Submit a course

Courses relevant to cardiovascular imaging can be submitted for inclusion on the BSCI/BSCCT website.

Members should be aware that advertising of courses on this site/page does not imply support or endoursement from the BSCI/BSCCT.

Listing of courses is free to BSCI/BSCCT members. A charge of £50 is required for non-members.

If you would like to submit a course to be considered for inclusion on the website please send the following information to This email address is being protected from spambots. You need JavaScript enabled to view it. :

Name of Course

Course director

When

Where

How to register

Other information (max 500 words)

Your name and BSCI/BSCCT membership number if a member (not for inclusion on the website)

Image of the Month April 2018 - Recurrent haemoptysis - but why?

Recurrent haemoptysis - but why?

Dr Jonathan Weir-McCall, University of Dundee.

Case History

A 59 year old female presented to clinic with a history of recurrent haemoptysis.  This had first occurred 14 years ago, with this being the 4th episode since that first occurrence.  Each time, the haemoptysis occurred without a prodrome and resulted in about half a cupful of fresh blood being produced.  She stopped smoking 2 years ago, prior to which she had a 30 pack year history.  She is otherwise fit and well.  The GP had performed FBC, U&Es, LFTs, CRP and a CXR prior to referral, all of which were normal.

Questions

Q1. Given the history and initial test results, which of the following is the most likely differential diagnosis?

  1. Chronic bronchitis
  2. Chronic thromboembolic pulmonary emboli
  3. Pulmonary AVM
  4. Bronchial carcinoma

The differential diagnosis for haemoptysis is wide, however has been somewhat narrowed down by the 14 year intermittent history, normal blood results and normal chest x-ray. 

In a recent smoker, bronchiectasis and chronic bronchitis are the most common causes of haemoptysis.1 Given the intermittent nature of the bleeding, a small AVM should be considered.  Vasculitis should also be in the differential although this is unlikely with no shortness of breath, and normal bloods.  While malignancy is always in the differential for a recent smoker presenting with haemoptysis this would be unusual given the 14 year history.  Given this range of differentials an ECG-gated pulmonary angiogram was performed.

Fig 1: ECG-gated pulmonary angiogram:

 IOTM May 2018 fig1

 

Q2. What does the CT image in Figure 1 show?

  1. Bronchopulmonary sequestration
  2. Chronic pulmonary thromboembolism
  3. Anomalous pulmonary venous drainage
  4. Unilateral absence of a pulmonary artery

The CT image is an axial slice of the thorax from a CT pulmonary angiogram study as evidenced by the dense enhancement of the pulmonary artery.

The right pulmonary artery courses in direct continuity from the pulmonary trunk, however the left pulmonary artery is not seen connecting with the pulmonary trunk.  In addition to this, the vessel in the region of the left pulmonary artery is poorly enhanced compared with the right pulmonary artery, and matches the enhancement seen in the descending aorta.  The combination of these features is in keeping with isolated unilateral absence of the pulmonary artery (IUAPA)2 with compensatory dilatation of the bronchial artery arising from the descending aorta.  As well as the dilated bronchial artery, the left internal mammary artery and intercostal arteries are also dilated, acting as further sources of collateral supply to the left lung.  The left lung is small compared with the right due to a degree of pulmonary atresia (Figure 2).

Figure 2: Annotated figure demonstrating the variant anatomy of this case of Isolated unilateral absence of a pulmonary artery

IOTM May 2018 fig2

Pul Trunk = Pulmonary trunk, Rt PAS = right pulmonary artery, Desc Ao = descending aorta, Bron A = Bronchial artery.  Filled in arrowhead points to a dilated Left internal mammary artery (cf the other side), Open arrows point to dilated intercostal arteries.

 

Q3: What complications is this patient at risk of?

