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Complications of myocardial infarction on multidetector-row computed tomography of chest
Clinical Radiology 65 (2010) 930e936
Contents lists available at ScienceDirect
Clinical Radiology journal homepage: www.elsevierhealth.com/journals/crad
Pictorial Review
Complications of myocardial infarction on multidetectorrow computed tomography of chest V. Raj a, K. Karunasaagarar a, J.H.F. Rudd b, N. Screaton a, D. Gopalan a, * a b
Department of Radiology, Papworth and Addenbrookes Hospital, Cambridge, UK Division of Cardiovascular Medicine, University of Cambridge, Cambridge, UK
article in formation Article history: Received 23 December 2009 Received in revised form 19 March 2010 Accepted 22 March 2010
Myocardial infarction (MI) secondary to coronary artery disease remains the leading cause of death in the western world. The advent of early reperfusion therapy has substantially decreased in-hospital mortality and has improved the outcome in survivors of the acute phase of MI. Complications of MI include ischaemic, mechanical, arrhythmic, embolic and inflammatory disturbances. Although some of these complications may be infrequent, their importance is underscored because of the potential ability to correct them with early diagnosis and appropriate treatment. The majority of these complications will be detected on clinical examination and confirmed by echocardiography. Some patients may undergo non-electrocardiogram (ECG)-gated thoracic multidetector-row computed tomography (MDCT) due to non-specific presentation. In this group, it is imperative for the radiologist to be aware of and be confident in diagnosing the complications secondary to MI. This review illustrates the spectrum and imaging features of acute and chronic complications of MI that can be visualized on both ECG-gated cardiac and non-ECG-gated thoracic MDCT. Ó 2010 The Royal College of Radiologists. Published by Elsevier Ltd. All rights reserved.
Introduction Rapid technological advances in multidetector-row computed tomography (MDCT) have lead to its applications in cardiac imaging becoming a practical reality at acceptable radiation dose. Although electrocardiogram (ECG) gating is a prerequisite for assessment of coronary arteries, non-ECGgated thoracic MDCT can also provide valuable morphological cardiovascular information that can modify patient management. The advent of early reperfusion therapy has substantially decreased in-hospital mortality and has improved the outcome in survivors of the acute phase of myocardial * Guarantor and correspondent: D. Gopalan, Papworth Hospital NHS Trust, Papworth Everard, Cambridge CB23 3RE, UK. Tel.: þ44 14808364562; fax: þ44 1480364403. E-mail address: [email protected] (D. Gopalan).
infarction (MI). Complications of MI can be secondary to ischaemia, mechanical dysfunction, arrhythmia, embolic and inflammatory disturbances. The majority of these complications will be detected on clinical examination and confirmed by echocardiography. A small proportion of patients, especially those who present with non-specific cardio-respiratory symptoms, such as atypical chest pain or unexplained shortness of breath, will require further imaging. In such patient cohorts, where chest radiography is unhelpful, MDCT of the chest may be required to guide further management. Therefore, it is important that the cardiac structures, even on ungated studies, are carefully scrutinized by both specialist as well as non-specialist radiologists and cardiologists interpreting these studies. This review illustrates the spectrum and imaging features of acute and chronic complications of MI (Table 1) that can be visualized on both ECG-gated cardiac and nonECG-gated thoracic MDCT.
0009-9260/$ e see front matter Ó 2010 The Royal College of Radiologists. Published by Elsevier Ltd. All rights reserved. doi:10.1016/j.crad.2010.03.017
V. Raj et al. / Clinical Radiology 65 (2010) 930e936
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Table 1 Complications of MI (1) Mechanical Free-wall rupture Ventricular septal rupture Mitral regurgitation Ventricular pseudoaneurysm Ventricular true aneurysm Cardiac failure and cardiogenic shock (2) Ischaemic (3) Embolic (4) Inflammatory Pericarditis Dressler’s syndrome (5) Arrhythmic
MI Cardiovascular disease kills nearly 200,000 people in the UK annually,1 although death rates have fallen by 40% since 1997. MI accounts for about half of those deaths and kills up to 50% of patients before they reach hospital. Initial treatment of all patients with MI is aimed at restoration of balance between myocardial oxygen demand and supply, pain relief, and prevention of complications of MI. For the purposes of determining appropriate treatment, MI can be categorized into ST segment elevation myocardial infarction (STEMI), non-ST segment elevation myocardial infarction (NSTEMI) and unstable angina. The primary focus in the management of MI is to recognize patients with STEMI so that early myocardial reperfusion therapy can be initiated. The means of accomplishing myocardial reperfusion has changed in the last decade, with primary percutaneous intervention now replacing thrombolytic therapy in most centres, driven by improved short and long-term mortality and morbidity.2 Patients with NSTEMI are not candidates for immediate thrombolysis but may be suitable for primary percutaneous intervention. Despite these advances in management techniques, early and late complications of MI do still occur.
Figure 1 CT axial image of a 65-year-old male patient with known ischaemic heart disease. There is thinning of the basal-mid lateral wall with sub-endocardial hypo-density (arrow) indicative of previous myocardial infarction. LA, left atrium; LV, left ventricle.
