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Multiple Myeloma an incurable disease, but I have spent the last 25 years in remission using a blend of conventional oncology and evidence-based nutrition, supplementation, and lifestyle therapies from peer-reviewed studies that your oncologist probably hasn't told you about.
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Chemotherapy-induced Cardiomyopathy Worsening!?
Is my chemotherapy-induced cardiomyopathy worsening? I was diagnosed with chemotherapy-induced cardiomyopathy in 2010. Once I did some research about CIC, developing this side effect made sense to me because of the many cardiotoxic regimens that I underwent before and during my autologous stem cell transplant.
Can Chemotherapy Damage Your Heart?
What I didn’t think about at the time was my prognosis. The cardio-oncologist who diagnosed my side effect prescribed metoprolol and sent on my way. I had a bad reaction to this therapy within a day or two, discontinued its use and set about identifying heart-healthy foods and supplements.
Long story short, I take a laundry list of non-conventional heart therapies ranging from cocoa powder to CQ10, vitamin D, curcumin, omega-3 fatty acids, and others. I exercise daily (modestly), eat nutritiously and I try not to sweat the little stuff, as the saying goes.
An annual echocardiogram tells me that my ejection fraction, A-fib, etc. remain stable. In my mind, my CIC is well-controlled by evidence-based non-conventional therapies.
What bothers me the most about this treatment-induced side effect is that it could have been prevented and once it occurred, conventional medications did little to help me. I’ve relied on non-conventional heart therapies for more than 15 years now.
Do you have chemotherapy-induced cardiomyopathy? If you’d like to learn more about my experiences, scroll down the page, post a comment or a question and I will reply to you ASAP.
Hang in there,
David Emerson
- MM Survivor
- MM Cancer Coach
- Director PeopleBeatingCancer
Navigating cancer therapy-induced cardiotoxicity: From pathophysiology to treatment innovations
Abstract
Every year, more than a million people in the United States undergo chemotherapy or radiation therapy for cancer, as estimated by the CDC. While chemotherapy has been an instrumental tool for treating cancer, it also causes severe adverse effects.
The more commonly acknowledged adverse effects include hair loss, fatigue, and nausea, but a more severe and longer lasting side effect is cardiotoxicity. Cardiotoxicity, or heart damage, is a common complication of cancer treatments. It can range from mild to severe, and it can affect some patients temporarily or others permanently, even after they are cured of cancer.
Dexrazoxane is the only FDA-approved drug for treating anthracycline-induced cardiotoxicity, but it also has drawbacks and adverse effects. There is no other type of chemotherapy-induced cardiotoxicity that has an approved treatment option. In this review, we discuss the pathophysiology of chemotherapeutic-induced cardiotoxicity, methods and guidelines of diagnosis, methods of treatment and mitigation, and current drug delivery approaches in therapeutic development.
Clinical perspective
Cardio-oncology is a rapidly growing interdisciplinary field at the nexus of cardiology and oncology that is dedicated to the prevention, detection, and management of cardiovascular complications in people with cancer. Cardio-oncologists most commonly care for patients who develop cardiovascular complications during or shortly after the completion of treatment for cancer, though the field also recognizes the importance of careful surveillance for incident cardiovascular disease in cancer…
Alternative methods of treatment in clinical trials
The Cardiovascular Cell Therapy Research Network’s SENECA (Stem Cell Injection in Cancer Survivors) is a major clinical trial that uses allogenic mesenchymal stem cells as a treatment strategy for anthracycline-induced cardiotoxicity. This clinical trial was the first study demonstrating safe trans-endocardial administration of allogeneic mesenchymal stem cells in AIC patients. Although the study confirmed the safety of stem cell administration, it showed little cardio-protective benefit. There
Small molecule drugs
In the past few years, researchers have investigated the potential of small molecules to protect the heart from anthracycline-induced cardiotoxicity. An allosteric inhibitor of the apoptotic protein Bax called BAI1 has been recently found to prevent cardiotoxicity in a doxorubicin exposure model in both zebrafish and mice. Bax is a protein responsible for multiple routes of cell death including apoptosis and necrosis. Bax protein expression is also linked to mitochondrial specific cell death,
Protein/peptide based therapeutics and protein based therapeutic targets
In a 2023 study that utilized both H9C2 cells and a murine model, C1q-tumor necrosis factor-5 protein (CTRP5) reduced doxorubicin cardiotoxicity through decreasing TLR/NLRP3 signaling. Using an adeno-associated virus system, C57BL/6 mice were genetically engineered to overexpress CTRP5 in only their hearts. CTRP5 has been previously shown to protect against ischemia–reperfusion injuries in mice. This is done via activation of the AMPKα signaling [72]. CTRP5 plays roles in glucose and lipid…
Future directions and conclusion
Chemotherapeutic-induced heart failure is a clear demonstration of an iatrogenic issue; the use of chemotherapeutics, such as anthracyclines, though very powerful for the treatment of cancer, are detrimental to the post cancer survival quality of life of patients. The primary issue with chemotherapeutic induced cardiotoxicity is the hugely limited number of dedicated therapeutic options; dexrazoxane as the lone option that is FDA approved for preventing anthracycline-induced cardiotoxicity is..
chemotherapy-induced cardiomyopathy worsening chemotherapy-induced cardiomyopathy worsening