  1. Left-sided pulmonary hypertension
  2. Right sided bronchiectasis
  3. Left sided haemoptysis
  4. Pulmonary embolism

Recurrent infections, dyspnoea and decreased exercise tolerance are the most common presentations of this condition.2  In addition to this there are several important sequalae.  Due to the increased blood through the single remaining pulmonary artery these patients are at high risk for developing pulmonary artery hypertension, this is especially pronounced during pregnancy, and indeed this can be the trigger that leads to the condition being discovered.4  Reduced blood supply to the side with the absent pulmonary artery predisposes it to recurrent infections with reports of bronchiectasis secondary to this.3 The dilated bronchial artery, internal mammary arteries and intercostal arteries are all at increased risk of bleeding due to the increased pressures running through them and their abnormal tortuous nature.  Patients with IUAPA are also at increased risk for high altitude pulmonary oedema and should be warned as such.  UAPA can occur with other congenital anomalies (in which case it is no longer “isolated”), in particular ASDs, VSDs and Tetralogy of Fallot.  Echocardiography is a useful adjunct in investigation as it can assess for these at the same time as measuring for pulmonary artery pressures to diagnose pulmonary hypertension.

References:

  1. Tsoumakidou M, Chrysofakis G, Tsiligianni I, Maltezakis G, Siafakas NM, Tzanakis N.  A prospective analysis of 184 hemoptysis cases: diagnostic impact of chest X-ray, computed tomography, bronchoscopy. Respiration. 2006;73(6):808-14. Epub 2006 Jan 27.
  2. Ten Harkel AD, Blom NA, Ottenkamp J. Isolated unilateral absence of a pulmonary artery: a case report and review of the literature. Chest. 2002 Oct;122(4):1471-7.
  3. Yiu MWC, Le DV, Leung Y, Ooi CGC.  Radiological features of isolated unilateral absence of the pulmonary artery.  J HK Coll Radiol 2001;4:277-280.
  4. Stiller RJ, Soberman S, Turetsky A, et al.  Agenesis of the pulmonary artery,: an unusual cause of dyspnea in pregnancy.  Am J Obstet Gynecol 1988; 158:172-173.

 


Image of the Month May 2018 - Absence doesn't make the heart grow fonder..

Absence doesn’t make the heart grow fonder:  an interesting case of partial pericardium.

Dr Tom Chance1, Dr Laura Duerden1, Dr Jonathan Rodrigues2, Dr Stephen Lyen1, Dr M Hamilton1, Dr N Manghat1.

Affiliations:

1 Department of Radiology, Bristol Royal Infirmary, United Kingdom

2 Department of Cardiothoracic Imaging, Toronto General Hospital, Toronto

 

Image focus:

A 45 year old man presented with atrial fibrillationA chest radiograph showed a slightly lobulated contour of the superior left heart border (see figure 1). Transthoracic echocardiography (performed at an outside institution) showed possible right ventricular (RV) mass.  Cardiovascular magnetic resonance was performed to clarify the echocardiographic appearances. It demonstrated abrupt pericardial discontinuity on axial HASTE sequence, with the right-sided pericardial edge causing focal, extrinsic RV compression (Fig 2A). Steady state free precession cine images demonstrated an impaired RV ejection fraction of 34%.  The RV indexed end diastolic volume was 77ml/m2 (normal age-matched range 67-111ml/m2). RV volumes quantified on short axis slices. Left ventricular (LV) morphology and function were normal (LV ejection fraction 45%). Cardiac CT was performed to provide higher spatial resolution detail of the pericardial abnormality. This was performed with retrospective gating with 20% mAs outside of diastolic reconstruction windows. This confirmed a large defect in the anterior and lateral pericardium with complete LV and partial RV herniation (Fig.2B and D). There were no discernible superior pericardial recesses (Fig. 2C) and also evidence of lung invaginating between left inferior pulmonary vein ostium and left atrium (Fig.2B, straight white line), indirectly inferring deficient pericardium in these regions.  There was differential contrast opacification in the RV apex, constrained by the pericardial herniation compared to the remaining RV, implying delayed RV apical emptying but no RV apical thrombus (Fig 2B, *). No other congenital abnormality was demonstrated.   The patient declined surgical pericardioplasty, accepting the risk of potential cardiac and/or vascular strangulation. The atrial fibrillation was medically managed.

Discussion:

Congenital pericardial absence is a rare condition, most frequently affecting the left-sided pericardium with either complete or partial absence and resultant LV herniation. Right-sided pericardial involvement is even less common. We present a rare case of partial absence of both left and right sides of the pericardium with complete LV herniation and partial RV herniation diagnosed non-invasively with multi-modality imaging.

