Signs on CT which are suggestive of pleural malignancy include: Irregular or nodular pleural thickening. \200 Circumferential pleural disease, involving the mediastinal surface. \200 Pleural thickening of > 1cm. CT can suggest pleural malignancy but is not in itself diagnostic, nor can it differentiate accurately between mesothelioma or metatstic pleural disease. It may be used to perform targeted pleural biopsy. MRI Limited role \200\224 sometimes used if surgical resection being considered but this i s rare. Nuclear medicine \200 PET-CT is not routinely used in mesothelioma unless curative surger y is being considered. Can be useful in cases of metastatic pleural malignancy of unknown primary. Information for the radiologist \200 Asbestos history. \200 Any previous malignancy. SUBASH KC/NMC-15TH/2014 MALIGNANT PLEURAL DISEASE 89 Fig. 4.43 right-chest pain. The scan reveals pleural thickening of encasing the lung. Biops y con \201 rmed mesothelioma. Axial CT slice from a patient who presented with shortness of breath and > 1cm in depth completely SUBASH KC/NMC-15TH/2014 90 CHAPTER 4 Respiratory conditions Mediastinal masses An abnormal soft tissue mass within the mediastinum. Clinical presentation Wide range of presentations depending on location and nature of the m ass. May present with chest pain, stridor, dyspnoea, dysphagia, SVC obstruction, hoarse voi ce, weight loss, back pain, or ruptured aneurysm, for example. May also be an incidental \201 nding. Imaging Plain \201 lm (Fig. PA and lateral chest radiographs may identify and localize th e mass and can help to guide further investigation. 4.44 ) CT (Fig. Usually performed for characterization and occasionally to guide biopsy. Identi \201 es calci \201 cation, cystic areas, and vascular structures better than plain \201 lm. Allows accurate localization of the mass which narrows the dif- ferential diagnosis: \200 Anterior mediastinum 4.45 ) \200\224 anterior to the pericardium, \200\230the 4 T \200\231s \200\231: Thymoma. \200 Thyroid. \200 Teratodermoid (germ cell tumors). \200 \200\230Terrible \200\231 lymphoma. Middle mediastinum \200\224 the heart, aortic root and pulmonary vessels: Bronchogenic cysts and tumors. \200 Ascending aortic aneurysm. \200 Lymphadenopathy. \200 Posterior mediastinum \200\224 posterior to the pericardium: Oesophageal tumor, achalasia, or duplication cysts. \200 Descending aortic aneurysm. \200 Neurogenic tumor. \200 Meningocoele. \200 Extramedullary haematopoiesis. Nuclear medicine Certain tumors show increased uptake on PET, e.g. lymphoma. Scintigraphy c an be used to identify thyroid goiter, ganglioneuromas and phaeochromocytomas. MRI Excellent at depicting neurogenic tumors and spinal abnormalities. Ultrasound Useful to assess the thyroid though will not visualize retrosternal areas adequa tely. Information for the radiologist \200 Age and sex of patient. \200 Presenting symptoms. \200 Previous imaging. \200 Management plan, e.g. biopsy. SUBASH KC/NMC-15TH/2014 MEDIASTINAL MASSES 91 Fig. 4.44 Note the descending aorta is well seen, as are the hilar structures, placing the mass within the anterior mediastinum. PA CXR showing a large soft tissue mass arising from the mediastinum. Fig. 4.45 the anterior mediastinum, enhances with contrast and contains some peripheral nec rosis. CT-guided biopsy con \201 rmed thymoma. CT of the same patient as Fig. 4.44 , con \201 rming the mass lies within SUBASH KC/NMC-15TH/2014 This page intentionally left blank SUBASH KC/NMC-15TH/2014 93 Chapter 5 Vascular differential diagnosis Global cardiomegaly 94 Enlarged left atrium 94 Enlarged left ventricle 94 Enlarged thoracic aorta 94 Enlarged pulmonary arteries 95 SUBASH KC/NMC-15TH/2014 94 CHAPTER 5 Vascular differential diagnosis Global cardiomegaly \200 Ischaemia. \200 Cardiomyopathy. \200 Pericardial effusion. \200 Multiple valvular disease. Enlarged left atrium \200 Increased pressure: \200 Mitral stenosis. \200 Atrial myxom a. \200 Left ventricular failure. Increased \202 ow: Mitral incompetence. \200 Right-to-left shunt. Enlarged left ventricle \200 Increased pressure: \200 Hypertension. \200 Aortic steno sis. \200 Coarctation. \200 Increased \202 ow: Aortic incompetence. \200 Mitral incompetence. \200 Right-to-left shunt. Weakened muscle: Ischaemia. \200 Cardiomyopathy. Enlarged thoracic aorta \200 Aortic stenosis: Post-stenotic dilatation of ascending aorta. Atherosclerosis. \200 Hypertension. \200 Infection: Syphilis. \200 Endocarditis. Coarctation. \200 Marfan \200\231s syndrome. \200 Dissection. \200 Post traumatic. SUBASH KC/NMC-15TH/2014 ENLARGED PULMONARY ARTERIES 95 Enlarged pulmonary arteries Dilated pulmonary trunk only \200 Post-stenotic dilatation (p ulmonary valve stenosis). Dilated central pulmonary arteries/small peripheral vessels \200 Primary pulmonary hypert ension. \200 Chronic pulmonary embolic