Korean J Radiol.  2019 Mar;20(3):333-351. 10.3348/kjr.2018.0280.

Assessment of Left Ventricular Myocardial Diseases with Cardiac Computed Tomography

Affiliations
  • 1Department of Radiology, Konkuk University Medical Center, Konkuk University School of Medicine, Seoul, Korea. ksm9723@yahoo.co.kr
  • 2Department of Radiology, Gangnam Severance Hospital, Yonsei University College of Medicine, Seoul, Korea.
  • 3Department of Radiology, Seoul National University Bundang Hospital, Seongnam, Korea.
  • 4Department of Radiology, Dongsan Medical Center, Keimyung University College of Medicine, Daegu, Korea.
  • 5Department of Radiology, Korea University Anam Hospital, Seoul, Korea.

Abstract

Rapid advances in cardiac computed tomography (CT) have enabled the characterization of left ventricular (LV) myocardial diseases based on LV anatomical morphology, function, density, and enhancement pattern. Global LV function and regional wall motion can be evaluated using multi-phasic cine CT images. CT myocardial perfusion imaging facilitates the identification of hemodynamically significant coronary artery disease. CT delayed-enhancement imaging is used to detect myocardial scar in myocardial infarction and to measure the extracellular volume fraction in non-ischemic cardiomyopathy. Multi-energy cardiac CT allows the mapping of iodine distribution in the myocardium. This review summarizes the current techniques of cardiac CT for LV myocardial assessment, highlights the key findings in various myocardial diseases, and presents future applications to complement echocardiography and cardiovascular magnetic resonance.

Keyword

Computed tomography; Myocardium; Myocardial perfusion imaging; Delayed enhancement

MeSH Terms

Cardiomyopathies*
Cicatrix
Complement System Proteins
Coronary Artery Disease
Echocardiography
Iodine
Myocardial Infarction
Myocardial Perfusion Imaging
Myocardium
Tomography, X-Ray Computed
Complement System Proteins
Iodine

Figure

  • Fig. 1 Anatomy of left ventricle. Three-chamber (A) and short-axis (B) MPR CCT images show mitral valve (short arrows), aortic valve (arrowheads), papillary muscles (thick arrows), and apical thinning (long arrow). Left ventricle is divided into three portions: inlet, apical, and outlet. Short-axis MPR image (B) is obtained at midventricular level. CCT = cardiac computed tomography, MPR = multiplanar reformat

  • Fig. 2 Changes in LV wall thickness during mid- and end-diastole. Wall thickness and chamber dimension of left ventricle need precise measurements, usually in end-diastole. Most CCT is performed in mid-diastole to evaluate coronary artery. Interpretation of LV wall thickness may be misleading in mid-diastole (A) compared with that in end-diastole (B). LV = left ventricular

  • Fig. 3 Infarct imaging using first pass and delayed-enhancement CCT in patient with acute MI in left circumflex territory. Short-axis MPR images of first pass (A) and delayed enhancement (B) show fixed subendocardial perfusion defect (arrows) and delayed transmural hyperenhancement (arrowheads) in mid-lateral LV wall. Curved MPR coronary CT angiography image (C) shows acute thrombotic occlusion (arrows) of proximal left circumflex artery. Subendocardial perfusion defect indicates microvascular occlusion and poor prognosis. MI = myocardial infarction

  • Fig. 4 Global and regional LV function assessment with CCT in 51-year-old man with previous MI. Precontrast CCT image (A) shows curvilinear fat deposition in subendocardium of LV myocardium (arrowheads). Short-axis MPR CCT images obtained during end-systole (B) and end-diastole (C) show akinesia, curvilinear fat deposition in subendocardium (arrowheads), and thinned myocardium (5 mm in thickness) in mid-anterior and anteroseptal LV wall (arrows). LV ejection fraction, end-diastolic, and end-systolic volumes were 57%, 137 mL, and 59 mL, respectively.

  • Fig. 5 Diagnostic approach based on LV wall thickness using CCT. AS = aortic stenosis, COA = coarctation of aorta, DCM = dilated cardiomyopathy, HCM = hypertrophic cardiomyopathy, IBSH = isolated basal septal hypertrophy, NCC = non-compaction cardiomyopathy

  • Fig. 6 IBSH of 67-year-old man with diabetes mellitus without hypertension. Three-chamber MPR CCT image shows focal hypertrophy of basal inter-ventricular septum (arrows) without hypertrophy elsewhere within myocardium in mid-diastole on LV outflow tract.

  • Fig. 7 HCM in 57-year-old man with chest pain. Short-axis MPR CCT images obtained during early (A) and delayed (B) contrast-enhancement phases show asymmetrical hypertrophy of mid anterior, anteroseptal, and anterolateral LV wall (A, arrows) in mid-diastole with multifocal mid-wall delayed enhancement (B, arrows).

