[Impacts of establishment of chest pain center on the door-to-balloon time and the short-term outcome after primary percutaneous coronary intervention of patients with ST segment elevated myocardial infarction].

OBJECTIVE: To investigate the impact of the establishment of chest pain center (CPC) model based on the pre-hospital real-time tele-12-lead electrocardiogram on the door-to-balloon (D-to-B) time and short-term outcome after primary percutaneous coronary intervention (PPCI) of patients with ST-segment elevated myocardial infarction (STEMI). METHODS: A regular CPC was established with pre-hospital transmitted real-time 12-lead electrocardiogram system for pre-hospital diagnosis of STEMI and enabled the STEMI patients to bypass the emergency room and directly treated in the catheter lab to shorten the D-to-B time. The mean D-to-B time, the short-term outcome and medical costs were compared in PPCI patients before (93 cases, group A) and after (149 cases, group B) the establishment of CPC. RESULTS: After the establishment of CPC, the annual mean D-to-B time was significantly shortened [(127 ± 79) min in group A vs.(72 ± 23 )min in group B, P < 0.01], the shortest monthly mean D-to-B time was remarkably reduced in group B than in group A [(56 ± 11) min vs. (73 ± 14) min, P < 0.01]. The annual ratio of D-to-B below 90 minutes was significantly increased from 62.4% (58/93) in group A to 91.9% (137/149) in group B (P < 0.05) . The in-hospital mortality rate tended to be lower and the incidence of heart failure during hospitalization was significantly reduced in group B compared with group A [3.4% (5/149) vs. 6.5% (6/93), P > 0.05; 14.1% (21/149) vs. 24.7% (23/93), P < 0.05]. The length of hospital stay was slightly shortened from (8.98 ± 4.89) days to (7.79 ± 5.43) days (P > 0.05). Corrected mean medical cost went down by 9.4% (P < 0.05). CONCLUSION: The establishment of CPC may significantly shorten the D-to-B time, improve the short-term outcome and reduce the hospitalization cost for PPCI patients with STEMI.

[Association between multi-noninvasive indexes and mild coronary stenosis].

OBJECTIVE: To observe the changes of multi-noninvasive indexes including endothelial function, arterial flexibility, carotid intima-media thickness (IMT) and serum inflammatory cytokines in patients with mild coronary stenosis. METHODS: One hundred and five patients were divided into three groups according to the result of coronary angiography: coronary heart disease (stenosis > or = 50% in at least one coronary segment), mild coronary stenosis (stenosis < 50% in at least one coronary segment) and control group (normal coronary). Brachial-ankle pulse wave velocity (baPWV) and ankle-brachial index (ABI), reflecting arterial flexibility and the lower extremity vascular disease respectively, were measured by a Colin system, carotid artery IMT was detected echocardiographically. Serum levels of NO, vWF, hs-CRP were measured before coronary angiography in all patients. RESULTS: baPWV [(1482 +/- 155) cm/s vs. (1249 +/- 158) cm/s] and carotid IMT [(0.88 +/- 0.18) mm vs. (0.72 +/- 0.20) mm] were significantly higher while serum levels of NO [(64 +/- 17) micromol/L vs. (83 +/- 17) micromol/L] was significantly lower in mild coronary stenosis group than those in control group (all P < 0.05). vWF, ABI and hs-CRP were similar between the two groups (all P > 0.05). Logistic regression analysis showed that NO, baPWV, smoking are independent predicting factors for mild coronary stenosis (all P < 0.05). CONCLUSIONS: Endothelial dysfunction, reduction of the arterial flexibility as well as increased serum inflammation were associated with mild coronary stenosis.

Characteristics of stress tests and symptoms in patients with myocardial bridge and coronary artery spasm.

BACKGROUND: A relationship between coronary artery spasm (CAS) and myocardial bridge (MB) has been noticed. This study was designed to investigate the differences of stress tests and symptoms between CAS patients with or without MB. METHODS: Two hundred and sixteen patients with atypical chest pain who underwent coronary angiography and acetylcholine provocation test were divided into MB group (n=68) and nonmyocardial bridge group (NMB, n=148). The results of acetylcholine test, treadmill exercise electrocardiography, myocardial scintigraphy, and levels of plasma endothelin-1 and nitric oxide were compared between the two groups. RESULTS: Among these atypical chest pain patients, CAS was induced by acetylcholine in 85% MB patients and 53% NMB patients (P<0.001). A positive exercise electrocardiogram was identified in 71% MB patients and 8% NMB patients (P<0.001). Myocardial scintigraphy revealed ischemic changes in 67% MB patients and 9% NMB patients (P<0.001) and reverse redistribution in 87 and 69% (P<0.01), respectively. MB patients experienced exertional chest pain as well as at rest more frequently than NMB patients. Endothelin-1 levels were elevated in MB group complicated with CAS (P<0.01), whereas nitric oxide levels were reduced in the same cohort (P<0.05) compared with NMB group. CONCLUSION: MB might predispose to CAS in which endothelial dysfunction may play a part. CAS patients with MB usually present mixed chest pain and positive stress tests as well as reversal redistribution on myocardial scintigraphy whereas CAS patients without MB displayed chest pain at rest, negative stress test and reversal redistribution.