Complications of MI Some complications of MI typically occur early in the course of MI (e.g., arrhythmia), whilst others generally cause deterioration later in the course of hospital admission (e.g., ventricular septal defect, cardiac rupture). Although most of these complications are readily diagnosed clinically or with echocardiography, some will first become apparent on MDCT. This review does not suggest using MDCT for the primary diagnosis of these complications; rather, we aim to highlight some important and potentially lethal conditions that might first become apparent using this technique.
Mechanical complications Mechanical complications of MI result from the dysfunction of ischaemic myocardium; rupture of infarcted myocardium, valvular incompetence or from the stretching of a scarred myocardial area.
Cardiac rupture
MI imaging with MDCT MDCT does not currently have an established role in imaging acute MI. However, the incidental detection of infarcted myocardium on a MDCT study performed for unrelated reasons is common. In both acute and chronic infarctions the myocardium has significantly lower attenuation than un-infarcted myocardium3 (Fig. 1). Decreased perfusion results in hypoenhancement of the myocardium and may imply ischaemia rather than infarction in the acute setting. In a more chronic state, the hypoenhancement may be due to a combination of hypoperfusion and fatty replacement. Chronic infarcts are usually accompanied by ancillary features such as myocardial thinning and wall motion abnormality.
Cardiac rupture most commonly involves the lateral wall of the left ventricle (LV). It occurs in 3e6% of MI patients and accounts for approximately 10% of mortality from all MI. Half of the ruptures occur within 5 days and 90% in the first 2 weeks following an acute MI4 (Fig. 2). Clinically the presentation is typical with sudden onset of chest pain, accompanied by arrhythmia, cardiogenic shock, and symptoms of pericarditis.4 Although often there is not enough time for diagnostic testing in managing these patients, echocardiography is the test of choice. If performed, MDCT features would include pericardial effusion with findings of cardiac tamponade, i.e., collapse of the right heart chambers and dilatation of the inferior vena cava and hepatic veins. It is important to identify free-wall rupture on cross-sectional imaging as it is universally fatal if untreated.5 Less frequently,
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Figure 2 CT short axis reconstruction in a 55-year-old patient with acute inferior MI. There is extravasation of contrast medium (arrow) from the inferior wall of the left ventricle in keeping with a contained leak secondary to cardiac rupture. Note the absence of pericardial effusion due to the contained nature of the free-wall rupture. RV, right ventricle; LV, left ventricle.
free-wall rupture is contained by adherent pericardium or scar tissue resulting in development of a pseudoaneurysm.
Ventricular septal rupture Ventricular septal rupture (VSR) post-MI has reduced in incidence to 0.2% (previously 1e2%) since the introduction of reperfusion therapy.6,7 Although most commonly seen at 2e5 days post-MI, it can occur any time after MI.8,9 Clinically the presentation is variable, ranging from asymptomatic to acute cardiogenic shock with a new pansystolic murmur. VSR usually occurs at the junction of preserved and infarcted myocardium. The location is often in the apical septum with anterior MI and the basal septum with inferior MI (Fig. 3). It almost always occurs in the setting of a transmural MI. A discrete gap in the myocardium might not be evident on MDCT as the VSR may be composed of a meshwork of serpiginous channels.4
Figure 3 Axial CT image in a 61-year-old female patient with an inferior MI. There is abnormal communication between the right and left ventricle (black arrow) resulting from a basal ventricular septal rupture. RV, right ventricle; LV, left ventricle.
cardiac failure. The diagnosis is usually readily made on echocardiography. On MDCT, there may be left-sided chamber dilatation; localized pulmonary oedema, especially in the right upper lobe when the regurgitant flow across the mitral valve is directed towards the right upper pulmonary vein; and rarely, papillary muscle rupture may be evident4 (Fig. 4).
Ventricular pseudoaneurysm Ventricular pseudoaneurysm results from a contained rupture of the LV free wall. The outer wall of the
Mitral regurgitation Mitral regurgitation, which is usually mild to moderate, is a common (13e45%) finding post-MI and is usually transient and self-limiting.4,10e12 Mitral regurgitation postMI can be caused by mitral valve annular dilatation secondary to ischaemia-related LV dilatation, papillary muscle dysfunction secondary to LV regional wall motion abnormality or papillary muscle rupture, which may occur following acute inferior MI with a median interval of 13 h after the primary event. This can be life threatening and accounts for 5% of deaths in acute MI patients.13,14
Papillary muscle rupture Papillary muscle rupture typically presents with sudden clinical deterioration with a new murmur and worsening
Figure 4 Coronal CT reconstruction showing upper-zone pulmonary opacification (black arrow) with relative sparing of the mid and lower zones due to oedema resulting from mitral regurgitation resulting in directional flow towards upper lobe pulmonary veins. LA, Left atrium; LSPV, Left superior pulmonary vein.
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Figure 5 Transaxial CT image in a 70-year-old man with infarction in the circumflex territory. There is a pseudoaneurysm (black arrow) in the basal postero-lateral wall of the left ventricle with calcified walls and thrombus (star). LA, left atrium; LV, left ventricle.
