Key result
In the senescence accelerated mouse (SAM) model, the incidence of senile cardiac amyloidosis was 46.0%, with amyloid deposition prominent around myocardial fibers and vascular walls.
No immediate clinical implications from SAM mouse data; leaves open human validation of age-related cardiac amyloidosis.
The characteristics of the senescence accelerated mouse (SAM), a new murine model for accelerated senescence, are early senescence and a high incidence of senile amyloidosis. This study was performed to clarify histopathologically the details of senile cardiac amyloidosis in SAM, and the incidence of amyloidosis in the heart of SAM (-P) was 46.0% (1+: 22.0; 2+: 16.0; 3+: 8.0%). Amyloid infiltrated the ventricular walls, interventricular septum, atrial walls and interatrial septum. Amyloid deposition was prominent around the myocardial fibers and in the vascular walls. Amyloid involvement was greater in the veins than in the arteries. Senile cardiac amyloidosis of SAM was mild or moderate and not severe, in general. The age dependency of amyloidosis incidence of the heart was confirmed. The heart/body weight ratio tended to parallel the grade of cardiac amyloidosis. SAM often had complications such as abscess, lymphoma, skin ulcer, etc. The incidence of amyloidosis was higher in SAM with these complications than in SAM without them. The complications seemed to promote the progress of cardiac amyloidosis and to superimpose secondary amyloidosis. In SAM senile cardiac amyloidosis is less frequent than renal amyloidosis (64.4%) or hepatic amyloidosis (63.3%).
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Hiromichi Ogawa (1988) studied Senile cardiac amyloidosis. Senescence accelerated mouse (SAM) model was evaluated on Incidence of senile cardiac amyloidosis. In the senescence accelerated mouse (SAM) model, the incidence of senile cardiac amyloidosis was 46.0%, with amyloid deposition prominent around myocardial fibers and vascular walls.
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