2019 BSCI/BSCCT Pre-course ”Introduction to Cardiac CT” with 50 cases

This elementary study day is aimed at clinicians (Cardiologists, Radiologists, Nuclear Physicians) who have little or no prior exposure to Cardiac CT.  There is no hands-on training as the aim is to provide basic knowledge about CT technique and introduce key concepts. The course material using 50 case demonstrations and 7 lectures would support application to Level 1 Accreditation.

Click here to download the program

The address for the Pre-course is:

Lecture Theatre 2

School of Medicine

University of Cambridge

Addenbrookes Hospital

Hills Road




Click here to download a map of the location. The Clinical school is highlighted in red. 


The pre-course is now full and no more registrations will be accepted. You can still register for the Thursday and Friday of the meeting at the top of the page.

Image of the Month - March 2019. Absent arm pulses and early-onset coronary disease.

Absent arm pulses and early-onset coronary disease 

Tarkin JM,1,2Gopalan D,Mason JC1

1National Heart & Lung Institute, Imperial College London

2Division of Cardiovascular Medicine, University of Cambridge

3Department of Radiology, Imperial College Healthcare NHS Trust

Case presentation

A 28-year-old woman presented with intermittent palpitations and atypical chest pain. She had been admitted to the intensive care unit at the age of 2 years with critical left arm ischemia, and subsequently developed chronic arm pain and weakness triggered by exercise. Past medical history was significant for postoperative pulmonary embolism, for which she received long-term oral anticoagulation. Her only other medication was aspirin once daily. She was a non-smoker, with no known risk factors for atherosclerotic coronary artery disease. There were no constitutional symptoms, rashes, joint pains, or jaw claudication. On examination, peripheral pulses were absent in the upper limbs, and blood pressure was un-recordable in the arms. Cardio-respiratory examination was otherwise normal. 

Blood investigations showed a mildly elevated cholesterol profile (total cholesterol 4.8 mmol/L, LDL cholesterol 3.1 mmol/L, total:HDL cholesterol ratio 4.1), Lipoprotein (a) 40 nmol/L (NR <35), and C-reactive protein 2 mg/L (NR<4). Serum immunoglobulin levels were normal, and antineutrophil cytoplasmic antibody (ANCA) screen was negative. Electrocardiogram and transthoracic echocardiogram were also within normal limits. A seven-day cardiac event recorder revealed sinus rhythm throughout, with occasional atrial ectopic beats. Exercise tolerance test, stopped due to fatigue after achieving 12 METs at 10 minutes of standard Bruce protocol, demonstrated no ST-segment changes or arrhythmia. Dobutamine stress echocardiography showed no stress-induced wall motion abnormality, but did, however, provoke mild chest pain. CT coronary angiography is shown in Figures 1 and 2. 


MArchIOM Fig1

Figure 1.CT coronary angiogram images orientated in axial plane, at the level of the (a) left and (b) right coronary ostia, showing coronary arterial abnormalities within the proximal left and right coronary arteries (arrows). 



Figure 2. CT coronary angiogram images in 3D multi-planar reconstruction showing (a) the origins of the right coronary artery (RCA) and left anterior descending (LAD) artery, the (b) length of the RCA and proximal-mid left circumflex artery (LCx), and (c) the proximal-mid LAD. 



  1. Name the abnormalities demonstrated in figures 1 and 2?
    1. Calcified coronary artery aneurysms associated with calcified mild (<50%) LAD and RCA stenoses
    2. Calcified coronary artery aneurysms associated with calcified mild (<50%) LCx and RCA stenoses 
    3. Calcified coronary artery aneurysms associated with non-calcified moderate (>50%) LAD and severe (>70%) RCA stenoses 
    4. Non-calcified coronary artery aneurysms associated with calcified mild (<50%) LAD and RCA stenoses
    5. Non-calcified coronary artery aneurysms associated with non-calcified moderate (>50%) LCx and severe (>70%) RCA stenoses

