Produção Nacional
Revisado por pares
Cardiovascular Effects of Androgen Deprivation Therapy for the Treatment of Prostate Cancer
2016; Lippincott Williams & Wilkins; Volume: 133; Issue: 5 Linguagem: Inglês
10.1161/circulationaha.115.012519
ISSN1524-4539
AutoresNirmanmoh Bhatia, Marília Harumi Higuchi dos Santos, Lee W. Jones, Joshua A. Beckman, David F. Penson, Amee Morgans, Javid J. Moslehi,
Tópico(s)Hormonal and reproductive studies
ResumoHomeCirculationVol. 133, No. 5Cardiovascular Effects of Androgen Deprivation Therapy for the Treatment of Prostate Cancer Free AccessResearch ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessResearch ArticlePDF/EPUBCardiovascular Effects of Androgen Deprivation Therapy for the Treatment of Prostate CancerABCDE Steps to Reduce Cardiovascular Disease in Patients With Prostate Cancer Nirmanmoh Bhatia, MD, Marilia Santos, MD, Lee W. Jones, PhD, Joshua A. Beckman, MD, David F. Penson, MD, MPH, Alicia K. Morgans, MD, MPH and Javid Moslehi, MD Nirmanmoh BhatiaNirmanmoh Bhatia From Cardiovascular Division (N.B., J.A.B., J.M.), Cardio-Oncology Program (N.B., J.M.), Vanderbilt-Ingram Cancer Center (D.F.P., A.K.M., J.M.), and Department of Urologic Surgery (D.F.P., A.K.M.), Vanderbilt University School of Medicine, Nashville, TN; Cardio-Oncology Service, Sirio-Libanes Hospital, Sao Paulo, Brazil (M.S.); Department of Cardiology, Sao Paulo Cancer Institute (ICESP), University of Sao Paulo, Brazil (M.S.); and Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY (L.W.J.). , Marilia SantosMarilia Santos From Cardiovascular Division (N.B., J.A.B., J.M.), Cardio-Oncology Program (N.B., J.M.), Vanderbilt-Ingram Cancer Center (D.F.P., A.K.M., J.M.), and Department of Urologic Surgery (D.F.P., A.K.M.), Vanderbilt University School of Medicine, Nashville, TN; Cardio-Oncology Service, Sirio-Libanes Hospital, Sao Paulo, Brazil (M.S.); Department of Cardiology, Sao Paulo Cancer Institute (ICESP), University of Sao Paulo, Brazil (M.S.); and Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY (L.W.J.). , Lee W. JonesLee W. Jones From Cardiovascular Division (N.B., J.A.B., J.M.), Cardio-Oncology Program (N.B., J.M.), Vanderbilt-Ingram Cancer Center (D.F.P., A.K.M., J.M.), and Department of Urologic Surgery (D.F.P., A.K.M.), Vanderbilt University School of Medicine, Nashville, TN; Cardio-Oncology Service, Sirio-Libanes Hospital, Sao Paulo, Brazil (M.S.); Department of Cardiology, Sao Paulo Cancer Institute (ICESP), University of Sao Paulo, Brazil (M.S.); and Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY (L.W.J.). , Joshua A. BeckmanJoshua A. Beckman From Cardiovascular Division (N.B., J.A.B., J.M.), Cardio-Oncology Program (N.B., J.M.), Vanderbilt-Ingram Cancer Center (D.F.P., A.K.M., J.M.), and Department of Urologic Surgery (D.F.P., A.K.M.), Vanderbilt University School of Medicine, Nashville, TN; Cardio-Oncology Service, Sirio-Libanes Hospital, Sao Paulo, Brazil (M.S.); Department of Cardiology, Sao Paulo Cancer Institute (ICESP), University of Sao Paulo, Brazil (M.S.); and Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY (L.W.J.). , David F. PensonDavid F. Penson From Cardiovascular Division (N.B., J.A.B., J.M.), Cardio-Oncology Program (N.B., J.M.), Vanderbilt-Ingram Cancer Center (D.F.P., A.K.M., J.M.), and Department of Urologic Surgery (D.F.P., A.K.M.), Vanderbilt University School of Medicine, Nashville, TN; Cardio-Oncology Service, Sirio-Libanes Hospital, Sao Paulo, Brazil (M.S.); Department of Cardiology, Sao Paulo Cancer Institute (ICESP), University of Sao Paulo, Brazil (M.S.); and Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY (L.W.J.). , Alicia K. MorgansAlicia K. Morgans From Cardiovascular Division (N.B., J.A.B., J.M.), Cardio-Oncology Program (N.B., J.M.), Vanderbilt-Ingram Cancer Center (D.F.P., A.K.M., J.M.), and Department of Urologic Surgery (D.F.P., A.K.M.), Vanderbilt University School of Medicine, Nashville, TN; Cardio-Oncology