ventilation. Structures at the posterior aspect of the heart are not well visualized. Optimal transoesophageal image quality is obtained at the posterior aspect of the heart, and so the apex of the heart is less well seen. Image quality may be compromised in patients with hiatus hernia. Not all patients tolerate the procedure, and so images relating to the suspected pathology should be acquired first in case the procedure has to be abandoned prematurely.
Normal anatomy is demonstrated to exclude congenital heart disease. Each cardiac chamber and its connections are systematically identified and the presence of any shunts excluded. The size of the cardiac chambers and walls are assessed. Normal values are shown in Table 6.3.
Table 6.3 Normal values for cardiac linear dimensions
| Parameter | Normal range |
| LAt diameter | |
| Left ventricular diastolic diameter | |
| Interventricular septum diastolic diameter | 0.6–1.2cm |
| Left ventricular posterior wall diastolic diameter | 0.6–1.2cm |
•LAt dilatation: mitral valve disease, systemic hypertension, coronary artery disease, dilated cardiomyopathy, restrictive cardiomyopathy, hypertrophic cardiomyopathy, AF.
•Left ventricular dilatation: mitral regurgitation, aortic regurgitation, severe aortic stenosis, systemic hypertension, IHD, dilated cardiomyopathy.
•Left ventricular hypertrophy: systemic hypertension, left ventricular outflow obstruction (aortic stenosis, supra-aortic membrane, subaortic membrane), hypertrophic cardiomyopathy (asymmetric), aortic coarctation, infiltrative cardiomyopathy (amyloidosis).
•Aortic root dilatation: systemic hypertension, collagen disorders, e.g. Marfan’s syndrome, syphilitic aortitis, aortic coarctation, aortic valve disease, aortic aneurysm, aortic dissection.
•Right atrial (RAt) dilatation: tricuspid valve disease, pulmonary valve disease, pulmonary hypertension, dilated cardiomyopathy, restrictive cardiomyopathy, constrictive pericarditis.
•Right ventricular dilatation: 1° pulmonary hypertension, 2° pulmonary hypertension (e.g. mitral stenosis, PEs, lung disease, left-to-right shunts), tricuspid regurgitation, pulmonary regurgitation, right ventricular cardiomyopathy (including arrhythmogenic), right ventricular infarction.
•Right ventricular hypertrophy: 1° pulmonary hypertension, 2° pulmonary hypertension (e.g. mitral stenosis, PEs, lung disease, left-to-right shunts), pulmonary stenosis, right ventricular outflow tract obstruction.
•Pulmonary trunk dilatation: pulmonary hypertension, collagen disorders, e.g. Marfan’s syndrome, pulmonary atresia, pulmonary valve disease, idiopathic PmA dilatation.
The size, shape, and function of the LV are evaluated with 2D/3D imaging ± contrast opacification. Commonly measured echocardiographic parameters of left ventricular function include EF, fractional shortening, stroke volume, and cardiac output. It should be remembered that, when calculated from the M-mode image, only the function of the base of the heart is assessed. This should not be extrapolated to global left ventricular function, unless the entire ventricle is normal. EF can also be calculated from apical diastolic and systolic views (using the modified Simpson’s rule). This is more reflective of global left ventricular function but is still limited since it is a 2D measurement and requires geometric assumptions. A more subjective assessment can be made by visually estimating left ventricular function as normal or as having mild, moderate, or severe impairment. Causes of impaired left ventricular systolic function are:
Regional wall motion abnormalities are confined to specific walls or segments of the LV. Systolic wall thickening is defined in Table 6.4.
Table 6.4 Categorization of regional wall motion
| Severity | Description |
| Normal | >50% ↑ in systolic wall thickness, compared with diastole |
| Hypokinetic | <50% ↑ in systolic wall thickness, compared with diastole |
| Akinetic | Absent systolic wall thickening |
| Dyskinetic | Outward wall motion during systole |
Dobutamine stress may be used in conjunction with left ventricular global and regional wall functional assessment. As well as allowing distinction between normal, ischaemic, and infarcted myocardium, it also permits the assessment of myocardial viability (regional dysfunction that will improve with revascularization) vs scar tissue (no effect on function from revascularization). It should be noted that CMR is now proven to be a superior technique for identification of myocardial scar/viability. Resulting interpretation with respect to regional wall motion responses to low-dose and peak-dose dobutamine stress is shown in Table 6.5.
Table 6.5 Interpretation of contractile responses to dobutamine stress
| Interpretation | Rest | Low dose | Peak dose |
| Normal | Normal | ↑ | Hyperdynamic |
| Inducible ischaemia | Normal or ↓ | No change or ↓ from baseline | ↓ from baseline |
| Scar tissue | Absent | Absent | Absent |
| Viability | Absent | Improved | Improved or ↓ compared with low dose (biphasic response) |
Left ventricular filling during diastole is an important component of left ventricular functional assessment. Normal LAt filling is passive throughout systole (S wave) and diastole (D wave) and is assessed from pulsed-wave (PW) Doppler sampling of pulmonary venous flow. Left ventricular filling is assessed from diastolic mitral valve flow. It is predominantly passive and early in diastole (E wave), with a small later contribution from atrial systole (A wave). Diastolic dysfunction results in elevated left ventricular end-diastolic pressure (LVEDP), and ultimately left atrial pressure (LAP), and so alters measured flow characteristics. There are three types of diastolic dysfunction (see Table 6.6), depending on the degree of raised LAP that occurs in order to drive flow across the mitral valve.
Right heart failure is depicted by a dilated, poorly functioning RV. Raised right-sided pressures are indicated by a dilated right atrium and IVC (seen on subcostal view).
Systolic PmA pressure, assuming there is no pulmonary valve stenosis, can be estimated from the pressure gradient between the right atrium and ventricle. This is measured from any tricuspid regurgitant jet (Bernoulli equation) summated with the estimated RAt pressure. Diastolic PmA pressure is measured by substituting the end-diastolic velocity of pulmonary regurgitation into the Bernoulli equation, again summated with the estimated RAt pressure. If the systolic PmA pressure is raised but the diastolic pressure is normal, this represents ↑ flow volume, rather than pulmonary hypertension. RAt pressure is assessed by IVC diameter evaluation and its calibre reduction with inspiration (see Table 6.7).
Table 6.6 Echo assessment of left ventricular diastolic dysfunction
| Characteristics | Abnormal relaxation | Pseudonormalization | Restrictive |
| Haemodynamics | |||
| Mitral valve | (E:A reversal E↓ A↑) | Normal | (E↑↑, sharp descent, A↓) |
| Pulmonary venous flow | Normal | Diminished S wave, deeper broader A wave | Diminshed S wave, deeper broader A wave |
| Doppler pattern (mitral valve above pulmonary vein below) |  |
 |
 |
| Left ventricular impairment | Mild | Moderate | Severe |
| Significance | Slow early left ventricular relaxation | Slow early relaxation, reduced compliance | Slow early left ventricular relaxation, severely reduced compliance |
| Symptoms | Well at rest, but shortness of breath if heart rate ↑ | Shortness of breath on exercise and limited exercise tolerance | Shortness of breath on minimal exertion |
Table 6.7 Estimation of right atrial pressure
| IVC size (cm) | IVC change with inspiration | Estimated RAt pressure (mmHg) |
| <1.5 | Collapse | 0–5 |
| 1.5–2.5 | ↓ >50% | 5–10 |
| 1.5–2.5 | ↓ <50% | 10–15 |
| >2.5 | ↓ <50% | 15–20 |
| 2.5 | No change | >20 |
Echocardiography can identify and quantify valve abnormalities to decide whether long-term follow-up or referral for valve surgery is necessary.
•Affected by other cardiac pathological processes, e.g. cardiomyopathy, carcinoid.
Aortic stenosis leads to left ventricular hypertrophy, ↑ left ventricular pressures, and, if untreated, LVF and risk of sudden death (see Table 6.8).
