Table of Contents  

Bergler-Klein: Acute chest pain and the value of echocardiography

Introduction

Acute chest pain is one of the most common symptoms in patients seeking aid from emergency medical departments.1 The differential diagnosis of thoracic pain comprises a number of entities (Table 1). Factors that may point to the aetiology of chest pain include the symptoms, onset and characteristics of the pain; the age of the patient; and risk factors such as smoking, diabetes mellitus, hypertension, hyperlipidaemia, obesity and family history of disease, as well as previous cardiovascular diseases. In acute myocardial infarction, early reperfusion therapy is crucial. For rapid diagnosis, an electrocardiogram (ECG) should always be obtained immediately. Serial plasma levels of troponin T, creatine kinase (CK) and CK-MB, as well as B-type natriuretic peptide (BNP, or its N-terminal proform NT-proBNP) and D-dimer should also be determined quickly. Other routine blood tests, including haemoglobin level, blood cell count, C-reactive protein, creatinine and electrolytes, should also be performed. However, it is some time before the results of these become available. Auscultation for cardiac murmurs or pulmonary rales, clinical examination for leg oedema, abdominal palpation and measurement of vital parameters including blood pressure, breathing rate and oxygen saturation are important in deciding the best course of action.

TABLE 1

Differential diagnoses of chest pain

Cause of chest pain Diagnoses
Cardiovascular Coronary artery disease: acute coronary syndrome, myocardial infarction
Aortic syndrome, aortic dissection, aneurysm
Pulmonary embolism
Valvular disease: aortic stenosis, endocarditis
Hypertensive crisis
Heart failure, cardiomyopathy (dilated, ischaemic, restrictive)
Takotsubo cardiomyopathy
Hypertrophic obstructive cardiomyopathy
Pericarditis, pericardial effusion
Myocarditis
Pulmonary hypertension
Pulmonary Pneumonia, pleural effusion, pleuritis
Pneumothorax
Tumour, mediastinal disease
Gastrointestinal Gastro-oesophageal reflux, oesophagitis, gastritis
Musculoskeletal Rheumatic disease, costochondritis, neuralgia
Chest trauma
Psychogenic

Transthoracic echocardiography can easily be performed at the bedside. The overall left ventricular (LV) function – one of the strongest predictors of outcome in emergency patients – is quickly determined, as are valvular function, segmental wall motion, right ventricular (RV) size and function, pulmonary arterial systolic pressure, pericardial effusion or cardiac tamponade and even pleural effusion.2,3

Recently published guidelines by the European Society of Cardiology (ESC) recommend that echocardiography be carried out in all patients with acute coronary syndromes, to assess LV function and wall motion abnormalities and to rule out other disease entities.4 This article discusses the main role of echocardiography in acute chest pain.

Acute coronary syndromes: non-ST-elevation myocardial infarction and ST-elevation myocardial infarction

Ischaemic wall motion abnormalities can be detected using echocardiography almost immediately, a mean of 12–19 seconds after experimental coronary occlusion.2 Wall motion abnormalities may even precede ST-segment changes on ECG or plasma troponin release. They are caused by transmural ischaemia of > 20% of the wall thickness and coronary stenosis > 80–85%. In addition, echocardiography can very quickly identify hypokinesia or akinesia of myocardial segments in patients with acute chest pain, and is very helpful in the diagnosis of acute coronary syndrome and distinguish it from other differential diagnoses (e.g. pulmonary embolism with dilated right ventricle, or aortic dissection with aortic regurgitation and pericardial effusion). Echocardiography should be readily available in all chest pain units.1,2,46

In the recent ESC Guidelines, it is highly recommended, based on a consensus of opinion among experts (defined as a Class I, level of evidence C, recommendation), that echocardiography be performed in all patients with suspected acute coronary syndrome or non-ST-elevation myocardial infarction.4 In acute ST-elevation myocardial infarction, echocardiography can help to rapidly rule out life-threatening mechanical complications such as papillary muscle rupture and severe acute mitral regurgitation, free ventricular wall rupture, pericardial effusion leading to cardiac tamponade and acute ventricular septal defect. Therefore, although echocardiography is not usually necessary if ST elevation can be clearly diagnosed by ECG, it is very useful to establish global LV function and plays a key role in determining the extent of myocardial damage in myocardial infarction.6

Echocardiography can rule in or rule out differential diagnoses such as aortic syndromes with aortic dissection, massive pulmonary embolism, aortic stenosis, hypertrophic cardiomyopathy, pericardial effusion or even pleural effusion in the context of chest pain.

Echocardiography should always be performed in patients with acute heart failure and in patients with myocardial infarction who are showing rapid clinical deterioration (an ESC Class I, level of evidence C, recommendation). This can help to distinguish the cause and severity of LV or RV dysfunction. RV infarction can be diagnosed quickly with transthoracic echocardiography. In cases of cardiogenic shock or cardiopulmonary resuscitation, echocardiography can help to establish the aetiology of cardiac failure.46

Resting transthoracic echocardiography is limited by a sensitivity of 93% and a much lower specificity of 66% for the detection of acute coronary syndrome in low-risk patients.2,3 In patients with obesity or pulmonary disease, the quality of imaging may be inadequate for reliable assessment of wall motion.

