Feature Article
By David M. Lavine, MD
This article was originally published in the July/August 2026 issue of Tarrant County Physician.
This article is about a personal medical journey which involves a four-year-long search to solve a problem which I hope will be an inspiration to those who read it.
The title comes from a grand rounds lecture given by Dr. Justin Grodin, a faculty member in advanced heart failure and cardiac amyloidosis at UT Southwestern.1 As the old saying goes, “When you hear hoofbeats you think of horses, but occasionally there is a zebra in the herd.” Well, my zebra is cardiac amyloidosis. When I was in medical school, this disease was hardly mentioned. Most doctors knew little to nothing about it.
My Reason
My reason for this article is personal and apparent. I could give you the detailed particulars of this disease, but suffice it to say, amyloidosis is caused by a protein misfolding/malformation which, in transthyretin amyloid cardiomyopathy (ATTR-CM), originates in the liver. The resulting amyloid infiltrates the myocardium, resulting in a thickening and stiffening of the heart muscle. The big problem is that the amyloid fibrils do their damage by concentrically thickening the muscle. The chest X-ray will not show cardiac hypertrophy, but the heart capacity is reduced, resulting in decreasing cardiac efficiency.
The most affected chamber is the left ventricle. Amyloid deposits make the walls stiff, preventing the chamber from relaxing and filling properly between beats. The next chamber most affected by the amyloid is the right ventricle impairing the right side’s ability to pump blood effectively. Because the ventricles become too stiff to accommodate blood entering the heart, pressure increases, causing the atria (the upper collecting chambers) to stretch and enlarge. This chamber enlargement leads to electrical disruption and arrhythmias such as atrial fibrillation. The more advanced the disease, the worse the outlook. The quicker the diagnosis, the more favorable the outcome.
The Journey to a Heart Biopsy
In 2021, I was beginning to have a general sense of malaise manifested by persistent fatigue and an ever-increasing intolerance to inclines. Needless to say, these symptoms were problematic. I had just retired and was looking forward to some active years. Yes, I was getting some answers for my symptoms piecemeal, but I felt a great urgency to complete this puzzle. With my medical background as an asset, I started a battery of tests. My PCP ordered an NT-proBNP biomarker. This measures the stress on your heart, which secretes a specific protein (NT-proBNP), especially during ischemic events. Normal is less than 450—mine was 1,402. What little information I could glean from the literature was sparse and, to say the least, gloomy. Survival rates were dismal. It made NO sense. I was a physically active person day in and day out.
My Quest
My pilgrimage to find the holy grail had begun. All my available sources of information created more questions than answers. As my quest for information grew, so did my sources. I even spoke with a past president of the American College of Cardiology, via a link with a medical classmate referral. A plethora of tests revealed nothing outstanding except ever-rising biomarker numbers. A follow-up Troponin level was 253, when normal is less than 47. Troponin also measures the stress of the heart following a sentinel event, but, I had never had an MI or outright cardiac failure; I was just feeling puny with an ever-decreasing activity level.
Corralling the Zebra
With no definitive answers and a situation that was getting worse, I pursued every medical connection I had. Nothing struck home, nothing was obvious, but persistence is my mantra. In Fort Worth and Charlottesville, Virginia, brilliant minds saw the discrepancies, but in over four years, found no good explanation. Even “Dr. Google” was stumped.
I Hear the Hoofbeats Coming
But the elusive mystery remained. I heard the hoofbeats and knew there was a zebra, but where was it? I had navigated a lot of “ifs and maybes” but found nothing definitive. No one could seem to explain the obvious incongruence of a 75-year-old active male and unexplained elevated biomarkers.
I Found the Zebra!
A new thought came from an old friend and internist. He had started on this journey with me in 2021. We had perused every pertinent fact and lab. After three years of continual dialogue, he queried about the possibility of my having cardiac amyloidosis. Because it was such a rare disease, 1:100,000, it seemed highly unlikely. But I wasn’t giving up . . . I was in the battle of my life. So on my next visit to my Fort Worth cardiologist, I asked if I could get a comparison echocardiogram. My last one in April 2025 was like the five previous ones. No zebras. I did ask him about the “rare” possibility of cardiac amyloidosis. His answer was definitive: “You don’t have cardiac amyloidosis.”