  1. What is the most likely diagnosis?
    1. Early-onset atheroscosclerosis because of familial hypercholesterolaemia  
    2. Late complications of Kawasaki’s disease 
    3. Granulomatosis with polyangiitis   
    4. Active large-vessel giant cell arteritis 
    5. Takayasu’s disease in clinical remission 

  1. What is the best course of management? 
    1. Conservative, symptom-guided management of stable coronary artery disease 
    2. High-intensity statins and lipid apheresis 
    3. High-dose steroids and tocilizumab 
    4. Dual anti-platelet therapy and percutaneous coronary intervention 
    5. Coronary artery bypass grafting surgery 


Q1, answer C. CT coronary angiography shows densely calcified coronary aneurysms involving the left main stem and RCA ostia (Figure 3a). In addition, there is a moderate non-calcified stenosis of the proximal LAD (50-70%), and a severe (>70%) RCA stenosis at the neck of the RCA aneurysm, with normal appearances of these vessels beyond. The LCx is disease free. 

Q2, answer E. Takayasu’s arteritis is a rare systemic inflammatory disease of unknown aetiology, which typically affects young females and results in large-vessel vasculitis characterised by granulomatous inflammation of the aorta and great vessels, as well as the coronary and renal arteries. Arterial narrowing or occlusion occurs in up to 90% of patients, often resulting in symptoms of limb claudication. Hence, Takayasu’s arteritis is known as the ‘pulseless’ disease. Aneurysms are also common. In this patient, there was a history of acute limb ischemia in childhood, as well as symptoms of arm claudication and absent upper limb pulses. MR angiography demonstrated bilateral subclavian artery occlusions, proximal right vertebral artery occlusion, and no abnormalities of the aorta, innominate or carotid arteries (Figure 3b). While Kawasaki’s disease and granulomatosis with polyangiitis vasculitis can affect the coronary arteries, these conditions are not typically associated with subclavian artery occlusion. Granulomatosis with polyangiitis vasculitis is also an ANCA-associated vasculitis. The lack of constitutional symptoms and normal C-reactive protein level suggest disease in remission. Takayasu’s arteritis is associated with accelerated atherosclerosis; there are no features in this case to indicate a diagnosis of familial hypercholesterolemia. 

MarchIOTM Fig3

Figure 3. (a) CT angiography in 3D volumetric reconstruction showing calcified bilateral coronary aneurysms (arrows); (b) MR angiography showing bilateral subclavian artery occlusions (solid arrows) and right vertebral artery occlusion (dashed arrow).


Q3, answer A. Management of coronary artery disease in patients with Takayasu’s arteritis can be challenging, particularly when there are ostial lesions. There have been no large randomised clinical trials evaluating outcomes of percutaneous coronary intervention (PCI) versus coronary artery bypass grafting (CABG) surgery in this setting. Small retrospective analyses indicate that CABG surgery may be associated with better long-term outcomes than PCI in patients with Takayasu’s arteritis. On the whole, coronary revascularisation is best avoided during an acute flare of the disease due to the friable nature of the inflamed vessels, and the risk of graft stenosis at the aortic insertion site. There may also be an increased risk of restenosis following PCI in patients with vasculitis-associated coronary artery disease, compared to stable atherosclerosis. When CABG surgery is needed, saphenous vein grafts are typically used because of possible inflammatory involvement of the internal thoracic arteries. In this patient, the clinical symptoms were not typical of effort-induced angina due to obstructive epicardial coronary artery disease, and non-invasive stress-imaging excluded significant inducible myocardial ischaemia that might indicate a need for coronary revascularisation. There were also no signs of active vasculitis that would require immunosuppression. The patient was managed conservatively, with a plan to monitor closely and consider further coronary investigations based on future clinical symptoms. 

Image of the Month January 2019 - Problem Solving using Cardiac CT by Modifying Technique

Problem Solving using Cardiac CT by Modifying Technique

Dr Ashley Thorpe, Dr Rajiv Singh and Dr Garrett McGann

An 80 year old presented to the emergency department after suffering syncope whilst sat in a chair with no prodromal features. Past medical history included COPD, bronchiectasis and hypothyroidism. 

