A Long Path to Diagnosis

After finally discovering the source of his medical maladies, Walt Feigenson has made it his mission to educate others about transthyretin amyloid cardiomyopathy (ATTR-CM).  Update 11/16/22: The American Heart Association team is saddened to learn of Walt’s recent passing. His wife, Trudi, let us know he was so grateful for every opportunity he had to help others dealing with amyloidosis and loved his role helping raise awareness of the condition.

Solving complex problems is nothing new for Walt Feigenson, 73, who enjoyed a long career in technology before he retired in 2010.

But neither Feigenson, nor his doctors, knew what to make of a series of seemingly unrelated health problems that began in 2007, when he was diagnosed with congestive heart failure.

Over the next decade, he went on to develop a dizzying array of seemingly unrelated health problems, including carpal tunnel syndrome, a ruptured biceps tendon, lumbar spinal stenosis and a heart arrhythmia that required two ablations. 

“Imagine living through all this, without knowing why,” Feigenson said. “None of the doctors put it together.” Finally, after several emergency room visits and numerous surgeries, in 2019, Feigenson sought help at a heart failure clinic. Upon reviewing Feigenson’s case, the cardiologist determined his symptoms were caused by a condition called transthyretin amyloid cardiomyopathy.

ATTR-CM is caused by amyloid proteins that build up in the heart. The amyloid protein deposits cause the heart walls to become stiff, resulting in the inability of the left ventricle to properly relax and fill with blood and adequately squeeze to pump blood out of the heart. As the muscle thickens, it becomes difficult for blood to enter the ventricle – so it pumps less blood and leads to congestion in the lung, causing shortness of breath.

In its early stages, ATTR-CM is often mistaken for other types of heart failure. There are two types of ATTR-CM:

·       Affecting about 1 in 25 African Americans, the inherited form results from a mutation in the transthyretin gene, resulting in amyloid deposits in the organs and nerves. Not all individuals with this mutation develop symptoms of hereditary ATTR-CM. In this form, symptoms begin anywhere between the ages of 20 and 80.

·       The wild type is caused not by a genetic mutation but by changes that come with age. The symptoms of wild-type ATTR-CM usually start after age 65. Genetic testing revealed that Feigenson had the wild type.

“The smartest thing I ever did was dumb luck,” he said of his decision to seek help at the clinic. “Even though it’s a fatal disease, I felt tremendous relief when I was diagnosed.”

Today he takes medication for his condition. While he doesn’t have any hard feelings that his condition went undiagnosed for so long, Feigenson wants to raise awareness about ATTR-CM, which can be managed by a cardiologist.

In addition to sharing his story with anybody who will listen, Feigenson has made himself available for medical tests that might reveal more about his condition. “I’m trying to push the envelope,” he said. “Besides making my partner Trudi happy by making her laugh, my efforts are devoted toward making the world a better place for people with amyloidosis.