Abnormalities in the function of arteries and small blood vessels may represent a key component of transthyretin amyloid cardiomyopathy (ATTR-CM) pathology and a potential therapeutic target, according to a recently published study in the Archives of Cardiovascular Diseases.
Most clinical manifestations of ATTR-CM are a direct consequence of the heart muscle becoming stiff due to the accumulation of amyloid deposits. Rigid cardiac walls impact how blood moves into the heart, which in turn leads to decreased cardiac output that eventually results in symptoms of heart failure, such as shortness of breath.
However, ATTR-CM can also affect the normal function of arteries in several ways, with important clinical implications.
Amyloid deposits in coronary arteries can cause ischemia
Ischemia refers to reduced blood supply to a specific organ. Sustained ischemia can result in permanent loss of function. Heart attacks and strokes are examples of prolonged ischemia leading to tissue death (necrosis). Several studies have shown that amyloid infiltration in the coronary arteries impairs their ability to expand, which can cause cardiac ischemia under certain conditions.
Amyloid deposits in pulmonary arteries can cause pulmonary hypertension
The loss of elasticity caused by amyloid deposits in the pulmonary arteries can lead to increased pulmonary arterial pressure. Pulmonary hypertension is associated with right heart failure, shortness of breath, exercise intolerance and fluid accumulation (edema). All of these factors contribute to reduced quality of life and increased mortality.
Read more about ATTR-CM signs and symptoms
ATTR-CM may cause eyesight abnormalities
The microscopic network of small blood vessels responsible for delivering oxygen to tissues and removing waste products is known as the microcirculation. Evidence suggests that amyloid infiltration may also affect retinal microcirculation, potentially resulting in visual impairment.
ATTR-CM and the metaboreflex
Arteries in the body dilate and contract in response to stimuli such as exercise. During physical activity, the body releases certain chemicals that normally interact with small blood vessels, causing them to contract appropriately. This mechanism is exaggerated in patients with ATTR-CM; such excessive contraction can lead to tissue ischemia during exercise.
Therapeutic implications of vascular abnormalities in ATTR-CM
As impaired dilation and excessive vasoconstriction contribute to the pathophysiology of ATTR-CM, some researchers hypothesize that vasodilating medications may have beneficial effects in these patients. However, further research in this area is needed.
“Whereas cardiac involvement determines prognosis in cardiac amyloidosis, vascular involvement is common and may contribute to the impaired cardiovascular profile observed in these patients,” the authors concluded.
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