Increased arterial intima-media thickness by B-M mode echodoppler ultrasonography in acromegaly.

BACKGROUND: Patients with acromegaly have an increased morbidity and mortality for cardiovascular diseases. Despite the increasing evidence for the existence of a specific cardiomyopathy in acromegaly, the presence of vascular abnormalities has been never investigated.

OBJECTIVE: To evaluate the cardiovascular risk and premature atherosclerosis in acromegaly.

SUBJECTS: Forty-five patients with acromegaly and 30 sex- and age-matched healthy subjects were included in this study: 30 patients were studied at the diagnosis of acromegaly and were in active disease (GH 59.3 +/- 10.2 mU/l, IGF-I 733 +/- 57.6 microg/l) while 15 patients were studied after surgery and/or radiotherapy and were cured from the disease (GH 4.5 +/- 0.7 mU/l, IGF-I 172.4 +/- 16.9 microg/l).

METHODS: Body mass index (BMI), systolic (SBP) and diastolic blood pressure (DBP), serum total, LDL- and HDL-cholesterol, triglycerides, and fibrinogen levels, prothrombin time (PT), activated partial thromboplastin time (APTT), glucose and insulin levels (fasting and after glucose load) were measured in all patients and controls. By echodoppler ultrasonography, blood systolic (SPV) and diastolic (DPV) peak velocity, and resistance index (RI) were measured at both common and internal carotid arteries where presence, size and location of atherosclerotic plaques were evaluated by B-Mode ultrasonography. Intima-media thickness (IMT) of both common carotids was measured by M-Mode ultrasonography.

RESULTS: SBP, but not DBP, was significantly higher in patients with active disease than in cured patients and controls (P = 0.003). Hypertension was found in nine (30%) patients with active disease, in two (13.3%) of those cured from acromegaly and in none of controls (chi2 = 10.81, P < 0.004). Fasting blood glucose levels were significantly higher both in patients with active disease and in those cured from the disease than in controls (P < 0.001). Circulating insulin levels were significantly higher in patients with active disease than in cured patients and controls (P < 0.001) and in cured patients than in controls (P < 0.001). Glucose tolerance abnormalities were found in 13 (43.3%) patients with active disease, in four (26.6%) patients with inactive disease and in four controls (13.3%) (chi2 = 6.71, P = 0.03). Total blood cholesterol levels were similar in the three groups, LDL-cholesterol and triglycerides levels were significantly higher, whereas HDL-cholesterol levels were significantly lower both in patients with active disease and in those cured from the disease than in controls (P < 0.001). Serum fibrinogen levels were significantly higher both in patients with active disease and in those cured from the disease than in controls (P < 0.001). No difference was found in PT and APTT levels among the three groups. At the level of right and left common carotid arteries, IMT was significantly higher both in patients with active disease and in those cured from the disease than in controls (P < 0.001). Both right and left SPV, but not DPV, were significantly higher in patients with active disease than in those cured from the disease and in controls (P < 0.01). Well defined carotid wall plaques were detected in two patients (6.6%) with active disease, in one patient cured from the disease (6.6%) and in two controls (6.6%). At the level of right and left internal carotid arteries, SPV, DPV and RI were similar among the three groups. Well defined carotid wall plaques were detected in three patients with active disease (10%), two patients cured from the disease (13.3%) and in one control (3.3%).

CONCLUSIONS: A significant increase of IMT of both common carotid arteries was observed in patients with active acromegaly, this was also found in those cured from acromegaly. However, the prevalence of well defined carotid plaques was not increased in both groups of patients with acromegaly as compared to controls. On this basis, heart more than vessels seems to be affected by chronic GH and IGF-I excess in acromegaly.