Service, Sirio-Libanes Hospital, Sao Paulo, Brazil (M.S.); Department of Cardiology, Sao Paulo Cancer Institute (ICESP), University of Sao Paulo, Brazil (M.S.); and Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY (L.W.J.). and Javid MoslehiJavid Moslehi From Cardiovascular Division (N.B., J.A.B., J.M.), Cardio-Oncology Program (N.B., J.M.), Vanderbilt-Ingram Cancer Center (D.F.P., A.K.M., J.M.), and Department of Urologic Surgery (D.F.P., A.K.M.), Vanderbilt University School of Medicine, Nashville, TN; Cardio-Oncology Service, Sirio-Libanes Hospital, Sao Paulo, Brazil (M.S.); Department of Cardiology, Sao Paulo Cancer Institute (ICESP), University of Sao Paulo, Brazil (M.S.); and Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY (L.W.J.). Originally published2 Feb 2016https://doi.org/10.1161/CIRCULATIONAHA.115.012519Circulation. 2016;133:537–541Case Presentation: A 74-year-old man with a new diagnosis of locally advanced prostate cancer is referred to the cardio-oncology clinic for optimization of his cardiovascular health after treatment with degarelix, a gonadotropin-releasing hormone (GnRH) receptor antagonist, for his prostate cancer. Two years ago, he had a myocardial infarction resulting in placement of a drug-eluting stent in his proximal left anterior descending artery. He has had no recurrent symptoms but lives a sedentary lifestyle. An electrocardiogram showed normal sinus rhythm. His most recent echocardiogram demonstrated a structurally normal heart with normal left ventricular ejection fraction. He takes aspirin 81 mg daily. He has hypertension, with the last recorded blood pressure of 160/90 mm Hg, and he is currently treated with metoprolol 25 mg twice daily and lisinopril 40 mg daily. He has diabetes mellitus that is treated with glipizide 10 mg daily, and his last hemoglobin A1c level was 7.4 mg/dL. He is also treated with pravastatin 40 mg daily; his low-density lipoprotein was 120 mg/dL at his most recent clinic visit. He continues to smoke 1 pack of cigarettes daily, and his body mass index is 30 kg/m2.OverviewProstate cancer is the most common noncutaneous cancer diagnosed in men in the United States and the second leading cause of cancer death.1 In 2015, there were an estimated 3 million prostate cancer survivors in the United States; this number will reach 4 million in the next decade.1 Because of the indolent, slowly progressive disease course of prostate cancer and advances in early detection and effective treatment, non–cancer-related deaths are the most common causes of mortality.2 In particular, given the prevalence of pre-existing and new cardiovascular disease (CVD), ischemic heart disease is the most common noncancer cause of death in patients with prostate cancer.2Androgen deprivation therapy (ADT) is the primary systemic therapy for locally advanced and metastatic prostate cancer, with as many as 50% of patients receiving ADT at some point during their disease course.3 Several observational studies suggest a link between ADT and increased risk of cardiovascular events.4 In 2010, the American Heart Association released a statement acknowledging the possible association between ADT and adverse cardiovascular events.5 More recently, the prostate cancer survivorship care guidelines by American Society of Clinical Oncology endorsed evaluation and screening of cardiovascular risk factors in men receiving ADT.6 Given the growing population of prostate cancer patients and survivors receiving ADT, it is crucial for practicing physicians to better understand ADT and the possible association with CVD.Mechanisms of ADTAfter synthesis in the testes, androgens (primarily testosterone) circulate in the serum and activate androgen receptor in target tissues, including muscle, adipose tissue, and prostate cancer cells. After activation by its ligand, androgen receptor induces a number of genes that are collectively referred to as the