Despite this, in August of 2025, I got my echo report: “amyloid myocardiopathy highly suspected.”
Pulling off the Stripes One by One
Now I consider myself to be a self-educated doctor of a disease that was once considered very rare. ATTR-CM is now becoming “the disease of the month.” Jack Nicklaus, the G.O.A.T. of golf, was recently diagnosed with the same disease. He has become a spokesperson for the drug Vyndamax, the same one I am on. I’m sure many people remain to be included in this group. Thus the goal of this article . . . to educate my peers.
Epilogue
As for me, I have accumulated a fine team of super specialists from Fort Worth to Charlottesville, Virginia and UTSW, Dallas. There is NO Way I am ever letting this transitioning zebra out of my sight—it took too long to find.
I am presently enrolled in Dr. Grodin’s clinic at UTSW and have agreed to participate in an intramural study that he is directing. Hopefully my numbers will help others. Also, I will continue to take super drug Vyndamax, which is a thyretein stabilizer. I also hope to enter a depleter study (Cleopattra), utilizing new technology, later this year. Research is abounding for this disease.
Last Thoughts—The Immortal Zebra May Not Be a Zebra After All
I shudder to think what might have been, had I not been so proactive, i.e., pushy. Everything I have researched is so “real time” that it is truly hard to separate the disease as part of the landscape of aging or a distortion/malformation of that landscape. If it is the latter, then hopefully growing old will be more unfettered with a diagnosis and an effective way to treat this disease.2
The Whole is Greater Than the Sum of its Parts
Once I had the results and diagnosis, I knew what was making me sick. I had caught the zebra, but as the name of this article implies, this cardiac amyloidosis may not be a zebra after all. As it turns out, I was the “poster child” for ATTR-CM wild type. This includes a plethora of musculoskeletal problems inherent in amyloid migration and infiltration. This can start with carpal tunnel syndrome (I had four procedures for this syndrome. The first release, which was endoscopic, was 20 years ago. I had a repeated open procedure, due to the same carpal tunnel symptoms, 10 years ago, obviously from continued amyloid infiltration.), ruptured bicep tendons, (I had two) and atrial fibrillation, which is resistant to cardioversion and ablation. This ultimately ended up with a pacemaker placement a year ago.
Finally, a heart biopsy in October of 2025 confirmed it. I would encourage you to look at the varied and sundry well-known end-organ systems of this not-so-rare disease. It may start with a simple carpal tunnel syndrome and work its way through the musculoskeletal complex and end with a definitive myocardial biopsy.
Early diagnoses, to confirm or negate, is as simple as getting a Congo red stain after a carpal tunnel, trigger finger, or residual cartilage disc diagnosis, as they are a few of the related conditions. A blood serum electrophoresis (SPEP) study is also important, or a 24-hour urine collection if you are considering a differential diagnosis.
My medical background (plastic surgery) afforded me contacts in the medical community. There is no doubt that I am here today and writing this article because of my medical connections. I hope and pray my education has been an enlightenment to you.
Please remember our Hippocratic Oath: “I will use my power to help the sick, to the best of my ability.” The life you save will be one grateful patient. It may even be your own.
References:
- Justin Grodin, Cardiac Amyloidosis: The Zebra Is Losing Its Spots, presentation, February 1, 2019.
- I gathered this information from a number of personal communications, including those with the Amyloid Cardiology Specialist Department of Cardiology, The University of Virginia Medical Center; Amyloid Cardiology Specialist, Health Resources, Heart & Vascular Specialists; Amyloid Cardiology Specialist, Department of Cardiology, UT Southwestern Medical Center; Amyloid Webinars ARC (Amyloid Research Consortium); the Amyloidosis Foundation Facebook page; and Mackinzie’s Mission.