Figure 6 Transaxial CT image in a 65-year-old man with a chronic LAD territory infarct. There is marked thinning of the apex and apical anteroseptum (white arrow) with aneurysmal dilatation of the apex (star). RV, right ventricle; LV, left ventricle; LAD, left anterior descending.
pseudoaneurysm is formed by thrombus and pericardium usually with a narrow neck communicating with the LV cavity. (Fig. 5) Unlike a true LV aneurysm, pseudoaneurysm contains no endocardium or myocardium. LV pseudoaneurysms can be clinically silent, or may cause arrhythmia, systemic embolization, or heart failure. If untreated the risk of subsequent cardiac rupture is approximately 30 to 45%, and mortality is as high as 23% if treated surgically and 48% if treated medically.15,16 Therefore, it is of paramount importance to identify and highlight the presence of these findings on MDCT, as ventricular pseudoaneurysms require surgical management.4
of myocardial calcification reflecting dystrophic calcification of infarcted myocardium. Dynamic imaging with retrospective cardiac gating may reveal focal dyskinesia. Cardiac failure and cardiogenic shock commonly result from myocardial dysfunction following an infarct. The degree of LV dysfunction depends on the extent of myocardial damage.17 Cardiogenic shock can be secondary to a multitude of causes, the most common of which is the haemodynamic compromise secondary to the MI. Other causes include myocardial rupture, as described above, and/or pharmacological depression of LV function and arrhythmia. In patients with no previous history of myocardial dysfunction, involvement of at least 40% of the LV mass is required to produce cardiogenic shock. However, this is not true in patients with pre-existing myocardial dysfunction where, smaller insults can have catastrophic consequences.18,19 On MDCT, features consist of direct cardiac signs, such as dilatation of the LV and possibly LA, hypoattenuation of the infarcted tissue and indirect signs including pleural/pericardial effusions and features of pulmonary interstitial and alveolar oedema. Many of these patients require both pharmacological and mechanical support to augment ventricular function. Mechanical support is most commonly given in the form of an intra-aortic balloon pump (IABP), which augments systemic pressure and increases coronary perfusion pressure. Ideally, the tip of the IABP should be in the descending thoracic aorta distal to the origin of the left subclavian artery. IABP malposition can result in complications such as limb ischaemia, embolization of platelet aggregates, haematoma, false aneurysm, and aortic dissection. Some patients with persisting LV compromise post-MI will be candidates for mechanical ventricular assist device (VAD) placement or transplantation. A VAD may augment either right or left ventricular function or both. It is usually
Ventricular true aneurysms Ventricular true aneurysms occur in the area of infarction and patients with apical transmural infarction are at a higher risk. The true aneurysm wall is composed of pericardium adherent to underlying epicardium and beneath the epicardium is the residual fibrous scar tissue of infarcted myocardium. Contrary to pseudoaneurysm, true aneurysm is connected to the ventricular cavity by a wide neck (Fig. 6). It rarely ruptures but if large, can cause significant haemodynamic consequences in the form of cardiac failure, due to disordered ventricular contraction, or ventricular thrombus formation leading to systemic embolization. Clinically patients present with cardiac failure and often systemic embolic episodes. Refractory arrhythmia is another mode of presentation that would alert the clinician to the possibility of aneurysm.4 Treatment ranges from prophylactic anticoagulation to surgical resection, depending on severity. True aneurysms are characterized by thinning and fusiform dilatation of the affected portion of the ventricular cavity. They may contain low attenuation thrombus or areas
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myocardium (Fig. 8). One in five patients with MI develops mural thrombus; this is more common in those with an anterior wall infarct.20 Most systemic emboli occur within 10 days of the acute event and commonly present as a stroke.4
Inflammatory complications Pericarditis Pericarditis occurs early after an acute MI in up to 10% of patients with the inflammation developing between 24 and
Figure 7 Transaxial CT image of a 58-year-old man. There is an eccentric thrombus (arrow) around the tip of the left ventricular assist device (star). The dilated enhancing structure in the right AV groove is the conduit between the aorta and ventricular assist device. Note the right-sided pacemaker leads. RV, right ventricle; LV, left ventricle.
used to bridge the critically ill heart failure patient to transplant but in some patients with reversible cardiomyopathy may be a bridge to cure. The device consists of an inflow and outflow line and a mechanical pump. The inflow is typically placed in the centre of the apex pointing towards the mitral valve while the outflow line is anastamosed to the ascending aorta. In patients with VAD, the tip of the ventricular catheter should be evaluated for position and adherent thrombus, the course of the device and lines for evidence of fluid collections (Fig. 7).
Embolic complications Patients are at higher risk of both venous and systemic thrombo-embolism after MI. The former is predominantly a consequence of immobility whilst arterial emboli are the result of mural thrombus arising from the area of infarcted
Figure 8 Transaxial CT image in a 55-year-old man with a history of alcohol abuse and previous MI. There is a large focal filling defect in the LV apex (black arrow) in keeping with thrombus.
Figure 9 (a) Transaxial CT in a 50-year-old male depicting a small pericardial (white arrow) and bilateral pleural effusions (star). There is no pericardial thickening or calcification. There were no CT features suggestive of tamponade. (b) Unenhanced transaxial CT image in a 64-year-old man with a small pericardial effusion (star). This has a radiodensity of 60 HU in keeping with a haemopericardium.