Two-dimensional speckle-tracking strain echocardiography is a promising new method of detecting ischaemia.2,3,710 Longitudinal systolic strain is very sensitive to coronary ischaemia. In cases of acute myocardial infarction, two-dimensional LV longitudinal strain has been shown to be useful for early risk and prognosis assessment. Typically, ischaemic regions show delayed, post-systolic thickening with reduced strain curves.9 The affected coronary segments can be easily identified using a bull’s eye plot of impaired peak systolic strain and post-systolic index (Figures 1 and 2). The global systolic strain reflects early subclinical LV dysfunction (normal values are between −18% and −20%), even in normal LV ejection fraction, and this is correlated with increased plasma levels of BNP. Strain analysis is easy to perform in addition to visual wall motion analysis, and can also be performed offline using digital storage workstations. After percutaneous coronary intervention, ischaemic areas may return to normal values; however, in a large transmural infarction with scarring, strain values may remain seriously impaired, as reflected by severely hypo- or akinetic wall motion areas.7,9

FIGURE 1

Bull's eye plot of peak systolic strain in acute anteroseptal ischaemia, shown by impaired values of longitudinal strain (light red) derived from the global longitudinal peak systolic strain (GLPSS) in the apical three-, four- and two-chamber transthoracic views (LAX, A4C and A2C). The average global strain was impaired by −12.3% (normal values are between −18% and −20%). AVC, aortic valve closure.

6-1-10-fig1.jpg
FIGURE 2

Bull's eye plot of the post-systolic index in a patient with anteroseptal ischaemia. The delayed peak strain after the aortic valve closure (post-systolic thickening) in ischaemia is indicated by the dark blue segments.

6-1-10-fig2.jpg

Aortic dissection

Aortic dissection is associated with a high mortality rate if not treated promptly. In many patients, adequate assessment – especially of the ascending aorta and aortic root, as well as the aortic arch and parts of the descending aorta – can be achieved with acceptable imaging quality using bedside screening with transthoracic echocardiography (TTE) as the initial modality.2,3,11,12 However, a negative transthoracic echo does not rule out aortic dissection, and computed tomography (CT) must be considered if clinical suspicion persists – for example, in patients with elevated plasma D-dimer, peripheral pulse deficit and tearing chest pain.

In haemodynamically unstable patients who cannot be subjected to CT, transoesophageal echocardiography (TOE) is the technique of choice in the diagnosis of aortic dissection, if an experienced examiner is available.11,12 With TOE, the site of the intimal tear in the aorta, false and true lumen, thrombus, pericardial effusion, severity of aortic valve regurgitation and LV function can quickly be visualized. The sensitivity and specificity of TTE and TOE can be improved by using contrast agents, and are higher in proximal dissections of the ascending aorta (type A dissections) than in the distal parts of the descending aorta (type B dissections).

Pulmonary embolism

The symptoms of pulmonary embolism can be similar to those of acute coronary syndrome, including dyspnoea, chest pain (which is often diffuse or experienced during inspiration), ECG changes and elevated biomarkers (D-dimer, BNP, and to a lesser degree troponin). The detection by bedside echocardiography of RV dysfunction and RV dilatation in a severely compromised patient can assist rapid treatment decisions. This is especially important if thrombolysis is indicated, particularly if this is accompanied by high troponin levels indicating myocardial injury.13,14 Suspected high-risk pulmonary embolism with cardiogenic shock or hypotension necessitates emergency CT or bedside echocardiography (depending on the availability of each). This is a Class I, level of evidence C, recommendation according to the ESC Guidelines.13 However, the sensitivity and specificity of echocardiography are only moderate, especially in normotensive, haemodynamically stable patients with suspected pulmonary embolism. In these patients, thoracic CT or ventilation–perfusion scintigraphy should be considered.

The major echocardiographic findings prognostic in pulmonary embolism are an enlarged right ventricle, typically with reduced basal and free wall RV function but with preserved RV apical contraction, and a small lumen of the left ventricle caused by reduced filling (Table 2 and Figure 3).

TABLE 2

Echocardiographic signs in pulmonary embolism

Direct: high specificity, low sensitivity
Thrombus in right heart: right atrium, right ventricle, paradoxical in patent foramen ovale
Pulmonary artery thrombus
Indirect: moderate specificity and sensitivity (40%)
RV dilatation (RV/LV > 1)
RV dysfunction (specificity 90% if high clinical probability)
McConnell sign: RV mid-wall hypo- or akinesia, but normal apical motion (94% specificity, even in pre-existing pulmonary disease)
D-sign, flattening of the interventricular septum, bowing towards left ventricle
Vena cava inferior dilation without inspiratory collapse
60/60 sign: pulmonary flow acceleration time < 60 milliseconds, pulmonary systolic arterial pressure < 60 mmHg
FIGURE 3

Dilated right ventricle and small lumen of left ventricle in a patient with pulmonary embolism. The inferior vena cava was also highly dilated.