disease. \200 Chronic lung disease. \200 Eisen menger \200\231s syndrome. Dilated central and peripheral vessels \200 Left-to-right shunt. SUBASH KC/NMC-15TH/2014 This page intentionally left blank SUBASH KC/NMC-15TH/2014 97 Chapter 6 Vascular presenting syndromes Intermittent claudication Rest pain 98 Acutely painful blue leg 99 98 SUBASH KC/NMC-15TH/2014 98 CHAPTER 6 Vascular presenting syndromes Intermittent claudication When atheroma narrows the blood vessels supplying the lower limb, blood \202 ow is reduced and with it the amount of oxygen that can be taken up by the ti ssues. Presentation Muscle ischaemia presents in the same basic way, whether it be cardiac (angina ) or in the lower limb (claudication). Patients suffer pain induced by exercise, relieved b y rest. In claudication the pain is typically felt in the calves, and is brought on by walk ing. Risk factors include: Increased age. \200 Smoking. \200 Hypertension. \200 Family history. Imaging Ultrasound Doppler ultrasound can be used in clinic to assess the patency of periph - eral vessels, and follow up treated areas, but is not accurate enough to be used as a sol e presurgical assessment. CT Can be used to visualize the peripheral vascular tree, but the radiation dose is high, a nd most centers prefer to use MRI. MRI Allows accurate assessment of the peripheral vasculature, identifying stenoses and occl usions in the main lower limb vessels down to the foot. Routinely used in the work-up of pa tients with claudication to plan intervention and follow-up patients after treatment. Angiography Diagnostic angiography has largely been superseded by MRI, but interven- tional radiologists have an ever increasing role in the treatment of these patients. Rest pain Once blood \202 ow to the foot becomes critical, oxygen supply cannot match dem and even at rest and the patient suffers continual pain in the lower limb. Imaging techniques are the same as for claudication. SUBASH KC/NMC-15TH/2014 ACUTELY PAINFUL BLUE LEG 99 Acutely painful blue leg Sudden occlusion of an artery results in acute ischaemia of the st ructures in that vascular territory. The commonest cause is thrombus, but cases can be iatr ogenic, traumatic, or due to other embolic phenomena. Presentation Patients present with an acutely swollen, painful, pulseless leg. Capillary re \201 ll will be reduced and the limb is cold to the touch. Risk factors include: \200 Atrial \201 brillation. \200 Atheroma elsewhere, particula rly the aorta. \200 Smoking. Imaging Plain \201 lm Little acute role but CXR may reveal cardiomegaly as a clue to an u nderlying cardiac cause. Ultrasound Echo should be performed to look for intra-cardiac thrombus, shunts, and valvula r vegetations. Peripheral Doppler ultrasound can be used to con \201 rm the clinical impression of absent \202 ow in the peripheral arteries. CT Can identify the level of occlusion, but more common role in the assess- ment of the aor ta for atheromatous disease which may account for embolus formation. MRI Accurate localization of the site of thrombus and the condition of the rest of the peri pheral vascular tree. Angiography In classic cases may still be used as the frontline diagnostic test, but this r ole now often given over to MRI. Angiography does allow catheters to be placed directly aga inst the causative thrombus however, allowing intra- arterial thrombolysis to be administer ed, or other mechanical treatments if appropriate. SUBASH KC/NMC-15TH/2014 This page intentionally left blank SUBASH KC/NMC-15TH/2014 101 Chapter 7 Vascular conditions Aortic dissection 102 Thoracic aneurysm 104 Acute myocardial infarction 106 Cardiomyopathy Coarctation of aorta Aortic stenosis Mitral valve disease 114 Congenital heart disease 116 Ischaemic heart disease 118 Cardiac tumors Abdominal aortic aneurysm 122 Peripheral vascula r disease: diagnosis Peripheral vascular disease: radiological treatments IVC \201 lter i nsertion 128 Arteriovenous \201 stula 108 110 112 120 124 126 130 SUBASH KC/NMC-15TH/2014 102 CHAPTER 7 Vascular conditions Aortic dissection Dissection occurs when blood is able to track between the layers of the v essel wall, creating a false lumen beneath the intima. Dissection is associated with hypertension, some connective tissue diseases, or may be iatrogenic. Clinical presentation Acute dissection will cause pain, often with associated neurological abnor- malities or pulse and blood pressure inequalities. Classically the pain is described as having a \200\230tearing \200\231 quality, between the shoulder blades. Aortic dissection classi \201 cation and treatment depends on whether or not the ascending aorta is affected: \200 Type A dissection involves the aorta proximal t o the origin of the left subclavian artery and normally requires surgical treatment. Type B dissection only involves the aorta distal to the