Hormonal therapy use for prostate cancer and mortality in men with coronary artery disease-induced congestive heart failure or myocardial infarction.
BACKGROUND
Hormonal therapy (HT) when added to radiation therapy (RT) for treating unfavorable-risk prostate cancer leads to an increase in survival except possibly in men with moderate to severe comorbidity. However, it is unknown which comorbid conditions eliminate this survival benefit.


OBJECTIVE
To assess whether neoadjuvant HT use affects the risk of all-cause mortality in men with prostate cancer and coronary artery disease (CAD)-induced congestive heart failure (CHF) or myocardial infarction (MI), CAD risk factors, or no comorbidity.


METHODS
A total of 5077 men (median age, 69.5 years) with localized or locally advanced prostate cancer were consecutively treated with or without a median of 4 months of neoadjuvant HT followed by RT at a suburban cancer center between 1997 and 2006 and were followed up until July 1, 2008. Cox regression multivariable analyses were performed assessing whether neoadjuvant HT use affected the risk of all-cause mortality, adjusting for age, year and type of RT, treatment propensity score, and known prostate cancer prognostic factors in each comorbidity group.


METHODS
Risk of all-cause mortality.


RESULTS
Neoadjuvant HT use was not associated with an increased risk of all-cause mortality in men with no comorbidity (9.6% vs 6.7%, adjusted hazard ratio [HR], 0.97; 95% confidence interval [CI], 0.72-1.32; P = .86) or a single CAD risk factor (10.7% vs 7.0%, adjusted HR, 1.04; 95% CI, 0.75-1.43; P = .82) after median follow-ups of 5.0 and 4.4 years, respectively. However, for men with CAD-induced CHF or MI, after a median follow-up of 5.1 years, neoadjuvant HT use was significantly associated with an increased risk of all-cause mortality (26.3% vs 11.2%, adjusted HR, 1.96; 95% CI, 1.04-3.71; P = .04).


CONCLUSIONS
Neoadjuvant HT use is significantly associated with an increased risk of all-cause mortality among men with a history of CAD-induced CHF or MI but not among men with no comorbidity or a single CAD risk factor.
Nanda
Akash
A
Harvard Radiation Oncology Program, Brigham & Women's Hospital-Dana-Farber Cancer Institute, 75 Francis St, ASB1 L2, Boston, MA 02115, USA. ananda@partners.org
Chen
Ming-Hui
MH
Braccioforte
Michelle H
MH
Moran
Brian J
BJ
D'Amico
Anthony V
AV
D000368:Aged; D000726:Androgen Antagonists / Q000627:therapeutic use; D018931:Antineoplastic Agents, Hormonal / Q000627:therapeutic use*; D001918:Brachytherapy; D015897:Comorbidity; D003324:Coronary Artery Disease / Q000453:epidemiology*; D003920:Diabetes Mellitus / Q000453:epidemiology; D007987:Gonadotropin-Releasing Hormone / Q000819:agonists; D006333:Heart Failure / Q000453:epidemiology*; D006801:Humans; D006937:Hypercholesterolemia / Q000453:epidemiology; D006973:Hypertension / Q000453:epidemiology; D053208:Kaplan-Meier Estimate; D008297:Male; D009203:Myocardial Infarction / Q000453:epidemiology; D020360:Neoadjuvant Therapy; D016016:Proportional Hazards Models; D011471:Prostatic Neoplasms / Q000401:mortality* / Q000628:therapy*; D012307:Risk Factors; D016896:Treatment Outcome
D000726:Androgen Antagonists; D018931:Antineoplastic Agents, Hormonal; D007987:Gonadotropin-Releasing Hormone