Relationship between tissue type plasminogen activator and coronary vulnerable plaque in patients with acute coronary syndrome: virtual histological study.

BACKGROUND: The association between vulnerability of plaque assessed with intravascular ultrasound (IVUS) and plasma levels of fibrinolytic biomarkers was determined in patients with acute coronary syndrome (ACS). However, few data are available on the relationship between the levels of tissue type plasminogen activator (t-PA) and virtual histological intravascular ultrasound (VH-IVUS) signs of plaque instability. METHODS: Eighty-nine patients with ACS were enrolled in the study. Blood was collected to measure t-PA levels by liquid phase bead flow cytometry. Eighty-nine nonbifurcate lesions (identified by coronary angiography and ECG) were investigated using IVUS before catheterization. IVUS radiofrequency data obtained with a 20 MHz catheter were analyzed with IVUS virtual histological software. The areas of plaque and media were calculated and lesions were classified into two groups: VH-IVUS derived thin cap fibroatheroma (VH-TCFA) and non-VH-TCFA plaque. RESULTS: Plasma t-PA level in the patients with TCFA was significantly lower than that with non-TCFA ((1489+/-715) pg/ml vs (2163+/-1004) pg/ml). Decreased plasma levels of t-PA were associated with plaque vulnerability. Plasma levels of t-PA correlated negatively with plaque plus media and necrotic core in plaque in patients with ACS. CONCLUSIONS: t-PA is an independent risk factor and a powerful predictor of vulnerable plaques. Decreased levels of t-PA may reflect instability of atherosclerotic plaques and might therefore serve as noninvasive determinants of those at high risk for consequent adverse events.

[Relationship between serum vasoactive factors and plaque morphology in patients with acute coronary syndrome].

OBJECTIVE: To investigate the relationship between vasoactive factors and plaque morphology in patients with acute coronary syndrome (ACS). METHODS: Intravascular ultrasound (IVUS) were performed and 7 serum vasoactive factors (sPE, tPA, MCP-1, IL-8, IL-6, sVCAM-1 and sCD40L) were measured through cytometric bead array, serum hs-CRP, HCY, glucose and lipid level were also determined in consecutively enrolled 56 patients with ACS. The changes of bio-factors were compared between vulnerable plaque and non-vulnerable plaque groups, AMI and UA patients, and patients with or without plaque rupture. RESULTS: Biomarkers were similar between patients with unstable angina pectoris and AMI. hs-CRP [(18.9 +/- 4.9) mg/l vs. (5.8 +/- 3.6) mg/L)] and IL-6 [19.5 pg/ml (9.2 - 44.6 pg/ml) vs. 5.3 pg/ml (2.3 - 13.4 pg/ml)] were significantly higher in the group of vulnerable plaque (P < 0.05) compared to non-vulnerable plaques group. sCD40L [(474 +/- 126) pg/ml vs. (238 +/- 35) pg/ml], sPE [(107.2 +/- 39.9) microg/ml vs. (49.1 +/- 5.6) microg/ml] and MCP-1 [(132 +/- 18) pg/ml vs. (127 +/- 13) pg/ml] were significantly increased in the plaque rupture group than that in non-plaque rupture group (all P < 0.05). Increasing of sCD40L, MCP-1, sPE and TC were independent risk factors for plaque rupture. CONCLUSIONS: IL-6 and hs-CRP are biomarkers for vulnerable plaques and diagnosis of acute myocardial infarction. sCD40L, MCP-1 and sPE may serve as the potential markers predicting plaque rupture in patients with ACS.

[Influence of catecholamines on myocardium in experimental septic shock].

OBJECTIVE: To study the influence of catecholamine on myocardium in rats with septic shock and its mechanism by biochemical and pathophysiological methods to evaluate the underlying pathophysiologic mechanism of myocardial damage and the influence of catecholamine on the myocardial injury. METHODS: Septic shock was replicated in rats by cecal ligation and puncture (CLP). Dobutamine (DB), norepinephrine (NE) and combination of DB and NE were used in the lowest dose. The rats were randomly divided into sham operations, CLP control group, CLP+DB group, CLP+NE group and CLP+DB+NE group, 8 rats in each group. Troponin I (cTnI) and total creatine kinase (CK) were measured, and myocardial tissue was examined under light microscopy and electron microscopy. RESULTS: An significantly increased cTnI level was found in CLP septic shock rats, compared with sham rats (P<0.05). In the present study, the use of DB or NE alone, or the combination of the two drugs, was not found to influence the cTnI levels. But, the total CK levels in catecholamine-treated group were significantly increased (P<0.05). There was no statistically significant correlation between cTnI and CK levels. Morphological study confirmed the results of cTnI. Findings that were common in the myocardium of CLP septic shock rats included extracellular and intracellular edema as well as mitrochondrial injury. However, no conclusive evidence was found for the influence of catecholamine on myocardial damage. CONCLUSION: No evidence of the influence of catecholamine on myocardial damage is found. Pathological study suggests that myocardial injury is the result of ischemia.