Mr MA

65y.o man presented with palpitation and presyncopal episode for past 3 hours. He also complained of worsening dyspnea and orthopnea for 1 month. He is a heavy smoker, has diabetes and hypertension with poor compliant to medication and follow up. In ED, vital signs were BP 108/80, HR 204, O²sats. 90%. There was bilateral lung crepitations up to mid zone. ECG showed VT. He was successfully cardioverted and intubated for respiratory distress. He was extubated after 4 days of IV diuresis in CCU.

In mmol/L: Urea 9.2, Creatinine 120, Na⁺ 134, K⁺ 4.2, Mg²⁺ 1.2, Ca²⁺ 2.3, Total Cholesterol 5.8, LDL-C 3.9, HDL-C 0.8, Triglyceride 2.4.HbA1c 8.8%Free T4 15.8 pmol/L. TSH 2.06 mIU/L.ECG: SR with PVC. Q waves over II,III,aVF. Poor R wave progression.Echocardiogram: LVEF 21%. Akinetic basal to apical inferolateral and inferior wall with hypokinetic the rest of LV. Presence of elliptical 46x75mm mass compressing right atrial and right basal ventricular wall with mixed echogenicity signal internally.
ECHO PLAX RWMA.mp4
ECHO A4C RWMA and mass.mp4
ECHO Subcostal echogenic mass.mp4

Diagnostic catheterization showed diffuse calcified coronary artery ectatic disease  with chronic total occlusion at distal LAD and proximal RCA. There is subtotal occlusion at the mid LCx with diffusely ectatic high OM1 disease.
ANGIO LAD RAO32 CRA24.mp4
ANGIO LCx CAU24.mp4
ANGIO RCA LAO44 CRA13.mp4

Further multimodality imaging were carried out to evaluate the pericardial mass and determine myocardial viability prior to revascularisation. Cardiac MRI showed a tubular mass under the pericardium adjacent to the right atrioventricular groove with internal heterogenous signal (Fig1a). Late gadolinium image showed transmural subendocardial enhancement of inferoseptal, inferolateral and inferior wall indicating non-viable RCA territories (Fig 1b,c). CT Coronary angiography showed a hypodense tubular mass measuring 10.3x6.6x4.5 cm adjacent to the right atrioventricular groove with coarse wall calcifications (Fig 2a). The superior margin of the mass communicates with the proximal RCA where it is patent but immediately thrombosed prior to its communication with the mass (Fig 2b). The inferior margin of the mass communicates with thrombosed and calcified distal RCA (Fig 2c). There is another smaller hypodense lesion with wall calcification measuring 1.7x2.0x1.9cm just after high OM1 branch which communicates with proximal and distal Lcx (Fig 2d). CT Aortography showed infrarenal fusiform abdominal aortic aneurysm (AAA) with mural thrombus measuring 5.6x6.1x12.7cm extending into iliac bifurcation (Fig 3a-d). Resection of giant CAA with CABG for the patient were discussed in heart team meeting but presence of concurrent AAA, non-viable RCA makes surgical option unsuitable. Patient was treated with anticoagulation and HFrEF guideline directed medical therapy for ischemic cardiomyopathy.

CT Coronary Angiography.mp4

Coronary artery aneurysms (CAA) are termed giant when the diameter exceeds the reference vessel diameter by more than 4 times. Atherosclerosis is the commonest cause of CAA in adults, whereas Kawasaki disease is responsible in pediatric population. RCA is the most affected artery (40%) followed by LAD (32%), LCx and LM being the least. This case demonstrated the usefulness of multiple imaging modalities in diagnosis and management of CAA. CT coronary angiography allows accurate evaluation of the aneurysm size and relation to other heart structures, degree of thrombus and calcification complementing the pitfall of endoluminal view from coronary catheterization alone.