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96 h after the primary event.21,22 Acute pericarditis is an inflammatory response to necrotic tissue and is more often seen in patients with transmural infarction.4 In early stages, patients may not experience any symptoms or those of acute infarction may mask them. As time goes by patients typically complain of progressive, severe, pleuritic chest pain, which must be differentiated from recurrent ischaemic chest pain and pulmonary embolism.
Dressler’s syndrome Dressler’s syndrome is thought to occur in 1e3% of patients in the first 8 weeks post-MI. The aetiology and pathophysiology is not known but an autoimmune response to myocardial necrosis is postulated. The syndrome is characterized by the presence of persistent low-grade fever, pleuritic chest pain, a pericardial rub, and pericardial effusion, which is usually exudative. There may be associated pericardial thickening (>4 mm) involving visceral and parietal pericardium with or without enhancement, Enlarging pericardial effusion can rarely lead to tamponade requiring pericardiocentesis. On imaging, pericardial effusion post-MI in the correct clinical setting should raise the suspicion of pericarditis or Dressler’s syndrome (Fig. 9).
Arrhythmias and conduction abnormalities Re-entry circuits occurring at the junction of necrotic, ischaemic, and viable myocardium are responsible for the majority of post-MI arrhythmias. The most feared is ventricular fibrillation, which is lethal without early defibrillation, and may occur at any stage of the infarction, although it is most common in the first 24 h.4 Heart block as a consequence of ischaemic damage affecting the
Figure 10 Transaxial CT image in a 60-year-old woman. The tip of the pacemaker has perforated the pericardium and lies in the lung (white arrow). There is a small pericardial effusion (star). RV, right ventricle; LV, left ventricle.
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ventricular conduction system occurs less commonly than prior to thrombolytic and primary percutaneous coronary intervention (PPCI), but may still occur, especially after large anterior MI. From an imaging point of view, patients may have temporary pacing wires present in the right ventricle. Infrequently the pacing wires are in an unexpected location and should be brought to the attention of the referring physician. (Fig. 10) Arrhythmia is readily appreciated on the ECG trace during cardiac-gated studies and staff should be appropriately trained to recognize this.
Conclusion MDCT technological advances are leading to a paradigm shift in the evaluation of cardiac disease using imaging. Although the incidence of MI is falling, it remains a common disease with a spectrum of both acute and delayed complications, many of which are life threatening. Echocardiography continues to be the frontline imaging technique in this patient group. We do not advocate the routine use of MDCT in imaging patients with acute MI; instead it should be used as a complementary test in patients who either have suboptimal or inconclusive echocardiography and/or cardiac MRI. On its own, MDCT can be particularly useful in imaging patients for whom it is important to delineate morphological abnormalities, such as differentiation of true and false ventricular aneurysm. As we have demonstrated, many MI-related complications can be picked up on non-ECG-gated thoracic MDCT. This emphasizes the importance of understanding the range of complications of MI and their imaging appearances. MDCT can potentially ensure accurate detection and early diagnosis leading to expedition of appropriate treatment.
References 1. Allender S, Peto V, Scarborough P, et al. Coronary heart disease statistics. BHF Statistics; 2008. 2. Andersen HR, Nielsen TT, Rasmussen K, et al. A comparison of coronary angioplasty with fibrinolytic therapy in acute myocardial infarction. N Engl J Med 2003;349:733e42. 3. Nikolaou K, Knez A, Sagmeister S, et al. Assessment of myocardial infarctions using multidetector-row computed tomography. J Comput Assist Tomogr 2004;28:286e92. 4. Brener SJ, Tschopp D. Complication of acute myocardial infarction. Cleveland Clinic, Disease Management Project; 2009. 5. Becker RC, Hochman JS, Cannon CP, et al. Fatal cardiac rupture among patients treated with thrombolytic agents and adjunctive thrombin antagonists: observations from the Thrombolysis and Thrombin Inhibition in Myocardial Infarction 9 Study. J Am Coll Cardiol 1999;33: 479e87. 6. Birnbaum Y, Wagner GS, Gates KB, et al. Clinical and electrocardiographic variables associated with increased risk of ventricular septal defect in acute anterior myocardial infarction. Am J Cardiol 2000;86: 830e4. 7. Crenshaw BS, Granger CB, Birnbaum Y, et al. Risk factors, angiographic patterns, and outcomes in patients with ventricular septal defect complicating acute myocardial infarction. GUSTO-I (Global Utilization of Streptokinase and TPA for Occluded Coronary Arteries) Trial Investigators. Circulation 2000;101:27e32. 8. Rhydwen GR, Charman S, Schofield PM. Influence of thrombolytic therapy on the patterns of ventricular septal rupture after acute myocardial infarction. Postgrad Med J 2002;78:408e12.