left subclavian and is commonly treated medically with antihypertensives. Imaging features Plain \201 lm CXR is often normal. Classical \201 ndings in dissection include: \200 Widened mediastinum or aortic arch. \200 Tracheal deviation. \200 Depr ession of the left main bronchus. \200 Left pleural effusion. Ultrasound TOE can be used to diagnose thoracic aortic aneurysms and dissections at the bed side; however, it is highly operator dependent, less accurate than CT, and not readily avai lable in many centers. CT Contrast-enhanced CT is the modality of choice for making the diagnosis and demonstratin g the relevant anatomy. Allows accurate visualization of the dissection \202 ap ( Figs. 7 .1 and 7.2 ), true and false lumens, and affected branches. May demonstrate hemorrhage into the aortic wall, a sign of impending dissection and managed in much the same way. CTA required for assessment prior to percutaneous stent placements. MRI Long procedure time and requirement for specialist (non-magnetic) moni- toring equipmen t severely limits its role in acutely unwell patients. Fluoroscopy No role in acute diagnosis, however endovascular stents may be used to treat di ssection \202 aps in the descending aorta. SUBASH KC/NMC-15TH/2014 AORTIC DISSECTION 103 Information for the radiologist \200 Time since onset of symptoms. \200 Blood pressure in both arms. \200 Signs of shock. \200 Previous history or risk factors for aneurysm. Fig. 7.1 Axial CT slice through the aortic arch in a patient presenting acutely with severe chest pain and signs of cardiovascular shock reveals a large dissection \202 ap extendin g the length of the arch. Fig. 7.2 root reveals a large pericardial effusion secondary to hemorrhage. Note also the d issection \202 ap in the descending thoracic aorta. Axial CT slice from the same patient as Fig. 7.1 at the level of the aortic SUBASH KC/NMC-15TH/2014 104 CHAPTER 7 Vascular conditions Thoracic aneurysm An aneurysm is present when the vessel diameter exceeds 150 normal. Thora cic aneurysms may be secondary to atherosclerosis, infec- tion, in \202 ammation, or traum a. % of Aneurysms of the arch and descending aorta are usually secondary to atherosclerosis, whilst those in the ascending aorta are seen in conditions such as aortic valve stenosis or Marfa n \200\231s syndrome. Risk of rupture increases with size, and is greater for aneurysms of the descending aorta than the ascending aorta. Clinical presentation \200 Many patients with thoracic aneurysms will be asymptomatic, di agnosed incidentally during investigation of other conditions. Ascending aortic aneurysms may involve the aortic root causing aortic regurgitation and congestive cardiac failure. Compression of local structures may cause wheeze or breathlessness (trachea), hoarseness (left recurrent laryngeal nerve) or dysphasia. \200 Rupture occurs most commonly into the left pleural space and presents with pain, hypotension, and shock. Thromboembolism is another potential complication, causing stroke, lower limb ischaemic or mesenteric ischaemia. Symptoms will depend upon the area affected. Imaging features Plain \201 lm Ascending aortic aneurysm may not be visible on plain \201 lm, or may give a bulge to the right mediastinum. The presence of curvilinear calci \201 cation in the aortic wall may be an indication of underlying aneurysm formation. Ultrasound TOE can be used to diagnose thoracic aortic aneurysms at the bedside; however, i t is highly operator dependent, less accurate than CT, and not readily available in many ce nters. CT Contrast-enhanced CT is the modality of choice for making the diagnosis, demonstrating t he relevant anatomy and is the modality of choice if acute rupture is suspected (Fig. 7.3 ) . CT is also used for accurate assessment prior to percutaneous stent placement. MRI Can be used to evaluate thoracic aneurysms, and allows interrogation of the aortic valv e if post-stenotic dilation or aortic regurgitation are factors. If long-term follow-up is required, allows accurate assessment without the radiation burden of CT. Long procedure time and requirement for specialist (non-magnetic) monitoring equipment severely limits its role in acutely unwell. SUBASH KC/NMC-15TH/2014 THORACIC ANEURYSM 105 Fluoroscopy No role in acute diagnosis, however endovascular management of thoracic aortic aneurysms is now commonplace. Information for the radiologist \200 Time since onset of symptoms. \200 Blood pressure in both arms. \200 Signs of shock. \200 Previous history or risk factors for aneurysm. Fig. 7.3 compromise, revealing active hemorrhage from an aneurysm of the proximal descendin g aorta, with blood accumulating in the left chest. The patient died in the CT suite. Axial CT from a patient who presented acutely with cardiovascular SUBASH KC/NMC-15TH/2014 106 CHAPTER 7 Vascular conditions Acute myocardial