Cerebral amyloid angiopathy-related cardiac injury: Focus on cardiac cell death

Cerebral amyloid angiopathy (CAA) is a kind of disease in which amyloid beta (A beta) and other amyloid protein deposits in the cerebral cortex and the small blood vessels of the brain, causing cerebrovascular and brain parenchymal damage. CAA patients are often accompanied by cardiac injury, involving A beta, tau and transthyroxine amyloid (ATTR). A beta is the main injury factor of CAA, which can accelerate the formation of coronary artery atherosclerosis, aortic valve osteogenesis calcification and cardiomyocytes basophilic degeneration. In the early stage of CAA (pre-stroke), the accompanying locus coeruleus (LC) amyloidosis, vasculitis and circulating A beta will induce first hit to the heart. When the CAA progresses to an advanced stage and causes a cerebral hemorrhage, the hemorrhage leads to autonomic nervous function disturbance, catecholamine surges, and systemic inflammation reaction, which can deal the second hit to the heart. Based on the brain-heart axis, CAA and its associated cardiac injury can create a vicious cycle that accelerates the progression of each other.

Automated summary

Cerebral amyloid angiopathy (CAA) is a disease characterized by the deposition of amyloid beta (A beta) and other amyloid proteins in the brain's blood vessels, leading to cerebrovascular and brain damage. CAA is often associated with cardiac injury, involving A beta, tau, and transthyroxine amyloid (ATTR). A beta acts as the main damaging factor, causing coronary artery atherosclerosis, aortic valve calcification, and cardiomyocyte degeneration. The progression of CAA can further impact the heart through amyloidosis, inflammation, and cerebral hemorrhage. The interaction between CAA and cardiac injury creates a vicious cycle that accelerates the progression of both conditions.