•Aetiology: congenital abnormality (bicuspid, unicuspid, or quadricuspid valve), calcific degenerative disease, rheumatic heart disease.
•Differential diagnosis: hypertrophic obstructive cardiomyopathy, subaortic membrane, supra-aortic membrane.
•2D/3D findings: thickened, calcified, and/or fused aortic cusps with reduced excursion, left ventricular outflow tract dimension (to calculate the aortic valve area), effects on the LV (hypertrophy/impaired systolic/diastolic function), post-stenotic dilatation of the ascending aorta/aortic coarctation.
•Colour Doppler findings: turbulent bright colour is seen through the valve.
•CW/PW Doppler findings: peak and mean valvular gradients; aortic valve area; the dimensionless severity index (DSI) is a useful parameter, particularly where left ventricular function is impaired.
Table 6.8 Parameters of aortic stenosis severity
| Mild | Moderate | Severe | |
| Mean gradient (mmHg) | <25 | 25–40 | >40 |
| Peak gradient (mmHg) | <36 | 36–64 | >64 |
| Effective orifice area (cm2) | 1.5–2.0 | 1.0–1.4 | <1.0 |
Aortic regurgitation leads to mild left ventricular hypertrophy, left ventricular dilatation, and LVF.
•Aetiology: congenital abnormality (bicuspid, unicuspid, or quadricuspid valve), rheumatic heart disease, aortic leaflet prolapse, calcific or idiopathic degeneration, subaortic VSD, infective endocarditis (presence of vegetations), aortic dissection (aortic root dissection flap), ascending aortic dilatation (hypertension, aortic stenosis, age), aortitis (syphilis, ankylosing spondylitis, GCA, RhA, Reiter’s syndrome), degenerative disease, including collagen disease, e.g. Marfan’s syndrome.
•2D/3D findings: aortic valve anatomy (including calcification, prolapse, vegetations, presence of subaortic VSD), size of aortic root/aortic dissection flap/aortic coarctation, effects on the LV (hypertrophy/impaired systolic/diastolic function).
•Colour Doppler findings: a diastolic regurgitant jet is seen. The width of the jet (colour M-mode) comparative with left ventricular outflow tract diameter and its extent into the left ventricular cavity is measured.
•CW/PW Doppler findings: the density of the diastolic signal is assessed, together with the pressure half-time. Diastolic flow reversal in the aortic arch or descending aorta is indicative of significant aortic regurgitation, unless the left ventricular diastolic pressure is high from a separate aetiology, e.g. MI. It can be difficult to differentiate between mild and moderate aortic regurgitation, especially with transthoracic imaging (see Table 6.9).
Table 6.9 Parameters of aortic regurgitation severity
| Mild | Moderate | Severe | |
| Jet width (as % of left ventricular outflow tract) | <25 | 65 | |
| Pressure half-time (ms) | >500 | <250 | |
| Vena contracta width (cm) | <0.3 | >0.6 | |
| Diastolic flow reversal | None | Aortic arch | Descending aorta |
Mitral stenosis causes LAt dilatation, ↑ pulmonary venous pressures, pulmonary oedema, pulmonary hypertension, right heart failure, and functional tricuspid regurgitation. TOE should be used to assess the suitability of the patient for percutaneous mitral valvuloplasty (see Table 6.10).
•Aetiology: rheumatic heart disease/calcification (valve leaflets, chordae, or papillary apparatus), congenital abnormality (very rare), SLE (rare).
•Differential diagnosis: LAt myxoma, obstruction of the valve by thrombus or vegetations.
•2D/3D findings: anatomy and degree of any calcification/fusion of the mitral valve leaflets and apparatus for suitability for valvuloplasty, effective orifice area (evaluated with planimetry), LAt size (dilated), presence of LAt thrombus, right heart size (hypertrophy) and function.
•Colour Doppler findings: turbulent flow is seen through the valve.
•CW/PW Doppler findings: peak and mean valvular gradients are calculated, the pressure half-time is measured, and the effective orifice area calculated. Pulmonary hypertension is estimated.
Table 6.10 Parameters of mitral stenosis severity
| Mild | Moderate | Severe | |
| Mean gradient (mmHg) | <5 | 5–10 | >10 |
| Pressure half-time (ms) | 71–139 | 140–219 | >219 |
| Mitral orifice area (cm2) | 1.6–2.0 | 1.0–1.5 | <1.0 |
Mitral regurgitation causes LAt dilatation, ↑ pulmonary venous pressures, pulmonary oedema, LVF, pulmonary hypertension, right heart failure, and functional tricuspid regurgitation. TOE gives an optimal assessment of severity (see Table 6.11).
•Aetiology: rheumatic heart disease, mitral valve prolapse/redundant tissue, IHD (papillary muscle rupture/infarction/restriction of posterior leaflet), dilated/ischaemic cardiomyopathy (annular dilatation), hypertrophic obstructive cardiomyopathy (systolic anterior motion), infective endocarditis (presence of vegetations), congenital abnormality (very rare; note the association of cleft mitral valve and primum atrial septal defect), SLE (rare).
•2D/3D findings: mitral valve anatomy (calcification, prolapse, redundant tissue, leaflet excursion, vegetations, annular size, apparatus integrity), left ventricular size and function (hypertrophy, dilatation), LAt size (dilatation), right heart function (hypertrophy, dilatation), and PmA pressures.
•Colour Doppler findings: an abnormal systolic jet is seen through the mitral valve into the left atrium. The size of this is assessed. This can be deceptive with very eccentric jets associated with mitral valve prolapse.
•CW/PW Doppler findings: signal density and shape are characterized. Analysis of pulmonary venous flow with PW Doppler can be helpful.
Table 6.11 Parameters of mitral regurgitation severity
| Mild | Moderate | Severe | |
| Jet area (cm2) | <4 | >10 | |
| Signal density on CW Doppler | + | ++ | +++ |
| Vena contracta width (cm) | <0.3 | 0.7 | |
| Pulmonary venous flow | Normal | Absent systolic component | Reversed systolic component |
Tricuspid stenosis causes RAt dilatation and ↑ systemic venous pressures.
•Aetiology: rheumatic heart disease (occurs in 10% of patients with mitral stenosis), carcinoid disease, endomyocardial fibrosis, SLE.
•2D/3D findings: tricuspid valve anatomy and degree of any doming, calcification, fusion of tricuspid valve leaflets and apparatus, size of the right atrium, and IVC (dilated).
•Colour Doppler findings: turbulent flow is seen through the valve.
•CW/PW Doppler findings: peak and mean valvular gradients are calculated, the pressure half-time is estimated, and the effective orifice area calculated. Pulmonary hypertension is calculated from the velocity of any tricuspid regurgitant jet. Peak E wave velocity is elevated (normal peak is <0.7ms−1) and there is a slow deceleration time. A mean gradient of 2–3mmHg may be clinically significant.
Tricuspid regurgitation leads to RAt dilatation, right ventricular hypertrophy, and failure (see Table 6.12).
•Aetiology: rheumatic heart disease, infective endocarditis (IV drug abuse), functional (2° to right ventricular dilatation, e.g. cardiac left-to-right shunts, right ventricular cardiomyopathy, pulmonary hypertension, permanent pacing system), carcinoid disease, Ebstein’s anomaly, SLE, myxomatous degeneration, cardiac amyloidosis.
•2D/3D findings: tricuspid valve anatomy (site, calcification, prolapse, redundant tissue, leaflet excursion, vegetations, annular size, apparatus integrity), right ventricular size (dilated) and function, size of the right atrium, IVC (dilated), presence of pacing wires.
•Colour Doppler findings: abnormal systolic jet is seen through the tricuspid valve into the right atrium. The size of this is assessed, compared with the right atrium.
•CW/PW Doppler findings: the density of the signal and shape is assessed. Analysis of hepatic flow with PW Doppler can be helpful. Pulmonary arterial pressure can be measured but may be underestimated if there is severe tricuspid regurgitation.
