The Relationship Of PTX3, RRI And Early Target Organ Damage In Primary Hypertension

BackgroundAt present, hypertension is recognized as the important risk factors of the heart, brain, kidney and peripheral vascular disease. According to the world Hypertension League (WTL), cardiovascular disease and stroke will become the primary cause of death and disability, which are mainly caused by hypertension. Diagnosing early target damage in hypertensive patients is very important to formulate prevention measures and prevent disease progression.As a traditional factor of atherosclerosis, hypertension early target damage is closely related to atherosclerosis. AS is consider to be an an immune-mediated inflammatory process. PTX3 is closely related to the occurrence and development of AS, which has the effect of protecting from cardiovascular by balancing the immune inflammation. PTX3 is indentified as the fist long pentraxin,which together with C-reactive protein, a short pentraxin belonging to be the highly conserved pentraxin family, playing important roles in innate immunity and inflammatory response. Related studies have shown that PTX3 may be an improtant indicator of vascular inflammation and damage, meanwhile PTX3 may also play a role in the innate immune response and inflammatory reactions in the kidney. PTX3 is expressed in human kidney and proximal renal tubular epithelial cells, which is related to endothelial function and urinary protein. While currently, no study reports about plasm PTX3 in hypertension patients. Due to the major source of PTX3 are macrophages and endothelial cells, the levels of PTX3 may better reflect the inflammatory status of the vascular bed, and may be an important marker of subclinical atherosclerosis and early renal injury in primary hypertension patients.Renal artery resistance index (RRI) is widely used in ultrasonic diagnosis of kidney disease, which believed can reflect changes in renal vascular resistance and diagnosis early kidney disease progression. Pathological examination confirmed that the increase of RRI is related to renal biopsy, vascular wall thickening and glomerular sclerosis. Recent studies have shown that positive correlation of RRI with cIMT in patients of essential hypertension, suggested that RRI may have more complicated pathophysiological significance and may reflect the changes in systemic vascular.Objectives:1. To investigate the association between PTX3, RRI and early target organ damage in primary hypertensive patients.2. Discuss the possible mechanism of PTX3 in atherosclerosis of hypertension.Method:In our study, We randomly recruited 60 subjects with primary hypertension from the outpatient cardiovascular clinics of Qilu hospital from June 2009 to November 2009, According to ultrasonography of carotid artery, the hypertensive patients were divided into two groups:hypertension +AS and hypertension-AS.At the same time,29 age-and sex- matched subjects were enrolled. All subjects completed a questionnaire on present condition.including blood press, heart rate.height, weight and so on.plasma PTX3 levels were determined by enzyme linked immunosorbent assay(ELISA). The diastolic and systolic lumen diameters (Dd and Ds) of carotid artery, cIMT and RRI were examined by ultrasonography.Data are expressed as means±SD. To evaluate statistic differences between groups, student's t test for unpaired values was used. Correlations among variables were based on analysis of Pearson's correlation, partial correlation. Moreover, to study whether there was an independent relationship between PTX3, RRI and markers of hypertension early target organ damage, multiple linear regression was performed. P <0.05 was accepted as significant.Results:1. The plasma PTX3 concentration was markedly higher in hypertension+AS, while no significant difference between hypertension-AS and control group.2. Relevant analysis revealed positive correlation with plasma PTX3 for cIMT, carotid stiffness and Microalbuminuria, and negative correlation for distensibility, strain and Glomerular filtration rate(eGFR).3. Multiple linear regression analysis showed that HDL, ACR and cIMT were independently associated with PTX34. RRI in hypertension+AS was significantly higher than hypertension-AS and control group, statistically significant difference(P<0.001).5. Relevant analysis revealed positive correlation with RRI for CIMT, age, systolic blood pressure, pulse pressure and serum creatinine, and negative correlation for diastolic blood pressure and eGFR.6. Multiple linear regression analysis indicated that age, pulse pressure and cIMT could influence RRI independently.7. Plasma PTX3 and RRI have no significant relevance in primary hypertension patients.Conclusions:1. Artery structure and function experienced significant changes in primary hypertension patients, expressed as common carotid artery intima-media thickness,stiffness and RRI increased, carotid tension and distensibility decreased.2. PTX3 in Hypertension+AS group significantly higher than normal control group and hypertension-AS group, indicating that PTX3 play a role in the process of atherosclerosis.3. Plasma PTX3 may not related to the level of blood pressure in hypertensive patients, but positively correlated with with cIMT and carotid artery stiffness, and negatively correlated carotid artery tension and expansion, indicating that plasma PTX3 may serve as a sensitive predictor of hypertensive target organ damage.4. The relationship of plasma PTX3, ACR and eGFR, indicateing PTX3 may be a stable marker of inflammation in hypertension patiants.5. Relevant analysis revealed positive correlation with RRI for cIMT, age, systolic blood pressure, pulse pressure and serum creatinine, and negative correlation for diastolic blood pressure and eGFR, demonstrating RRI is related to the change of cardiovascular morphology and hemodynamics, and may be a useful indicator for diagnosing early target damage in hypertensive patients.6. There are no significant correlation between PTX3 and RRI in essential hypertension patients, showing that they may make actions through different mechanisms.