infarction Acute myocardial infarction (MI) is caused by sudden occlusion of a coro- nary artery leading to ischaemia and death of cardiac myocardium. Risk factors i nclude increasing age, previous ischaemic heart disease, cigarette smoking, diabetes, hyper tension, and hypercholesterolaemia. Clinical presentation Central chest pain is the sine qua non of acute myocardial infarction . The pain is usually centered over the lower left hemithorax, radiating to the left should er, jaw, and left arm. However, features may be atypical and occa- sionally present as uppe r abdominal pain. An ECG will usually demonstrate ST-T changes con \201 rming the diagnosis. A subset of patients present without any chest pain or ECG changes and the diagnosis is made based on serum troponin rise. Apart from intrathoracic conditions such as aortic dissection, pulmonary embolism, pneumoni a, re \202 ux oesophagitis, and pleural effusion, upper abdominal diseases such as peptic ulcer exacerbation, acute cholecystitis, and perforation peritonitis may all mimic an acute MI. Imaging Traditionally, imaging used to be of limited value in the initial evaluation of acu te MI. However, with the advent of primary percutaneous intervention (PCI) and \200\230tri ple rule-out \200\231, this is changing. Plain \201 lm Chest radiographs may be completely normal unless patient develops acute le ft ventricular failure. Echocardiogram May demonstrate: \200 Regional wall motion abnormalities. \200 Mitral in suf \201 ciency. \200 Ventricular septal rupture. \200 Pericardial effusion. Measured ejection fraction (EF) will provide an indication of the effect of the MI on cardi ac function, which has prognostic relevance. Coronary angiography With the advent of primary PCI, coronary angiography and left ventricu - lography are performed in the acute setting with a view to proceed to appropriate interve ntion. It is performed usually by puncturing a femoral or (if necessary) brachial artery. Using highly selective catheters and under \202 uoroscopic guidance, the coronary ostia a re selectively engaged and small volumes of contrast agent injected to demonstrate the coro nary arteries and any occlusion or stenoses. This then acts as a road map for further inter vention. Nuclear medicine No role in the imaging of acute MI. SUBASH KC/NMC-15TH/2014 ACUTE MYOCARDIAL INFARCTION 107 Have a greater role in ischaemic heart disease (see disease, p. 118). b Ischaemic heart CT CT scanning does not have an established role in the management of acute ST elevation MI . However, research is continuing into the use of CT to investigate patients who present with acute chest pain without ECG changes of MI as it can be used to s imultaneously assess the coronary arteries, aorta, and pulmonary arterial tree to exclude s igni \201 cant coronary artery disease, aortic dissection, and acute pulmonary embolism. A t present this remains a specialized investigation and is not widely available. Information for the radiologist \200 Duration of symptoms. \200 Risk factors. \200 EC G changes. \200 Blood results. \200 Heart rate and rhythm. Fig. 7.4 resistant heart failure following MI, demonstrating a post infarct VSD. CT reconstructed in the plane of the cardiac short axis in a patient with SUBASH KC/NMC-15TH/2014 108 CHAPTER 7 Vascular conditions Cardiomyopathy A structural or functional disease of heart muscle that is not secondary to ischaemia, valvular pathology, hypertension, or congenital abnormality. There are several distinct forms, including: Enlargement of the cardiac chambers (dilated cardiomyopathy, DCM). \200 Hypertrophy of th e cardiac muscle (hypertrophic CM, HCM). \200 Loss of elasticity in the ventricle and red uced capacity to expand (restrictive CM, RCM). Clinical presentation \200 Clinical presentation is variable and includes fatigue, dyspno ea, chest pain, palpitations, and syncope. Diagnosis may occur through investigation of other family members after a sudden death or newly con \201 rmed diagnosis. Causes of DCM include myocarditis (viral and bacterial), pregnancy, alcohol, and muscular dystrophies. Autosomal dominant inheritance is found in HCM; however, 50 % of cases are sporadic. Examination \201 ndings include a displaced or forceful apex beat (in DCM and HCM respectively). HCM is associated with an ejection systolic murmur. \200 Kussmaul \200\231s sign (elevati on of JVP on inspiration) is found in RCM. \200 Progression leads to signs and symptoms o f cardiac failure. Imaging features Plain \201 lm (Fig. \200 Cardiomegaly is present in DCM and is a late feature of HCM. \200 Heart failure develops with progressive disease. 