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Doxorubicin-induced Heart Damage Prevention
If doxorubicin aka adriamycin is a part of your therapy plan, please consider doxorubicin-induced heart damage prevention.
I say this because my mantra is “I wish I knew then what I know now.” I am a cancer survivor who developed chemotherapy-induced cardiomyopathy 15 years after my doxorubicin/adriamycin administration.
The list below demonstrated both conventional (FDA approved) and evidence-based non-conventional therapies cited to prevent the heart damage created by dox.
What therapies can prevent doxorubicin-induced heart damage?
- Dexrazoxane:
- An iron chelator that reduces the formation of free radicals and prevents cardiac damage. It is often used in conjunction with doxorubicin to protect the heart.
- Antioxidants:
- Coenzyme Q10: An antioxidant that helps protect cardiac cells from oxidative damage.
- Vitamin E and Vitamin C: These vitamins help reduce oxidative stress and may offer some protection to cardiac cells.
- Beta-Blockers:
- Drugs like carvedilol can reduce the incidence of cardiomyopathy by reducing oxidative stress and improving cardiac function.
- Angiotensin-Converting Enzyme (ACE) Inhibitors:
- Medications such as enalapril can help prevent the remodeling of cardiac tissue and reduce the risk of heart failure.
- Angiotensin II Receptor Blockers (ARBs):
- Similar to ACE inhibitors, ARBs like losartan can protect against cardiac damage.
- Statins:
- These drugs, commonly used to lower cholesterol, have been shown to reduce oxidative stress and inflammation, offering cardioprotection.
- Liposomal Doxorubicin:
- Encapsulating doxorubicin in liposomes can reduce its cardiotoxic effects by altering its distribution in the body, leading to lower concentrations in cardiac tissue.
- Lifestyle and Monitoring:
- Regular cardiovascular monitoring before, during, and after treatment can help detect early signs of cardiotoxicity.
- Lifestyle modifications, such as a heart-healthy diet, regular exercise, and avoiding smoking, can support overall heart health.
- Other Medications:
- Aldosterone antagonists: Medications like spironolactone can help reduce cardiac fibrosis and improve heart function.
- Neprilysin inhibitors: These drugs, often combined with ARBs, may provide additional cardioprotective effects.
- Nutritional Supplements:
- L-carnitine: An amino acid derivative that may help protect the heart by improving mitochondrial function and reducing oxidative stress.
- Omega-3 fatty acids: Found in fish oil, these may help reduce inflammation and improve cardiac function.
- Gene Therapy:
- Although still experimental, gene therapy approaches are being explored to directly counteract the molecular mechanisms underlying doxorubicin-induced cardiotoxicity.
My personal belief is that every cancer patient who has any amount of cardiotoxic chemotherapy develops heart damage. Some patients will develop heart damage immediately, some in the months that follow and some like me who don’t exhibit heart damage for years.
man hand holding his nutritional supplemets, healthy lifestyle background.
But everyone who undergoes cardiotoxic chemo can benefit from doxorubicin-induced heart damage prevention.
If you would like to learn more about therapies shown to protect your heart from damage email me at David.PeopleBeatingCancer@gmail.com
thank you,
David Emerson
- Cancer Survivor
- Cancer Coach
- Director PeopleBeatingCancer
Tufts researchers uncover immune cell link to doxorubicin-induced heart damage
“The research team found that, once in the heart, the CD8+ T-cells can cause changes to the organ, leaving the cardiac tissue
- scarred,
- highly fibrotic,
- and less able to perform.
Their research showed that in mice the T-cells are releasing molecules that are meant to cause cell death, which are normally intended to combat viruses and other invaders, but these molecules cause fibrosis and stiffen the heart, preventing it from contracting well…
In addition to investigating how to block CD8+ T-cells from entering the heart without affecting doxorubicin’s ability to fight cancer, future research from the team will also explore whether the molecules that attract T-cells to the heart, called chemokines, could serve as biomarkers to monitor or predict cardiac damage, allowing for more personalized and safer treatment plans for patients…”
Cytotoxic T cells drive doxorubicin-induced cardiac fibrosis and systolic dysfunction
“Doxorubicin, the most prescribed chemotherapeutic drug, causes dose-dependent cardiotoxicity and heart failure. However, our understanding of the immune response elicited by doxorubicin is limited.
Here we show that an aberrant CD8+ T cell immune response following doxorubicin-induced cardiac injury drives adverse remodeling and cardiomyopathy. Doxorubicin treatment in non-tumor-bearing mice increased circulating and cardiac IFNγ+CD8+ T cells and activated effector CD8+ T cells in lymphoid tissues.
Moreover, doxorubicin promoted cardiac CD8+ T cell infiltration and depletion of CD8+ T cells in doxorubicin-treated mice decreased cardiac fibrosis and improved systolic function. Doxorubicin treatment induced ICAM-1 expression by cardiac fibroblasts resulting in enhanced CD8+ T cell adhesion and transformation, contact-dependent CD8+degranulation and release of granzyme B.
Canine lymphoma patients and human patients with hematopoietic malignancies showed increased circulating CD8+ T cells after doxorubicin treatment.
In human cancer patients, T cells expressed IFNγ and CXCR3, and plasma levels of the CXCR3 ligands CXCL9 and CXCL10 correlated with decreased systolic function…”