Congenital pericardial absence is believed to result from pleuro-pericardial hypoxia and agenesis due to premature atrophy of the left common cardiac vein and is frequently associated with other congenital anomalies. The unusual pattern of pericardial absence and lack of concomitant congenital defect raises the possibility that the abnormality was acquired in early development, but after completion of cardiac organogenesis in this patient.

 cxr partial pericardium1

 

Figure 1 - PA chest radiograph. The heart appears enlarged with evidence of indentation in the superior leftward cardiac contour.

  

 figure abcd final 2

Figure 2 A. Axial HASTE image showing pericardium exerting extrinsic mass effect on the RV and apical RV herniation. B. Axial ECG-triggered cardiac CT image confirming the partial pericardial absence and demonstrating retained contrast in the herniated RV apex (*). There is lung invaginating between the left inferior pulmonary vein and left atrium (solid white arrow). C. 2-chamber reformat from ECG-gated cardiac CT showing deficient superior pericardial recesses and the inferior extent of the pericardium (solid white arrow). D. Volume-rendered ECG-triggered CT reconstruction demonstrating the point of RV partial herniation (*).

 

Multiple choice questions

Question  1) Congenital pericardial absence most often occurs in which geographic pattern

A-    Complete absence of the pericardium

B-     Absence of the left pericardium

C-     Absence of the right pericardium.

Answer:  B- Absence of the left pericardium. Most common defect is absence of the left pericardium (up to 70% of cases), followed by right pericardium (17%), and then total absence of the pericardium (9%).

Question 2) Of the above geographic patterns of pericardial absence, which has the best prognosis?

A-    Complete absence of the pericardium

B-     Absence of the left pericardium

C-     Absence of the right pericardium

Answer: A- Complete absence of the pericardium. Herniation of the heart through focal pericardial defects can lead to several complications including tricuspid regurgitation, myocardial strangulation, ischaemia and sudden death. Complete absence of pericardium does not normally require intervention unless complications occur[i].

Question 3) Congenital pericardial defects result from the premature atrophy of which structure?

A-    Left common cardinal vein

B-     Right common cardinal vein

C-     Left primitive jugular vein

D-    Left vitelline vein

Answer: A- Left common cardinal vein (duct of Cuvier). As a result, reduced blood supply to the left pleuro-pericardial membrane results in pericardial agenesis[ii].

Question 4 ) Which echocardiographic finding is not typically seen in congenital partial pericardium?

A-    Cardioptosis

B-     Abnormal interventricular septal motion

C-     Apparent right ventricular dilatation

D-    Pulmonary regurgitation

Answer: D- Pulmonary regurgitation. Echocardiographic findings are related to increased cardiac mobility within the chest cavity[iii].

References


[i] Congenital absence of the pericardium. Hyun-Jin Kim, Young-Seok Cho et al. J Cardiovasc Ultrasound. 2014 Mar;22(1):36-39.

[ii] Congenital absence of the pericardium presenting as acute myocardial necrosis. Brulotte S, Roy L et al. Can J Cardiol. 2007 Sep; 23(11): 909-912.

[iii] Congenital absence of left pericardium. Victor AR, Osorio P et al. Rev Port Cardiol. 2003 Jun;22(6):801-10.

Safeguarding

Click here to download the BSCI/BSCCT Safeguarding Policy Statement.

Image of the Month - March 2018 - Progressive dyspnoea in a patient with a bioprosthetic AVR

Progressive dyspnoea in a patient with a bioprosthetic AVR

Jack PM Andrews, Marc R Dweck, Alastair J Moss.

Centre for Cardiovascular Science, University of Edinburgh, Chancellor’s Building, Royal Infirmary of Edinburgh, 51 Little France Crescent, Edinburgh EH16 4TJ, UK. 

Corresponding Author: Dr. Jack PM Andrews. E-mail: This email address is being protected from spambots. You need JavaScript enabled to view it.

