Presentation
Increased work of breathing.
Patient Data
Peribronchial cuffing and Kerley B-lines compatible with interstitial pulmonary edema.
Systemic venous distension.
Enlarged heart shadow on the PA projection.
On the lateral projection there is an oreo cookie sign due to pericardial effusion outlined by lung anteriorly and epicardial fat posteriorly.
Negative study for pulmonary embolus.
There is a left ventricular aneurysm extending superiorly from the mid to apical left ventricle.
Although contrast timing is not optimized for the assessment of myocardium, there is a suspected thrombus within the aneurysmal left ventricle.
The sagittal reformats demonstrate the layers of the oreo cookie sign: lung, pericardial effusion and epicardial fat.
Pasted from cardiac catheter report:
Right radial artery access was achieved a 6 French sheath was inserted standard 5 French diagnostic catheters were taken for the coronary angiogram. 5000 units of heparin were given as an anticoagulant
Left mainstem large in caliber and unobstructed
The LAD was in fact a short and very vestigial type I vessel. Very early bifurcation into a high very large first diagonal was seen with ongoing LAD which is almost functionally a large septal and very likely intramyocardial heart and severe 80% proximal stenosis followed by a short aneurysmal segment and a further 60 to 70% stenosis beyond which the vessel petered out to a very small target.
The first diagonal is a large vessel arising very early from the proximal LAD. This had a 40% mid-vessel stenosis
The circumflex gave rise to a very large first obtuse marginal branch which was unobstructed. The ongoing circumflex had mild atheroma.
RCA very large dominant vessel ectatic and unobstructed throughout.
CTCA was performed to clarify apparent aberrant LAD anatomy.
CAD-RADS 2.0 score: CAD-RADS 5/P3/HRP/E
Suspected dual LAD with truncated/vestigial LAD proper supplying the septal perforator branches and terminating high in the interventricular groove. It has a proximal severe stenosis with post-stenotic aneurysmal dilatation followed by moderate stenosis.
Dominant first diagonal branch which could also be interpreted as a long duplicated LAD1 which demonstrates a complete occlusion of its main branch. This occluded branch was not visible on the preceding catheter angiogram.
The circumflex supplies the anterolateral basal and midventricular wall and has one dominant obtuse marginal branch which is unobstructed.
The RCA appears ectatic with a coronary plaque proximally with high-risk plaque features including positive remodeling, 'spotty' calcification and low attenuation. It supplies the posterior descending and posterolateral branch which demonstrates at most mild stenosis.
Significant non-coronary findings: LAD territory infarct which involves the mid anterior and anterior septal walls extending to the apical anterior and septal walls. This is associated with a thick and significant LVH apical thrombus. This thrombus measures approximately 2.7 cm in thickness along the anterior wall.
The left ventricle is dilated with akinetic mid to apical anteroseptal to anterior LV with an ejection fraction of ~27%.
The late gadolinium enhancement of the apical and anterior mid-ventricular and thinned akinetic/dyskinetic myocardium is transmural to a larger extent and subendocardial to a much lesser extent at its margins. This is compatible with a largely non-viable LAD distribution infarct.
The infarcted mid to apical anterior myocardium is aneurysmal, containing a wall-mounted thrombus.
Case Discussion
In this case, catheter angiography was performed prior to the CT and illustrates the complementary role CT coronary angiography can have in the assessment of coronary artery disease.
The LAD anatomy is complex in this case. The 'LAD proper' is shortened and appears to terminate high in the interventricular groove. The first early branch of the 'LAD proper' in this case has been defined as a dual LAD type 1 1, but could also be described as a dominant D1 branch. The complete occlusion of its major branch was not visible on catheter angiography and has resulted in the mid to apical LAD infarct and subsequent left ventricular aneurysm.
Subsequent to the CCTA, a cardiac MRI was ordered to assess for viability. This confirmed the aneurysmal dilatation of the LAD territory infarct was non-viable.
Finally, an important point to remember when reporting chest radiographs: enlargement of the heart shadow is non-specific and can be due to chamber dilatation and/or pericardial effusion and this distinction is important. Acute pericardial effusion can be fatal if not recognized and treated. In this case, the presence of interstitial pulmonary edema indicates left ventricular failure while systemic venous distension can be due to congestive heart failure and/or cardiac tamponade. The oreo cookie sign is valuable as it establishes the presence of pericardial effusion.
Pericardial effusion can rarely occur as an early reperfusion phenomenon after myocardial infarction. Dressler syndrome occurs weeks after MI and is due to autoimmune pericarditis. Contained LV perforation is a differential diagnosis to consider.
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