Table 6.12 Parameters of tricuspid regurgitation severity
| Mild | Moderate | Severe | |
| Jet area (cm2) | <5 | 5–10 | >10 |
| Vena contracta width (cm) | <0.7 | >0.7 | |
| Signal density on CW Doppler | + | ++ | +++ |
| Shape of CW Doppler signal | Pansystolic | Pansystolic | Triangular |
| Hepatic venous flow reversal | None | Absent systolic component | Pansystolic flow reversal |
Pulmonary stenosis causes right ventricular hypertrophy and, if left untreated, right heart failure (see Table 6.13).
•Aetiology: congenital, rheumatic heart disease, carcinoid.
•Differential diagnosis: right ventricular outflow obstruction (infundibular stenosis).
•2D/3D findings: pulmonary valve anatomy (calcification, leaflet thickening, doming), size of the pulmonary trunk (post-stenotic dilatation), effects on the RV (hypertrophy/impaired function).
•Colour Doppler findings: turbulent systolic flow through the pulmonary valve.
•CW/PW Doppler findings: The maximum gradient and pulmonary valve area are calculated.
Table 6.13 Parameters of pulmonary stenosis severity
| Mild | Moderate | Severe | |
| Peak gradient (mmHg) | <40 | 40–75 | >75 |
•Aetiology: congenital, infective endocarditis (IV drug abuse), pulmonary hypertension, PmA dilatation, carcinoid disease, post-pulmonary valvotomy.
•2D/3D findings: pulmonary valve anatomy (calcification, prolapse, vegetations), size of the pulmonary trunk, effects on the RV (hypertrophy/impaired function).
•Colour Doppler findings: a diastolic regurgitant jet is seen. The width of the jet and its extent into the right ventricular outflow tract and cavity are measured.
•CW/PW Doppler findings: the density of the diastolic signal and its duration are estimated. Pulmonary regurgitation is haemodynamically significant if the jet is broad relative to the width of the PmA, extends >2cm into the right ventricular outflow tract, and persists throughout diastole.
Echocardiography is used for follow-up of prosthetic heart valves and potential dysfunction. It is important to consult tables of normal flow pattern values for each valve type according to its make and size. TOE is superior to TTE. The following parameters are assessed:
•Direct 2D/3D imaging of the valve ring and leaflets.
•Presence of any rocking motion suggestive of valvular dehiscence.
•Forward blood flow through the valve.
•Valvular regurgitation (typical regurgitation on valve closure is normal).
The following features are characteristic of infective endocarditis:
•Predisposing abnormal structure (valve lesion/congenital abnormality).
•Mobile echogenic masses (vegetations, usually in the path of regurgitant jets).
•Spread of infection to other valves (usually along the path of a regurgitant jet).
•Abscess (particularly around the aortic root, prosthetic valves).
•Embolic potential (large, mobile vegetations, especially the aortic valve).
•Valve destruction (degree of regurgitation and effect on cardiac chamber size and function).
•Chamber perforation and shunting.
The normal pericardium is poorly visualized with echocardiography, since it is a very thin structure. Pericardial abnormalities that may be identified are:
•Pericardial effusion (fluid between the pericardial layers).
•Pericardial thickening or calcification (constrictive pericarditis).
•Pericardial masses, e.g. cysts or tumour.
A pericardial effusion gives rise to echo-free space around the heart. The anatomical relationship of pericardial fluid with the descending aorta distinguishes pericardial (anterior) and pleural (posterior) effusions. If the effusion is organizing or contains a thrombus or tumour, then echodense structures may be identified within it. The width of this space is measured to give a rough guide as to the size of the effusion:
The most important assessment is whether fluid is causing any haemodynamic compromise, i.e. cardiac tamponade. This may occur regardless of the size of the effusion, particularly if it has accumulated rapidly. Features suggestive of a tamponade include:
•Dilatation of the IVC (>2.5cm), poor collapse with inspiration (<50%).
•Exaggerated reduction in transmitral velocities on inspiration (>40%).
•Right ventricular diastolic collapse.
•Low-volume, poorly filled LV.
This is typically caused by TB and constrains left and right ventricular filling. On 2D imaging, the pericardium is thickened and appears bright when calcification is present. The period of left ventricular diastolic function is shortened. Systolic function is normal. Doppler shows:
•Exaggerated reduction of transmitral E wave velocity with inspiration.
•Shortened transmitral E wave deceleration time.
•Exaggerated flow reversal in the superior vena cava (SVC) on expiration.
The commonest intra-cardiac masses are thrombi and vegetations (infective endocarditis). Thrombus formation is ↑ in conditions causing slow blood flow such as mitral or tricuspid valve stenosis or cardiomyopathy. The commonest cardiac tumours are atrial myxomas and metastatic deposits. An atrial myxoma is typically a pedunculated, frond-like mass that arises from the interatrial septum. Metastatic deposits can be found anywhere within the heart, including the pericardium. Extrinsic masses may cause compression of cardiac structures. Atrial pectinate muscles, Eustachian valve, Chiari network, papillary muscles, fibrin strands, sutures on prosthetic valves, large vascular structures, such as the aorta, coronary sinus, or left ventricular aneurysms, may be incorrectly interpreted as cardiac masses.
•Atrial masses: thrombus, myxoma, lipomatous hypertrophy of the interatrial septum, ruptured mitral valve apparatus, 1° benign tumour, 1° malignant tumour, 2° tumour.
•Ventricular masses: thrombus, ruptured mitral valve apparatus, 1° benign tumour (fibroma, lipoma, rhabdomyoma, haemangioma), 1° malignant tumour (rhabdomyosarcoma, fibrosarcoma, angiosarcoma), 2° tumour.
•Valvular masses: vegetations, thrombus/pannus, fibroelastoma.
The aorta is a predominantly posterior structure, and so the arch and descending aorta are best visualized by TOE.
•2D findings: integrity of the walls is assessed for atheroma (irregular wall thickening), intramural haematoma, or dissection flap. The latter may be indirectly suspected from the presence of pericardial effusion or aortic regurgitation. Its anatomy and extent are noted to allow classification. Presence of regional left ventricular wall motion abnormalities may indicate coronary artery involvement. The size of the aorta is measured at several sites to assess dilatation or coarctation (see Table 6.14). The normal aortic wall thickness is 4mm.
Table 6.14 Normal aortic dimensions
| Site | Normal range (mm) |
| Annulus | 20–31 |
| Sinus of Valsalva | 29–45 |
| Sinotubular junction | 22–36 |
| Tubular ascending aorta | 22–36 |
| Descending | 20–30 |
•Doppler findings: colour, CW, and PW Doppler can all be used to distinguish between true (normal systolic velocity flow) and false (low or absent systolic flow) lumens in aortic dissection, to identify and determine the severity of aortic regurgitation and aortic coarctation.
It is important to recognize situs and connections of cardiac chambers and great vessels.
•The RV is recognized by the following features:
•It is associated with the tricuspid valve.
•The tricuspid valve is sited more towards the apex than the mitral valve.
•The tricuspid and pulmonary valves are not continuous (compare the aortic and mitral valves).
•It is trabeculated and contains a moderator band.
•The ventricles should be connected to the correct outflow tract:
•The aorta is a single vessel.
•The PmA bifurcates soon after its origin, unless hypoplasia/atresia is present.
•The atria should be connected to the correct inflow:
•The pulmonary veins normally drain into the left atrium. Drainage into alternative structures, e.g. SVC or IVC, hepatic veins, is referred to as anomalous pulmonary venous drainage and is associated with a left-to-right shunt.
There should be no shunts between systemic and pulmonary systems; such shunts include atrial septal defect (abnormal connection between the left and right atria; see Table 6.15), VSD (abnormal connection between the LV and RV; see Table 6.16), or patent ductus arteriosus (abnormal connection between the aorta and PmA).