6-1-10-fig3.jpg

Conclusion

Echocardiography is very useful in the differential diagnosis of most causes of chest pain in the emergency and bedside settings, and for this reason should be performed in all patients. Experience on the part of the examiner and adequate imaging quality are both necessary; however, the latter may be lacking in patients with obesity or pulmonary disease. New hand-held ultrasound machines may be of value in emergencies. However, these have very small screens and the findings should be interpreted with caution; nor should they be considered a substitute for a later, full echocardiographic examination. Echocardiography should be made available in all chest pain units to diagnose – or help rule out – acute coronary syndromes, aortic dissection and pulmonary embolism.

References

1. 

Kontos MC, Diercks DB, Kirk JG. Emergency department and office-based evaluation of patients with chest pain. Mayo Clin Proc 2010; 85:284–99. http://dx.doi.org/10.4065/mcp.2009.0560

2. 

Sechtem U, Achenbach S, Friedrich M, Wackers F, Zamorano JL. Non-invasive imaging in acute chest pain syndromes. Eur Heart J Cardiovasc Imaging 2012; 13:69–78. http://dx.doi.org/10.1093/ejechocard/jer250

3. 

Flachskampf FA, Daniel W. Cardiac imaging in the patient with chest pain: echocardiography. Heart 2010; 96:1063–72. http://dx.doi.org/10.1136/hrt.2009.172114

4. 

Hamm CW, Bassand JP, Agewall S, et al. ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation: The Task Force for the management of acute coronary syndromes (ACS) in patients presenting without persistent ST-segment elevation of the European Society of Cardiology (ESC). Eur Heart J 2011; 32:2999–3054. http://dx.doi.org/10.1093/eurheartj/ehr236

5. 

Anderson JL, Adams CD, Antman EM, et al. 2011 ACCF/AHA Focused Update Incorporated Into the ACC/AHA 2007 Guidelines for the Management of Patients With Unstable Angina/Non-ST-Elevation Myocardial Infarction: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation 2011; 123:e426–579. http://dx.doi.org/10.1161/CIR.0b013e318212bb8b

6. 

Van de Werf F, Bax J, Betriu A, et al. Management of acute myocardial infarction in patients presenting with persistent ST-segment elevation: the Task Force on the Management of ST-Segment Elevation Acute Myocardial Infarction of the European Society of Cardiology. Eur Heart J 2008; 29:2909–45. http://dx.doi.org/10.1093/eurheartj/ehn416

7. 

Munk K, Andersen NH, Terkelsen CJ, et al. Global left ventricular longitudinal systolic strain for early risk assessment in patients with acute myocardial infarction treated with primary percutaneous intervention. J Am Soc Echocardiogr 2012; 25:644–51. http://dx.doi.org/10.1016/j.echo.2012.02.003

8. 

Bergler-Klein J, Binder T. 2D strain imaging in the setting of acute myocardial infarction. Arch Cardiovasc Dis 2008; 101:72–3. http://dx.doi.org/10.1016/S1875-2136(08)70260-2

9. 

Gorcsan J III, Tanaka H. Echocardiographic assessment of myocardial strain. J Am Coll Cardiol 2011; 58:1401–13. http://dx.doi.org/10.1016/j.jacc.2011.06.038

10. 

Blessberger H, Binder T. Two dimensional speckle tracking echocardiography: clinical applications. Heart 2010; 96:2032–40. http://dx.doi.org/10.1136/hrt.2010.199885

11. 

Nienaber CA, Powell JT. Management of acute aortic syndromes. Eur Heart J 2012; 33:26–35b. http://dx.doi.org/10.1093/eurheartj/ehr186

12. 

Evangelista A, Flachskampf FA, Erbel R, et al. Echocardiography in aortic diseases: EAE recommendations for clinical practice. Eur J Echocardiogr 2010; 11:645–58. http://dx.doi.org/10.1093/ejechocard/jeq056

13. 

Torbicki A, Perrier A, Konstantinides S, et al. Guidelines on the diagnosis and management of acute pulmonary embolism: the Task Force for the Diagnosis and Management of Acute Pulmonary Embolism of the European Society of Cardiology (ESC). Eur Heart J 2008 29:2276–315. http://dx.doi.org/10.1093/eurheartj/ehn310

14. 

Lankeit M, Gómez V, Wagner C, et al. A strategy combining imaging and laboratory biomarkers in comparison with a simplified clinical score for risk stratification of patients with acute pulmonary embolism. Chest 2012; 141:916–22. http://dx.doi.org/10.1378/chest.11-1355





Add comment 





Home  Editorial Board  Search  Current Issue  Archive Issues  Announcements  Aims & Scope  About the Journal  How to Submit  Contact Us
Find out how to become a part of the HMJ  |   CLICK HERE >>
© Copyright 2012 - 2013 HMJ - HAMDAN Medical Journal. All Rights Reserved         Website Developed By Cedar Solutions INDIA