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9. Yip H-K, Fang C-Y, Tsai K-T, et al. The potential impact of primary percutaneous coronary intervention on ventricular septal rupture complicating acute myocardial infarction. Chest 2004;125:1622e8. 10. Birnbaum Y, Chamoun AJ, Conti VR, et al. Mitral regurgitation following acute myocardial infarction. Coron Artery Dis 2002;13:337e44. 11. Carasso S, Sandach A, Beinart R, et al. Usefulness of four echocardiographic risk assessments in predicting 30-day outcome in acute myocardial infarction. Am J Cardiol 2005;96:25e30. 12. Hillis GS, Møller JE, Pellikka PA, et al. Prognostic significance of echocardiographically defined mitral regurgitation early after acute myocardial infarction. Am Heart J 2005;150:1268e75. 13. Davis N, Sistino JJ. Review of ventricular rupture: key concepts and diagnostic tools for success. Perfusion 2002;17:63e7. 14. Hochman JS, Buller CE, Sleeper LA, et al. Cardiogenic shock complicating acute myocardial infarctiondetiologies, management and outcome: a report from the SHOCK Trial Registry. SHould we emergently revascularize Occluded Coronaries for cardiogenic shocK? J Am Coll Cardiol 2000;36:1063e70. 15. Frances C, Romero A, Grady D. Left ventricular pseudoaneurysm. J Am Coll Cardiol 1998;32:557e61.
16. Gan HL, Zhang JQ. Diagnosis and surgical treatment of post-infarction left ventricular pseudoaneurysm. Chin Med J (Engl) 2009;122:232e5. 17. Menon V, White H, LeJemtel T, et al. The clinical profile of patients with suspected cardiogenic shock due to predominant left ventricular failure: a report from the SHOCK Trial Registry. Should we emergently revascularize Occluded Coronaries in cardiogenic shocK? J Am Coll Cardiol 2000;36:1071e6. 18. Alonso DR, Scheidt S, Post M, et al. Pathophysiology of cardiogenic shock. Quantification of myocardial necrosis, clinical, pathologic and electrocardiographic correlations. Circulation 1973;48:588e96. 19. Mendes LA, Picard MH, Sleeper LA, et al. Cardiogenic shock: predictors of outcome based on right and left ventricular size and function at presentation. Coron Artery Dis 2005;16:209e15. 20. Mollet NR, Dymarkowski S, Volders W, et al. Visualization of ventricular thrombi with contrast-enhanced magnetic resonance imaging in patients with ischemic heart disease. Circulation 2002;106:2873e6. 21. Hutchcroft BJ. Dressler’s syndrome. BMJ 1972;3:49. 22. Shahar A, Hod H, Barabash GM, et al. Disappearance of a syndrome: Dressler’s syndrome in the era of thrombolysis. Cardiology 1994;85: 255e8.
Contents lists available at ScienceDirect
Clinical Radiology journal homepage: www.elsevierhealth.com/journals/crad
Pictorial Review
Complications of myocardial infarction on multidetectorrow computed tomography of chest V. Raj a, K. Karunasaagarar a, J.H.F. Rudd b, N. Screaton a, D. Gopalan a, * a b
Department of Radiology, Papworth and Addenbrookes Hospital, Cambridge, UK Division of Cardiovascular Medicine, University of Cambridge, Cambridge, UK
article in formation Article history: Received 23 December 2009 Received in revised form 19 March 2010 Accepted 22 March 2010
Myocardial infarction (MI) secondary to coronary artery disease remains the leading cause of death in the western world. The advent of early reperfusion therapy has substantially decreased in-hospital mortality and has improved the outcome in survivors of the acute phase of MI. Complications of MI include ischaemic, mechanical, arrhythmic, embolic and inflammatory disturbances. Although some of these complications may be infrequent, their importance is underscored because of the potential ability to correct them with early diagnosis and appropriate treatment. The majority of these complications will be detected on clinical examination and confirmed by echocardiography. Some patients may undergo non-electrocardiogram (ECG)-gated thoracic multidetector-row computed tomography (MDCT) due to non-specific presentation. In this group, it is imperative for the radiologist to be aware of and be confident in diagnosing the complications secondary to MI. This review illustrates the spectrum and imaging features of acute and chronic complications of MI that can be visualized on both ECG-gated cardiac and non-ECG-gated thoracic MDCT. Ó 2010 The Royal College of Radiologists. Published by Elsevier Ltd. All rights reserved.
Introduction Rapid technological advances in multidetector-row computed tomography (MDCT) have lead to its applications in cardiac imaging becoming a practical reality at acceptable radiation dose. Although electrocardiogram (ECG) gating is a prerequisite for assessment of coronary arteries, non-ECGgated thoracic MDCT can also provide valuable morphological cardiovascular information that can modify patient management. The advent of early reperfusion therapy has substantially decreased in-hospital mortality and has improved the outcome in survivors of the acute phase of myocardial * Guarantor and correspondent: D. Gopalan, Papworth Hospital NHS Trust, Papworth Everard, Cambridge CB23 3RE, UK. Tel.: þ44 14808364562; fax: þ44 1480364403. E-mail address: [email protected] (D. Gopalan).
infarction (MI). Complications of MI can be secondary to ischaemia, mechanical dysfunction, arrhythmia, embolic and inflammatory disturbances. The majority of these complications will be detected on clinical examination and confirmed by echocardiography. A small proportion of patients, especially those who present with non-specific cardio-respiratory symptoms, such as atypical chest pain or unexplained shortness of breath, will require further imaging. In such patient cohorts, where chest radiography is unhelpful, MDCT of the chest may be required to guide further management. Therefore, it is important that the cardiac structures, even on ungated studies, are carefully scrutinized by both specialist as well as non-specialist radiologists and cardiologists interpreting these studies. This review illustrates the spectrum and imaging features of acute and chronic complications of MI (Table 1) that can be visualized on both ECG-gated cardiac and nonECG-gated thoracic MDCT.
