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OPINION |
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Year : 2020 | Volume
: 2
| Issue : 1 | Page : 3-4 |
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Atherosclerosis and oncology: Shared mechanisms, shared treatment principles
Sorin C Danciu, Enrique Padilla Campos
Department of Cardiology, Advocate Illinois Masonic Medical Center, Chicago, IL, USA
Date of Submission | 22-Apr-2020 |
Date of Acceptance | 23-Apr-2020 |
Date of Web Publication | 16-Jun-2020 |
Correspondence Address: Dr. Sorin C Danciu Room 1303, 836 W Wellington Ave., Chicago, IL 60657 USA
 Source of Support: None, Conflict of Interest: None
DOI: 10.4103/ACCJ.ACCJ_8_20
Atherosclerosis and cancer are two chronic, progressive entities with major global disease burden that shares several mechanistic features. Despite these similarities, treatment strategies for malignancy and atherosclerosis differ significantly from each other. We propose that cardiovascular therapies can be optimized with the implementation of established cancer treatment principles.
Keywords: Atherosclerosis, Cancer, Treatment principles
How to cite this article: Danciu SC, Campos EP. Atherosclerosis and oncology: Shared mechanisms, shared treatment principles. Ann Clin Cardiol 2020;2:3-4 |
Introduction | |  |
Atherosclerosis and cancer are two chronic, progressive entities with major global disease burden that shares several mechanistic features. Inflammatory processes, genetic alterations, and oxidative stress are just a few of the many underlying mechanisms that drive both conditions.[1] Despite these similarities, treatment strategies for malignancy and atherosclerosis differ significantly from each other. We propose that cardiovascular therapies can be optimized with the implementation of established cancer treatment principles.
Screening | |  |
Risk factor screening is recommended for atherosclerotic disease. However, recent data suggest that screening only high-risk individuals may be insufficient. Recent evidence suggests that the Fuster Blood pressure, Exercise, Weight, Eating fruits and vegetables, Tobacco (BEWAT) score is able to predict subclinical atherosclerosis.[2] In addition, the Multi-Ethnic Study of Atherosclerosis study[3] has shown the significant extent of subclinical atherosclerosis present even in subjects considered at low risk. We propose that a systemic atherosclerosis risk score should be calculated and recorded annually for subjects starting at the age of 45.
In oncology, imaging plays a well-defined role in establishing disease and is paramount to assessing progression. A similar vision should be evaluated in cardiology, where the patient would be involved in the care plan and followed by imaging to support decisions on continuing long-term treatment. A classification system based on the systemic spread of disease –analogous to metastasis in oncologic terms– is likely to afford better prognostication at risk at the time of the diagnosis of atherosclerotic heart disease. As an example, the use of atherosclerosis imaging to identify vulnerable plaques and guide therapy may reveal an important clinically relevant potential similar to oncological schemes, although these modalities require further study.[4]
Treatment | |  |
Dietary and pharmacologic interventions have been clearly shown to have significant effects on the reduction and prevention of atherosclerotic disease. Most recently, the Evaluation of Cardiovascular Outcomes after an Acute Coronary Syndrome During treatment with Alirocumab (ODYSSEY trial)demonstrated a reduction in all-cause mortality and recurrent myocardial infarction (MI) in postMI patients who were treated with alirocumab and high-intensity statin therapy to a target low-density lipoprotein (LDL) 25–50 mg/dL. Despite strong clinical data, Garg et al. demonstrated, in 2014, that in certain practices, <50% of patients are prescribed optimal medical therapy postpercutaneous coronary intervention.[5] Furthermore, the current guidelines are unclear on the optimal duration of therapy, and most trials involving lipid-lowering agents have not been carried out beyond 4–5 years.
In cancer care, the treatment of metastatic disease often focuses on palliation, and these individuals are maintained on lifelong therapies. For localized disease, once remission is achieved, treatment is stopped or reduced, and serial surveillance imaging is continued. We believe that it is reasonable to apply the same treatment approach to cardiology patients who have diffuse and localized atherosclerosis. Compared to aggressive induction chemotherapy, the treatment of cardiovascular disease differs, whereas the current guidelines recommend gradual treatment, such as moderate-intensity statin for a patient that may already have moderate atherosclerosis. In theory, the concept of induction could be applied by using a multidrug regimen–similar to chemotherapy–combining statin, cholesterol absorption inhibitors, bempedoic acid, icosapent ethyl, fibrates, anti-inflammatory agents, and Proprotein convertase subtilisin/kexin type 9 (PCSK-9) inhibitors, aggressively given for 6 months to atherosclerotic patients.[6] If this concept proves beneficial, an intense regimen of shorter duration would make patients more likely to accept it, follow it, and it may also be economically impactful in an era of limited resources.
Finally, the role of lifestyle modification cannot be understated in the treatment of atherosclerosis. Considering the mechanistic similarities between oncologic and atherosclerotic disease processes, it is not surprising that both diet and abstinence from smoking play a significant role in modifying both disease processes.
Conclusion | |  |
The concept of inducing “remission” of atherosclerosis would be a pivotal change in the future of preventive cardiology [Table 1]. A randomized controlled trial studying the long-term cardiovascular effects of an aggressively lowered LDL level could help develop new treatment algorithms for atherosclerosis. Allied to advancements in intravascular imaging to monitor for disease burden, a treatment paradigm similar to those seen in oncology practice may not be too far out of our grasp.[7],[8]
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
References | |  |
1. | Tapia-Vieyra JV, Delgado-Coello B, Mas-Oliva J. Atherosclerosis and cancer; A resemblance with far-reaching implications. Arch Med Res 2017;48:12-26. |
2. | Fernandez-Alvira JM, Pocock S, Fernandez-Ortiz A, Ibanez B, Fernandez-Jimenez R, Sanz J, et al. Predictive values of the Ideal cardiovascular health and the Fuster-BEWAT scores for detecting subclinical atherosclerosis in healthy individuals – J Am Coll Cardiol 69, 11 Supplement March 2017, DOI 10.1016/S0735-1097(17)35067-2. |
3. | Mortensen MB, Falk E, Li D, Nasir K, Blaha MJ, Sandfort V, et al. Statin trials, cardiovascular events, and coronary artery calcification. JACC Cardiovasc Imaging 2018;11:221-30. |
4. | Tarkin JM, Dweck MR, Evans NR, Takx RA, Brown AJ, Tawakol A, et al. Imaging atherosclerosis. Circ Res 2016;118:750-69. |
5. | Garg P, Wijeysundera HC, Yun L, Cantor WJ, Ko DT. Practice patterns and trends in the use of medical therapy in patients undergoing percutaneous coronary intervention in Ontario. J Am Heart Assoc. 2014;3:e000882 doi: 10.1161/ JAHA.114.000882. |
6. | Preiss D, Tobert JA, Hovingh GK, Reith C. Lipid-modifying agentsm from statins to PCSK9 inhibitors. JACC 2020;76:1945-55. |
7. | Arnett DK, Blumenthal RS, Albert MA, Michos ED, Buroker AB, Miedema MD, et al. ACC/AHA Guideline n the Primary Prevention of Cardiovascular Disease. J Am Coll Cardiol 2019. doi: https://doi.org/10.1016/jacc.2019.03.010. |
8. | Dittrich C, Kosty M, Jezdic S, Pyle D, Berardi R, Bergh J, et al. ESMO/ASCO Recommendations for a global curriculum in medical oncology edition 2016. ESMO Open 2016;1:e000097. |
[Table 1]
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