Transthyretin-mediated amyloid cardiomyopathy (ATTR-CM) is a progressive, irreversible, and debilitating disease affecting an estimated 240,000 people worldwide1

ATTR-CM is the result of a protein called transthyretin (TTR) that misfolds into clusters called amyloid deposits. These amyloid deposits build up in the cardiac muscle, causing debilitating heart damage and resulting in progressive heart failure—this damage can be disabling, and life-threatening.1

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These amyloid deposits build up in the heart causing the heart wall to stiffen, resulting in progressing heart damage.

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Hereditary ATTR-CM (hATTR-CM) is the result of an inherited genetic mutation that causes a protein called transthyretin (TTR). hATTR-CM accounts for roughly 80% of all hereditary ATTR cases, with symptoms appearing as early as age 20, or as late as age 80.

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Wild-type ATTR-CM (wtATTR-CM) develops sporadically, meaning there is no genetic TTR mutation passed on through families. Symptoms for wtATTR-CM, which may initially be mild, typically emerge after age 65.1

What can you do?

The CARDIO-TTRansform study is currently enrolling to evaluate the safety and effectiveness of an investigational antisense drug for people living with hereditary and wild-type ATTR-CM.

  1. What is Transthyretin Amyloid Cardiomyopathy (ATTR-CM)? American Heart Association. 2019. Accessed October 31, 2019.