Table 6.15 Types of atrial septal defect
| Atrial septal defects | Site | Associations |
| Ostium secundum | Fossa ovalis | Mitral valve prolapse |
| Ostium primum | Low septum | AV valve abnormalities |
| Sinus venosus | Upper septum | Anomalous pulmonary venous drainage |
Table 6.16 Types of ventricular septal defect
| VSD | Site | Associations |
| Membranous | Infundibular septum | |
| Subaortic | Below aortic valve | |
| Muscular | Muscular septum | |
| AV | Posterior septum near AV valves | AV valve abnormalities |
If shunts are identified, they are quantified. Pulmonary artery pressure is assessed, together with evidence of shunt reversal (right to left), indicating Eisenmenger’s syndrome. Fallot’s tetralogy is a relatively common congenital condition, composed of a subaortic VSD, an overriding aorta, right ventricular outflow tract or pulmonary valve stenosis, and right ventricular hypertrophy.
•Aortic valve: may be unicuspid, bicuspid, quadricuspid, or associated with a subaortic or supra-aortic membrane.
•Pulmonary valve/right ventricular outflow tract: may be obstructed.
•Mitral valve: cleft leaflet associated with primum atrial septal defect, mitral stenosis, parachute valve.
•Tricuspid valve: ventricularization of site = Ebstein’s anomaly.
•Aortic and pulmonary arteries: should be normal situs, size, and anatomy, and unobstructed:
•Left-sided aortic arch, aortic coarctation.
•Pulmonary hypoplasia, atresia, affecting either of the PmAs after trunk bifurcation.
Further reading
British Society of Echocardiography. 
http://www.bsecho.org.
Houghton AR.Making Sense of Echocardiography, 2nd edn. Boca Raton: CRC Press, 2014.
Leeson P, Augustine D, Mitchell ARJ, Becher H.Echocardiography, 2nd edn. Oxford: Oxford University Press, 2012.
Otto CM.Textbook of Clinical Echocardiography, 5th edn. Philadelphia: Elsevier Saunders, 2013.
The ECG records the heart’s electrical activity. It can provide valuable information about not just arrhythmias, but also a host of other disorders that affect the electrical activity of the myocardium such as ischaemia, cardiomyopathy, and electrolyte disturbances.
•Investigation of suspected arrhythmias, both to ‘capture’ the cardiac rhythm, whilst the patient is experiencing symptoms, and also to look for predisposing abnormalities, e.g. short PR interval, ventricular pre-excitation (delta waves), conduction abnormalities, long QT interval.
•Investigation of chest pain, e.g. myocardial ischaemia or infarction, pericarditis, PE.
•Assessment of suspected cardiomyopathy and/or LVF (a normal ECG is unusual in the presence of left ventricular systolic dysfunction).
•Assessment of electrolyte disturbances, particularly where these might have pro-arrhythmic potential, e.g. hyperkalaemia.
•Assessment of drug effects on the heart, e.g. digoxin, tricyclic antidepressants.
None. However, always check if the patient has a known allergy to the self-adhesive pads used to attach the electrodes to the skin.
•Explain what the procedure involves.
•Ask the patient to lie supine on a bed or examination couch.
•Prepare the skin by shaving, where necessary, and cleaning with alcohol wipes.
•Ask the patient to relax and lie still, whilst the recording is in progress.
•Having prepared the patient for the test, attach the chest and limb electrodes in the appropriate positions.
•Before recording the ECG, check that the calibration settings of the ECG machine are appropriate. Standard settings are an amplitude of 10mm/1mV and a paper speed of 25mm/s. Ensure that these settings are noted on the ECG.
•After recording the ECG, ensure that the patient’s identification details and the time and date of the recording are noted on it.
•It is good practice to make a record on the ECG of any symptoms (e.g. chest pain, palpitations) that the patient was experiencing at the time of the recording or to write ‘asymptomatic’ where appropriate.
•Ensure that the ECG is seen and reported by an appropriate staff member as soon as practicable.
Always use a systematic approach to ECG reporting to ensure nothing is overlooked.
•Heart rate: bradycardia vs tachycardia.
•Rhythm: regular vs irregular, supraventricular vs ventricular, broad complex vs narrow complex.
•QRS axis: left or right axis deviation.
•P wave: presence or absence, inverted, tall (peaked), or wide (bifid).
•P–R interval: long, short, or variable.
•Q waves: are pathological Q waves present?
•QRS complex: large, small, broad, or abnormally shaped.
•ST-segment: elevated or depressed.
•T wave: tall, small, or inverted.
•U wave: are prominent U waves present?
•Additional waves: are delta waves or J waves present?
•By counting the number of large squares between two successive QRS complexes and dividing this number into 300, e.g. four large squares = 300/4 = 75bpm. This method is preferred when the heart rhythm is regular.
•By counting the number of QRS complexes along a 25cm rhythm strip (50 large squares) and multiplying this number by 6, e.g. 14 complexes in 25cm = 14 × 6 = 84bpm. This method is preferred when the heart rhythm is irregular.
Bradycardia is arbitrarily defined as a heart rate <60bpm, and tachycardia as a heart rate >100bpm.
•Second- and third-degree AV block.
•Escape rhythms, e.g. AV junctional escape rhythms, ventricular escape rhythms, asystole, and drug-induced conditions.
•Narrow complex tachycardia: e.g. sinus tachycardia, atrial tachycardia, atrial flutter, AF, AV re-entry tachycardias.
•Broad complex tachycardia: e.g. narrow complex tachycardia with aberrant conduction, ventricular tachycardia, accelerated idioventricular rhythm, torsades de pointes.
•Is ventricular activity (QRS complexes) present?
•What is the ventricular rate?
•Is the ventricular rhythm regular or irregular?
•Are the QRS complexes narrow or broad?
•Are there P waves (atrial activity)?
•What is the correlation between P waves and QRS complexes?
Being able to describe the cardiac rhythm in these terms will narrow down the range of possible diagnoses in most cases and you will, at least, be able to describe the key features of the rhythm clearly over the telephone to an expert.
•Atrial flutter (see Fig. 6.17).
•AF (see Fig. 6.18).
•AV re-entry tachycardias (see Fig. 6.19).
•Accelerated idioventricular rhythm.
•Ventricular tachycardia (see Fig. 6.20).
•Polymorphic ventricular tachycardia (torsades de pointes; see Fig. 6.21).
•Ventricular fibrillation (see Fig. 6.22).
•Left axis deviation: left anterior hemiblock, Wolff–Parkinson–White syndrome, inferior MI, ventricular tachycardia (with left ventricular apical focus).
•Right axis deviation: left posterior hemiblock, right ventricular hypertrophy, Wolff–Parkinson–White syndrome, anterolateral MI, dextrocardia.
•P waves absent: AF, sinus arrest or sinoatrial block (persistent or intermittent), hyperkalaemia.
•P waves inverted: dextrocardia, retrograde atrial depolarization, electrode misplacement.
•Tall or peaked P waves: RAt enlargement.
•Wide, often bifid P waves: LAt enlargement.
•Short PR interval (<0.12s): AV junctional rhythm, Wolff–Parkinson–White syndrome (see Fig. 6.23).
•Long PR interval (>0.2s): first-degree AV block (see Fig. 6.24), e.g. IHD, hypokalaemia, acute rheumatic myocarditis, Lyme disease, digoxin, β-blockers, certain calcium channel blockers.
•Variable PR interval: second-degree AV block (Mobitz type I (see Fig. 6.25), Mobitz type II, 2:1 AV block), third-degree AV block (see Fig. 6.26).
•Pathological Q waves: MI, left ventricular hypertrophy, bundle branch block.
•Large R or S waves: incorrect ECG calibration, left ventricular hypertrophy, right ventricular hypertrophy, posterior MI, Wolff–Parkinson–White syndrome (left-sided accessory pathway), dextrocardia, bundle branch block.
•Small QRS complexes: incorrect ECG calibration, obesity, emphysema, pericardial effusion.
•Broad QRS complexes (>0.12s): bundle branch block, ventricular rhythms, hyperkalaemia.
•Abnormally shaped QRS complexes: incomplete bundle branch block, fascicular block, Wolff–Parkinson–White syndrome.
