MRI for patients with pacemakers and implantable cardioverter-defibrillators

The British Cardiovascular Society and the Clinical Imaging Board (the Society and College of Radiographers, the Institute of Physics and Engineering in Medicine, and the Royal College of Radiologists) recently published a joint letter on MRI for patients with pacemakers and implantable cardioverter-defibrillators.

It stated that they “jointly believe that patients with cardiac devices should no longer be disadvantaged and have the same access to MRI scanning in the NHS as everyone else. Addressing this will require local champions, new working practices (clinical, financial), and partnerships – especially between cardiology and radiology and medical physics departments. But there are no fundamental barriers - we as a community are capable of making this happen. We encourage you to help make this a reality in the NHS.”

Click here to download the letter

Image of the Month July 2018 -Fluttering between imaging modalities

Fluttering between imaging modalities

Dr Jamie Kitt, Dr Andrew Kelion  and Dr Elizabeth Orchard.

Department of Cardiology, Oxford Heart Centre, John Radcliffe Hospital, Oxford, United Kingdom

A 46-year-old civil servant was referred to us by a local district general hospital (DGH) in April 2018.  He had been admitted in October 2017 after developing rapid palpitations whilst in the shower. He attended his local Emergency Department and was found to be in atrial flutter with 2:1 block and a ventricular rate of 140 beats per minute. He was seen by the on-call cardiologist and started on Bisoprolol and Apixaban. He was referred to the local Electrophysiologist. An A&E bedside scan (GE V-scan) done locally was ‘reportedly normal’ and he went on to have a successful flutter (cavo-tricuspid isthmus) ablation in December 2017.  

At our clinic in June 2018, he reported no further palpitations, but mentioned fatigue with reduced exercise tolerance compared to early 2017. On reflection, he felt that he had always struggled to keep up with his peers at school and university. He had no other past medical history of note, and was a non-smoker who drank only occasional alcohol. He took only Apixaban 5mg bd.

On examination, oxygen saturation was 99% on room air. Pulse rate was 66 and regular, with normal character and volume, and blood pressure was 115/60. Jugular venous pulse was normal. He had wide fixed splitting of the second heart sound, and a pan-systolic murmur loudest at the lower left sternal edge. The chest was clear.

12-lead electrocardiogram (ECG) demonstrated sinus rhythm, with partial right bundle branch block (RBBB) and a QRS duration of 100ms.

Question 1: What is the likely diagnosis at this point based on the current information?

  1. Ventricular septal defect (VSD)
  2. Atrio-ventricular septal defect (AVSD)
  3. Mitral regurgitation
  4. Atrial septal defect (ASD)
  5. Pulmonary stenosis

Answer: 4. Atrial septal defect (ASD). The combination of long-standing exercise intolerance, an atrial arrhythmia, wide fixed splitting of the second heart sound and RBBB morphology on the ECG is highly suggestive of an ASD1.

At follow up in the DGH, he had eventually had a formal trans-thoracic echo and a dilated right heart was noted as well as an atrial septal defect which prompted the referral to us. A transthoracic echocardiogram (TTE) at our clinic was reported as a primum ASD with a left to right shunt (Figure 1).  There was also moderate mitral regurgitation due to prolapse of the anterior mitral valve leaflet (AMVL) with thickening of the leaflet tips (Figure 2). The right ventricle (RV) was moderately dilated, with severe bi-atrial dilatation.

Figure 1. Trans-thoracic echo apical 4 chamber view A :  Severely enlarged left atrium  B: Severely dilated RA with evidence of RA pressure overload at end systole (arrow) C: RV dilatation (albeit in snap-shot at end-systole) D (arrow): Elongated AMVL with prolapse

2018 july fig1

Figure 2.  A: Zoomed apical 4 chamber of the inta-atrial septum showed a defect (measured as 1.3cm) reported as a primum ASD. B: Corresponding colour flow Doppler through the defect confirming left to right shunt

2018 july Fig 2 

Transoesophageal echocardiography (TOE) was performed a few weeks later, and the images were reviewed at our Adult Congenital Heart Disease (ACHD) Multidisciplinary Team (MDT) Meeting. The study was felt to show a primum ASD, with an accompanying bubble study which appeared to show a left to right shunt (Figures 3A and 3B). However, the atrial defect itself was not clearly visualised, so cardiac magnetic resonance (CMR) imaging was advised to define the anatomy more precisely.

