[Diagnostic value of ischemia-modified albumin in patients with acute coronary syndrome].

OBJECTIVE: To investigate the diagnostic value of ischemia-modified albumin (IMA) for patients with acute coronary syndrome (ACS). METHODS: We detected the IMA levels by albumin cobalt-binding (ACB) test and observed its dynamic changes in 492 patients with ACS, 74 patients with high blood pressure, 78 patients with viral myocarditis (VMC), 395 patients with acute chest pain (133 patients with acute ACS and 262 follow-up patients due to chest pain), 68 patients underwent percutaneous coronary intervention (PCI) and 830 healthy controls. Cardiac troponin I (cTnI) levels were assayed and electrocardiogram (ECG) recorded in patients with ACS. RESULTS: The optimal diagnostic cutoff point for IMA in this study population was found to be 0.45 ABSU by ROC analysis. The IMA level (ABSU) in ACS group (0.55 +/- 0.11) was significantly higher than that in VMC group (0.38 +/- 0.11) and IMA levels in ACS and VMC groups were both higher than that in control and high blood pressure groups (0.34 +/- 0.08 and 0.35 +/- 0.08, all P < 0.05). IMA levels and the positive rates in patients with ACS were significantly higher (0.54 +/- 0.12 vs 0.44 +/- 0.12, 77.4% vs 39.3%, all P < 0.01) than those in chest pain follow-up group. In 133 patients with ACS, positive rate for IMA was significantly higher than that for cTnI within 1 h of admission (82.0% vs 40.6%, P < 0.01), and was similar at 6 - 24 h after admission (96.2% vs. 95.5%, P > 0.05). In 72 patients presenting to the emergency center within 3 h of acute chest pain and with negative cTnI, positive rate for IMA was 86.1% and for ECG 72.2%, the sensitivity for ACS diagnosis rised to 93.1% with both methods. The IMA leve was higher immediately after PCI than that before PCI (P < 0.05). IMA levels peaked 1d after hospitalization, then decreased gradually and returned to normal 14 days later. CONCLUSIONS: IMA was a useful biochemical marker for the early diagnosis of ACS.

[Effects of tetramethylpyrazine on fibrosis of atrial tissue and atrial fibrillation in a canine model of congestive heart failure induced by ventricular tachypacing].

OBJECTIVE: To explore the effects of tetramethylpyrazine (TMP) on fibrosis of atrial tissue and atrial fibrillation in a canine model of congestive heart failure (CHF) induced by ventricular tachypacing. METHODS: Twenty-one healthy mongrel dogs were randomly divided into three groups, which were normal control group, untreated group and TMP-treated group. Atrial fibrillation (AF) was induced by burst of atrial pacing, after the canine model of CHF was established. The atrial tissues were sampled and stained with Mallory's trichromic stains, then the fibrosis in the atrial tissues was analyzed. The left ventricular ejection fraction (LVEF) was evaluated by echocardiography. The levels of angiotensin II (AngII), aldosterone (ALD), amino-terminal peptide of type III procollagen (PIIINP)ìlaminin (LN) and hyaluronic acid (HA) in peripheral blood were examined by radioimmunoassay. RESULTS: The LVEF was significantly decreased in the untreated group as compared with that in the normal control group (P<0.01), while the frequencies of AF and sustaining AF were significantly increased and the AF duration was obviously prolonged in the untreated group as compared with those in the normal control group (P<0.01). The fibrosis degree in the left or right atrial tissue in the untreated group was more serious than that in the normal control group (P<0.01). The AF duration was positively correlated with the fibrosis degree in the left atrial tissue (r=0.84, P=0.018). The levels of AngII, ALD, PIIINP and HA in peripheral blood were significantly higher in the untreated group than those in the normal control group (P<0.05 or P<0.01). The level of AngII was positively correlated with the level of ALD in peripheral blood (r=0.759, P=0.048). The LVEF and the frequency of sustaining AF were both significantly improved in the TMP-treated group as compared with those in the untreated group (P<0.05). The fibrosis in the left or right atrial tissue in the untreated group was more serious than that in the untreated group (P<0.01). The levels of AngII and PIIINP in peripheral blood were also markedly higher in the TMP-treated group than those in the untreated group (P=0.05, P=0.01). CONCLUSION: Tetramethylpyrazine has the effect of reducing the fibrosis degree of atrial tissue in dogs with CHF, and this efficacy may be related to the mechanism of decreasing the frequency of AF and shortening the AF duration.

[Collagen type I and interleukin-1 beta gene expression in human atria during atrial fibrillation].

OBJECTIVE: To determine whether gene expression of collagen type I and interleukin-1 beta (IL-1beta) is altered in patients with atrial fibrillation (AF). METHODS: Right atrial tissue samples were taken from 75 patients with rheumatic heart disease who underwent heart valve replacement surgery. 34 patients had no history of AF, 11 patients had paroxysmal AF and 30 patients had persistent AF. The mRNA content of collagen type I and IL-1beta was measured with semi-quantitative RT-PCR. RESULTS: The mRNA content of collagen type I was significantly increased in the persistent AF group (P < 0.001) and increased in the paroxysmal AF group (P < 0.05) as compared with that in the sinus rhythm group. The mRNA content of IL-1beta was up-regulated in the persistent AF group (P < 0.05), but the trend of increase did not reach statistical significance in the paroxysmal AF group (P > 0.05). The mRNA content of IL-1beta was significantly correlated with the mRNA content of collagen type I (r = 0.295, P = 0.011), left atrial dimension (r = 0.385, P = 0.001) and AF duration (r = 0.326, P = 0.004). CONCLUSION: The upregulation of IL-1beta gene expression in atrium may contribute to the atrial fibrosis during AF through influencing collagen metabolism.