androgen response, driving prostate cancer growth, among other things (Figure 1). Thus, the major goal of ADT in the treatment of prostate cancer is to reduce serum testosterone levels to <50 ng/dL, with many men achieving levels <20 ng/dL.3Download figureDownload PowerPointFigure 1. Schematic of the hypothalamic-pituitary-gonadal axis and sites of action of antiandrogen therapies. AR indicates androgen receptor; DHT, dihydrotestosterone; GnRH, gonadotropin-releasing hormone; and LH, luteinizing hormone.ADT can be achieved by surgical or pharmacological castration, bilateral orchiectomies, or GnRH agonist or antagonist treatment (Table 1). GnRH agonists ultimately downregulate luteinizing hormone (LH) secretion from the anterior pituitary after causing an initial surge of LH levels in the first weeks of treatment (Figure 1). In contrast, GnRH antagonists bind GnRH receptors on the anterior pituitary gland and inhibit LH release, avoiding a surge in LH and potential associated complications. Diminished LH levels suppress androgen synthesis by the testes (Figure 1). Antiandrogens work at the level of the prostate cancer cells to directly block activation of the androgen receptor and can be used to augment the effectiveness of GnRH agonist or antagonist suppression of androgen receptor activation (Figure 1).Table 1. List of Antiandrogen DrugsGnRH AgonistsGnRH AntagonistsAntiandrogensAdrenal Androgen InhibitorsEstrogensLeuprolideDegarelixFlutamideKetoconazoleEstradiolGoserelinBicalutamideCorticosteroidsPremarinTriptorelinNilutamideAbiraterone acetateHistrelinEnzalutamideGnRH indicates gonadotropin-releasing hormone.Effects and Pathophysiology of ADT on the Cardiovascular SystemThe effects of ADT on the cardiovascular system are driven largely by indirect modifications of cardiovascular risk factors. Most data, derived predominantly from GnRH agonists (eg, leuprolide, goserelin) demonstrate an association between ADT and increased low-density lipoprotein and triglyceride levels, increased fat and decreased lean body mass, increased insulin resistance and decreased glucose tolerance, and a general metabolic state similar to the metabolic syndrome (although with heightened high-density lipoprotein levels). These changes can accelerate systemic atherosclerosis and predispose to coronary artery disease. ADT has also been associated with both arterial and venous thromboembolic events, including deep vein thrombosis, pulmonary emboli, arterial thrombosis, and stroke.3,4 No clear effect of ADT on blood pressure has been delineated. Indeed, counterintuitively, ADT improves vascular endothelial function; therefore, the mechanism of atherogenesis is unclear.7 The effects of ADT on various cardiovascular risk parameters are summarized in Table 2.Table 2. Pathophysiology of Adverse Cardiovascular Effects of GnRH AgonistsIndirect EffectsDirect EffectsLow Testosterone↑Fat mass↓Cardiac contractility?↓Vasodilation↓Lean body mass↑T-cell activation and destabilization of fibrous cap/plaque rupture↓HDL↑Insulin resistance/hyperinsulinemia↑Visceral obesity↑LDL, ↑HDL, and ↑triglycerides↑Prothrombotic state↑Diabetes mellitus↑Metabolic syndrome↑Arterial wall thicknessGnRH indicates gonadotropin-releasing hormone; HDL, high-density lipoprotein; and LDL, low-density lipoprotein.Interestingly, there may be differences between GnRH agonists and antagonists in terms of cardiovascular risk. GnRH antagonists suppress both LH and follicle-stimulating hormone, as opposed to GnRH agonists, which suppress primarily LH. This might influence how these molecules affect endothelial function, lipid metabolism, and fat accumulation. Interestingly, a recent pooled analysis of 6 randomized, controlled trials found that among men with pre-existing CVD, the risk of cardiac events was twice as high in men treated with a GnRH agonist as in men treated with GnRH antagonists.8 Prospective studies are necessary to provide more definitive