It is well recognized that amyloid protein can infiltrate many regions of the body. This can include the peripheral nerves, the liver, kidney, spleen, the gastrointestinal tract, and most importantly the myocardium. The amyloid proteins that cause cardiomyopathy may come from genetically altered liver genes (transthyretin amyloid, ATTR) or from the bone marrow with malignant plasma cells (light chain amyloid, AL) generating the aberrant protein. These two types of amyloidosis cause significant damaging effects on both the myocardial cells as well as the conduction system of the heart. The resultant changes can produce dyspnea and exercise intolerance which is thought to be secondary to diastolic dysfunction and reduced stroke volume. This subclinical decompensation poses a significant problem for members of a care team as it often goes unrecognized. In the operating room patients are exposed to dramatic hemodynamic changes and may have difficult airways, autonomic dysfunction, and conduction abnormalities. Although the topic of amyloidosis is well described in cardiology literature, it is underdiagnosed. The purpose of this review is to describe some of the pathophysiology behind the principle proteins that cause cardiac amyloidosis and to comprehensively describe perioperative considerations for anesthesia providers.
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