7.5 ) Ultrasound/echocardiography DCM \200 Diffuse 4-chamber dilatation. \200 Poor systolic f unction with normal left ventricular wall (LV) thickness. HCM \200 Asymmetric or symmetric LV wall thickening. \200 Systolic anterior motion of t he mitral valve. DCM and HCM are both associated with mitral valve regurgitation. RCM \200 Poor late diastolic \201 lling of the left ventricle. \200 Dilatation of the left atrium with normal systolic function. CT \200 Can assess muscle thickness and heart size. \200 Non-calci \201 ed pericardium <3mm thick helps exclude constrictive pericarditis as a differential for RCM. MRI \200 Similar to CT in terms of anatomical detail but gives better idea of ventricular and valvular function (Fig. 7.6 ). MRI can also be used to identify amyloid deposition, sarcoidosis (high T2), and haemochroma tosis (low T1 and T2) as causes of DCM. SUBASH KC/NMC-15TH/2014 CARDIOMYOPATHY 109 Angiography \200 Ventricular volumes are increased in DCM and reduced in HCM. EF can be assessed and ischaemic causes excluded. RCM causes rapid early diastolic \201 lling and poor late diastolic \201 lling. \200 Finally endomyocardial biopsy can be obtained in order to con \201 rm the diagnosis. Information for the radiologist \200 Clinical history, family history, and differential d iagnosis including ECG and echocardiography \201 ndings are helpful. Electrolytes prior to contrast-enhanced CT. \200 Heart rate and rhythm if gated studies b eing considered. \200 Remember patients with pacemakers can \200\231t have MRI. Fig. 7.5 PA CXR of a 23-year-old man presenting with dyspnoea revealing gross cardiomegaly. Echo con \201 rmed enlargement of all 4 cardiac chambers in keeping with idiopathic cardi omyopathy. Fig. 7.6 enlargement of all 4 cardiac chambers. Still image from a cardiac MRI study of the same patient as Fig. 7.5 revealing SUBASH KC/NMC-15TH/2014 110 CHAPTER 7 Vascular conditions Coarctation of aorta Coarctation is a localized narrowing of the aorta, normally occurring at the junction of the arch and descending thoracic aorta, resulting in an obstruction to b lood \202 ow. Clinical presentation Clinical presentation is dictated by the severity and extent of the n arrowing, and features such as the presence of collateral vessels. Severe coarctation can present with heart failure in the newborn. Associated cardiac anomal ies such as patent ductus arteriosus (PDA) and ventricular septal defect (VSD) are common. Patients in whom the narrowing is less severe often present as older children or young adul ts with uncontrolled upper limb hypertension and weak femoral pulses. The \201 nal subset is asymptomatic patients in whom coarctation is detected incidentally. Imaging Plain \201 lm (Fig. \200 In the neonatal group, the features are those of heart failure. \200 The typical \201 nding in the older age group is of a \200\230 \201 gu re of 3 \200\231 appearance 7.7 ) of the proximal descending aorta. Bilateral rib notching seen on the under-surface of the ribs posteriorly is caused by enlarged intercostal arteries due to collateralization. It is best appreciated in the 3 rd and 4 th ribs. Echocardiogram Often the only imaging required in neonates, as it demonstrates: \200 The coarctation segment, and its relationship with the ductus arteriosus. The pressure gradient across the narrowed segment. \200 Associated cardiac anomalies. In adults, the main value is to look for left ventricular hypertrophy (LVH) and associated anomalies such as bicuspid aortic valve. CT (Fig. \200 Of value in adults who cannot undergo MRI. \200 Gives excellent anatomica l detail, but not the functional information of MRI. 7.8 ) MRI Can provide anatomical detail, assess for intracardiac defects, and also provide inform ation on the severity of the narrowing. Angiography With the increasing use of MRI, the diagnostic role of catheterization and angi ography has reduced but is used therapeutically in cases where a balloon angioplasty or ste nt of the coarctation segment is possible. Information for the radiologist \200 Blood pressure difference between the 2 arms. \200 Results of previous imaging such as echo. \200 Detailed information regarding previous i nterventions and surgery. \200 Details of the planned surgery. SUBASH KC/NMC-15TH/2014 COARCTATION OF AORTA 111 Fig. 7.7 problem revealing marked focal dilatation of the aortic arch. PA CXR of a 20-year-old man presenting to A&E with an unrelated Fig. 7.8 a tight, previously unsuspected coarctation with a large post-stenotic aneurysm of the aorta. Note the calci \201 cation in the aneurysm wall. Surface rendered CT image from the same patient as Fig. 7.7 demonstrating SUBASH KC/NMC-15TH/2014 112 CHAPTER 7 Vascular conditions Aortic stenosis Narrowing of the aortic valve (normal area 2.5 \200\2233.5cm increased left ventricular work load and hypertrophy. Usually the valve area decreases to <1cm 2 ) resulting in 2 before the patient becomes symptomatic. Clinical presentation Aortic stenosis (AS) is seen mainly in an elderly population as a con sequence of degenerative disease in