As a result, a transthoracic echocardiogram (TTE) was arranged as an outpatient which demonstrated a mildly dilated left atrium at 60mls and an echogenic structure visualised within the left atrium with a possible attachment to the atrial septum. Colour flow is seen to contour the structure.  (Figure 1A &B)

Question 1: What is the most common cardiac tumor?

  1. Lipoma 
  2. Myxoma
  3. Metastases
  4. Sarcoma


C) Metastases – Metastases are estimated to be 30 times more common than primary cardiac tumors. Common tumors which frequently metastasize to the heart include breast, melanoma and lymphoma. (1)

A CT cardiac angiogram was arranged to further investigate the ultrasound abnormality. A transoesophageal ultrasound was considered, however a CT was chosen due to its less invasive nature. A modified protocol was used to include both a prospective ECG-gated coronary artery study and a 10 second delayed phase.

During the arterial phase there was the impression of a filling defect within a mildly dilated left atrial appendage suspicious for a mass or thrombus. (Figure 1C) The critical phase in this series, the delayed 10 second phase, which showed the filling defect had disappeared suggesting the arterial phase anomaly, was caused by incomplete mixing of contrast. (Figure 1D)


This case highlights the importance of protocoling and making use of a delayed phase to differentiate a pseudo filling defect from true mass or thrombus. In this case the patient avoided further invasive investigation and treatment and any potential morbidity and complications they may bring. It has been shown that using a 2 phase acquisition significantly reduces pseudo filling defect detection when compared to single phase (2) and has a favourable sensitivity, specificity, positive and negative predictive values in detecting true thrombus when compared to the reference standard, trans-oesophageal echo. (3)

Question 2: What percentage of patients who have atrial fibrillation and a recent embolic event are shown to have LAA clot?

  1. 10%
  2. 15%
  3. 20%
  4. 30%
  5. 50%


C)  ≈20%. In a study of 317 patients with AF and a recent embolic event, 21-23% were found on transoesophageal echo to have left atrial appendage clot. (5)

30-40% of strokes have no demonstrable cause. The left atrium and specifically the left atrial appendage has been studied to shed light specifically on cryptogenic stroke. Specific LAA morphologies have been shown to increase the risk of LAA thrombus and stroke. LAA function has also been assessed and poorer function has been linked to LAA thrombus and stroke.   (6)

Question 3: What are common causes of mass mimics on transthoracic echocardiography?

  1. Crista terminalis
  2. Right ventricular moderator band
  3. Atrioventricular groove fat
  4. Hiatal hernia
  5. All of the above


E) The crista terminalis can appears as a hyperechoic structure against the right atrial wall. A thickened right ventricular moderator band can appear as a mass within the right ventricle. Lipomas of the atrioventricular groove can protrude into the atria or the ventricles and appear as an intracardiac mass. A hiatal hernia large enough can impress upon the heart and can cause a pseudomass within the left atrium. (7)

Figure 1: (A) TTE 4 chamber view demonstrating an echogenic structure within the left atrium possibly attaching to the atrial septum. (B)TTE 4 chamber view with colour flow contouring the echogenic structure within the left atrium. (C) Arterial phase CT showing a filling defect within the left atrial appendage (Arrow). (D) 10 second delay phase demonstrating resolution of the filling defect within the left atrial appendage.

Problem solving using modifying CT technique




  1. Klatt EC, Heitz DR, et al. Cardiac metastases.Cancer1990; 65:1456-1459
  2. Pavitt, C& Lazoura, O, Lindsay A, et al. The Use of Cardiac CT for the Detection of Left Atrial Appendage Thrombus: A Quality Improvement Project. Heart 2014;100:A86-A87.
  3. Hur J, Kim YJ, Lee HJ, et al. Left Atrial Appendage Thrombi in Stroke Patients: Detection with Two-Phase Cardiac CT Angiography versus Transesophageal Echocardiography. Radiology 2009 251:3, 683-690.
  4. Burke A, Jeudy J, Virmani R. Cardiac tumours: an update. Heart 2008;94:117-123. 
  5. Stoddard MF, Dawkins PR, Prince CR, Ammash NM. Left atrial appendage thrombus is not uncommon in patients with acute atrial fibrillation and a recent embolic event: a transoesophageal echocardiographic study. J Am Coll Cardiol 1995;25(2):452-9.
  6. Goldman ME, Pearce LA, Hart RG. Pathophysiologic correlates of thromboembolism in nonvalvular atrial fibrillation: reduced flow velocity in the left atrial appendage. J Am Soc Echocardiogr. 1999;12(12):1080-7.
  7. Malik, S. Chen, N. et al. Transthoracic echocardiography: Pitfalls and Limitations as Delineated at Cardiac CT and MR imaging. Radiographics 2017; 37:383-406




