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Computed Tomography for Coronary Anatomy and Perfusion - Guiding Therapy in a Patient with an Occluded Left Anterior Descending Coronary Artery

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A 79-year-old male was resuscitated from ventricular fibrillation, which occurred during the recovery phase of an exercise stress test. His past history included sick sinus syndrome treated with a dual-chamber pacemaker and a patent foramen ovale, which was closed percutaneously after a transient ischemic attack.

Emergent coronary angiography showed a right dominant coronary circulation with collaterals from the right coronary artery (RCA) flowing toward the left anterior coronary artery (LAD) (see Figure 1A), which was completely occluded after giving off a diagonal branch (see Figures 1A and 1B). There was also a 50% stenosis of the mid-RCA, a 50% ostial stenosis of the left main coronary artery stenosis, and 90% proximal stenosis of the first diagonal branch of the LAD. The left ventriculogram showed normal wall motion in all segments.

The patient was referred for computed tomography angiography (CTA) to determine whether the caliber of the distal LAD was suitable for bypass grafting. Multidetector electrocardiographic gated CTA of the heart and coronary arteries was obtained on a 64-channel scanner with standard 120kV at 0.8mm slice thickness with MAS 800 at 0, 40, 70, 75, and 80% phases. The patient was given 100mg of oral metoprolol two hours prior to the study. Sublingual nitroglycerin (0.4mg) was administered at 25, 15, and five minutes prior to the study to produce coronary artery dilation and enhance collateral flow. Angiography was performed with 120ml iopamidol injected at 6ml/sec followed by 50ml of saline injected at 5ml/sec.

The left main coronary artery ostium had a moderate eccentric stenosis. The LAD had ostial and proximal calcified plaques with mild stenosis. The mid-LAD was occluded after the origin of the second septal and first diagonal arteries. The mid LAD was reconstituted after skip area of 21mm. The initial 15mm of the mid LAD after reconstitution was mildy stenotic. The second diagonal branch arose from this diseased segment. After the second diagonal branch, the mid LAD was a 2mm vessel that was free of disease (see Figure 2). The distal LAD was directly visualized to connect with the posterior descending branch of the distal RCA, consistent with a well developed collateral flow. Left ventricular wall motion was normal.

Left ventricular diastolic-phase images, windowed to show myocardial perfusion, revealed reduced contrast enhancement of the anterolateral endocardial wall segment (see Figure 3). Exercise dual-isotope nuclear stress test confirmed a reversible perfusion defect of the anterolateral wall (see Figure 4).

Multidetector electrocardiographic gated CTA of the heart and coronary arteries demonstrated an adequate target for bypass graft placement to the mid to distal LAD. CTA showed better collateral filling of the distal LAD than demonstrated by intra-arterial angiography. CTA further demonstrated that the distal anterior wall of the left ventricle suffered diminished subendocardial perfusion despite this collateral flow. Reversible ischemia was documented by stress testing with myocardial perfusion imaging. The patient underwent uneventful surgery with anastamosis of the left internal mammary artery to the distal LAD and a saphenous vein graft to the diagonal.

This case demonstrates the usefulness of CTA in visualizing the epicardial coronary arteries beyond their proximal occlusion, detecting collaterals not visualized after standard intra-arterial injections,1 and in demonstrating functional abnormalities of myocardial perfusion.2 While not all totally occluded coronary arteries can or should be opened,3 selected patients in whom symptomatic residual ischemia can be documented and revascularization is technically feasible may benefit from intervention. CTA may have a role in identifying such patients.

References

  1. Hoe J, Int J Cardiovasc Imaging, 2009;25:43–54.
  2. Blankstein R, et al., J Am Coll Cardiol, 2009;54:1072–84.
  3. Hochman JS, et al., N Engl J Med, 2006;355:2395–2407.