0009-9260/$ e see front matter Ó 2010 The Royal College of Radiologists. Published by Elsevier Ltd. All rights reserved. doi:10.1016/j.crad.2010.03.017
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Table 1 Complications of MI (1) Mechanical Free-wall rupture Ventricular septal rupture Mitral regurgitation Ventricular pseudoaneurysm Ventricular true aneurysm Cardiac failure and cardiogenic shock (2) Ischaemic (3) Embolic (4) Inflammatory Pericarditis Dressler’s syndrome (5) Arrhythmic
MI Cardiovascular disease kills nearly 200,000 people in the UK annually,1 although death rates have fallen by 40% since 1997. MI accounts for about half of those deaths and kills up to 50% of patients before they reach hospital. Initial treatment of all patients with MI is aimed at restoration of balance between myocardial oxygen demand and supply, pain relief, and prevention of complications of MI. For the purposes of determining appropriate treatment, MI can be categorized into ST segment elevation myocardial infarction (STEMI), non-ST segment elevation myocardial infarction (NSTEMI) and unstable angina. The primary focus in the management of MI is to recognize patients with STEMI so that early myocardial reperfusion therapy can be initiated. The means of accomplishing myocardial reperfusion has changed in the last decade, with primary percutaneous intervention now replacing thrombolytic therapy in most centres, driven by improved short and long-term mortality and morbidity.2 Patients with NSTEMI are not candidates for immediate thrombolysis but may be suitable for primary percutaneous intervention. Despite these advances in management techniques, early and late complications of MI do still occur.
Figure 1 CT axial image of a 65-year-old male patient with known ischaemic heart disease. There is thinning of the basal-mid lateral wall with sub-endocardial hypo-density (arrow) indicative of previous myocardial infarction. LA, left atrium; LV, left ventricle.
Complications of MI Some complications of MI typically occur early in the course of MI (e.g., arrhythmia), whilst others generally cause deterioration later in the course of hospital admission (e.g., ventricular septal defect, cardiac rupture). Although most of these complications are readily diagnosed clinically or with echocardiography, some will first become apparent on MDCT. This review does not suggest using MDCT for the primary diagnosis of these complications; rather, we aim to highlight some important and potentially lethal conditions that might first become apparent using this technique.
Mechanical complications Mechanical complications of MI result from the dysfunction of ischaemic myocardium; rupture of infarcted myocardium, valvular incompetence or from the stretching of a scarred myocardial area.
Cardiac rupture
MI imaging with MDCT MDCT does not currently have an established role in imaging acute MI. However, the incidental detection of infarcted myocardium on a MDCT study performed for unrelated reasons is common. In both acute and chronic infarctions the myocardium has significantly lower attenuation than un-infarcted myocardium3 (Fig. 1). Decreased perfusion results in hypoenhancement of the myocardium and may imply ischaemia rather than infarction in the acute setting. In a more chronic state, the hypoenhancement may be due to a combination of hypoperfusion and fatty replacement. Chronic infarcts are usually accompanied by ancillary features such as myocardial thinning and wall motion abnormality.
Cardiac rupture most commonly involves the lateral wall of the left ventricle (LV). It occurs in 3e6% of MI patients and accounts for approximately 10% of mortality from all MI. Half of the ruptures occur within 5 days and 90% in the first 2 weeks following an acute MI4 (Fig. 2). Clinically the presentation is typical with sudden onset of chest pain, accompanied by arrhythmia, cardiogenic shock, and symptoms of pericarditis.4 Although often there is not enough time for diagnostic testing in managing these patients, echocardiography is the test of choice. If performed, MDCT features would include pericardial effusion with findings of cardiac tamponade, i.e., collapse of the right heart chambers and dilatation of the inferior vena cava and hepatic veins. It is important to identify free-wall rupture on cross-sectional imaging as it is universally fatal if untreated.5 Less frequently,
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Figure 2 CT short axis reconstruction in a 55-year-old patient with acute inferior MI. There is extravasation of contrast medium (arrow) from the inferior wall of the left ventricle in keeping with a contained leak secondary to cardiac rupture. Note the absence of pericardial effusion due to the contained nature of the free-wall rupture. RV, right ventricle; LV, left ventricle.
free-wall rupture is contained by adherent pericardium or scar tissue resulting in development of a pseudoaneurysm.
