title: Relation among left ventricular mass, insulin resistance, and hemodynamic parameters in type 2 diabetes.
abstract: Increased left ventricular mass (LVM) is an independent cardiovascular risk marker, which often occurs independently of arterial blood pressure in type 2 diabetes. To investigate the factors related to the disproportionate increase in LVM in type 2 diabetes, we conducted a cross-sectional study. We studied 40 male type 2 diabetic patients aged 36 to 70 years with controlled blood pressure. Magnetic resonance imaging was used to measure LVM accurately. Radial arterial waveforms were recorded non-invasively by applanation tonometry to assess the hemodynamic status, radial augmentation index (AI) and time from forward peak to reflection peak (TPP). Glycemic control status and insulin resistance were evaluated by plasma HbA1c and homeostasis model assessment (HOMA) score, respectively. E/E', an echocardiographic parameter for left ventricular (LV) diastolic function, was also analyzed by echocardiography. Univariate analyses showed that HbA1c and TPP had trends toward a positive correlation with LVM indexed for body surface area (LVMI), whereas AI did not. When patients' age, heart rate, and systolic blood pressure were simultaneously included in the linear regression model, the TPP and HOMA score were independently related to LVMI (p<0.05 for each variable). Increased LVMI was accompanied with impaired LV diastolic function assessed by E/E'. In conclusion, the TPP and HOMA score were associated with a modest but clinically relevant increase in LVM in type 2 diabetes independently of arterial blood pressure. Pulse wave analysis may reveal hemodynamic alterations that affect LVM but that cannot be identified using a sphygmomanometer.
authors.affiliation: Department of Cardiovascular Medicine, Kyoto University Graduate School of Medicine, Kyoto, Japan.
authors.forename: Neiko
authors.initials: N
authors.lastname: Ozasa
authors.forename: Yutaka
authors.initials: Y
authors.lastname: Furukawa
authors.forename: Takeshi
authors.initials: T
authors.lastname: Morimoto
authors.forename: Eiji
authors.initials: E
authors.lastname: Tadamura
authors.forename: Toru
authors.initials: T
authors.lastname: Kita
authors.forename: Takeshi
authors.initials: T
authors.lastname: Kimura
mesh_terms: D000328:Adult; D000368:Aged; D001794:Blood Pressure / Q000502:physiology*; D003430:Cross-Sectional Studies; D003924:Diabetes Mellitus, Type 2 / Q000473:pathology / Q000503:physiopathology*; D004562:Electrocardiography; D006442:Glycated Hemoglobin / Q000378:metabolism; D006339:Heart Rate / Q000502:physiology; D006706:Homeostasis / Q000502:physiology; D006801:Humans; D006973:Hypertension / Q000473:pathology / Q000503:physiopathology; D017379:Hypertrophy, Left Ventricular / Q000473:pathology* / Q000503:physiopathology*; D007333:Insulin Resistance / Q000502:physiology*; D016014:Linear Models; D008279:Magnetic Resonance Imaging; D008297:Male; D008875:Middle Aged; D018487:Ventricular Dysfunction, Left / Q000473:pathology / Q000503:physiopathology
chemical_list: D006442:Glycated Hemoglobin