•Elevated ST-segments: acute STEMI (see Fig. 6.27), left ventricular aneurysm, Prinzmetal’s (vasospastic) angina, pericarditis (concave ‘saddle-shaped’ appearance), high take-off.
•Depressed ST-segments: myocardial ischaemia, acute posterior MI, drugs, e.g. digoxin (reverse tick), ventricular hypertrophy with ‘strain’.
•Tall T waves: hyperkalaemia, acute MI.
•Small T waves: hypokalaemia, pericardial effusion, hypothyroidism.
•Inverted T waves: normal (aVR, V1, sometimes V2–V3 and III), myocardial ischaemia, MI, ventricular hypertrophy with ‘strain’, digoxin toxicity.
•Short QT interval: hypercalcaemia, digoxin effect, hyperthermia.
•Long QT interval: hypocalcaemia, drug effects, acute myocarditis, hereditary syndromes (Jervell and Lange–Nielsen syndrome, Romano–Ward syndrome).
•Prominent U waves: hypokalaemia, hypercalcaemia, hyperthyroidism.
•A common error is to interpret an ECG in isolation. To avoid this error, always consider the clinical context in which it was recorded. Begin your assessment of the ECG by asking, ‘How is the patient?’ before rushing to conclusions about the clinical relevance of any abnormalities that may be present.
•A normal ECG does not necessarily exclude a significant cardiac problem, particularly when recorded whilst the patient is asymptomatic. This is particularly the case when investigating palpitations and chest pain.
•Technical artefacts are often mistaken for significant abnormalities. Ensure adequate patient preparation and correct electrode placement to minimize the risk of artefact.
Further reading
Houghton AR, Gray D.Making Sense of the ECG, 4th edn. Boca Raton: CRC Press, 2014.
ECG monitoring allows continuous observation of a patient’s ECG in an ambulatory setting over an extended period of time. This is typically from 24h all the way up to a year or more, depending upon the technique used. There are three types of device available for ambulatory ECG monitoring:
•24h ambulatory ECG (Holter) monitor.
•Insertable cardiac monitor (e.g. Medtronic Reveal LINQ™).
The choice of device is largely determined by how frequently the patient experiences symptoms, as the key to successful ECG monitoring is to maximize the chances of capturing a typical symptomatic event during the monitoring period. A Holter monitor is typically worn for 24–48h but becomes somewhat impractical over longer periods. It is therefore ideally suited to patients with frequent (daily) symptoms. An external loop recorder (often called an event monitor) is carried for around 7 days and is therefore used for patients with less frequent symptoms. Instead of recording a continuous ECG, they capture brief periods of the ECG, usually when activated by the patient. Transtelephonic monitors allow captured loops to be relayed to a cardiac centre by telephone, allowing an immediate analysis of the recorded ECG.
An insertable cardiac monitor (ICM) is used to detect infrequent events. It is used to monitor a patient’s cardiac rhythm over an extended period (up to its battery life, usually around 3 years). An ICM is implanted SC and contains a battery, a digital memory, and diagnostic software to analyse the ECG recording. It records the ECG on a digital ‘loop’, continuously overwriting older ECG data with the most current data. Should a symptomatic event occur, the patient can ‘freeze’ the loop using an external hand-held device that is held over the ICM (‘patient-activated’ recordings). Additionally, the device can be programmed to detect and store abnormal cardiac rhythms automatically (‘auto-activated’ recordings). The device will usually store the ECG leading up to an event and also a short segment of ECG following the event. Stored ECG loops can subsequently be downloaded for further analysis via a telemetry device at the hospital clinic or via a wireless device in the patient’s own home.
Where patients have symptoms suggestive of a paroxysmal arrhythmia (palpitation and/or dizziness/syncope), ECG monitoring can provide a diagnosis by capturing the cardiac rhythm during a typical event. This allows the underlying arrhythmia to be identified or, where the rhythm proves to be normal, an arrhythmic aetiology to be ruled out. The choice of method depends upon the frequency of the symptoms.
None. However, always check if the patient has a known allergy to the self-adhesive pads used to attach the electrodes to the skin.
For external monitoring, no specific preparation is required, apart from ensuring that the electrodes make good contact with the patient’s skin, so that an ECG of diagnostic quality can be recorded. For the implantation of an ICM:
•Explain what the procedure involves.
•Obtain written informed consent.
•Check the FBC (and clotting profile if bleeding risk).
•Sedation if the patient is anxious.
The best site for the device is established by optimal ECG signal measurement prior to insertion.
External monitors are attached to the patient’s skin via electrodes, ensuring good contact is maintained. The recorder itself is carried on a belt or in a pouch. The patient should be given a diary with clear instructions on how to operate the monitor and how to note the timing and nature of any symptoms that occur. Some event monitors are carried by the patient and only applied to the skin during symptomatic episodes. The patient should be given clear instructions on how to operate such a monitor and a ‘test run’ should be conducted.
An ICM is implanted SC under aseptic technique and using LAn. The implantation takes around 15min and can be done as a day case procedure. The device is self-contained since, unlike a pacemaker, there are no associated leads. The ICM is commonly implanted near the left deltopectoral groove or below the left breast. Once implanted, the device is interrogated using an external programmer to ensure that a high-quality ECG is being recorded. The incision is closed using surgical glue or butterfly closures.
External monitoring carries no significant risks. Implantation of an ICM carries a risk of:
•Erosion through the skin (if the patient is thin).
Depending upon the underlying cause of the patient’s symptoms, almost any cardiac rhythm disturbance (or indeed no rhythm disturbance whatsoever) may be revealed by ECG monitoring. The most important aspect of interpreting the results is to correlate recordings with symptoms. Patient-activated recordings are, as one might expect, usually made in relation to a symptomatic episode. In this case, it is essential to find out precisely what symptoms were experienced at the time (including a witness account where appropriate). Auto-activated recordings may be asymptomatic and made by the device without the patient being aware of a problem. The most useful outcome is to assess the ECG recorded during a typical symptomatic event. It is then usually straightforward to make a diagnosis and plan further treatment as appropriate.
Ambulatory ECG monitoring allows the chance of capturing paroxysmal arrhythmias, an opportunity that is unlikely to arise with a 12-lead ECG recording unless the patient happens to be symptomatic at the time. Each of the methods of ECG monitoring has advantages over the others. External monitoring is non-invasive but can only be performed for relatively short periods. An ICM allows continuous ECG monitoring over a much longer period, making it extremely useful for investigating patients with infrequent, but nonetheless troublesome, symptoms. It does, however, involve an invasive procedure (with the attendant risks) and is more expensive than other forms of ambulatory monitoring. It can, however, prove very cost-effective if it avoids the need for multiple short-term ambulatory recordings.
As with any other form of ambulatory monitoring, failure to correlate symptoms with recorded events can lead to inappropriate diagnoses.
Further reading
Crawford MH, Bernstein SJ, Deedwania PC, et al. ACC/AHA guidelines for ambulatory electrocardiography: executive summary and recommendations. Circulation 1999; 100: 886–93.
National Institute for Health and Care Excellence (2010). Transient loss of consciousness (‘blackouts’) in over 16s. Clinical guideline CG109. http://www.nice.org.uk/guidance/cg109.
Task Force for the Diagnosis and Management of Syncope; European Society of Cardiology (ESC); European Heart Rhythm Association (EHRA); Heart Failure Association (HFA); Heart Rhythm Society (HRS), Moya A, Sutton R, Ammirati F, et al. Guidelines for the diagnosis and management of syncope (version 2009). Eur Heart J 2009; 30: 2631–71.
Exercise testing permits the dynamic assessment of cardiac function. There are many different indications for exercise testing, but the commonest is the investigation of suspected or known CHD.
•Assessment of likelihood of CHD in patients with chest pain.
•Risk stratification of patients with known CHD and hypertrophic cardiomyopathy.
•Evaluation of response to treatment or revascularization in CHD.
•Assessment of exercise-induced arrhythmias.
