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Calcified embolus mimics patent middle cerebral artery on CT angiogram
  1. Vignan Yogendrakumar1,
  2. Satya Patro2,
  3. Dar Dowlatshahi1,
  4. Grant Stotts1,
  5. Daniela Iancu2
  1. 1 Department of Medicine (Neurology), University of Ottawa, Ottawa, Ontario, Canada
  2. 2 Department of Diagnostic Imaging, University of Ottawa, Ottawa, Ontario, Canada
  1. Correspondence to Dr Daniela Iancu; diancu{at}toh.ca

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Case report

A 61-year-old woman presented with acute symptoms of right middle cerebral artery ischaemia, with left face/arm/leg weakness, right gaze preference and homonymous hemianopia. A non-contrast CT scan of the head showed a calcified Y-shaped hyperdensity at the right middle cerebral artery bifurcation (figure 1A). We did not identify any contraindications for thrombolytic therapy, and the patient was treated with intravenous tissue plasminogen activator.

Figure 1

Hyperdense calcific thrombus at the right middle cerebral artery bifurcation.

We used a multi-phase CT angiogram to assess her cerebrovascular status. We expected a role for endovascular intervention given the clinical deficits and corresponding right middle cerebral artery bifurcation hyperdensity, which we assumed to be thrombus. However, the initial phase of the CT angiogram did not show the expected occlusion (figure 1B), prompting the question of whether the observed calcification was extraluminal.

A multi-phase CT angiogram involves two repeat scans of the head (without additional contrast) to try to detect delayed collateral filling.1 These later phase scans showed persistent lack of contrast in the artery just distal to the calcification, and delayed arterial collaterals in the ipsilateral hemisphere, consistent with flow obstruction at the expected site from the original scan (figure 2). We determined that the calcification was intra-luminal and therefore initiated thrombectomy, successfully removing a calcific clot. (figure 1C). The likely source of the embolus was her heavily calcified aortic arch.

Figure 2

Multiphase CT angiogram.

Spontaneous calcific emboli are an uncommon but increasingly recognised cause of ischaemic stroke.  They can arise from aortic stenosis, aortic arch atherosclerosis and mitral valve calcification.2  Calcific emboli often show as a hyperdense vessel sign on non-contrast CT and as a bright hyperdensity on CT angiography. The hyperdense vessel sign is a focal density of the middle cerebral artery seen on non-contrast CT and predicts the presence of thromboembolic material.3 In our case, a calcific embolus presented as a hyperdense vessel on non-contrast CT but without the contrast cut-off normally expected with arterial occlusion. The vessel appeared isodense with iodinated contrast, simulating vessel patency.  

There are similar reports of false patency in the literature.4 5   In these cases, MRI or digital subtraction catheter angiography was used to verify vessel occlusion but with an associated delay in treatment. In the present case, careful inspection with multi-phase CT angiogram detected this “pseudo-patency”, allowing us to verify the finding at the time of initial assessment without the delay from further testing.

In cases where the clinical presentation suggests a large vessel occlusion that can not be seen on conventional CT angiography, we recommend considering alternative modalities such as multiphase CT angiography. Other imaging options include, CT perfusion, a rapid MRI diffusion-weighted imaging/apparent diffusion coefficient protocol, and verification with catheter angiography.1

Key points

  • Calcific emboli, generally hyperdense on non-contrast CT scans and CT angiography, can appear isodense to iodinated contrast on CT angiography, creating a sense of false vessel patency ('pseudo-patency').

  • Multiphase CT angiography assesses the collateral circulation at different time points; the finding of delayed backfilling of arteries distal to a proximal artery suggests occlusion.

  • In cases where there is not the expected cut-off, multiphase CT angiography and assessment of delayed collateral flow can verify arterial occlusion.

References

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Footnotes

  • Contributors VY and GS were responsible for drafting the manuscript and subsequent revisions. SP and DD provided critical revision for intellectual content. DI is guarantor of the paper.

  • Competing interests None declared.

  • Patient consent Detail has been removed from this case description/these case descriptions to ensure anonymity. The editors and reviewers have seen the detailed information available and are satisfied that the information backs up the case the authors are making.

  • Provenance and peer review Not commissioned; externally peer reviewed. Reviewed by William Whiteley, Edinburgh, UK and Joshua Klein, Boston, USA.

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