Recently Diagnosed or Relapsed? Stop Looking For a Miracle Cure, and Use Evidence-Based Therapies To Enhance Your Treatment and Prolong Your Remission
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.
Click the orange button to the right to learn more about what you can start doing today.
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Got Myeloma? Got Afib?
Got myeloma? Got Afib? I have been diagnosed with everything the article below mentions that can increase my risk of atrial fibrillation, aka Afib. I was diagnosed with MM in 1994, developed my first DVT shortly after I began induction therapy in ’95, and then flipped into Afib fully 15 years after my ASCT.
So if you’re an MM survivor, you may develop atrial fibrillation, aka Afib, too.
The solution? In my experience, anyway. First and foremost, get a baseline echocardiogram. Before you have induction therapy or an ASCT. Develop a relationship with a cardio-oncologist.
Can Chemo Cause Afib? – Oncology Support Network
Discuss a heart-healthy lifestyle with your oncologist. By this I mean heart-healthy nutrition, supplementation, and lifestyle therapies.
If you have questions about my heart-healthy diet or supplements, scroll down the page, post a question or a comment, and I will reply to you ASAP.
Thanks,
David Emerson
- MM Survivor
- MM Cancer Coach
- Director PeopleBeatingCancer
Cancer, Inflammation, and Thrombosis: Drivers of Atrial Fibrillation in Oncology Patients
Background
Atrial fibrillation (AF) is a frequent and serious cardiovascular complication in oncology patients, driven by shared pathophysiological mechanisms of inflammation, thrombosis, and cardiac remodeling. Cancer and its therapies significantly increase AF risk, impacting survival, quality of life, and management complexity.
Methods
This narrative review synthesizes current evidence on the epidemiology, pathogenesis, and management of AF in cancer, emphasizing inflammatory and prothrombotic pathways, treatment-related cardiotoxicity, and cardio-oncology strategies. Literature was retrieved from PubMed and recent cardio-oncology guidelines to provide an integrated overview of mechanistic insights and therapeutic implications.
Results
Cancer patients exhibit up to a 10-fold higher risk of AF than the general population, particularly with esophageal, lung, and hematologic malignancies. Mechanistically, the NLRP3 inflammasome, neutrophil extracellular traps, and hypercoagulability promote atrial fibrosis and electrical instability.
Cancer therapies—including anthracyclines, platinum agents, tyrosine kinase inhibitors, immunotherapies, and thoracic radiation—further potentiate AF. Management is challenging due to drug–drug interactions, bleeding risks, and altered pharmacokinetics.
Evidence supports the use of direct oral anticoagulants when feasible and emphasizes multidisciplinary cardio-oncology collaboration. Personalized anticoagulation, vigilant rhythm monitoring, and shared decision-making are key to optimizing outcomes.
Conclusion
AF in cancer arises from a convergence of inflammation, thrombosis, and therapy-induced injury. A structured, multidisciplinary cardio-oncology approach integrating early risk stratification, tailored anticoagulation, and preventive strategies is essential.Future research should focus on oncology-specific risk prediction tools, biomarker-guided management, and randomized trials to refine evidence-based care for this high-risk population…
Atrial fibrillation (AF), the most common cardiac arrhythmia, is becoming more widespread. The prevalence was predicted to be 50 million worldwide. This increasing burden emphasizes how crucial it is to treat AF as a serious cardiovascular complication in cancer patients, who are already at higher risk because of their comorbidities and cancer treatments.1
Conclusion
This narrative review has set out to integrate current evidence on how cancer, inflammation, thrombosis, and cancer-directed therapies converge to promote atrial fibrillation, and to outline practical implications for clinical evaluation, anticoagulation, rhythm control, and preventive strategies in oncology patients. Taken together, existing data support viewing AF in cancer not as an incidental comorbidity, but as a phenotype of shared inflammatory and prothrombotic pathways, treatment-related injury, and competing risks that demand oncology-specific risk stratification and coordinated cardio-oncology care.
However, our conclusions are inherently constrained by the narrative, non-systematic design. Relevant studies may have been missed, selection of evidence may be influenced by availability and reporting bias, and heterogeneity in cancer types, treatments, AF definitions, and follow-up across the included literature limits comparability. Robust oncology-focused risk scores, randomized trials of anticoagulation and rhythm strategies, and prospective mechanistic studies are needed before uniform treatment algorithms can be defined.
In the interim, individualized, multidisciplinary decision-making -grounded in current guidelines but adapted to tumour biology, treatment phase, platelet dynamics, and patient priorities- remains the most rational approach for managing AF in this high-risk population.
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