Earlier application of loading doses of aspirin and clopidogrel decreases rate of recurrent cardiovascular ischemic events for patients undergoing percutaneous coronary intervention.

BACKGROUND: Aspirin and clopidogrel resistance plays a significant role in the development of cardiovascular ischemic events for ninety patients undergoing percutaneous coronary intervention. Recent studies have indicated that increasing the dose of antiplatelet drugs maybe a potent method to improve the inhibition of platelet aggregation. METHODS: Thrombelastograph (TEG) determinations were used to evaluate the effect of antiplatelet therapy. According to the results, 90 patients were divided into three groups and given different doses of aspirin and clopidogrel. Thirty patients with both an inhibition rate of aspirin > 50% and an inhibition rate of clopidogrel > 50% were defined as the control group. Sixty patients with an inhibition rate for aspirin < 50% and an inhibition rate for clopidogrel < 50% were defined as the resistance group. Patients in resistance group were randomly assigned to be given a routine dose (100 mg aspirin plus 75 mg clopidogrel per day, which we called a resistance plus routine dose group, R + R) and a loading dose (200 mg aspirin and 150 mg clopidogrel per day, which we called resistance plus loading dose group, R + L) of antiplatelet therapy. A 12-month follow-up was observed to examine the change of inhibition rate of antiplatelet therapy and to estimate the relationship between inhibition rate and the occurrence of cardiovascular ischemic events. RESULTS: After 6 months of antiplatelet therapy, the inhibition rate of aspirin in the R + L group increased from (31.4 ± 3.7)% to (68.6 ± 7.1)%, which was significantly higher than that in R + R group, (51.9 ± 8.2)% (P < 0.01). The inhibition rate of clopidogrel in the R + L group increased from (22.1 ± 3.8)% to (60.2 ± 7.4)%, which was significantly higher than in the R + R group, (45.9 ± 4.3)% (P < 0.01). The occurrence rates of cardiovascular ischemic events, stent thrombosis, recurrent unstable angina and myocardial infarction in the R + R group were 20%, 36% and 17%, respectively. Occurrence was significantly increased compared with that in the control group, 3%, 10% and 1%, respectively (P < 0.01). In contrast, the occurrence rates in the R + L group (10%, 23% and 6%, respectively) were attenuated compared with those in the R + R group (P < 0.01), although still higher than in the control group (P < 0.01). CONCLUSIONS: Almost all of the cardiovascular ischemic events occurred in the first six months after percutaneous coronary intervention. According to the result of TEG determinations, earlier application of a loading dose of aspirin and clopidogrel can decrease the rate of recurrent cardiovascular ischemic events.

[Time-course changes of myogenic tone of mesenteric small artery in spontaneously hypertensive rat].

To investigate the time-course changes of myogenic tone in mesenteric small artery (MSA) of spontaneously hypertensive rat (SHR), thirty-two 7-week aged SHR rats were randomly divided into four groups (8, 16, 24, 32 weeks of age), and 32 sex- and age-matched Wistar-Kyoto (WKY) rats were assigned to control groups (CON). On the day of the study, segments of MSA were isolated and then cannulated to the two pipettes. Vascular diameters in response to the increased intraluminal pressure (from 0 mmHg to 150 mmHg, by 25 mmHg steps) of isolated MSA under no-flow conditions were recorded by a Pressure Myograph System both in physiologic salt solution (PSS) (active diameter, Da) and calcium-free PSS (passive diameter, Dp). The myogenic tone was calculated by (Dp - Da)/Dp × 100%. The tail artery pressure and vascular myogenic tone in SHR rats were significantly higher than those of the CON rats. Before 24 weeks, the vascular myogenic tone of MSA in SHR group increased monotonically, but at the end of 32 weeks, the vascular myogenic tone decreased in comparison with that in 24-week group, but was significantly higher than that in CON group. The tail artery pressure in SHR group slowly increased monotonically with increasing weeks of age, and the tail arterial pressure in 32-week group remained significantly higher than that in 24-week group. Vascular myogenic tone may participate in the whole process of hypertension. Early in the development of hypertension, because of the compensatory role of vascular tone, the vascular function has been partially compensated, thus guaranteeing adequate blood supply to organs. Late in the development of hypertension, because of the decompensation of myogenic tone, the vascular function is damaged, leading to the occurrence of severe vascular disease.

[Effects of bisoprolol on serum interleukin-6 and tumor necrosis factor-alpha level in patients with congestive heart failure].

AIM: To investigate the levels of the serum interleukin-6(IL-6)and tumor necrosis factor-alpha (TNF-alpha) in patients with congestive heart failure (CHF) and to evaluate the beneficial effects of beta-blockers on the above variables. METHODS: Studied 110 patients with CHF randomly treated with routine drugs (ACE Inhibitors, diuretics and vasodilator drugs, n=55) or additional beta-blocker bisoprolol (n=55). The levels of serum IL-6 and TNF-alpha in above patients with CHF at the different period of the course and in 50healthy humans were determined by radioimmunoassay. Simultaneously, the left ventricular ejective fraction (LVEF) of above patients were measured by nuclide ventricular imagery. RESULTS: Compared with control group, the levels of serum IL-6 and TNF-alpha in patients with CHF were significantly increased during the course. There was a significantly negative correlation between IL-6, TNF-alpha and LVEF at 12 weeks after the treatment, and there were significant differences of serum IL-6 and TNF-alpha level among NYHA II, III and IV in CHF patients. The level of serum IL-6 and TNF-alpha were decreased more significantly in the bisoprolol group than in the routine group (P<0.05 ) . CONCLUSION: Serum IL-6 and TNF-alpha level might play an important role in pathogenesis of CHF. Beta-blockers had suppress neurohumoral over activation in patients with CHF.