association with atherosclerosis. The other subset is y ounger patients, in whom the onset of stenosis is due to a congenitally bicuspid valve. Rhe umatic involvement is uncommon in the Western world, but should still be considered in case s of multivalve disease. Patients usually present with progressive exertional dyspnoea, syncopal attacks, chest pain, and heart failure. Whilst valvular AS is by far the commonest cause, supravalvular stenosis (narrowing of the proximal ascending aorta in William \200\231s syndrome) and subvalvular s tenosis (idiopathic hypertrophic subaortic stenosis) are alternatives and can be dif \201 cult to differentiate clinically. Congenital bicuspid aortic valve leading to AS is associated with coarctation of aorta in conditions such as Turner \200\231s syndrome. Imaging Plain \201 lm \200 Often normal although LCH and aortic valve calci \201 catio n can be seen. \200 Post-stenotic dilatation of the ascending aorta can be appreciated as a smooth prominence in the mid-right mediastinal outline (Fig. 7.9 ). Cardiomegaly is unusual, except when heart failure develops and its presence usually indicates mixed aortic valve disease or associated mitral valve disease. Echocardiogram Echocardiogram is the mainstay of diagnosis. It provides information on: \200 The presence and severity of stenosis including the gradient across the aortic valve. Valve thickening and calci \201 cation. \200 The effect on the left ventricle (wall thic kness and chamber volumes). \200 Associated valvular heart disease. It is often useful in differentiating valvular AS from both the supravalvular and subvalvul ar types. MRI (Fig. Little advantage over echo in most cases, however it is useful in patients with s ubvalvular stenosis to help identify the site, extent, and severity of stenosis and guide i ntervention. 7.10 ) CT Little role in the assessment of valve function or stenosis but can exclude coexisting c oronary artery disease, and is also useful in assessing aortic calci \201 cation prior to newer endovascular valve replacement techniques. Angiography Most patients with AS undergo cardiac catheterization for assessment of severit y of disease and to exclude signi \201 cant coronary artery disease. SUBASH KC/NMC-15TH/2014 AORTIC STENOSIS 113 Information for the radiologist \200 Clinical presentation. \200 Presence of other valv ular disease, especially mitral disease. \200 Previous imaging details to look for progre ssion of disease. Fig. 7.9 apex suggests LVH and the ascending aorta is dilated. CXR from a middle-aged man with dyspnoea. The curve of the cardiac Fig. 7.10 in a plane to allow assessment of the aortic valve. Signi \201 cant AS was con \201 rmed. Still image from cardiac MRI study of the same patient as Fig. 7.9 obtained SUBASH KC/NMC-15TH/2014 114 CHAPTER 7 Vascular conditions Mitral valve disease Mitral stenosis (MS), mitral regurgitation (MR), and mixed mitral dise ase represent the spectrum of mitral valve disease. Normal mitral valve area is between 4 \200\2236cm to <2cm 2 . 2 . Symptoms of MS develop once the valve area narrows Clinical presentation \200 Mitral valve disease presents with progressive dyspnoea. \200 Patients with severe disease develop orthopnoea and paroxysmal nocturnal dyspnoea. Haemoptysis is a rare manifestation. \200 Disease progression and physiological stress (e .g. pregnancy) may precipitate pulmonary oedema. Development of atrial \201 brillation may result in worsening of symptoms. \200 Patient s are at risk of developing left atrial thrombus and associated thromboembolic complications. Isolated mitral stenosis is usually due to rheumatic heart disease. Rarely it may be the re sult of valve involvement in carcinoid or collagen vascular disease and even more rarely a congenital malformation. Mixed mitral disease is usually due to rheumatic heart disease. MR has a much wider etiolog y: It can develop acutely following rupture of a papillary muscle after MI or bacterial endocarditis. Chronic MR may be due to: \200 Stretching of the valve ring in patients with LV failure. \200 Mitral valve prolapse. \200 Myxomatous involvement. \200 Rheumatic fever. \200 Papillary muscle dysfunction with ischaemic heart disease. \200 Congenital abnormalities of the mitral apparatus. Imaging Plain \201 lm Signs of left atrial enlargement include: \200 Double heart shado w. \200 Splaying of carina (sub-carinal angle more than 75 \200 Elevation of left main bronchus. \200 Enlargement of left atrial appendage (Fig. ). 