On Wednesday morning, billionaire and former New York Mayor Michael Bloomberg put an end to his bid for the presidency, while also endorsing Joe Biden.
And another one bites the dust.
In a statement released on his 2020 campaign site, Bloomberg acknowledged that staying in the race would make achieving his ultimate goal of defeating Donald Trump more difficult.
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“After yesterday’s results, the delegate math has become virtually impossible – and a viable path to the nomination no longer exists,” Bloomberg said in the statement. “But I remain clear-eyed about my overriding objective: victory in November. Not for me, but for our country. And so while I will not be the nominee, I will not walk away from the most important political fight of my life.”
And in choosing not to walk away from that political fight, Bloomberg took the same opportunity to endorse “a great American”, Joe Biden.
“I am immensely proud of the campaign we ran, the issues we raised, and the sweeping and achievable plans we proposed – including our Greenwood Initiative to right historic wrongs, fight racial inequality and make the promise of equal opportunity real for the Black communities that have endured centuries of exploitation and discrimination,” he added. “That work is fundamental to the future of our country – and to the more perfect union that each generation is called to build.”
Of course, Bloomberg, who spent about $500 million of his own money toward his campaign, couldn’t leave the race without former New Yorker Donald Trump taking a shot.
“Mini Mike Bloomberg just “quit” the race for President,” the current president tweeted. “I could have told him long ago that he didn’t have what it takes, and he would have saved himself a billion dollars, the real cost. Now he will pour money into Sleepy Joe’s campaign, hoping to save face. It won’t work!”
If you or someone you love has heart failure and unresolved, seemingly unrelated symptoms such as carpal tunnel syndrome, shortness of breath, irregular heartbeat, or even lower back pain, it could be a sign of something more serious.1
It could be transthyretin cardiac amyloidosis, or ATTR-CM.1
Discover more about this rare and underdiagnosed condition that affects our community, and how you and your loved one can start a proactive conversation with your doctor.
What Is It? ATTR-CM is a rare, serious, and underdiagnosed type of amyloidosis that affects the heart and is associated with heart failure.2 Amyloidosis is a group of diseases in which certain proteins change shape, or “misfold,” and can build up in different parts of the body.3 When these misfolded proteins build up in your heart, it may lead to ATTR-CM.2
There are two different types.2 Wild-type ATTR-CM is the most common form and is associated with aging.2,4 There is also hereditary ATTR-CM, which is caused by a gene change, also known as a mutation.2 In the U.S., the most common type (V122I) is found almost exclusively in African Americans.5,6 Approximately 3% to 4% of African Americans in the U.S. are thought to be carriers of the mutation.5 However, not all individuals with the V122I mutation develop symptoms of hereditary ATTR-CM.6
Who is Affected? You are more likely to find hereditary ATTR-CM in our own communities, as it is primarily seen in people with Black, African American, and Afro-Caribbean heritage.7 It is a hereditary condition that affects both men and women.1 People can start to see and experience symptoms as early as their 50s or 60s.1
What Can You Do? Advocating for yourself or your loved one begins with a simple conversation with your doctor. Here are some sample questions to get you started:
Based on my symptoms, medical history, and family history, do you think ATTR-CM could be the cause of my heart failure?
Do you have experience diagnosing ATTR-CM, or can you recommend a local specialist?
I understand this condition can affect different parts of the body. Should I seek additional specialists to be a part of my care team?
Are there any patient support or advocacy groups you recommend for emotional and mental support or additional information on ATTR-CM?
1 Jain, A., & Zahra, F. (2023, April 27). Transthyretin amyloid cardiomyopathy (ATTR-CM). In StatPearls [Internet]. StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK574531/
2 Rozenbaum, M. H., Large, S., et al. (2021). Impact of delayed diagnosis and misdiagnosis for patients with transthyretin amyloid cardiomyopathy (ATTR-CM): A targeted literature review. Cardiology and Therapy, 10(1), 141–159. https://doi.org/10.1007/s40119-021-00219-5
4 Ruberg, F. L., Grogan, M., et al. (2019). Transthyretin amyloid cardiomyopathy: JACC state-of-the-art review. Journal of the American College of Cardiology, 73(22), 2872–2891. https://doi.org/10.1016/j.jacc.2019.04.003
5 Goyal, A., Lahan, S., et al. (2022). Clinical comparison of V122I genotypic variant of transthyretin amyloid cardiomyopathy with wild-type and other hereditary variants: A systematic review. Heart Failure Reviews, 27(3), 849–856. https://doi.org/10.1007/s10741-021-10098-6
6 Buxbaum, J. N., & Ruberg, F. L. (2017). Transthyretin V122I (pV142I) cardiac amyloidosis: An age-dependent autosomal dominant cardiomyopathy too common to be overlooked as a cause of significant heart disease in elderly African Americans. Genetics in Medicine: Official Journal of the American College of Medical Genetics, 19(7), 733–742. https://doi.org/10.1038/gim.2016.200
7 Spencer-Bonilla, G., Njoroge, J. N., et al. (2021). Racial and ethnic disparities in transthyretin cardiac amyloidosis. Current Cardiovascular Risk Reports, 15(6), 8. https://doi.org/10.1007/s12170-021-00670-y
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