LAD occlusion – acute or chronic?

Laurian Copel, MD

Department of Radiology, Shamir (Assaf Harofeh) Medical Center, Tzrifin, Israel

A 62-year-old male patient, suffering from progressive chest pain, general weakness and dyspnea for the past 3 weeks, was admitted to the hospital. On physical exam, the patient was dyspneic, sweating, with peripheral cyanosis and signs of pulmonary congestion. His risk factors of ischemic heart disease (IHD) include hypertension and dyslipidemia. Upon admission, he had sinus tachycardia with 120 bpm, a blood pressure of 170/110 mmHg, oxygen saturation of 87% and a Troponin value of 1.43 ngr/mL. An ECG exam showed an elevated ST on the anterolateral wall with large Q waves (V1 – V6). An echocardiography exam revealed hypokinesia of the anterolateral wall of the left ventricle (LV), with an ejection fraction (EF) of 20%. An intra-mural hematoma or intra-ventricular thrombi was suspected due to the appearance of an apical filling defect adhered to the wall. The clinical workup suggested a recent myocardial infarction. A coronary CT angiography (cCTA) was then performed to evaluate the coronaries and to rule out an intra-mural hematoma of the myocardium.
CT images showed a right coronary artery (RCA) dominant system. A total occlusion of the left anterior descending artery (LAD) was revealed at the site of the first diagonal branch, with multiple calcified plaques in the occluded segment and no contrast in the distal lumen. The antero-septal wall, mid- and distal lateral wall, as well as the periapical region of the LV were hypo-enhanced, demonstrating contrast perfusion defects. The LV wall thickness was preserved. Multiple calcified and non-calcified plaques were shown in the proximal and mid segment of the RCA, causing no significant stenosis. No signs of an intra-mural hematoma of the myocardium were seen. A filling defect was noticed adhered to the anterior wall of the LV, consistent with LV thrombi. Multiple triangular filling defects in the peripheral spleen were shown in an immediate follow-up CT scan of the upper abdomen, suggesting multiple infarcts. A subacute or chronic LAD occlusion was diagnosed and, after a team consultation, it was decided not to perform an interventional coronary angioplasty.
MPR, MIP and cVRT images show a LAD occlusion with multiple calcified plaques in the occluded segment and no contrast in the distal lumen. Multiple calcified and non-calcified plaques are shown in the proximal and mid segments of the RCA, causing no significant stenosis.
Courtesy of Department of Radiology, Shamir (Assaf Harofeh) Medical Center, Tzrifin, Israel
Fig. 1: MPR (Figs. 1a and 1b). MIP (Fig. 1c) and cVRT (Figs. 1d and 1e) images show a LAD occlusion (arrows) with multiple calcified plaques in the occluded segment and no contrast in the distal lumen. Multiple calcified (arrowheads) and non-calcified (dotted arrows) plaques are shown in the proximal and mid segments of the RCA (Fig. 1b), causing no significant stenosis.
An axial image using a narrow window setting shows the hypo-enhanced area of the anterior wall and the septum compared to the normal area of the LV wall. A hybrid view, containing the coronary tree and myocardial enhancement, as well as an ACC 17 regions enhancement pie chart show hypo enhancement of the entire antero-septal wall, lateral mid- and distal segments and the periapical region, demonstrating contrast perfusion defects.
Courtesy of Department of Radiology, Shamir (Assaf Harofeh) Medical Center, Tzrifin, Israel
Fig. 2: An axial image using a narrow window setting (Fig. 2a) shows the hypo-enhanced area of the anterior wall and the septum (arrows) compared to the normal area (arrowheads) of the LV wall. A hybrid view (Fig. 2b), containing the coronary tree and myocardial enhancement, as well as an ACC 17 regions enhancement pie chart (Fig. 2c) show hypo enhancement of the entire antero-septal wall (highlighted in blue), lateral mid- and distal segments and the periapical region, demonstrating contrast perfusion defects.
A filling defect is shown adhered to the anterior wall of the LV, consistent with LV thrombi. An immediate follow-up CT scan shows multiple triangular filling defects in the peripheral spleen, suggesting multiple infarcts.
Courtesy of Department of Radiology, Shamir (Assaf Harofeh) Medical Center, Tzrifin, Israel
Fig. 3: A filling defect (arrow) is shown adhered to the anterior wall of the LV (Fig. 3a), consistent with LV thrombi. An immediate follow-up CT scan (Fig. 3b) shows multiple triangular filling defects (arrowheads) in the peripheral spleen, suggesting multiple infarcts.
The distinction between acute and chronic coronary occlusion has particular importance for the management of patients presenting with acute chest pain.[1] cCTA has the potential to demonstrate the characteristic features for differential diagnosis. The challenges presented in this case are three fold – the patient is dyspneic and unable to comply with breathing instructions; he has a higher and irregular heart rate varying between 68 and 176 bpm with multiple atrial premature beats (APBs) and there is no time for beta blocker administration in such a stat examination. A retrospective ECG gated spiral scanning was performed with pre-programed “Mindose Auto” to reduce the radiation exposure. The system identifies the “Best diastole” (at 63%) and the “Best systole” (at 31%) phase intelligently and reconstructs the images in each phase automatically. Demonstration and understanding of the coronary anatomy can be facilitated by cinematic volume rendering technique (cVRT). A hybrid view of the coronaries and the ventricular wall enhancement allow a three-dimensional display of the LAD occlusion and the corresponding myocardial infarct. We are confident that optimal image quality can be achieved even with irregular and higher heart rates.

Scanner

Scan area

Heart

Scan mode

Retrospective ECG gated spiral scan

Scan length

159.3 mm

Scan direction

Cranio-caudal

Scan time

3 s

Tube voltage

110 kV

Effective mAs

289 mAs

Dose modulation

CARE Dose4D

CTDIvol

35.6 mGy

DLP

646 mGy*cm

Rotation time

0.28 s

Pitch

0.33

Slice collimation

128 x 0.6 mm

Slice width

0.6 mm

Reconstruction increment

0.3 mm

Reconstruction kernel

I26f

Heart rate

91 – 96 bpm

Contrast

350 mg/mL

Volume

90 mL + 25 mL saline

Flow rate

5 mL/s

Start delay

Bolus tracking with 100 HU at the ascending aorta + 10 s