data on the type of ADT to use or to avoid for men at high cardiovascular risk.Despite well-known adverse effects on cardiovascular risk factors and a possible association between ADT exposure and increased cardiovascular morbidity, no single prospective study has definitively established that ADT exposure increases the risk of CVD or cardiovascular mortality. However, a preponderance of the evidence suggests that men with pre-existing CVD, including a history of congestive heart failure or myocardial infarction, are at the highest risk of cardiovascular events with ADT exposure, especially during the first 6 months of ADT initiation, and close follow-up is warranted.4ManagementWe have developed the "ABCDE" paradigm (Figure 2) to control cardiovascular risk factors in cancer survivors.9 Here, we have adapted this approach for prostate cancer survivors in the absence of formal guidelines specifically for the prevention and management of CVD in patients on ADT (Table 3 and Figure 3).Table 3. ABCDE Algorithm for Prostate Cancer SurvivorsAAwarenessIncreased awareness of patients of cardiovascular signs and symptomsAspirinAspirin 81 mg daily for primary or secondary prevention of cardiovascular eventsBBlood pressureGoal blood pressure <140/90 mm HgCCholesterolHigh-intensity statin therapy for preexisting CVD or hyperlipidemiaCigarettesSmoking cessation counseling, therapyDDiabetes mellitusFrequent blood glucose monitoringMetformin for diabetes mellitus if possibleDietDiet rich in fruits, vegetables, and whole grain and low in saturated fat with 600 IU vitamin D daily and adequate calcium (1200 mg/d)Avoidance of excessive alcoholEExercise150 min/wk of moderate-intensity physical activity or 75 min/wk of vigorous exerciseCVD indicates cardiovascular disease.Download figureDownload PowerPointFigure 2. "ABCDE" algorithm for prostate cancer survivors.Download figureDownload PowerPointFigure 3. Algorithm to manage patients on androgen deprivation therapy (ADT) in the cardio-oncology clinic. ACC/AHA indicates American College of Cardiology/American Heart Association; ACE, angiotensin-converting enzyme; ADA, American Diabetes Association; CHF, congestive heart failure; CV, cardiovascular; and HbA1c, hemoglobin A1c.Awareness and AspirinIncreasing awareness of patients of the signs and symptoms of CVD and screening for undiagnosed metabolic and cardiovascular risk factors are essential during an initial clinic visit with a primary care provider or cardio-oncologist (Figure 3). Evidence suggests that in patients diagnosed with high-risk prostate cancer, aspirin may be associated with lower prostate cancer–specific mortality (hazard ratio, 0.60; 95% confidence interval, 0.37–0.97).10 Although this has yet to be validated in other populations, it is possible that select patients may benefit from aspirin for primary and secondary prevention of CVD and possibly for reduced cancer-related mortality.Blood PressureHypertension is a known cardiovascular risk factor, and a treatment goal is attaining a blood pressure <140/90 mm Hg. We recommend angiotensin-converting enzyme inhibitors as first-choice agents because of their mortality benefit in patients with diabetes mellitus and CVD and possibly improved outcomes in cancer patients, including those with prostate cancer (delayed prostate-specific antigen failure).11Cholesterol and CigarettesHyperlipidemia should be treated with high-intensity statin therapy independently of goal low-density lipoprotein levels, especially in the presence of diabetes mellitus or CVD. Tobacco products should be completely avoided because smoking is an independent and negative prognostic factor for both prostate cancer–specific and all-cause mortality in patients with prostate cancer.12Diabetes, Diet, and ExerciseBecause glycemic control can worsen with ADT, frequent monitoring of blood glucose and appropriate adjustment of diabetes therapy are recommended. Metformin is