•Assessment of symptoms in valvular heart disease.
•Objective assessment of exercise capacity.
The absolute and relative contraindications to exercise testing are listed in Box 6.1.
Box 6.1 Absolute and relative contraindications to exercise testing
•Unstable angina (rest pain within previous 48h)
•Uncontrolled cardiac arrhythmias (causing symptoms or haemodynamic compromise)
•Symptomatic severe aortic stenosis
•Uncontrolled symptomatic heart failure
•Acute PE or pulmonary infarction
•Acute myocarditis or pericarditis
•Left main stem coronary stenosis
•Uncontrolled hypertension (systolic >200mmHg, diastolic >110mmHg)
•Tachyarrhythmias or bradyarrhythmias
•Outflow obstruction, e.g. hypertrophic cardiomyopathy
Unless the exercise test is being performed to assess response to treatment, patients should be advised to discontinue anti-anginal drugs, e.g. β-blockers, calcium channel blockers, long-acting nitrates, nicorandil, and also digoxin 48h prior to the test. Patients should attend for the test wearing suitable clothing and footwear.
The test should be carefully explained to the patient, so that they are familiar with the exercise protocol being used. A resting ECG is recorded, and the patient’s BP measured. An appropriately trained team comprising at least two personnel, trained in advanced life support, should supervise the test. Full resuscitation and defibrillation facilities must be readily available. Exercise can be performed using either an exercise treadmill or an exercise bicycle. A variety of protocols are available, of which the commonest are the Bruce protocol and the modified Bruce protocol (see Table 6.17). The workload during exercise normally ↑ at 3min intervals, with the BP and ECG being recorded at each stage. The patient should be asked to report any symptoms during the test.
Table 6.17 Modified Bruce and Bruce protocols
| Protocol | Modified Bruce | Standard Bruce | ||||||
| Stage | 01 | 02 | 03 | 1 | 2 | 3 | 4 | 5 |
| Speed (kph) | 2.7 | 2.7 | 2.7 | 2.7 | 4.0 | 5.5 | 6.8 | 8.0 |
| Slope (°) | 0 | 1.3 | 2.6 | 4.3 | 5.4 | 6.3 | 7.2 | 8.1 |
•A fall of >10mmHg in systolic BP from baseline associated with ischaemia.
•↑ ataxia, dizziness, or near syncope.
•Difficulty in monitoring the ECG or BP.
•Onset of arrhythmias (ventricular tachycardia, supraventricular tachycardia, AF, worsening ventricular ectopics).
•1.0mm or more ST elevation (in leads without Q waves, other than V1 or aVR).
•A request from the patient to stop the test.
•A fall of >10mmHg in systolic BP from baseline, even in the absence of ischaemia.
•>3mm of ST-segment depression or marked axis shift.
•Development of bundle branch block that cannot be distinguished from ventricular tachycardia.
•Fatigue, breathlessness or wheezing, leg cramps, claudication.
At the end of the exercise, the patient may be permitted to sit. Monitoring of the ECG and BP must continue until the heart rate and BP have returned to baseline and any ECG changes have resolved.
Exercise testing is generally well tolerated, with a morbidity of 2.4 in 10,000 and a mortality of 1 in 10,000 (within 1 week of testing). Risks include arrhythmias and cardiac arrest, MI, and cardiac rupture, and are more likely in those with a recent history of ACS. Facilities for resuscitation and defibrillation must be immediately available.
Myocardial ischaemia is indicated by 1mm horizontal or downsloping ST-segment depression 80ms after the J point. Some cardiologists use 2mm of ST-segment depression as the diagnostic criterion—this ↑ the specificity of the test but reduces the sensitivity. Upsloping ST-segment depression and T wave changes are not reliable indicators of ischaemia. A fall in BP (or a failure of BP to rise) during exercise can also indicate ischaemia, particularly if accompanied by ST-segment depression and chest pain.
Generally speaking, the earlier and the more marked the ST-segment changes, the more severe the underlying coronary artery disease. The prognostic value of exercise testing is well established. Patients can be risk-stratified using the Duke treadmill score, calculated as follows:
where: 0 = no exercise angina; 1 = exercise angina; 2 = exercise angina that led to termination of the test.
The Duke treadmill score defines a high-risk group with a score of ≥−11, with an annual cardiovascular mortality of 5%. Low-risk patients have a score of ≥+5, with an annual cardiovascular mortality of 0.5%.
Almost any arrhythmia or conduction disturbance can occur during exercise testing. If the exercise test is being performed to investigate arrhythmias, this can indicate a diagnostic result.
Exercise testing is a relatively simple and inexpensive investigation, with a strong evidence base that it is useful in a large number of clinical situations. Alternative tests for myocardial ischaemia include stress echocardiography, CMR, and myocardial perfusion imaging.
Exercise test results are commonly reported as ‘positive’ or ‘negative’, giving the erroneous impression that the results are ‘black or white’. The sensitivity and specificity of exercise testing vary widely between different patient populations, and false −ve and false +ve results are not uncommon. If the pretest probability of CHD is low, e.g. an asymptomatic young woman, exercise testing is of little value as even a ‘positive’ result is unlikely to be true. Similarly, if the pretest probability of CHD is high, e.g. a ♂ in his 60s with typical anginal symptoms, a ‘negative’ result is also unlikely to be true. Guidelines from NICE state that exercise testing should not be used for the de novo diagnosis of IHD, but only for the assessment of patients with known IHD.
National Institute for Health and Care Excellence (2016). Chest pain of recent onset: assessment and diagnosis. Clinical guideline CG95. http://www.nice.org.uk/guidance/cg95.
Since myocardial perfusion abnormalities occur early following the onset of ischaemia, evaluation of regional myocardial perfusion heterogeneity is a sensitive marker for the presence of coronary artery disease. Myocardial perfusion imaging is most commonly performed with radionuclide imaging. Alternative modalities include contrast echocardiography and contrast CMR imaging.
The radioisotopes thallium-201 or technetium-99m are taken up by the myocardium in proportion to blood flow. Images are then acquired by a gamma camera. The images are processed to provide colour mapping of myocardial perfusion. Information is obtained regarding the presence of reversible or fixed myocardial ischaemia. Late repetition of image acquisition allows redistribution of the isotope in areas of slow blood flow for assessment of myocardial viability.
As with all investigational methods for evaluation of ischaemia, perfusion imaging is enhanced by the addition of cardiac stress. This may be in the form of physical exercise, e.g. treadmill or bicycle, or with use of pharmacological stressors. The latter are particularly useful if the patient is physically unable to exercise sufficiently or has ECG abnormalities that prohibit accurate interpretation, e.g. left bundle branch block or ventricular pacing. The most commonly used pharmacological stressor is the vasodilator adenosine, which has a very short half-life. Dobutamine can also be used in patients with contraindications to adenosine, but it is a less effective vasodilator. Adenosine gives rise to a 4- or 5-fold hyperaemia, whereas dobutamine only has a 2-fold vasodilatory effect. During adenosine stress, there is a 4- to 5-fold ↑ in blood flow to normal myocardial territories, compared with the basal state. In the presence of coronary artery stenosis, there is impaired vasodilatation and a reduction in the stress:rest ratio, precipitating a myocardial perfusion mismatch.
•To assess the presence and degree of coronary artery stenoses in patients with suspected coronary artery disease.
•To assist in the management of patients with known coronary artery disease:
•To determine the likely prognosis and probability of future cardiac events, e.g. following MI or during proposed non-cardiac surgery.
•To guide proposed revascularization procedures by determining the physiological significance of known coronary artery lesions, including the effects of anomalous coronary arteries, muscle bridging, and coronary artery ectasia in Kawasaki’s disease.
•To assess the success of performed revascularization strategies.
•To differentiate between areas of myocardial scar tissue and viable myocardium prior to proposed revascularization.
Pregnancy is a contraindication to nuclear imaging. Contraindications to physical exercise testing are listed in Box 6.1.
