Transthyretin Amyloid Cardiomyopathy: Impact of Transthyretin Amyloid Deposition in Myocardium on Cardiac Morphology and Function

Figures

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  Figure 1. The figure shows the distribution of patient results according to the four geometries of the American Society of Echocardiography [23]: (A) concentric LVH, (B) eccentric LVH, (C) concentric LV remodeling, and (D) normal. LV, left ventricular; LVH, left ventricular hypertrophy; LVM, left ventricular mass; RWT, relative wall thickness.

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  Figure 2. Pathological features and their association with echocardiographic parameters in patients with ATTR-CM. Relationship between the percentage of TTR area and (A) percentage of non-cardiomyocyte area, (B) LVEF, (C) E/e’ (septal) ratio, and (D) RWT. Relationship between the portion of non-cardiomyocyte area and (E) LVEF, (F) E/e’ (septal) ratio, and (G) RWT. ATTR-CM, transthyretin amyloid cardiomyopathy; E/e’ (septal) ratio, early transmitral filling velocity (E)/peak early diastolic velocity of the septal mitral annulus (e’) ratio; LVEF, left ventricular ejection fraction; RWT, relative wall thickness; TTR, transthyretin.

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  Figure 3. The association between immunostaining of 8-hydroxy-2′-deoxyguanosine (8-OHdG) and echocardiographic parameters in patients with ATTR-CM. (A) Immunostaining for 8-OHdG, visualized by diaminobenzidine (brown). 8-OHdG was found to be expressed in cardiomyocyte nuclei (Arrowheads). The relationship between the percentage of 8-OHdG stained cardiomyocyte nuclei and (B) percentage of TTR area, (C) the percentage of non-cardiomyocyte area, (D) LVEF, (E) E/e’ (septal) ratio, and (F) RWT. ATTR-CM, transthyretin amyloid cardiomyopathy; E/e’ (septal) ratio, early transmitral filling velocity (E)/peak early diastolic velocity of the septal mitral annulus (e’) ratio; LVEF, left ventricular ejection fraction; RWT, relative wall thickness; TTR, transthyretin.

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  Figure 4. Schematic representation of the mechanism of cardiac dysfunction in ATTR-CM. In hearts displaying ATTR-CM, increased TTR amyloid deposition might be involved in the enlargement of the non-cardiomyocyte area, resulting in LV hypertrophy and LV diastolic dysfunction. Furthermore, the increased TTR amyloid deposition and subsequent enlargement of the non-cardiomyocyte area might lead to increased ROS accumulation, thus causing LV systolic dysfunction. ATTR-CM, transthyretin amyloid cardiomyopathy; LV, left ventricular; ROS, reactive oxygen species; TTR, transthyretin.