  • Fig. 8 Cardiac sarcoidosis in 61-year-old woman with irregular cardiac rhythm and dyspnea. Short-axis MPR CCT images obtained during early (A) and delayed (B) contrast-enhancement phases show concentrically hypertrophied mid-LV wall in mid-diastole with diffuse transmural and mesocardial delayed enhancement (arrows). Delayed-enhancement CMR image (C) shows diffuse mesocardial enhancement in septum and multifocal patchy mesocardial enhancement in mid anterior, lateral, and inferior LV wall (arrows). Delayed-enhancement CMR is superior to delayed-enhancement CCT for differentiating patterns of delayed myocardial enhancement. CMR = cardiovascular magnetic resonance

  • Fig. 9 LV metastasis from lung cancer in 93-year-old man. Contrast-enhanced chest CT image (A) shows 13-mm lobulated nodule with heterogeneous enhancement in anterior segment of left lower lobe (arrow). Mid-diastolic short-axis MPR CCT image (B) shows large infiltrating mass with homogeneous hypoenhancement as focal hypertrophied mid inferoseptal and inferior LV wall (arrows).

  • Fig. 10 Severe aortic valve stenosis in 79-year-old man with chest discomfort and shortness of breath. Double oblique MPR image of aortic valve (A) shows thickened and calcified cusps (arrowheads) of tricuspid aortic valve with severely reduced opening (aortic valve area of 0.98 cm2) during early-systole. Short-axis MPR image (B) shows hypertrophied mid-LV wall, particularly asymmetric septal hypertrophy (arrows). Delayed-enhancement CCT image (C) shows extensive mesocardial delayed hyperenhancement in middle LV wall (arrows).

  • Fig. 11 Cardiac amyloidosis in 74-year-old male who presented with chest pain. Four-chamber MPR delayed enhancement image obtained during mid-diastole shows hypertrophy of LV myocardial wall and diffuse, concentric subendocardial and transmural enhancement (arrowheads) in LV myocardial wall. Case courtesy of HJ Lee, Yonsei University Severance Hospital.

  • Fig. 12 DCM in 63-year-old man. Four-chamber MPR image (A) obtained during end-diastole shows all cardiac chamber dilatation. Short-axis MPR CCT images obtained during end-systole (B) and end-diastole (C) show LV dilation, thinned myocardium (5 mm in thickness), and global severe hypokinesia. LV ejection fraction, end-diastolic, and end-systolic volumes were 12%, 137 mL, and 59 mL, respectively.

  • Fig. 13 NCC in 48-year-old woman with dyspnea and cough pain. End-diastolic short-axis MPR image shows increased thickness of noncompacted layer in anterior, lateral, and inferior segments of mid-LV wall with ratio of noncompacted (black arrow, 15 mm in thickness) to compacted myocardium (white line, 6 mm in thickness) > 2.3:1.

  • Fig. 14 LV aneurysm with intracavitary thrombus in 53-year-old man with chronic MI. Axial CCT image shows thin-walled apical aneurysm (arrowheads) and extensive intracavitary thrombus formation (arrows).

  • Fig. 15 LV pseudoaneurysm in 65-year-old man with stable angina. Two-chamber MPR CCT image shows LV inferior wall outpouching with relatively narrow neck (arrowheads), intracavitary thrombus (arrows), and multiple calcifications along its wall.

  • Fig. 16 LV crypt in 68-year-old man with HCM. End-diastolic (A) and end-systolic short-axis (B) MPR CCT images show sharp-edged disruption of normal compacted myocardium penetrating basal inferior LV wall (A, arrow) with near complete obliteration during end-systole (B, arrow).

  • Fig. 17 V diverticulum. Three-chamber MPR CCT image shows finger or hook-like pouch of entire LV myocardial wall (arrow) arising from LV apex in mid-diastole.

  • Fig. 18 Myocarditis in 69-year-old man with dyspnea for 10 days. Initial chest CT (A) shows hypoenhancement in apical to mid interventricular septum (arrows) with preserved myocardial thickness. Short-axis MPR CCT image (B) obtained 3 weeks later shows thinned myocardium at anterior, septal, and inferior segments of middle LV wall (arrows). Delayed-enhancement cardiac magnetic resonance image (C) obtained 5 weeks later shows transmural hyperenhancement at mid-anterior and septal LV wall and subendocardial hyperenhancement at middle inferior LV wall (arrows).

  • Fig. 19 Nonspecific myocardial fat in 51-year-old woman without cardiac symptoms. Axial precontrast CCT image shows fat (arrow) in LV apical septum.


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