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Updated: Jan 21, 2026

Transthoracic Speckle Tracking Echocardiography for the Quantitative Assessment of Left Ventricular Myocardial Deformation
Published on: October 20, 2016
The Further Negative Effect of Hyperuricemia on Left Ventricular Structure and Function in Patients with Type 2
Qingqing Wang1, Kaibin Tan2, Hongmei Xia3
1Department of Ultrasound, Affiliated Hospital of Southwest Medical University, Luzhou, China.
Abstract:
The aims of this study were to explore the left ventricular (LV) structural abnormality and its risk factors in type 2 diabetes mellitus (T2DM) patients with or without hyperuricemia (HU) and to compare their LV function using three-dimensional speckle tracking echocardiography (3DSTE). Eighty T2DM patients with preserved LV ejection fraction were included, 40 of whom had HU as co-morbidity. Forty age- and gender-matched controls were also recruited. The risk factors and corresponding diagnostic values for LV remodeling (LVR) were, respectively, determined using multifactor logistic regression and area under the receiver operating characteristic curves (AUC). LV global longitudinal strain (GLS), global circumferential strain (GCS), global area strain (GAS), and global radial strain (GRS) were measured by 3DSTE. LV morphology constituent ratio showed significant differences among groups (P = 0.0001). Compared with the controls, more abnormal LV patterns were found in the two T2DM groups, while LV hypertrophy was the most prevalent in those with T2DM and HU. Fasting plasma glucose and serum uric acid were two significant risk factors for LVR in T2DM patients (AUC values: 0.678 and 0.672). The patients with T2DM alone had significantly lower GLS than the controls (P < 0.05). The patients with T2DM and HU had significantly lower GLS, GCS, GAS, and GRS than the controls (all P < 0.01), and they also had significantly lower GLS, GCS, and GAS than the patients with T2DM alone (all P < 0.05). Conventional echocardiography combined with 3DSTE could detect subclinical LV structural abnormality and dysfunction in T2DM patients with or without HU.
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