[A study of the relationship between remodeling of left ventricle and endothelial injury and pro-inflammatory mediators in different stages of essential hypertension].

Objective: To explore the relationship between left ventricular remodeling and vascular endothelial injury and pro-inflammatory mediators in different stages of essential hypertension.

Methods: Patients were grouped in according to the duration of the disease. The control group consisted of patients with history of hypertension for 6 months to 1 year (35 cases), patients with a history of 3 years were categorized as group A (38 cases), patients with 5-year history as group B (32 cases), 8-year history as group C (33 cases), 13-year history as group D (34 cases), 15-year history as group E (32 cases). Ultrasonic measurements included left atrial diameter (LAD), interventricular septal thickness (IVST), left ventricular posterior wall thickness (PWT). Nitric oxide (NO, nitrate reductase method), plasma endothelin-1 (ET-1, radioimmunoassay), tumor necrosis factor-alpha (TNF-alpha, radioimmunoassay), high-sensitivity C-reactive protein (hs-CRP, turbidimetry method) and interleukin-6 (IL-6, enzyme linked immunosorbent assay) were determined.

Results: There was no significant difference in ultrasonic measurements, vascular endothelial function and pro-inflammatory factors between control group and group A (all P>0.05). With prolongation of disease, there was obvious change in left ventricular remodeling, and the level of NO lowered, but the levels of ET-1, hs-CRP, TNF-alpha, IL-6 were elevated (F(LAD)=5.89, F(IVST)=6.58, F(PWT)=9.84, F(NO)=7.58, F(ET-1)=6.21, F( hs-CRP)=9.80, lzF(TNF-alpha)=12.45, F(IL-6)=6.53, all P<0.01). Compared with the control group, LAD, IVST, PWT, and the levels of NO, ET-1, hs-CRP, TNF-alpha, IL-6 showed statistically significant differences (P<0.05 or P<0.01). There were significant differences among groups B, C, D and E when compared one another (all P<0.01).

Conclusion: The longer the duration of essential hypertension, the more obvious changes are found in left ventricular remodeling and endothelial injury. Pro-inflammatory factors promote endothelial injury and left ventricular remodeling. The vascular endothelial injury and pro-inflammatory mediators are the main promoters of atherosclerosis.