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Vascular disease prevention and management after cancer therapy
KEY POINTS
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Vascular disease after completion of cancer therapy can be due to (1) the continuum of preexisting vascular disease and/or (2) as a new development owing to cancer therapy exposure.
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The first category requires optimal, guideline-directed therapies in the overall context of the patient’s care, conditions, and goals.
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The second category needs definition of the contributing role of the cancer therapy, thereby allowing for appropriate management.
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Cancer therapies, such as cisplatin, BCR-ABL inhibitors, and radiation, can have a direct long-lasting effect on the vasculature.
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Vascular changes can also be an indirect consequence of cancer and its therapy (e.g., via reduction in physical activity, weight increase, hypothyroidism, kidney disease).
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Promoting vascular health and preventing vascular disease is a key mandate.
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For patients requiring treatment, this is to be disease- and guideline-directed.
Historically vascular disease after cancer therapy had not been a topic of relevance given the generally very poor survival prognosis of many malignancies. This has changed over the past two decades. An illustrating example is chronic myeloid leukemia (CML), the prognosis of which has changed completely. The advent of inhibitors that target the molecular arrangement underlying this disease has provided a “cure.” Indeed, as long as patients are responding to therapy they enjoy a life expectancy similar to their peers and, in fact, they are more likely to die of non-CML diseases, one of these being vascular disease. In addition to this specific example, it has also been recognized that in general cardiovascular disease (CVD), including myocardial infarction and stroke, has a significant impact on the overall outcome of patients with cancer ( Fig. 29.1 ).
A. Survival of patients without cancer and cancer survivors with and without concomitant cardiovascular disease (CVD). B. Cumulative incidence of arterial occlusive disease in patients with chronic myeloid leukemia on nilotinib (observed) versus risk factor-matched controls. Peripheral arterial disease is four times more commonly seen than coronary artery disease. C. Cumulative incidence of CVD after chest radiation in patients with Hodgkin lymphoma. D. Burden of coronary artery disease in patients with Hodgkin lymphoma after mediastinal radiation.
General considerations
Vascular disease after completion of cancer therapy can be caused by (1) the continuum of vascular disease that was present even before the cancer treatment, and/or (2) the new development of vascular disease during or after completion of cancer therapy. This distinction helps with the direction of therapy. Whereas the first scenario requires follow up and treatment in keeping with published guidelines, the second scenario must take into account the uniqueness of the cancer therapy the patient has received. For instance, vascular toxicity risk with cancer therapeutics such as 5-FU is expected to be limited to the time of exposure. On the contrary, cisplatin and BCR-ABL inhibitors, such as nilotinib and ponatinib, as well as radiation therapy can have long-lasting effects even beyond the active treatment period. , These nuances have implications for the association of vascular presentations with the cancer therapy and the duration of preventive efforts. For example, it would be unlikely that a patient develops chest pain one year after colon cancer treatment because of 5-FU exposure. Rather, it is more likely that the patient is experiencing progression of underlying coronary artery disease (CAD) that is now becoming clinically apparent. In this setting, contrary to the acute 5-FU therapy scenario, vasodilator therapy would not be the first line of management. As in the other two chapters of vascular diseases in patients with cancer, there is merit to focus on the three main modes of presentation as follow up, screening, prevention, and treatment differ. Cultivating an understanding of the most likely clinical course in any given patient and focusing on the underlying mechanism (i.e., a pathophysiology directed approach) is likely the most efficient and effective way. At the same time, there needs to be an openness of mind for differential diagnoses, the impact of additional factors, and the comorbidities of the patient that can contribute to the presentations.
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