Figure 3A.  Trans-oesophageal echocardiohgram (TOE) mid-oesophageal at 71 degrees focusing on the intra-atrial septum (IAS) A: Severely enlarged right atrium. B: IAS with small primum ASD suspected but unable to clearly visualise at any angulation C: Off axis tri-leaflet aortic valve D: Partial view of a dilated RV

2018 july fig3a

Figure 3B. Bubble study during TOE at 3rd cardiac cycle after injection into left arm (unaware of left sided SVC at this time) consistent with large left to right shunt.

2018 july fig3b

CMR was performed in July 2018, including a detailed atrial stack and a twist angiogram in addition to the standard set of sequences. The study reportedly showed a moderate secundum ASD located antero-inferiorly (Figure 4A and 4B), resulting in a 2:1 left to right shunt. A comment was made that no primum ASD was seen. There was a mildly dilated RV when indexed to his body surface area (235mls) with normal RV function, normal LV function, and mild mitral regurgitation. Normal pulmonary venous (PV) drainage was noted, but a persistent left-sided superior vena cava (SVC) was seen on the twist angiogram though it was unclear whether this was draining into the right atrium (RA).

 

Figure 4. Cardiac MRI performed using Siemens 1.5T magnet. 4A Atrial stack A:Severely dilated left atrium. B: Severely dilated right atrium. C (arrow): Atrial Septal defect visualised reported as moderate sized secundum atrial septal defect (ASD) measuring (21x17mm) which is located very antero-inferiorly. Flows subsequently  confirmed Qp:Qs 2:1. 4B Horizontal long axis (HLA) view also showing significant atrial septal defect (arrow) and D: moderately dilated RV

2018 july fig4a and b

Question 2: What is the commonest variation in the thoracic venous system?

  1. Anomalous drainage of right sided superior vena cava (SVC) to the left atrium (LA)
  2. Persistent left-sided SVC (bilateral SVCs aka SVC duplication)
  3. Isolated left sided SVC

Answer: 2. Persistent left-sided SVC, is the most common congenital venous anomaly in the chest.

It accounts for 10% of thoracic vein anomalies and is present in 0.3-0.5% of the general population2. It is only seen in isolation in 10% of cases since in the vast majority of cases (82-90%) a normal (but small) right-sided SVC is also present, and a persistent bridging vein (left brachiocephalic vein) is seen in 25-35% of cases.

 On further discussion at the ACHD MDT Meeting in August 2018, there was still no agreement on the exact anatomy despite TTE, TOE with a bubble study, and CMR. He was duly referred for a gated cardiac X-ray computed tomographic (CT) study, which resolved the confusion. CT demonstrated a right-sided SVC and inferior vena cava (IVC) draining normally into the RA. The persistent left-sided SVC (figure 5B in Powerpoint) drained into a completely de-roofed coronary sinus and LA (Figure 5), creating a large effective "ASD". An additional small secundum ASD was also evident. PV drainage was normal. The right ventricle and both atria were dilated. The coronary arteries were normal. 

 

Figure 5 . Gated Cardiac CT which was performed on a GE Revolution with 16cm detector, using Omnipaque 350 50ml at 5ml/s, saline 50ml at 5ml/s. No metoprolol or GTN was administered. Prospective gating at 70-80% as well as 0-100% at 20% current. 100kVp. Heart rate 64bpm. DLP 223mGy.cm.

5A: A: Deroofed coronary sinus creating large ‘ASD’ as well as a B: Secundum ASD and 5B shows C: Left sided SVC draining into De-roofed coronary sinus and Left atrium (LA).

2018 july fig5

 

Question 3: What is the commonest associated congenital lesion seen with a left sided SVC

  1. Atrial septal defect (ASD)
  2. Ventricular septal defect (VSD)
  3. Coarctation of the aorta
  4. Pulmonary stenosis
  5. Anomalous pulmonary venous return

Answer: 1. ASD. Congenital heart defects are present in 4.4% of patients with left-sided SVC3. ASDs are the most common by far but it can also occur with a single atrium, VSDs, Tetralogy of Fallot, coarctation of the aorta, anomalous pulmonary venous drainage and pulmonary stenosis. These should be thus searched for if a left sided SVC is present. There are a number of possible drainage sites. Left-sided SVCs are often functionally insignificant with 92% draining into coronary sinus since venous return from the head, neck and upper limbs is delivered to the right atrium 3. In the other 8%, although drainage into the LA results in a right to left shunt, it is usually not large enough to cause cyanosis or symptoms 3 but, in this case the coronary sinus ASD and second secundum ASD resulted in a large left to right shunt.