the preferred agent for the initial treatment of diabetes mellitus in this population because of its favorable effects on metabolic syndrome. The prostate cancer survivorship guidelines from the American Society of Clinical Oncology6 recommend health promotion by encouraging maintenance of a healthy weight through caloric restriction and regular physical activity. There is increasing evidence supporting the efficacy of structured exercise training (ie, endurance training, resistance training, or their combination) as an effective strategy to offset or attenuate some of the common side effects of ADT.13 National guidelines recommend that patients with cancer participate in at least 150 min/wk of moderate exercise (eg, brisk walking, light swimming) or 75 min/wk of vigorous exercise (eg, jogging, running, hard swimming).13 American College of Sports Medicine guidelines recommend that patients with cancer participate in at least 150 min/wk of moderate exercise (eg, brisk walking, light swimming) or 75 min/wk of vigorous exercise (eg, jogging, running, hard swimming).13 However, this recommendation is a long-term goal and is not advised as an initial prescription for most sedentary patients either during or immediately after ADT. A generalized approach to individualized exercise prescription is available.14Dietary goals include increasing the intake of fruits, vegetables, and whole grains; decreasing the intake of saturated fats; and consuming adequate vitamin D (≥600 IU/d) and calcium (not exceeding 1200 mg/d). Alcohol should be limited to ≤2 drinks a day. We recommend lifestyle modification counseling at follow-up clinic visits. Because cancer diagnosis and treatment are a significant source of psychological stress, a factor independently associated with adverse cardiovascular events, screening and counseling to manage stress may also be helpful15 (Figure 3).ADT may prolong QTc, and a baseline electrocardiogram should be obtained. If initial screening reveals evidence of congestive heart failure or valvular or other structural heart disease, an echocardiogram should be obtained.The physician's focus should be to optimize the cardiovascular and metabolic risk profile as much as feasible over the course of survivorship. Once ADT is initiated, we recommend close follow-up at least every 3 months during the first year of therapy.Case ConclusionA detailed discussion about cardiovascular risks of ADT was undertaken. Our patient was counseled to quit smoking and to adopt the above recommended diet and exercise regimen. An electrocardiogram was obtained that revealed normal sinus rhythm. His statin was changed to atorvastatin 80 mg daily, and metformin 500 mg twice daily was substituted for glipizide for his diabetes mellitus. The dose of metoprolol was increased to 50 mg twice daily, and he was advised to maintain a blood pressure diary at home. He was screened for stress and offered counseling. He was scheduled for a follow-up visit in 1 month, and he received a pamphlet with the new modified ABCDE algorithm (Figure 2).Sources of FundingDr Jones receives research grants from the National Cancer Institute and Aktiv Against Cancer. Dr Beckman receives grant support from Bristol-Myers Squibb. Dr Penson receives research support from Medivation/Astellas.DisclosuresDr Jones is the cofounder of Exercise by Science, Inc. Dr Beckman is a consultant for Merck, Novartis, Bristol-Myers Squibb, and AstraZeneca. Dr Morgans is a consultant for Dendreon and Myriad. Dr Moslehi is a consultant for Novartis, Pfizer, Takeda, ARIAD Pharmaceuticals, Bristol-Myers Squibb, and Acceleron. The other authors report no conflicts.FootnotesCorrespondence to Alicia K. Morgans, MD, MPH, or Javid Moslehi, MD, Cardio-Oncology Program, Vanderbilt University Medical Center, 2220 Pierce Ave, Nashville, TN 37232. E-mail [email protected] or [email protected]References1. 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