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Original Studies |
Departments of Molecular and Clinical Endocrinology and Oncology (A.C., P.M., D.F., G.L.) and Internal Medicine I (M.P.), Federico II University of Naples; Department of Clinical Science, Section of Endocrinology, University La Sapienza (R.B., E.F., P.G., G.T.), Rome; and Division of Endocrinology, S. Giuseppe Hospital, IRCCS, Istituto Auxologico Italiano (A.L.), Verbania, Italy
Address all correspondence and requests for reprints to: Annamaria Colao, M.D., Ph.D., Department of Molecular and Clinical Endocrinology and Oncology, Federico II University of Naples, via S. Pansini 5, 80131 Naples, Italy. E-mail: colao{at}unina.it
Increased mortality from cardiovascular diseases has been reported in acromegaly. Our objective was to evaluate the impact of glucose tolerance abnormalities and/or systemic hypertension in further worsening the acromegalic cardiomyopathy. The study design was open transversal. The subjects studied were 130 consecutive naive acromegalic patients (74 women and 56 men; age, 1780 yr). Interventricular septum (IST) and left ventricular (LV) posterior wall thickness (PWT), LV mass index (LVMi), maximal early to late diastolic flow velocity ratio (E/A), isovolumic relaxation time (IRT), and LV ejection fraction (EF) were measured by echocardiography. The results were analyzed in line with the presence of glucose tolerance abnormalities (normal in 60, impaired in 38, diabetes mellitus in 32) and the presence (in 46) or absence (in 84) of hypertension. Patients with impaired glucose tolerance and diabetes mellitus had significantly higher age (P = 0.01), and systolic (P = 0.01) and diastolic (P = 0.01) blood pressures and lower E/A (P = 0.01) and EF (P = 0.01) than those with normal glucose tolerance. Disease duration, circulating GH and insulin-like growth factor I (IGF-I) levels, IST, LVPWT, LVMi, and IRT were similar in the 3 groups. Normotensive patients had significantly lower age (P < 0.001), LVPWT (P < 0.001), IST (P = 0.003), LVMi (P < 0.001), and IRT (P = 0.02) and significantly higher E/A (P < 0.001) and EF (P < 0.001) than hypertensive subjects. Disease duration, circulating GH, and IGF-I levels were similar in the 2 groups.
Multiple regression analysis showed that systolic blood pressure was the strongest predictor of LVMi (P = 0.0004), followed by GH levels (P = 0.02), whereas diastolic blood pressure was the strongest predictor of LVEF reduction (P < 0.0001), followed by glucose tolerance status (P = 0.02). Age was the strongest predictor of both E/A impairment (P < 0.0001) and IRT (P = 0.01), followed by IGF-I levels (P = 0.02).
Compared to patients with uncomplicated acromegaly, those with hypertension but without abnormalities of glucose tolerance had an increased prevalence of LV hypertrophy (75% vs. 37.2%) as well as of impaired diastolic (50% vs. 7.8%) and systolic function (18.7% vs. 3.9%), whereas patients with glucose tolerance abnormalities but without hypertension had only an increased prevalence of impaired diastolic (39.7%) and systolic function (31.7%). The subgroup of acromegalic patients suffering from hypertension and diabetes mellitus had the highest prevalence of LV hypertrophy (84.6%), diastolic filling abnormalities (69.2%), and impaired systolic function at rest (53.9%). A careful cardiac investigation should thus be performed in all acromegalic patients showing these complications.
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