Figure 1 Comparison of In Vivo CE-MRI and Histological Sections in LVNC
(A) Contrast-enhanced magnetic resonance imaging (CE-MRI) in short-axis view demonstrated that diffuse delayed enhancement occurred in the interventricular septum, left ventricular free wall, and the trabecular meshwork region of the left ventricle. (B) The histological section in isolated left ventricular noncompaction (LVNC) from the apical segment of the left ventricle demonstrated that fibrosis presented within trabeculations (arrow) as well as in compacted myocardium (arrowhead). In addition, mucoid degeneration (asterisk) was identified in endocardium. (Masson's Trichrome stain, original magnification x1).
J Am Coll Cardiol, 2011; 58:311-312,
© 2011 by the American College of Cardiology Foundation
RESEARCH CORRESPONDENCE
Histopathological Features of Delayed Enhancement Cardiovascular Magnetic Resonance in Isolated Left Ventricular Noncompaction
Yan Chaowu, PhD, MD*, Li Li, PhD and Zhao Shihua, PhD, MD
Contrast-enhanced magnetic resonance imaging (CE-MRI) is an important imaging modality for the evaluation of isolated left ventricular noncompaction (LVNC). The delayed gadolinium enhancement has been identified in both compacted and noncompacted myocardium, and it may correlate with the clinical severity of LVNC (1–3). However, little is known about the histological basis of myocardial delayed enhancement in LVNC patients, especially in the noncompacted myocardium. In this study, we made a comparison between the myocardial delayed enhancement and histological findings in a patient with LVNC who underwent heart transplantation.
A 27-year-old man was admitted with exertional dyspnea. Chest roentgenogram showed cardiomegaly with pulmonary venous congestion, and the cardiothoracic ratio was 72%. The LVNC was diagnosed by echocardiography, and the ratio of the noncompacted to compacted myocardium was 3.2. The left ventricular end-diastolic dimension was 63 mm, and left ventricular ejection fraction was 18%. Contrast-enhanced MRI was performed, and deep intertrabecular recesses presented in the apical and lateral wall of the left ventricle. The near-transmural delayed enhancement occurred in the interventricular septum, and diffuse enhancement presented in the free wall and the trabecular meshwork region of the left ventricle. In addition, CE-MRI detected the left ventricular thrombus and pericardial and pleural effusions. One week later, informed consent was obtained, and heart transplantation was carried out. The pathological findings of the explanted heart were compared with the previous in vivo CE-MRI (Fig. 1 ). In the compacted myocardium with delayed enhancement, extensive fibrosis was identified and predominantly localized in the mid-myocardial wall. The collagen volume fraction was 27.9% in the histological section, which came from the region of near-transmural delayed enhancement in the interventricular septum. In the noncompacted myocardium with delayed enhancement (the trabecular meshwork region of left ventricle), however, 2 types of pathological findings presented: mucoid degeneration in the endocardium and fibrosis within the trabeculations. The collagen volume fraction of trabeculations was 37.4% in the left ventricular apex and 32.8% in the lateral wall of the left ventricle. In the myocardial regions without delayed enhancement, there was no significant increase in the amount of fibrosis. The epicardial coronary arteries were normal in the patient.
The results of this study demonstrated that fibrosis was identified histologically in both compacted and noncompacted myocardium. In the compacted myocardium, the regions of delayed enhancement corresponded well with the focally increased fibrosis. Furthermore, CE-MRI may overestimate the degree of fibrosis replacement, as we found in the interventricular septum. In the noncompacted myocardium, delayed enhancement was associated with fibrosis within the trabeculations as well as mucoid degeneration in the endocardium.
Previous studies have showed that myocardial delayed enhancement presented in patients with LVNC, and it has been proposed that the regions of delayed enhancement probably reflected the regions of increased myocardial fibrosis (1,2). Pathological analysis also demonstrated that fibrosis occurred in the left ventricular myocardium of LVNC patients (4,5). However, further research was lacking to assess the histopathological correlation of myocardial delayed enhancement in LVNC. In the present study, our findings show that the fibrosis is the histological basis in the delayed enhancement of compacted myocardium; however, it is still unknown which mechanism plays the leading role in the delayed enhancement of noncompacted myocardium.
© 2011 by the American College of Cardiology Foundation
RESEARCH CORRESPONDENCE
Histopathological Features of Delayed Enhancement Cardiovascular Magnetic Resonance in Isolated Left Ventricular Noncompaction
Yan Chaowu, PhD, MD*, Li Li, PhD and Zhao Shihua, PhD, MD
Contrast-enhanced magnetic resonance imaging (CE-MRI) is an important imaging modality for the evaluation of isolated left ventricular noncompaction (LVNC). The delayed gadolinium enhancement has been identified in both compacted and noncompacted myocardium, and it may correlate with the clinical severity of LVNC (1–3). However, little is known about the histological basis of myocardial delayed enhancement in LVNC patients, especially in the noncompacted myocardium. In this study, we made a comparison between the myocardial delayed enhancement and histological findings in a patient with LVNC who underwent heart transplantation.
A 27-year-old man was admitted with exertional dyspnea. Chest roentgenogram showed cardiomegaly with pulmonary venous congestion, and the cardiothoracic ratio was 72%. The LVNC was diagnosed by echocardiography, and the ratio of the noncompacted to compacted myocardium was 3.2. The left ventricular end-diastolic dimension was 63 mm, and left ventricular ejection fraction was 18%. Contrast-enhanced MRI was performed, and deep intertrabecular recesses presented in the apical and lateral wall of the left ventricle. The near-transmural delayed enhancement occurred in the interventricular septum, and diffuse enhancement presented in the free wall and the trabecular meshwork region of the left ventricle. In addition, CE-MRI detected the left ventricular thrombus and pericardial and pleural effusions. One week later, informed consent was obtained, and heart transplantation was carried out. The pathological findings of the explanted heart were compared with the previous in vivo CE-MRI (Fig. 1 ). In the compacted myocardium with delayed enhancement, extensive fibrosis was identified and predominantly localized in the mid-myocardial wall. The collagen volume fraction was 27.9% in the histological section, which came from the region of near-transmural delayed enhancement in the interventricular septum. In the noncompacted myocardium with delayed enhancement (the trabecular meshwork region of left ventricle), however, 2 types of pathological findings presented: mucoid degeneration in the endocardium and fibrosis within the trabeculations. The collagen volume fraction of trabeculations was 37.4% in the left ventricular apex and 32.8% in the lateral wall of the left ventricle. In the myocardial regions without delayed enhancement, there was no significant increase in the amount of fibrosis. The epicardial coronary arteries were normal in the patient.
The results of this study demonstrated that fibrosis was identified histologically in both compacted and noncompacted myocardium. In the compacted myocardium, the regions of delayed enhancement corresponded well with the focally increased fibrosis. Furthermore, CE-MRI may overestimate the degree of fibrosis replacement, as we found in the interventricular septum. In the noncompacted myocardium, delayed enhancement was associated with fibrosis within the trabeculations as well as mucoid degeneration in the endocardium.
Previous studies have showed that myocardial delayed enhancement presented in patients with LVNC, and it has been proposed that the regions of delayed enhancement probably reflected the regions of increased myocardial fibrosis (1,2). Pathological analysis also demonstrated that fibrosis occurred in the left ventricular myocardium of LVNC patients (4,5). However, further research was lacking to assess the histopathological correlation of myocardial delayed enhancement in LVNC. In the present study, our findings show that the fibrosis is the histological basis in the delayed enhancement of compacted myocardium; however, it is still unknown which mechanism plays the leading role in the delayed enhancement of noncompacted myocardium.
