| Background and objectiveThe incidence of coronary artery disease in hypertensive patients is still high, even if blood pressure are properly controlled. And so is left ventricular hypertrophy even after using full dosage angiotensin converting enzyme inhibitor. The mechanism is not clear. Obesity and glycose-lipid metabolic disorder always accompany with hypertension. Insulin resistance, as the core factor of metabolic symptom, correlates with hyperleptinmia. Leptin and insulin resistance are considered to be associated with the incidence of cardiovascular diease in hypertensive patients recently. And the correlation of leptin, insulin resistance and platelet aggregation, left ventricular hypertrophy becomes a study spot.Platelet plays an important role in the physiological hemostasis and pathological thrombogenesis. Animal experiment showed that thrombi forming in the obese mice which defect leptin were generally less stable and embolized more frequently than those of WT mice after arterial injury. And the median time to complete thrombotic arterial occlusion after injury was significantly prolonged in ob mice compared with their lean counterparts. Exploring the relation of leptin and platelet aggregation will help to make clear the etiology of cardiovascular incidence in hypertensive patients.More than 40% hypertensive patients accompany with left ventricular hypertrophy. Retroconversion of this condition can help to delay or prevent the occurrence of heart failure, coronary artery diease and sudden death. Recent observations showed that insulin resistance and leptin may correlate with left ventricular hypertrophy, but their founds contradicted.This study tested the level of platelet aggregation, left ventricular hypertrophy, insulin resistance and the concentration of serum leptin in patients with essential hypertention, and explored whether serum leptin, insulin resistance were associated with platelet aggregation and left ventricular hypertrophy.Materials and methodsHypertensive patients We investigated 61 hypertensive patients who all coincided with 1999 WHO diagnostic standard ( 32 male and 29 female, mean age 48.33±6.05 years). Patients with secondery hypertension, gout, hematopathy, diabetes mellitus, coronary heart disease, heart failure, renal failure or cerebrovascular disease were excluded. All patients should be away from anti-platelet drugs, e.g. aspirin, clopidogrel more than two weeks before enrollment.Controls 45 healthy controls were selected from subjects in outpatient department who underwent regular check-up examinarion (24 male and 21 female, mean age 46.69±6.71 years). The controls had no history of CHD, EH, DM. They had normal electrocardiograms.All of them were measured blood pressure, height, weight and waist circumference, calculated BMI. Peripheral venous blood samples were collected. Tested fasting serum leptin with ELISA, fasting serum insulin with chemoluminescence assay and lipids, glucose with automatic biochemistry analyzer. Platelet aggregation rate was tested using natrium citricum-anticoagulated plasm with turbidity method. Measured left ventricular end-diastolic dimension(LVEDd), left ventricular posterior wall thickness(LVPWT) and interventricular septal thickness(IVST) with two dimensional echocardiography. Left ventricular mass index was calculated.Analysis of variance, t test, Pearson's correlation analysis and multiple linear regression analysis were used for statistic analysis with SPSS 11.01 software .Results 1 The serum concentration of leptin in hypertensive patients was significantly higher than that of control group[(10.64±3.79)ng/ml VS (6.82±2.28) ng/ml, P<0.01]. FL was positively correlated with SBP. FL in patients with EH and LVH was higher than that of hypertensive patients without LVH [(11.16±2.02)ng/ml VS (9.73±4.33)ng/ml, P<0.05].2 Platelet aggregation induced by ADP, COL, ADR were higher in hypertensive patients than in control group, (77.46±9.38)% VS (65.77±5.49)%, (79.43±3.9)% VS (69.15±3.47)%, (80.07±4.4)% VS (62.17±1.8)% separately; P < 0.05 .3 IRI in hypertensive patients was higher than in control group[(1.68±0.37)VS (1.05±0.51); P<0.05], while ISI was lower[(-3.63±0.41) VS (-2.51±0.38); P<0.05]; The two groups had no difference in FINS.4 FL was higher in obese individuals than in non-obesity ones of control group. And lower in male than in female.5 FL was significantly positively correlated with the ratio of female and male, BMI, WC, TG, SBP, DBP, FINS, UA, IRI (P<0.05); but inversely correlated with ISI, HDL(P<0.01). After adjusting for sex and BMI, the correlation between FL(r=-0.6280, P<0.01), IRI(r=0.7013, P<0.01), FINS(r=0.5078, P<0.01), SBP(r=0.3470, P<0.05) and HDL(r=-0.4720, P<0.01) also existed. But in female patients, the correlation of FINS, ISI and FL was not found.6 Pearson's correlation analysis showed that, after adjusting for BMI, LVMI was positively correlated with SBP(r=0.8630, P<0.01), FL(r=0.6926, P<0.01) and FINS (r=0.4532, P<0.05). Platelet aggregation induced by ADP was effected by FL, FINS and ISI; but that induced by COL, ADR only correlated with FINS and ISI.Conclusions1 The increase of leptin is correlated with blood pressure, and it probably aggravates blood pressure and left ventricular hypertrophy.2 There is a high platelet aggregation in hypertensive patients, and the high level of serum leptin and insulin resistance may have effects on it.3 Insulin resistance in hypertensive patients may contribute to left ventricular hypertrophy. 4 Serum leptin is higher in female and obesity than male.5 Serum leptin may interfere the metabolism of lipids and uric acid.
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