Image of the Month February 2019 - When a curry gives you more than heartburn..

When a curry gives you more than heartburn: A rare cause of myocardial infarction. 


Dr. S. Ahmed, Dr. A. Appaji, Dr. A. Large, Dr. S. Duckett Department of Cardiology, Royal Stoke University Hospital, Stoke-on-Trent. 

A fifty-six year old female was admitted to accident and emergency (A&E) with a witnessed collapse at home. She had a background history of recurrent urinary tract infections and an eleven pack year history of smoking. She had diarrhoea and vomiting for two days prior to admission after having a home-cooked curry and recalled feeling dizzy and nauseous with chest discomfort before passing out. 

On arrival to A&E, her blood pressure was 88/62 mmHg with symptoms of feeling light-headed and clammy. On examination her jugular venous pressure was elevated, normal heart sounds and bibasal crepitations on chest auscultation. Electrocardiogram (ECG) showed normal sinus rhythm with ST segment depression in leads III, aVF and V4 to V6 with a subsequent troponin rise of > 50000. CXR showed evidence of pulmonary oedema. 

A cardiac MRI was performed which showed mild impairment of left ventricular function, a limited basal infero-septal myocardial infarction. An incidental finding of a small (5X8mm) mobile mass was seen in the proximal ascending aorta, fixed to the aortic wall superior to the ST junction and above the RCA origin which was felt to be thrombus. It was dark on the early gadolinium image (image C) and non-enhancing on the late gadolinium (image B). 

CT coronary angiography was performed to further assess the coronary arteries which revealed a dissection flap (image D see arrow) causing moderate stenosis at the right coronary artery (RCA) ostium with further mild stenosis caused by a long soft tissue plaque in the proximal vessel. The images and cases were discussed with the interventional cardiology team and conservative management was felt to be the best option. 

The patient was discharged with dual antiplatelet therapy for 12 months and an ACE inhibitor, statin and beta blocker. A follow up CT imaging revealed resolution of the RCA ostial dissection flap with no significant stenosis. (image E see arrow) 


IOM case Dr Saba

Discussion: Spontaneous coronary artery dissection is a rare cause of non-atherosclerotic myocardial infarction with an incidence of 0.1% to 0.4% of all acute coronary syndromes.It is more commonly described in young females and known to be associated with fibromuscular dysplasia, connective tissue disease and peri-partum status. Frequently identified triggers include catecholamine release mediated by physical exertion, intense emotional stress and increased abdominal pressures induced by coughing, retching or vomiting.Both these mechanisms increase the shearing stress on the coronary artery wall. A conservative approach towards management with standard medical therapy is usually preferred compared to invasive angiography as most cases resolve spontaneously. 


1. Mortensen KH, Thuesen L, Kristensen IB, Christiansen EH. Spontaneous coronary artery dis- section: a Western Denmark Heart Registry study. Catheter Cardiovasc Interv. 2009 Nov 1;74(5):710-7. 2. Saw J, Aymong E, Sedlak T, Buller CE, Starovoytov A, Ricci D, Robinson S, Vuurmans T, 

Gao M, Humphries K, Mancini GB. Spontaneous coronary artery dissection: association with predisposing arteriopathies and precipitating stressors and cardiovascular outcomes. Circ Cardiovasc Interv. 2014 Oct;7(5):645-55. 

