Cardiovascular Risk Factors in Patients with Uncontrolled and Long-Term Acromegaly: Comparison with Matched Data from the General Population and the Effect of Disease Control

Context: Data on cardiovascular risk in acromegaly are scanty and lack a clear correlation to epidemiological data. Objective: Our aim was an evaluation of cardiovascular risk factors in patients with active acromegaly, a calculation of the Framingham risk score (FRS) compared with age-and gender-matched controls of the general population, and an evaluation of the effect of IGF-I normalization. Design and Setting: We conducted a retrospective, comparative study at a university referral center. Patients: A total of 133 patients with acromegaly (65 men, aged 45-74 yr) from the German Pegvisomant Observational Study were matched to 665 controls from the general population. Main Outcome Measures: Risk factors were measured at baseline and after 12 months of treatment with pegvisomant (n = 62). Results: Patients with acromegaly had increased prevalence of hypertension, mean systolic and diastolic blood pressure (BP), history of diabetes mellitus and glycosylated hemoglobin (all P < 0.001) and decreased high-density lipoprotein, low-density lipoprotein, and total cholesterol (all P < 0.001). FRS was significantly higher in patients with acromegaly compared with controls (P < 0.001). At 12 months, systolic BP (P = 0.04) and glycosylated hemoglobin (P = 0.02) as well as FRS (P = 0.005) decreased significantly. IGF-I was normalized in 62% (41 of 62). In these patients, glucose and systolic and diastolic BP was significantly lower than in partially controlled patients. Summary: We found an increased prevalence of cardiovascular risk factors in acromegalic patients compared with controls. Control of acromegaly led to a significant decrease of FRS, implying a reduced risk for coronary heart disease. This was most significant in those patients who completely normalized their IGF-I levels. Conclusion: Disease control is important to reduce the likelihood for development of coronary heart disease. (J Clin Endocrinol Metab 95: 3648-3656, 2010)