Senile cardiac amyloidosis

As early as 1850, Virchow discovered a deposit between tissue cells in the human body that, upon contact with iodine, showed a starch-like color reaction. Virchow called it amyloid substance (amyloid), and tissues in which this substance was deposited were called amyloid degeneration. It has now been proven that the so-called amyloid substance is actually a protein composed of different components. Therefore, it is more appropriate to call it amyloid protein. Systemic amyloidosis refers to amyloid deposition in various tissues and organs throughout the body, but some patients have deposition only locally; some of these patients may be in the early stage of systemic amyloidosis, with subsequent progression to amyloid deposition in other tissues or organs. Amyloidosis is relatively rare and occurs more often in men over 40 years of age, and less frequently in women. The clinical manifestations are extremely heterogeneous and are related to the type, the site of amyloid deposition, the properties of the amyloid protein, and the degree of damage to the affected organs. The commonly affected organs and tissues are the liver, kidneys, heart, blood vessels, skin, and bone marrow. Amyloidosis of the circulatory system is mainly due to amyloid deposition in the intercellular spaces of myocardial cells, together with amyloid deposition in the basement membrane of myocardial nutrient vessels, causing basement membrane thickening and narrowing of the vascular lumen. These factors lead to myocardial cell dysfunction. Clinical manifestations include arrhythmias, angina pectoris, congestive heart failure, and sudden death. Primary, systemic, senile, and TTR isoleucine-122 mutation types often involve cardiac involvement. Some patients may develop angina despite normal coronary angiography, possibly due to decreased coronary blood supply. The ECG may show a pseudo-myocardial infarction pattern. After intravenous injection of thallium-201 (201TL), the washout rate can be as high as 57%–61%. This examination can determine the survival of viable myocardial cells; the higher the washout rate, the fewer viable myocardial cells and the worse the cardiac function (assessed by echocardiography), with death often occurring within less than one year. AA-type amyloidosis can cause giant cell arteritis.