Cardiac amyloidosis
Updates to Case Attributes
Although there seems to be concentric left ventricular hypertrophy, this would be a misnomer as there is merely thickening of the LV wall due to amyloid deposition in the extracellular space. The myocardium itself is not hypertrophied. The amyloid results in a reduced capability of the heart to contract (restrictive pattern).
Also note that there is reduced signal intensity of the blood pool due to pooling of contrast in the enlarged extracellular space of the ventricular walls.
Cardiac amyloidosis carries a very poor prognosis.
- +<p>Although there seems to be concentric left ventricular hypertrophy, this would be a misnomer as there is merely thickening of the LV wall due to amyloid deposition in the extracellular space. The myocardium itself is not hypertrophied. The amyloid results in a reduced capability of the heart to contract (restrictive pattern). </p><p>Also note that there is reduced signal intensity of the blood pool due to pooling of contrast in the enlarged extracellular space of the ventricular walls.</p><p><a title="Cardiac amyloidosis" href="/articles/cardiac-amyloidosis">Cardiac amyloidosis</a> carries a very poor prognosis. </p>
Systems changed:
- Cardiac
Updates to Study Attributes
Patient characteristics:Length 184 cm, weight 77 kg, BSA 2,00 m²
Diameters:- LV: 46 mm- RV: 44 mm- Septum: 18 mm, lateral wall 10 mm, anterior wall 14 mm, inferior wall 13 mm
Functional analyses:Left ventricle:- EDV: 187 mL (94 mL/m²)- ESV: 75 mL (37 mL/m²)- SV: 113 mL (56 mL/m²)- EF: 60%- CO: 6.6 L/min (3.3 L/min/m²)
Right ventricle:- EDV: 170 mL (85 mL/m²)- ESV: 69 mL (34 mL/m²)- SV: 101 mL (51 mL/m²)- EF: 60%- CO: 5.9 L/min (3.0 L/min/m²)
Concentric hypertrophy of LV wall, most prominent septally. Enlarged atria. No signs of LV outflow tract obstruction or systolic anterior motion (SAM) of the mitral valve. Synchronous contraction of both ventricles. No focal wall motion abnormalities. No valvular insufficiencies. No signs of iron deposition (T2* value 23 ms).
On early and late enhancement series diffuse enhancement of the myocardium with concentric subendocardial apical and mid-ventricular ring enhancement in the late phase. There is also enhancement of papillary muscles, RV wall and both atria. Low signal intensity of the blood pool compared to myocardium. Pericardial effusion. Bilateral pleural effusion. Haemangioma in vertebral body T8.
Conclusion:Images in keeping with cardiac amyloidosis.
Image MRI (cine images) ( update )
Image MRI (cine images) ( update )
Image MRI (cine video) ( update )
Image MRI (cine images) ( update )
Image MRI (cine images) ( update )
Image MRI (cine video) ( update )
Image MRI (cine images) ( update )
Image MRI (viability) ( update )
Image MRI (viabilty) ( update )
Image MRI (late viability) ( update )
Image MRI (real time) ( update )
Image MRI (LookLocker) ( update )
Image MRI (early viability) ( update )
Image MRI (BB SPIR C+) ( update )
Image MRI (T2 BB SPIR) ( update )
Image MRI (T2 BB SPIR) ( update )
Image MRI (cine images) ( update )
Image MRI (cine images) ( update )
Image MRI (cine images) ( update )
Image MRI (cine images) ( update )
Image MRI (BB SPIR C+) ( update )
Image MRI (LookLocker) ( update )
Image MRI (viabilty) ( update )
Image MRI (early viability) ( update )
Image MRI (late viability) ( update )
Image 1 MRI (cine video) ( create )
Image 2 MRI (cine images) ( create )
Image 3 MRI (cine video) ( create )
Image 4 MRI (cine images) ( create )
Image 5 MRI (real time) ( create )
Image 6 MRI (cine images) ( create )
Image 7 MRI (cine images) ( create )
Image 8 MRI (cine images) ( create )
Image 9 MRI (BB SPIR C+) ( create )
Image 10 MRI (LookLocker) ( create )
Image 11 MRI (viability) ( create )
Image 12 MRI (viabilty) ( create )
Image 13 MRI (early viability) ( create )
Image 14 MRI (late viability) ( create )
Image 15 MRI (T2 BB SPIR) ( create )
Unable to process the form. Check for errors and try again.