title: Can insulin action induce myocardial texture alterations in essential hypertension?
abstract: The prevalence of hyperinsulinemia/insulin resistance in hypertensive individuals, as well as the effects of insulin on myocytic and fibroblastic growth, are well known in both epidemiologic and animal models. To check whether there are any links between ultrasonic myocardial texture parameters and insulin level in essential hypertensives, we compared 18 essential hypertensive men (Group 1, H) with 18 age- and gender-matched healthy controls (Group 2, C) (age, 57 +/- 10 years). For all study subjects we performed ambulatory blood pressure monitoring (ABPM); conventional 2-D Doppler echocardiography for the assessment of the left ventricular mass index (LVMi) and function; quantitative analysis of digitized echocardiographic images for evaluation of cyclic variation (CVI) of mean gray level (MGL) at the septum and posterior wall levels; and 75-g 3-h oral glucose tolerance test (OGTT) for analysis of area under glycemic curve (AUGC, g/min/dL) and insulinemic curve (AUIC, mU/min/mL), as well as serum glucose and insulin peaks. Both the daily mean blood pressure (H: 109 +/- 4.6 v C: 94.6 +/- 4.6, P < .0001) and LVMi (adjusted for body surface) (H: 133 +/- 24 v C: 97 +/- 21 g/m2, P < .0001) were significantly higher in hypertensives. Values for AUIC were significantly higher in hypertensives (10.37 +/- 5.53 v 6.33 +/- 5.28), P < .032); CVI was also significantly higher in group C, for both septum (C: 40.2 +/- 16.9 v H: 15.9 +/- 18.1, P < .0001) and posterior wall (C: 44.5 +/- 19.6 v H: 20 +/- 17.5; P < .0001). There was a significant inverse correlation between AUIC and CVI for both septum (r: -0.57, P < .001) and posterior wall (r: -0.50, P < .002). The significantly higher impairment of myocardial ultrasonic texture and the higher level of the AUIC insulinemia in hypertensives, as well as the significant inverse relationship between CVI and hyperinsulinemia, are our major findings. Hyperinsulinemia/insulin resistance could cause an altered collagen/muscular ratio, which could potentially explain, at least in part, the CVI alterations detected in hypertensive patients.
authors: Dipartimento di Medicina Interna, Centro di Medicina Nucleare, Università di Pisa, Italy. dibellov@po.ifc.pi.cnr.it
authors: V
authors: V
authors: Di Bello
authors: O
authors: O
authors: Giampietro
authors: R
authors: R
authors: Pedrinelli
authors: E
authors: E
authors: Matteucci
authors: D
authors: D
authors: Giorgi
authors: A
authors: A
authors: Bertini
authors: M
authors: M
authors: Bianchi
authors: M
authors: M
authors: Ferdeghini
authors: E
authors: E
authors: Boldrini
authors: G
authors: G
authors: Dell'Omo
authors: M
authors: M
authors: Paterni
authors: C
authors: C
authors: Giusti
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D001786:Blood Glucose / Q000378:metabolism; D018660:Blood Pressure Monitoring, Ambulatory; D016022:Case-Control Studies; D004452:Echocardiography; D006801:Humans; D006973:Hypertension / Q000097:blood* / Q000473:pathology / Q000503:physiopathology; D007328:Insulin / Q000097:blood*; D007333:Insulin Resistance; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000473:pathology*; D016277:Ventricular Function, Left
chemical_list: D001786:Blood Glucose; D007328:Insulin