•Known hypersensitivity to adenosine.
•Untreated second- or third-degree heart block, sick sinus syndrome, long QT syndrome.
•Asthma, chronic obstructive airways disease with known bronchospasm.
•Hypotension (systolic BP <90mmHg).
•ACS not successfully stabilized with medical therapy.
•Concomitant use of dipyridamole (within last 24h) or xanthines (within last 12h).
•Known hypersensitivity to dobutamine.
•Concomitant use of β-blockade.
β-blockers and rate-limiting calcium antagonists should be withdrawn for 48h prior to the test if physical exercise or dobutamine stress is planned. Xanthines and dipyridamole should be withdrawn for 24h prior to adenosine stress, and any foods or drugs containing caffeine should be avoided. Peripheral IV access should be sited.
The stress study is generally performed first, since if this is normal, there may be no need to acquire resting images. The radioisotope is injected at peak stress, so that myocardial uptake of the tracer reflects maximal blood flow and optimizes visualization of any perfusion deficit. The protocols for the varying forms of stress are given in Table 6.18.
Table 6.18 Radionuclear exercise and imaging protocols
| Stress | Protocol | Injection time of radioisotope |
| Physical exercise | As directed by physician, e.g. Bruce, Sheffield, to 85% max predicted heart rate (MPHR) | 1–2min prior to cessation of peak exercise |
| Adenosine | 140µg/kg/min for 6min | 3–4min after start of infusion |
| Dipyridamole* | 140µg/kg/min for 4min | 4min after infusion completion |
| Dobutamine | In 3min stages: 5–10, 20, 30, 40µg/kg/min | When 85% MPHR and/or maximal dose dobutamine |
* See Pellika PA, Nagueh SF, Elhendy AA, et al. American Society of Echocardiography recommendations for performance, interpretation, and application of stress echocardiography. J Am Soc Echocardiogr 2007; 20: 1021–41.
Heart rate and BP should be measured throughout physical or pharmacological stress. A 12-lead ECG should be observed continuously for evidence of ST-segment or T wave changes suggestive of ischaemia and arrhythmias.
Redistribution imaging for assessment of myocardial viability can be performed 3–4h after stress imaging. To enhance redistribution imaging, particularly if any perfusion deficits seen with stress are severe, sublingual nitrate can be given, followed by a further resting injection of the radioisotope and image acquisition an hour later. This is known as a stress–redistribution–reinjection protocol.
A single- or dual-head gamma camera is used for image acquisition. This rotates 180° round the patient from 45° in the right anterior oblique position to 45° in the left posterior oblique position. The tomographic data are reconstructed into double oblique imaging planes. Stress and rest images are aligned carefully with accurate image registration for comparison. Image quality is assessed, and then the long and short axis images are evaluated for myocardial perfusion deficits.
It should be remembered that the patient is exposed to ionizing radiation, especially if sequential studies are planned. Physical or pharmacological stress may induce severe myocardial ischaemia, infarction, and potentially life-threatening arrhythmias (0.01–0.05%).
•ST-segment elevation of >0.1mV in leads without Q waves.
•A fall in systolic BP >10mmHg below baseline.
•A severe hypertensive response (BP >250/115).
•Clinical loss of peripheral perfusion, i.e. pallor or cyanosis.
Perfusion deficits are identified as areas of reduced tracer uptake. These may be assessed qualitatively or semi-quantitatively. Semi-quantitative classification expresses regional myocardial uptake as a percentage of the maximal uptake seen, according to the following scale:
Perfusion deficits may be categorized as either reversible (present on stress imaging alone) or fixed (present on stress and rest imaging). When the redistribution protocol is followed, areas of reduced perfusion can be examined for the presence of viability (revascularization will improve regional function) or scar tissue (revascularization is futile). The size of the LV and RV can also be determined (see Table 6.19).
Table 6.19 Possible results for myocardial perfusion imaging
| Stress | Rest | Clinical conclusion | |
| Myocardial perfusion | Normal/↑ | Normal | Normal |
| Reduced | Normal | Myocardial ischaemia (reversible defect) | |
| Reduced/absent | Reduced/absent | MI (fixed defect) | |
| Late redistribution | Reduced | ↑ from baseline | Viable myocardium |
| Reduced | Reduced | MI (scar) |
Radionuclide imaging is readily available and non-invasive. It is inexpensive, compared with coronary angiography. In contrast to MRI, where the number of imaging planes that can be acquired may be limited, radionuclide imaging provides full myocardial coverage. There are many studies supporting the ability of the technique to give accurate diagnostic information and prognostic data.
Qualitative or semi-quantitative analytical techniques, whereby signal intensity is compared with the area of maximal myocardial uptake, may limit accuracy in the presence of triple-vessel disease where there is globally reduced myocardial perfusion. Additionally, the study may be suboptimal if peak stress is not achieved. Radionuclide imaging has poor spatial resolution in comparison with other techniques. Perfusion defects limited to the subendocardium may not be visualized. Image quality can be degraded by patient movement and artefacts. Such artefacts include attenuation from breast tissue in the anterior wall and inferior signal loss.
Further reading
Anagnostopoulos C, Harbinson M, Kelion A, et al. (2004) Procedure guidelines for radionuclide myocardial perfusion imaging. Heart 2004; 90(Suppl 1): i1–10.
Bourque JM, Beller GA. Stress myocardial perfusion imaging for assessing prognosis: an update. JACC Cardiovasc Imaging 2011; 4: 1305–19.
Hendel RC, Berman DS, Di Carli MF, et al. ACCF/ASNC/ACR/AHA/ASE/SCCT/SCMR/SNM 2009 appropriate use criteria for cardiac radionuclide imaging. Circulation 2009; 119: e561–87.
Radionuclide ventriculography (RNV) is a technique to provide accurate assessment of cardiac chamber size, morphology, and function. The patient’s RBCs are radiolabelled with 99mtechnetium pertechnate in vitro or in vivo. The labelled blood pool within the cardiac chambers is then imaged with a gamma camera, gated to the ECG. Multiple image acquisitions are acquired throughout the cardiac cycle, typically over at least 16 systolic and 32 diastolic frames. These images can be assessed either based on either the radioactive count or by geometric analysis.
•Prognostic estimation in patients with heart failure or coronary artery disease.
•Estimation of operative coronary risk for non-cardiac surgery.
•Diagnosis of coronary artery disease where conventional exercise testing is inadequately performed or result equivocal.
•Evaluation of the efficacy of revascularization or medical management strategies in patients with coronary artery disease.
•Monitoring of cardiac function in patients undergoing chemotherapy.
The technique is contraindicated in pregnant or lactating women.
No special preparation is required for a resting study. If an exercise study is to be performed, the patient should fast for 3–4h prior to the procedure. If pharmacological stress agents are used, the same preparation as for myocardial perfusion imaging should be followed. A resting ECG is helpful to exclude arrhythmias.
For a resting study, the patient lies supine whilst anterior and left anterior oblique images are acquired. Stress studies may be performed with either physical exercise, e.g. bicycle ergometry, or pharmacological stressors, e.g. dobutamine. Images are acquired at intervals once the heart rate has stabilized at each new level of exercise or stress. The patient should have haemodynamic and ECG monitoring throughout. Cardiopulmonary resuscitation facilities should be available. Images are then analysed to obtain the required morphological and functional parameters. High activity areas, such as the spleen or aorta, may be filtered out for optimal assessment of cardiac parameters.
Technetium has a 6h half-life. Although the heart receives the largest dose, 5% of the total radiation dose is sequestered by the BM, the most radiosensitive body tissue. Radiation dose is up to 1100MBq, and so a typical examination carries a fatal cancer risk of 1 in 3300. Serial studies should be avoided where alternative forms of imaging suffice.
•Dilatation or hypertrophy of the cardiac chambers and great vessels may be identified.
•Left and right ventricular EFs can be measured. Normal left ventricular EF is 60–80% at rest and slightly more during exercise. Right ventricular EF is 46–70%. Both values decline with age. The extent of any global left ventricular dysfunction can therefore be identified.