Discussion:

This case highlights the importance of comprehensive cardiological assessment of patients with new onset atrial arrhythmias, including a detailed TTE, particularly in young adults, before jumping to treat the rhythm disorder. It also highlights the importance of searching for other lesions once one congenital lesion has been identified. Moreover, it emphasises the strengths and limitations of the various imaging modalities used in assessment of complex congenital heart disease. Echocardiography and CMR provide excellent functional information. However, when the anatomy is uncertain, gated cardiac CT offers the unparalleled ability to perform extensive reorientation of a true three-dimensional dataset with high spatial resolution. There is no requirement for images to have been acquired in precisely the right plane, as for echo and CMR. Modern CT scanners such as the GE REVOLUTION also allow easy dose modulation across the entire cardiac cycle, so that even LV and RV systolic function can be calculated to complement the anatomical assessment.

References:

  1. S Martin, E Shapiro and M Mukherjee. Atrial Septal Defects – Clinical Manifestations, Echo Assessment, and Intervention. Clin Med Insights Cardiol. 2014; 8 (Suppl 1): 93–98. PMCID: PMC4373719
  2. Padhani AR, Hale HL. Mediastinal venous anomalies: potential pitfalls in cancer diagnosis. Br J Radiol. 1998; 71 (847): 792-8Br J Radiol
  3. Pretorius PM, Gleeson FV. Case 74: right-sided superior vena cava draining into left atrium in a patient with persistent left-sided superior vena

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Image of the Month - June 2018 - An unusual cause of extensive bilateral lower limb oedema

An unusual cause of extensive bilateral lower limb oedema

Rachael Forsythe and Orwa Falah, Edinburgh

An 84 year old male presented with sudden onset massive bilateral lower limb swelling and a 4 day history of vague abdominal pain and swelling.  He had no previous similar episodes; otherwise fit and well.  Still working as a farmer. Treated for hypertension (bisoprolol), atrial fibrillation (recently commenced on apixaban) but no other relevant past medical history.  No personal or family history of thrombophilia.  He was haemodynamically stable on admission. Relevant bloods: Hb 118, platelets 160, creatinine 169, urea 16.6, eGFR 33.

Urgent CTA was performed (images 1-3).

2018 jun fig1

Image 1: Large AAA (red arrow) rupturing into IVC (green arrow) via aorto-caval fistula.

2018 jun fig2

Image 2: Contrast from the AAA (red arrow) is seen within the inferior vena cava and iliac veins (orange arrow)

2018 june fig3

Image 3: Contrast from the AAA (red arrow) is seen within the inferior vena cava (green arrow), which also contains thrombus (blue arrows)

Question 1:

What are the diagnoses?

Question 2:

What effect does acute renal failure have on apixaban clearance?

  1. a.no effect – apixaban does not undergo renal excretion and would therefore be cleared within 48 hours
  2. b.increases the clearance time; dose should be reduced if serum creatinine >133micromol/litre or age >80 or weight <61kg
  3. c.increases the clearance time by an extra 72 hours but only when the eGFR is below 30

           Question 3:

 Why might a patient with aorto-caval fistula present with breathlessness and syncope?

  1. a)aorto-caval fistula can cause a left-to-right shunt resulting in high output congestive cardiac failure
  2. b)breathlessness and syncope is a manifestation of haemorrhagic shock
  3. c)they may develop acute aortic stenosis due to elevated right ventricular systolic pressure

The optimal approach to this would be urgent open repair, however in the context of acute renal failure, apixaban assay confirmed that clearance was markedly reduced. It was therefore not felt safe to proceed with open repair in the acute period due to the risk of being unable to achieve haemostasis.  The patient therefore had a trans-jugular inferior vena caval filter inserted followed by standard EVAR the following day (image 4). 

2018 jun fig4

Image 4: 3D reconstruction following EVAR (thick green arrow), with IVC filter visible (thin green arrow)

Despite successful EVAR deployment, the fistula remained patent with a type 2 endoleak due to patent lumbar arteries.  However, renal function rapidly returned to normal and the patient experienced rapid symptomatic relief.  He was discharged home on warfarin with plans for early follow up imaging.

Answers:

  1. Ruptured abdominal aortic aneurysm with large aorto-caval fistula and concurrent bilateral ilio-femoral DVTs extending into the IVC
  2. B
  3. A

 

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.