[Clinical features of coronary artery spasm patients with or without myocardial bridge].

OBJECTIVE: To investigate the clinical features of coronary artery spasm patients with or without myocardial bridge and explore the roles of endothelial dysfunction in these patients. METHODS: One hundred eighteen patients undergone acetylcholine provoking test were divided into myocardial bridge (MB) group (n = 26) and non-myocardial bridge (NMB) group (n = 92). The results of acetylcholine test, treadmill exercise electrocardiography, stress myocardial perfusion scintigraphy, plasma level of endothelin-1 and nitric oxide were compared between MB group and NMB group. RESULTS: Coronary artery spasm was induced in 21 patients in MB group (81%) and 52 patients in NMB group (57%, P < 0.05). Positive treadmill electrocardiography was obtained in 19 patients in MB group (73%) and 7 patients in NMB group (8%, P < 0.001). Ischemic perfusion defect in 20 (77%) and 9 patients (10%, P < 0.001) and reverse redistribution in 23 (88%) and 68 patients (74%, P > 0.05). Patients showed different clinical features in MB group and NMB group (more short-duration exertional angina and could not be readily released by nitroglycerine in MB group while more patients experienced long-lasting variant angina and symptoms could be readily released by nitroglycerine). Plasma endothelin-1 level was significantly higher [(132.1 +/- 6.5) ng/L vs. (108.5 +/- 8.2) ng/L, P < 0.01] while nitric oxide was significant lower [(84.7 +/- 17.5) ng/L vs. (99.8 +/- 18.2) ng/L, P < 0.05] in MB group compared to NMB group. CONCLUSION: MB patients were prone to coronary artery spasm partly due to endothelial dysfunction. Patients with MB and coronary artery spasm also showed classic clinical symptoms and positive stress tests for ischemia.

[Relationship between dehydroepiandrosterone and arteriosclerosis in premenopausal and postmenopausal women].

OBJECTIVE: To investigate the correlation between dehydroepiandrosterone and arteriosclerosis in premenopausal and postmenopausal women. METHODS: Forty premenopausal and 40 postmenopausal women were examined for serum concentrations of dehydroepiandrosterone and intima-media thickness of the carotid artery, and the serum concentrations of lipids, estrogen, endothelin, and E-selectin were also measured. RESULTS: Compared with premenopausal women, the mean intima-media thickness was increased but dehydroepiandrosterone and estrogen levels were decreased in postmenopausal women. A significant inverse correlation was detected between the intima-media thicknesses and dehydroepiandrosterone level. The postmenopausal women had decreased antioxidation and elevated low-density lipoprotein level. CONCLUSION: Arteriosclerosis is more likely to occur in women with low dehydroepiandrosterone level which causes decreased antioxidation and elevation of blood lipid levels.

[A new synthetic tripeptide inhibits L-arginine transport in macrophages].

OBJECTIVE: To observe the effect of a new synthetic tripeptide [Arg(NO(3))- Lys(OCH(3))- Arg(NO(3))] on L-arginine/NO pathway in the macrophage cell strain RAW246.7. METHODS: The cultured macrophages exposed to lipopolysaccharide (LPS, 1 microg/L) treatment were randomly divided into 3 groups (n=6) and treated with distilled water, 1x10(-4) mol/L tripeptide and 1x10(-4) mol/L L-arginine, NG-monomethyl-L-arginine (L-NMMA) for 24 h, respectively. The macrophages were incubated for 24 h with LPS (1 microg/L) and in the presence of different concentrations of L-arginine (0 to 2 mmol/L), or in normal culture medium (containing 0.5 mmol/L L-arginine) for 24 h with LPS (1 microg/L) and in the presence of tripeptide of 0 to 10x10(-4) mol/L. The changes of [(3)H]-L-arginine transport and NO production from the macrophages were measured. RESULT: NO release from macrophages incubated in the LPS-containing culture medium was 50 folds, and [(3)H]-L-arginine uptake 2.7 folds that in cells in normal culture medium. Tripeptide (1x10(-4) mol/L) inhibited [(3)H]-L-arginine transport and NO production by 67% and 71% respectively. The effect of tripeptide was stronger than L-NMMA (P<0.05). Extracellular L-arginine caused a concentration-dependent increase in nitrite production, which reached the maximum at concentrations above 0.5 mmol/L Km for nitrite production of 0.162+/-0.015 mmol/L and Vmax of 91.2+/-2.3 micromol/(24h.10(6) cells). L-arginine transport and NO production were inhibited by tripeptide, but their dose-dependent pattern of changes was different with EC50 of 0.21x10(-4) mol/L and 1.27x10(-4) mol/L, respectively. CONCLUSIONS: Activation of macrophages with LPS induces nitrite accumulation in the culture medium, which is dependent on the presence of extracellular L-arginine. The tripeptide induces dysfunction of L-arginine/NO pathway in macrophages, potently inhibits L-arginine transport and competitively combine the active sites of nitric oxide synthase.