7.11 ). Progressive mitral valve disease will lead to pulmonary venous hypertension (see b Left ven tricular failure, p. 52). Occasionally mitral valve calci \201 cation may be appreciated. Rare features include ill- de \201 ned nodules (haemosiderosis) or densely calci \201 ed nodules in the middle or lo wer zones (pulmonary ossi \201 cation). Echocardiogram Provides information about: \200 The anatomy of the mitral valve and the s ubvalvular apparatus. \200 Valve thickening and calci \201 cation. \200 Mitral valve a rea. \200 Papillary muscle status. SUBASH KC/NMC-15TH/2014 MITRAL VALVE DISEASE 115 Left atrial dimensions. \200 Pulmonary hypertension and right ventricular function. \200 Any associated cardiac abnormalities. Further imaging is often not required. The left atrium is the cardiac chamber closest to the esophagus and TOE provides exquisite detail of the left atrium and mitral valve. It is often used to look for signs of endocarditis and in theater for the perioperative ass essment of the mitral valve and the submitral apparatus. MRI \200 Occasionally in patients with previous surgery or congenital mitral disease MR m ay be performed to assess the intracardiac and major vascular anatomy (e.g. when MS is a pa rt of hypoplastic left heart syndrome) but in general adds little to echo. Another role of cardiac MRI is in patients with ischaemic MR to assess myocardial viability. Angiography \200 Mainly reserved for patients > 40 years or those with signs of associated ischaemic heart disease. Essential, however, as a part of percutaneous mitral valvotomy, prior to balloon valvotomy. Information for the radiologist \200 Clinical details including duration of symptoms. Fig. 7.11 of left atrial enlargement the carina, and enlargement of the left atrial appenda ge. PA CXR showing dense calci \201 cation of the mitral valve annulus and signs \200\224 left atrial contour overlying the right heart, splaying of SUBASH KC/NMC-15TH/2014 116 CHAPTER 7 Vascular conditions Congenital heart disease This group of diseases include a wide spectrum of cardiovascular d isor- ders of varying complexities and often associated with genetic syndromes and multisys tem abnormalities. The age of presentation varies from before birth to adulthood depending on the nature of the abnormality. Clinical presentation CHD is broadly divided into 2 groups: \200 Acyanotic lesions, which include left-to-right shunts such as atrial septal defect (ASD), VSD, PDA, and left-sided valvular diseases such as congenital MS and A S. Cyanotic lesions, which are typically right-to-left shunts such as tetralogy of Fallot or complex lesions leading to admixture of oxygenated and de-oxygenated blood such as total anomalous pulmonary venous drainage (TAPVD), truncus arteriosus, and s ingle ventricle states. Acyanotic lesions commonly present with failure to thrive, recurrent res- piratory infectio ns, \200\230attacks of asthma \200\231, and heart failure. If undetected they progress to pulmonary hypertension which may result in shunt reversal and the development of cyanosis ( Eisenmengerization). Cyanotic heart diseases typically present with cyanotic spells and failure to thrive. Those due to admixture lesions will often present with heart failure as well. Patients may have associated syndromes and congenital anomalies affecting other organs and systems. Imaging Plain \201 lm (Fig. The CXR will not make a speci \201 c anatomical diagnosis, b ut combined with an appropriate history will allow broad categorization of disease and guid e more specialized investigation. 7.12 ) Pulmonary plethora (increased vascular markings seen all the way to the periphery of the \201 lm) is seen in acyanotic heart disease. With progression of disease the lungs become d arker and \200\230pruning \200\231 of the vessels is seen. Echocardiography \200 This is the mainstay of imaging for congenital heart disease. \200 Outlines the anatomical abnormality and secondary changes such as chamber enlargement, wall hypertrophy, and cardiac function. Cardiac catheterization Using a peripheral (usually femoral) venous or arterial approach, a llows assessment of cardiac anatomy, ventricular function, ventricular and pulmonary artery pressures. Cardiac CT \200 Has a limited but evolving role. \200 May be used in patients with pace makers or other metallic devices which preclude MRI. SUBASH KC/NMC-15TH/2014 CONGENITAL HEART DISEASE 117 Provides useful anatomical detail but little functional information compared with echo or MRI. Advantages of CT over MRI include the demonstration of associated lung abnormality, speed of acquisition, and high spatial resolution. Cardiac MRI \200 Has an ever-expanding role, allowing assessment of: Intra- and extracardiac anatomy. \200 Valvular function and pressure gradients. \200 Ve ntricular function and volumes. The lack of ionizing radiation is another advantage over CT in this group of patients, who are often young children needing follow-up imaging over a long perio d of time. Information for the radiologist \200 The suspected abnormality, echo results, exact infor mation sought, and detail regarding previous intervention and surgery. It is important to know about pacemakers