Cardiac amyloidosis due to transthyretin (ATTR) protein is a common cause of cardiomyopathy. ATTR amyloidosis results from misfolded TTR protein deposits in the heart, leading to heart failure, conduction block, and arrhythmias. The TTR protein is synthesized mainly by the liver and transports thyroid hormone and vitamin A. Misfolding leads to amyloid fibril formation, which deposits in the heart and other tissues. ATTR can be wild-type (normal TTR sequence) or variant (abnormal TTR sequence). Wild-type ATTR primarily causes cardiomyopathy, while variant ATTR can also cause polyneuropathy. Approximately 50,000 to 150,000 people in the US have ATTR-related heart failure. Without treatment, survival is about 5 years. Tafamidis, a TTR stabilizer, reduces mortality and hospitalizations in ATTR cardiomyopathy. It is the only currently approved therapy for ATTR amyloidosis. Other treatments include loop diuretics for fluid overload and management of arrhythmias. Diagnosis involves imaging and blood tests to exclude other types of amyloidosis. ATTR amyloidosis is more common in older individuals and is associated with specific genetic variants. Treatment options include TTR stabilizers and therapies that suppress TTR production. Prognosis varies based on the variant and treatment response. This review summarizes the clinical presentation, diagnosis, and treatment of ATTR cardiomyopathy.Cardiac amyloidosis due to transthyretin (ATTR) protein is a common cause of cardiomyopathy. ATTR amyloidosis results from misfolded TTR protein deposits in the heart, leading to heart failure, conduction block, and arrhythmias. The TTR protein is synthesized mainly by the liver and transports thyroid hormone and vitamin A. Misfolding leads to amyloid fibril formation, which deposits in the heart and other tissues. ATTR can be wild-type (normal TTR sequence) or variant (abnormal TTR sequence). Wild-type ATTR primarily causes cardiomyopathy, while variant ATTR can also cause polyneuropathy. Approximately 50,000 to 150,000 people in the US have ATTR-related heart failure. Without treatment, survival is about 5 years. Tafamidis, a TTR stabilizer, reduces mortality and hospitalizations in ATTR cardiomyopathy. It is the only currently approved therapy for ATTR amyloidosis. Other treatments include loop diuretics for fluid overload and management of arrhythmias. Diagnosis involves imaging and blood tests to exclude other types of amyloidosis. ATTR amyloidosis is more common in older individuals and is associated with specific genetic variants. Treatment options include TTR stabilizers and therapies that suppress TTR production. Prognosis varies based on the variant and treatment response. This review summarizes the clinical presentation, diagnosis, and treatment of ATTR cardiomyopathy.