Key result
T2DM with hyperlipidemia is linked to lower LV strain than T2DM alone or healthy controls.
Why the study?
Does concomitant hyperlipidemia worsen subclinical left ventricular systolic dysfunction in patients with type 2 diabetes mellitus and normal LVEF?
Observational (n=121)
Does concomitant hyperlipidemia worsen subclinical left ventricular systolic dysfunction in patients with type 2 diabetes mellitus and normal LVEF?
p-value: p=<0.001
In patients with type 2 diabetes and normal LVEF, concomitant hyperlipidemia is associated with more pronounced subclinical left ventricular systolic dysfunction and hypertrophy as detected by 3D speckle tracking echocardiography.
Hyperlipidemia may compound subclinical LV impairment in T2DM; hypothesis-generating for lipid control effects on strain.
AIMS: The aims of the current study were to analyze and compare the left ventricular (LV) structure and function in type 2 diabetes mellitus (T2DM) patients with or without hyperlipidemia using conventional echocardiography and real-time three-dimensional speckle tracking echocardiography (3DSTE) and to determine the variables that could affect LV strain values in these patients. METHODS: Eighty-one T2DM patients with normal LVEF (≥55%) were included, 41 of whom had hyperlipidemia as comorbidity. Forty age- and gender-matched healthy volunteers were recruited as the control group. Conventional echocardiography and 3DSTE were performed, and LV global longitudinal strain (GLS), global circumferential strain (GCS), global area strain (GAS), and global radial strain (GRS) were measured. RESULTS: Significant differences in two-dimensional LV geometry were found among three groups (P = .015). Compared with the control group, LV remodeling was more prevalent in the patients with T2DM, and LV hypertrophy was most prevalent in the T2DM patients with hyperlipidemia. GLS and GCS values decreased significantly in the T2DM patients without hyperlipidemia relative to the control group (P < .01 and P < .05). The GLS, GCS, GAS, and GRS values in the T2DM patients with hyperlipidemia were all significantly lower than those in the control group (all P < .001) and were also significantly lower than those in the T2DM patients without hyperlipidemia (P < .01 or P < .05). Both fasting plasma glucose (FPG) and hyperlipidemia were independently associated with all strain values in patients with T2DM. CONCLUSIONS: The combination of conventional echocardiography and 3DSTE could detect subclinical LV abnormalities in T2DM patients with or without hyperlipidemia.
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Wang et al. (2018) conducted an observational in Type 2 diabetes mellitus with or without hyperlipidemia (n=121). Hyperlipidemia vs. T2DM without hyperlipidemia and healthy volunteers was evaluated on Left ventricular strain values (GLS, GCS, GAS, GRS) (p=<0.001). T2DM patients with hyperlipidemia had significantly lower left ventricular strain values compared to healthy controls (P<0.001) and T2DM patients without hyperlipidemia (P<0.05).
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