and metallic devices that preclude an MRI examination. Fig. 7.12 pulmonary arteries, cardiomegaly, and plethoric lungs. Note also how the aortic a rch appears smaller than usual. Echo con \201 rmed a large ASD. CXR of an 18-year-old woman reveals marked enlargement of the SUBASH KC/NMC-15TH/2014 118 CHAPTER 7 Vascular conditions Ischaemic heart disease A range of cardiac abnormalities caused by insuf \201 cient blood supply reaching the myocardial muscle mass, usually secondary to atherosclerotic narrowing of the coronary arteries. Associated with smoking, hyperten- sion, diabetes, family history , hypercholesterolaemia. Clinical presentation May manifest acutely with severe central chest pain and breathlessnes s, either acute MI or unstable angina. May have a more protracted course with occasional chest pain (angina) especially stress or exercise related, heart failure, ischaemic CM or cardiac arrhythmias. Imaging Plain \201 lm \200 Chest radiographs may be completely normal. \200 Cardiomeg aly with left ventricular enlargement is often seen. \200 Occasionally myocardial calci \201 cation due to a previous transmural infarct and calci \201 ed ventricular aneurysm may be apparent. May be signs of heart failure in the lung and pleural effusions. Echocardiogram Provides useful diagnostic and prognostic information including: \200 Regi onal wall motion abnormalities. \200 Chamber hypertrophy and enlargement. \200 Identi \201 cation of ventricular aneurysm and associated thrombus. \200 EF. It is valuable in follow-up after both medical treatment and percutaneous or surgical inter vention. Coronary angiography (Fig. 7.13) Provides details of signi \201 cant stenoses and occlusio ns in the coronary arteries and helps plan further percutaneous or surgical intervention. Radionuclide perfusion studies \200 Limited use in the acute setting but proven role in e valuating ischaemic damage to the heart and excluding ischaemia as a cause of non speci \201 c chest pain. Stress and rest Tl-201 and Tc99 m (MIBI scan) provides re-distribution information thus helping to identify viable but ischaemic muscle. MUGA scan using Tc-99 m labeled red blood cells can evaluate wall motion and EF. Cardiac CT \200 Calcium-scoring identi \201 es the burden of coronary artery disease by looking at the calcium load in the coronary arteries and is useful in patients where the ca use of chest pain is not established. CT coronary angiogram with contrast is not yet established as the modality of choice for im aging the coronaries prior to intervention but repeated studies show a high negative predic tive value \200\224 i.e. is useful in excluding coronary artery disease. SUBASH KC/NMC-15TH/2014 ISCHAEMIC HEART DISEASE 119 ECG-gated MRI \200 MRI has a tremendous potential in the imaging of ischaemic heart disease. Cine MRI is an accurate method of assessing cardiac function. \200 Gadolinium-enhanced MR I can help identify areas of ischaemia, predict myocardial viability, and delineate areas of subendocardial infarction. Information for the radiologist \200 Duration of symptoms. \200 Associated illnesses. \200 Smoking history, medical history. \200 ECG \201 ndings including cardiac rhythm. (a) (b) Fig. 7.13 stenosis in the right coronary artery. (b) Same patient following endovascular st enting of the stenosis, which resulted in maintained symptom relief. (a) Coronary angiogram of a man with severe angina reveals a signi \201 cant SUBASH KC/NMC-15TH/2014 120 CHAPTER 7 Vascular conditions Cardiac tumors Cardiac tumors may be primary or secondary. Metastatic disease from an extra cardiac tumor is the most common cause of an intracardiac mass. Lung and breast are the mo st common primary sites. Primary cardiac tumors are rare and more often benign than malignant. Some of the more common primary tumors include: \200 Myxoma: the most common primary card iac tumor, and benign (Fig. 7.14 ). Usually occurs in left atrium, often arising from a \200\230stalk-like \200 \231 pedicle. Lipoma. \200 Rhabdomyoma: most common primary tumor in pediatric group, associated with tuberous sclerosis. Sarcoma: the most common primary malignant cardiac tumor is angiosarcoma but there are many other types of sarcoma. Clinical presentation Present at any age with palpitations, shortness of breath, cough, che st pain, or syncope. Clinically there may be a heart murmur, arrhythmia, or evidence of car diac failure. May present with complications such as pulmonary emboli or endocarditis. Imaging Plain \201 lm Rarely able to detect the tumor but may reveal cardiomegaly, left a trial enlargement, calci \201 cation, or pulmonary oedema. Ultrasound (echocardiogram) Usually the initial specialist investigation, offers real-time imaging of the tumor throughout the cardiac cycle and good anatomical detail. Provides info rmation on cardiac and valvular function.