Image of the Month August 2018 - A Complicated Infarct

A Complicated Infarct

I Harries1, B Berlot1, R Ascione2, M Hamilton3, C Bucciarelli-Ducci1

1. Department of Cardiology, Bristol Heart Institute, United Kingdom

2. Department of Cardiothoracic Surgery, Bristol Heart Institute, United Kingdom

3. Department of Radiology, Bristol Royal Infirmary, United Kingdom

A 53 year old male ex-smoker with no other cardiovascular risk factors presented to a local hospital with progressive dyspnoea following an episode of chest pain that had occurred six weeks prior. ECG showed sinus rhythm with anterior Q waves. Coronary angiography demonstrated a proximal occlusion of the left anterior descending (LAD) artery and mild non-flow limiting disease in the right and left circumflex coronary arteries. The patient was commenced on appropriate medical therapy and transferred to our institution for cardiac magnetic resonance (CMR) imaging to evaluate LAD territory viability.

Figure 1. Mid ventricular short and 2 chamber long axis PSIR late Gadolinium enhancement sequences of the left ventricle.

 Nov18 IOM Figure 1 cropped 

  1. Is the LAD territory viable?
    1. No
    2. Yes


  1. No. The LAD territory is not viable. There is transmural late enhancement of the mid antero-septal, mid-anterior and mid anterolateral walls on the short axis view, and of the mid and apical anterior walls and apical cap on the long axis (2 chamber) view. The likelihood of functional recovery following revascularisation is very low in segments with >75% hyperenhancement 1.

Figure 2. Mid ventricular short axis and long axis 2 chamber balanced SSFP cine stills of the left ventricle.

Nov18 IOM Figure 2 cropped

  1. What complication of myocardial infarction is demonstrated?
    1. Left ventricular aneurysm
    2. Ventricular septal defect
    3. Papillary muscle rupture
    4. Left ventricular pseudoaneurysm
    5. Left ventricular thrombus


d.         Left ventricular pseudoaneurysm.  Myocardial rupture is evidenced by the abrupt discontinuation of the myocardium in the mid anterior segment (white arrow) with containment by the overlying pericardium (red arrow).


Figure 3. Zoomed mid ventricular short axis balanced SSFP cine still of the left ventricle.

Nov18 IOM Figure 3 cropped

 A pseudoaneurysm or ‘false aneurysm’ is formed when cardiac rupture is contained by adherent pericardium or scar tissue. Unlike true aneurysms, pseudoaneurysms contain no endocardium or myocardium and are significantly more likely to rupture than true aneurysms, which rarely rupture because of the densely fibrotic tissue found in the wall of true aneurysms 2.

  1. What is the appropriate management strategy?
    1. Surgical repair
    2. Medical therapy
    3. Revascularisation of the LAD (CABG or PCI)
    4. Cardiac transplant


  1. Surgical repair. If feasible, surgical repair is the preferred therapeutic option because conservative management of pseudoaneurysms carries a 30-45% risk of rupture and a mortality of almost 50%3. Perioperative mortality is less than 10% with greater risk for patients requiring concomitant mitral valve repair2.


The patient successfully underwent left ventricular aneurysmectomy (Figure 4.), was established on appropriate medical therapy, had a primary prevention ICD implanted and is making a good recovery.

Figure 4. Mid ventricular short axis and long axis 2 chamber balanced SSFP cine stills of the left ventricle following left ventricular aneurysmectomy.

Nov18 Figure 4 cropped


  1. Kim RJ, Wu E, Rafael A, Chen EL, Parker MA, Simonetti O, Klocke FJ, Bonow RO, Judd RM. The use of contrast-enhanced magnetic resonance imaging to identify reversible myocardial dysfunction. N Engl J Med. 2000 Nov 16;343(20):1445-53.
  2. Shapira O. (2017, Nov 27) Left ventricular aneurysm and pseudoaneurysm following acute myocardial infarction. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4900369/.
  3. Frances C, Romero A, Grady D. Left ventricular pseudoaneurysm. J Am Coll Cardiol. 1998 Sep;32(3):557-61.