•Regional wall dysfunction at rest, at low- and peak-dose stress, and during recovery may be described in a manner analogous to stress echocardiography, in order to identify areas of reversible myocardial ischaemia, myocardial hibernation, or scar.
RNV is non-invasive and repeatable and provides serial measurements, especially in patients who are difficult to scan echocardiographically or who cannot tolerate MRI. It can be used in critically ill patients soon after an acute MI.
Patients receive a significant radiation dose. Echocardiography is safer, and CMR is likely to replace this technique as the gold standard. Red cell labelling may be inefficient in chronic renal failure. Technical factors are important; in particular, radioactivity in the left atrium must be separated from that in the LV to obtain an accurate EF. A poor ECG signal and inappropriate gating may render data uninterpretable; heart rate variability may compromise diastolic filling indices, and inadequate frame counts ↓ statistical reliability.
Further reading
Hendel RC, Berman DS, Di Carli MF, et al. ACCF/ASNC/ACR/AHA/ASE/SCCT/SCMR/SNM 2009 appropriate use criteria for cardiac radionuclide imaging. Circulation 2009; 119: e561–87.
A PmA (Swan–Ganz) catheter is a multi-lumen catheter that is passed percutaneously from a central vein, e.g. femoral, subclavian, or jugular, to the right heart structures. It can be used to measure venous, RAt, right ventricular, PmA, and LAt (indirect) pressures to obtain blood samples for O2 saturation estimation, to measure cardiac output and systemic vascular resistance, and additionally to act as a central venous infusion port.
•Aid in the diagnosis of cardiovascular shock and pulmonary oedema.
•Management of complicated acute MI, especially right ventricular infarction, cardiogenic shock.
•Management of patients with cardiac failure.
•Fluid therapy/inotropic delivery in severely ill patients, e.g. sepsis, burns, multi-organ failure, cardiac surgery, trauma.
•Diagnostic right heart catheterization, including congenital heart disease, pulmonary hypertension, intra-cardiac shunts.
•Prosthetic tricuspid or pulmonary valve.
•Right heart tumour or thrombus.
•Unstable ventricular arrhythmia.
LAn is injected into the skin at the site of venous access. The patient is positioned flat on a couch, generally with a head-down orientation if cephalad access is to be used. Pressure transducers are made ready and zeroed for accurate measurements. Fluoroscopic screening should be available, if required.
An access sheath is placed in the vein using a Seldinger technique. The PmA triple-lumen catheter is flushed with saline, and the integrity of the flotation balloon assessed by inflation with air. Under fluoroscopic guidance or by observation of intra-cardiac pressure traces, the catheter is passed through the venous system towards the right heart and into a branch of the PmA. At each stage, pressure and O2 samples can be measured. The balloon can be inflated to assist passage through the right heart. The balloon is wedged briefly into a PmA branch to obtain an assessment of indirect pressure (PmA wedge pressure). Cardiac output can be calculated using a thermodilution method. Iced saline at a known temperature is injected through the proximal lumen and a thermistor at the catheter tip measures the temperature rise in the blood-warmed saline as it passes through the tricuspid valve, RV, and pulmonary valve. Systemic peripheral resistance can also be estimated.
•Arterial puncture, pneumothorax, haemothorax.
•PE or infarction (if the right heart contains masses or if the balloon remains inflated in wedge pressure position).
•PmA rupture (balloon over-inflation).
PmA catheterization can be used to assess pulmonary and systemic venous filling pressures and fluid status, right and left cardiac function, and also, where indicated, to provide information on valve dysfunction, intra-cardiac shunts, tamponade, and pulmonary hypertension.
This technique has traditionally been a useful adjunct to patient monitoring in the intensive care setting, in particularly for accurate pressure evaluation of the right heart and left atrium and for continuous cardiac output assessment. However, recently several less invasive devices have been designed for cardiac output monitoring, e.g. oesophageal Doppler.
The procedure is generally well tolerated, but it is an invasive procedure not without risk. It is essential that the PmA catheter is inserted only by suitably trained individuals to assist diagnosis and monitor treatment in carefully selected patients. If a non-invasive alternative is available, then this should be preferentially employed. Care must be taken in data interpretation, as misleading results may be obtained if the system is not systematically and accurately zeroed for serial measurements. Indirect LAt pressure measurements may be inaccurate in patients with pulmonary disease.
Further reading
Kelly CR, Rabbani LE. Pulmonary-artery catheterization. N Engl J Med 2013; 369: e35.
On standing, gravity redistributes up to 800mL of blood to the legs. The normal compensatory response is ↑ sympathetic and ↓ parasympathetic stimulation, which maintains BP with a small ↑ in heart rate. Head-up tilt table testing uses gravity-induced venous pooling to assess autonomic control and to attempt to reproduce symptoms of autonomic dysfunction of dizziness or collapse, i.e. neuro-cardiogenic (vasovagal) syncope.
Testing is appropriate in the investigation of sudden, unpredictable loss of consciousness thought to be neurally mediated (vasovagal syncope, carotid sinus syncope, or situational syncope) in the absence of structural heart disease.
•Severe left ventricular outflow tract obstruction.
•Severe proximal cerebral or coronary artery disease.
•Testing is not appropriate for frail patients who cannot weight-bear for up to an hour.
Fasting is not required. Patients should continue all suspected culprit medications.
The test should take place in a quiet room at a constant temperature. The patient is lightly strapped to a table with a weight-bearing footboard. Pulse and beat-to-beat BP are recorded throughout the test. The patient is laid supine for 10min (20min, if cannulated), and then the table is mechanically tilted to 70° for 20min of passive tilt. If positivity or discontinuation criteria have not been reached by this point, 400μg of sublingual glyceryl trinitrate (GTN) are administered whilst upright, and the tilt is continued for a further 15min. If the patient has a history of adverse reaction to nitrates, or if a diagnosis of psychogenic or hyperventilation syncope is suspected, then a 40min tilt protocol should be used instead with no GTN provocation.
Syncopal symptoms (or, in extreme cases, loss of consciousness), hypotension, and bradycardia may be induced, albeit transiently, so full cardiopulmonary resuscitation facilities and an appropriately trained supervising team should be available.
A normal response is a <20% ↓ in BP associated with a modest rise in pulse rate. The test is −ve in the absence of a fall in BP, fall in heart rate, and lack of syncopal symptoms, and +ve if syncopal symptoms are induced by hypotension and/or bradycardia. A cardio-inhibitory response is characterized by a fall in heart rate (asystole in extreme cases), a vasodepressor response by a fall in BP with no pulse change, and a mixed response by a fall in both pulse and BP. A diagnosis of postural orthostatic tachycardia syndrome (POTS) is indicated by a rise in heart rate of ≥30bpm and/or to ≥120bpm, within 10min of upright tilt.
Monitoring of ECG and BP during a 24h ambulatory period or during a Valsalva manoeuvre—measurements of plasma catecholamines, mineralocorticoids, and glucose have a role in the investigation of autonomic dysfunction and syncope, but only tilt table testing provides a dynamic objective, witnessed assessment.
The test is time-consuming and requires technical and medical personnel trained in the conduct and interpretation of the procedure and in resuscitation.
National Institute for Health and Care Excellence (2010). Transient loss of consciousness (‘blackouts’) in over 16s. Clinical guideline CG109. www.nice.org.uk/guidance/cg109.
Parry SW, Reeve P, Lawson J, et al. The Newcastle protocols 2008: an update on headup tilt table testing and the management of vasovagal syncope and related disorders. Heart 2009; 95: 416–20.
Task Force for the Diagnosis and Management of Syncope; European Society of Cardiology (ESC); European Heart Rhythm Association (EHRA); Heart Failure Association (HFA); Heart Rhythm Society (HRS), Moya A, Sutton R, Ammirati F, et al. Guidelines for the diagnosis and management of syncope (version 2009). Eur Heart J 2009; 30: 2631–71.