Introduction

An 85-year old woman presented to the cardiology service with exertional dyspnoea whilst walking on the flat. She underwent a bioprosthetic surgical aortic valve replacement (stentless 25 mm Kohler Elan, Vascuetec) 12 years ago for calcific aortic stenosis. She was otherwise systemically well and had not undergone any recent dental procedures. On examination, she had a collapsing pulse (BP 120/30 mmHg) and grade 3 early diastolic murmur in the aortic area. Electrocardiogram (ECG) demonstrated sinus rhythm with voltage criteria for left ventricular hypertrophy and routine bloods returned a normocytic anaemia with a mildly elevated serum bilirubin (27 umol/L). A transoesophageal echocardiogram (TOE) was performed. (Figure 1)

2018 March IOM 1

Figure 1. Transoeophageal echocardiogram mid-oesophageal AV long axis view (A). 3D echocardiogram short axis view (B).

  

2018 March IOM 2

Figure 2. Cardiac magnetic resonance demonstrated transprosthesis laminar regurgitation jet (A). 3D  cardiac computed tomography coronal reconstruction of the aortic bioprosthesis confirmed the left cusp prolapse [inset] that is independent from a septated LVOT aneurysm (B). Pre TAVR deployment aortogram showing substantial volume of contrast within the left ventricle confirming significant aortic incompetence (C). Post TAVR deployment aortogram; note the lack of contrast within the left ventricle indicating the return of valvular competence and successful TAVR deployment (D).

Clinical Question

What is the aetiology of the bioprosthetic aortic valve dysfunction?

  1. Infective endocarditis
  2. Late suture dehiscence
  3. Leaflet prolapse
  4. Thrombus formation
  5. LVOT aneurysm formation

  Answer – C

 The correct answer is leaflet prolapse. TOE demonstrated a severe central regurgitant jet at the level of the prosthesis, confirmed by the large width of the colour flow jet (>65% of LVOT diameter) and colour M-mode holodiastolic flow reversal across the prosthesis (Figure 1A & B). Pathological regurgitation of prosthetic heart valves can either be central or paravalvular. Paravalvular regurgitation is often related to position of the sewing ring and anchoring tissue in the outflow tract with latent failure of the suture line due to age-related deterioration or LVOT aneurysm formation. Central regurgitation is a common feature of structural valve dysfunction. Distortions in leaflet anatomy due to perforations or thickening of the cusps ultimately result in leaflets prolapsing below the annular plane.

Whilst echocardiography remains the initial first line investigation, adjuvant imaging using cardiac magnetic resonance is increasingly utilised to confirm the severity and location of regurgitant jets (Figure 2A). [1] Bioprosthetic valve thrombosis and infective endocarditis are important differential diagnoses to exclude using modalities with superior spatial resolution such as cardiac computed tomography (Figure 2B). [2]

Figure 2C and 2D demonstrate aortograms both pre and post deployment of transcathether aortic valve replacement (TAVR) illustrating the immediate cessation of valvular incompetence.  The advent of valve-in-valve interventions offers novel strategies for high-risk patients with failing stentless bioprostheses. [3] Confirming the specific aetiology of bioprosthesis dysfunction with multi-modality imaging is a priority to select the most appropriate therapeutic strategy. This patient underwent transcatheter aortic valve implantation (26mm CoreValve Evolut R, Medtronic) with an immediate improvement in symptoms.

REFERENCES

[1]       Salaun E, Jacquier A, Theron A, Giorgi R, Lambert M, Jaussaud N, Hubert S, Collart F, Bonnet JL, Habib G, Cuisset T, Grisoli D. Value of CMR in quantification of paravalvular aortic regurgitation after TAVI. Eur Heart J – Cardiovascular Imaging. 2016;17:41-50.

[2]       Moss AJ, Dweck MR, Dreisbach JG, Williams MC, Mak SM, Cartlidge T, Nicol ED, Morgan-Hughes GJ. Complementary role of cardiac CT in the assessment of aortic valve replacement dysfunction. Open Heart. 2016;3:e000494. Doi: 10.1136/openhrt-2016-000494.

[3]       Duncan A, Davies S, Di Mario C, Moat N. Valve-in-valve transcatheter aortic valve implantation for failing surgical aortic stentless bioprosthetic valves: A single-center experience. J Thorac Cardiovasc Surg. 2015;150:91-98.