[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.