Ventricular septal rupture Ventricular septal rupture (VSR) post-MI has reduced in incidence to 0.2% (previously 1e2%) since the introduction of reperfusion therapy.6,7 Although most commonly seen at 2e5 days post-MI, it can occur any time after MI.8,9 Clinically the presentation is variable, ranging from asymptomatic to acute cardiogenic shock with a new pansystolic murmur. VSR usually occurs at the junction of preserved and infarcted myocardium. The location is often in the apical septum with anterior MI and the basal septum with inferior MI (Fig. 3). It almost always occurs in the setting of a transmural MI. A discrete gap in the myocardium might not be evident on MDCT as the VSR may be composed of a meshwork of serpiginous channels.4
Figure 3 Axial CT image in a 61-year-old female patient with an inferior MI. There is abnormal communication between the right and left ventricle (black arrow) resulting from a basal ventricular septal rupture. RV, right ventricle; LV, left ventricle.
cardiac failure. The diagnosis is usually readily made on echocardiography. On MDCT, there may be left-sided chamber dilatation; localized pulmonary oedema, especially in the right upper lobe when the regurgitant flow across the mitral valve is directed towards the right upper pulmonary vein; and rarely, papillary muscle rupture may be evident4 (Fig. 4).
Ventricular pseudoaneurysm Ventricular pseudoaneurysm results from a contained rupture of the LV free wall. The outer wall of the
Mitral regurgitation Mitral regurgitation, which is usually mild to moderate, is a common (13e45%) finding post-MI and is usually transient and self-limiting.4,10e12 Mitral regurgitation postMI can be caused by mitral valve annular dilatation secondary to ischaemia-related LV dilatation, papillary muscle dysfunction secondary to LV regional wall motion abnormality or papillary muscle rupture, which may occur following acute inferior MI with a median interval of 13 h after the primary event. This can be life threatening and accounts for 5% of deaths in acute MI patients.13,14
Papillary muscle rupture Papillary muscle rupture typically presents with sudden clinical deterioration with a new murmur and worsening
Figure 4 Coronal CT reconstruction showing upper-zone pulmonary opacification (black arrow) with relative sparing of the mid and lower zones due to oedema resulting from mitral regurgitation resulting in directional flow towards upper lobe pulmonary veins. LA, Left atrium; LSPV, Left superior pulmonary vein.
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Figure 5 Transaxial CT image in a 70-year-old man with infarction in the circumflex territory. There is a pseudoaneurysm (black arrow) in the basal postero-lateral wall of the left ventricle with calcified walls and thrombus (star). LA, left atrium; LV, left ventricle.
Figure 6 Transaxial CT image in a 65-year-old man with a chronic LAD territory infarct. There is marked thinning of the apex and apical anteroseptum (white arrow) with aneurysmal dilatation of the apex (star). RV, right ventricle; LV, left ventricle; LAD, left anterior descending.
pseudoaneurysm is formed by thrombus and pericardium usually with a narrow neck communicating with the LV cavity. (Fig. 5) Unlike a true LV aneurysm, pseudoaneurysm contains no endocardium or myocardium. LV pseudoaneurysms can be clinically silent, or may cause arrhythmia, systemic embolization, or heart failure. If untreated the risk of subsequent cardiac rupture is approximately 30 to 45%, and mortality is as high as 23% if treated surgically and 48% if treated medically.15,16 Therefore, it is of paramount importance to identify and highlight the presence of these findings on MDCT, as ventricular pseudoaneurysms require surgical management.4
of myocardial calcification reflecting dystrophic calcification of infarcted myocardium. Dynamic imaging with retrospective cardiac gating may reveal focal dyskinesia. Cardiac failure and cardiogenic shock commonly result from myocardial dysfunction following an infarct. The degree of LV dysfunction depends on the extent of myocardial damage.17 Cardiogenic shock can be secondary to a multitude of causes, the most common of which is the haemodynamic compromise secondary to the MI. Other causes include myocardial rupture, as described above, and/or pharmacological depression of LV function and arrhythmia. In patients with no previous history of myocardial dysfunction, involvement of at least 40% of the LV mass is required to produce cardiogenic shock. However, this is not true in patients with pre-existing myocardial dysfunction where, smaller insults can have catastrophic consequences.18,19 On MDCT, features consist of direct cardiac signs, such as dilatation of the LV and possibly LA, hypoattenuation of the infarcted tissue and indirect signs including pleural/pericardial effusions and features of pulmonary interstitial and alveolar oedema. Many of these patients require both pharmacological and mechanical support to augment ventricular function. Mechanical support is most commonly given in the form of an intra-aortic balloon pump (IABP), which augments systemic pressure and increases coronary perfusion pressure. Ideally, the tip of the IABP should be in the descending thoracic aorta distal to the origin of the left subclavian artery. IABP malposition can result in complications such as limb ischaemia, embolization of platelet aggregates, haematoma, false aneurysm, and aortic dissection. Some patients with persisting LV compromise post-MI will be candidates for mechanical ventricular assist device (VAD) placement or transplantation. A VAD may augment either right or left ventricular function or both. It is usually
Ventricular true aneurysms Ventricular true aneurysms occur in the area of infarction and patients with apical transmural infarction are at a higher risk. The true aneurysm wall is composed of pericardium adherent to underlying epicardium and beneath the epicardium is the residual fibrous scar tissue of infarcted myocardium. Contrary to pseudoaneurysm, true aneurysm is connected to the ventricular cavity by a wide neck (Fig. 6). It rarely ruptures but if large, can cause significant haemodynamic consequences in the form of cardiac failure, due to disordered ventricular contraction, or ventricular thrombus formation leading to systemic embolization. Clinically patients present with cardiac failure and often systemic embolic episodes. Refractory arrhythmia is another mode of presentation that would alert the clinician to the possibility of aneurysm.4 Treatment ranges from prophylactic anticoagulation to surgical resection, depending on severity. True aneurysms are characterized by thinning and fusiform dilatation of the affected portion of the ventricular cavity. They may contain low attenuation thrombus or areas
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myocardium (Fig. 8). One in five patients with MI develops mural thrombus; this is more common in those with an anterior wall infarct.20 Most systemic emboli occur within 10 days of the acute event and commonly present as a stroke.4
Inflammatory complications Pericarditis Pericarditis occurs early after an acute MI in up to 10% of patients with the inflammation developing between 24 and
Figure 7 Transaxial CT image of a 58-year-old man. There is an eccentric thrombus (arrow) around the tip of the left ventricular assist device (star). The dilated enhancing structure in the right AV groove is the conduit between the aorta and ventricular assist device. Note the right-sided pacemaker leads. RV, right ventricle; LV, left ventricle.
