title: Are left ventricular mass, geometry and function related to vascular changes and/or insulin resistance in long-standing hypertension? ICARUS: a LIFE substudy.
abstract: Vascular hypertrophy and insulin resistance have been associated with abnormal left ventricular (LV) geometry in population studies. We wanted to investigate the influence of vascular hypertrophy and insulin resistance on LV hypertrophy and its function in patients with hypertension. In 89 patients with essential hypertension and electrocardiographic LV hypertrophy, we measured blood pressure; insulin sensitivity by hyperinsulinaemic euglucaemic clamp; minimal forearm vascular resistance (MFVR) by plethysmography; intima-media cross-sectional area of the common carotid arteries (IMA) by ultrasound; and LV mass, relative wall thickness (RWT), systolic function and diastolic filling by echocardiography after two weeks of placebo treatment. LV mass index correlated to IMA/height (r=0.36, P=0.001), serum insulin (r=-0.25, P<0.05), plasma glucose (r=-0.34, P<0.01), and showed a tendency towards a correlation to insulin sensitivity (r=0.21, P=0.051), but was unrelated to MFVR. Deceleration time of early diastolic transmitral flow positively correlated to IMA/height (r=0.30, P<0.01). The ratio between early and atrial LV filling peak flow velocity negatively correlated to MFVR(men) (r=-0.30, P<0.05). Endocardial and midwall systolic LV function were not related to vascular hypertrophy, plasma glucose, serum insulin or insulin sensitivity. In conclusion, insulin resistance was not related to LV hypertrophy or reduced LV function. However, high thickness of the common carotid arteries was associated with LV hypertrophy and high deceleration time of early diastolic transmitral flow. High MFVR was associated with low ratio between early and atrial LV filling peak flow velocity. This may suggest that systemic vascular hypertrophy contributes to abnormal diastolic LV relaxation in patients with hypertension and electrocardiographic LV hypertrophy.
authors.affiliation: Department of Clinical Physiology and Nuclear Medicine, Glostrup University Hospital, Copenhagen, Denmark. mho@dadlnet.dk
authors.forename: M H
authors.initials: MH
authors.lastname: Olsen
authors.forename: E
authors.initials: E
authors.lastname: Hjerkinn
authors.forename: K
authors.initials: K
authors.lastname: Wachtell
authors.forename: A
authors.initials: A
authors.lastname: Høieggen
authors.forename: J N
authors.initials: JN
authors.lastname: Bella
authors.forename: S D
authors.initials: SD
authors.lastname: Nesbitt
authors.forename: E
authors.initials: E
authors.lastname: Fossum
authors.forename: S E
authors.initials: SE
authors.lastname: Kjeldsen
authors.forename: S
authors.initials: S
authors.lastname: Julius
authors.forename: H
authors.initials: H
authors.lastname: Ibsen
mesh_terms: D000368:Aged; D001783:Blood Flow Velocity / Q000502:physiology; D001786:Blood Glucose / Q000378:metabolism; D001794:Blood Pressure / Q000502:physiology; D017536:Carotid Artery, Common / Q000503:physiopathology; D003718:Denmark; D003971:Diastole / Q000502:physiology; D004452:Echocardiography; D005260:Female; D006352:Heart Ventricles / Q000000981:diagnostic imaging / Q000378:metabolism / Q000503:physiopathology; D006801:Humans; D006973:Hypertension / Q000378:metabolism / Q000503:physiopathology*; D017379:Hypertrophy, Left Ventricular / Q000378:metabolism / Q000503:physiopathology; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance / Q000502:physiology*; D008297:Male; D008875:Middle Aged; D009664:Norway; D012737:Sex Factors; D013223:Statistics as Topic; D013318:Stroke Volume / Q000502:physiology; D013599:Systole / Q000502:physiology; D014481:United States; D014655:Vascular Resistance / Q000502:physiology; D016277:Ventricular Function, Left / Q000502:physiology*; D020257:Ventricular Remodeling / Q000502:physiology
chemical_list: D001786:Blood Glucose; D007328:Insulin