used to bridge the critically ill heart failure patient to transplant but in some patients with reversible cardiomyopathy may be a bridge to cure. The device consists of an inflow and outflow line and a mechanical pump. The inflow is typically placed in the centre of the apex pointing towards the mitral valve while the outflow line is anastamosed to the ascending aorta. In patients with VAD, the tip of the ventricular catheter should be evaluated for position and adherent thrombus, the course of the device and lines for evidence of fluid collections (Fig. 7).
Embolic complications Patients are at higher risk of both venous and systemic thrombo-embolism after MI. The former is predominantly a consequence of immobility whilst arterial emboli are the result of mural thrombus arising from the area of infarcted
Figure 8 Transaxial CT image in a 55-year-old man with a history of alcohol abuse and previous MI. There is a large focal filling defect in the LV apex (black arrow) in keeping with thrombus.
Figure 9 (a) Transaxial CT in a 50-year-old male depicting a small pericardial (white arrow) and bilateral pleural effusions (star). There is no pericardial thickening or calcification. There were no CT features suggestive of tamponade. (b) Unenhanced transaxial CT image in a 64-year-old man with a small pericardial effusion (star). This has a radiodensity of 60 HU in keeping with a haemopericardium.
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96 h after the primary event.21,22 Acute pericarditis is an inflammatory response to necrotic tissue and is more often seen in patients with transmural infarction.4 In early stages, patients may not experience any symptoms or those of acute infarction may mask them. As time goes by patients typically complain of progressive, severe, pleuritic chest pain, which must be differentiated from recurrent ischaemic chest pain and pulmonary embolism.
Dressler’s syndrome Dressler’s syndrome is thought to occur in 1e3% of patients in the first 8 weeks post-MI. The aetiology and pathophysiology is not known but an autoimmune response to myocardial necrosis is postulated. The syndrome is characterized by the presence of persistent low-grade fever, pleuritic chest pain, a pericardial rub, and pericardial effusion, which is usually exudative. There may be associated pericardial thickening (>4 mm) involving visceral and parietal pericardium with or without enhancement, Enlarging pericardial effusion can rarely lead to tamponade requiring pericardiocentesis. On imaging, pericardial effusion post-MI in the correct clinical setting should raise the suspicion of pericarditis or Dressler’s syndrome (Fig. 9).
Arrhythmias and conduction abnormalities Re-entry circuits occurring at the junction of necrotic, ischaemic, and viable myocardium are responsible for the majority of post-MI arrhythmias. The most feared is ventricular fibrillation, which is lethal without early defibrillation, and may occur at any stage of the infarction, although it is most common in the first 24 h.4 Heart block as a consequence of ischaemic damage affecting the
Figure 10 Transaxial CT image in a 60-year-old woman. The tip of the pacemaker has perforated the pericardium and lies in the lung (white arrow). There is a small pericardial effusion (star). RV, right ventricle; LV, left ventricle.
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ventricular conduction system occurs less commonly than prior to thrombolytic and primary percutaneous coronary intervention (PPCI), but may still occur, especially after large anterior MI. From an imaging point of view, patients may have temporary pacing wires present in the right ventricle. Infrequently the pacing wires are in an unexpected location and should be brought to the attention of the referring physician. (Fig. 10) Arrhythmia is readily appreciated on the ECG trace during cardiac-gated studies and staff should be appropriately trained to recognize this.
Conclusion MDCT technological advances are leading to a paradigm shift in the evaluation of cardiac disease using imaging. Although the incidence of MI is falling, it remains a common disease with a spectrum of both acute and delayed complications, many of which are life threatening. Echocardiography continues to be the frontline imaging technique in this patient group. We do not advocate the routine use of MDCT in imaging patients with acute MI; instead it should be used as a complementary test in patients who either have suboptimal or inconclusive echocardiography and/or cardiac MRI. On its own, MDCT can be particularly useful in imaging patients for whom it is important to delineate morphological abnormalities, such as differentiation of true and false ventricular aneurysm. As we have demonstrated, many MI-related complications can be picked up on non-ECG-gated thoracic MDCT. This emphasizes the importance of understanding the range of complications of MI and their imaging appearances. MDCT can potentially ensure accurate detection and early diagnosis leading to expedition of appropriate treatment.
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