Basic fibroblast growth factor changes in response to coronary angioplasty in patients with stable angina

Basic fibroblast growth factor (bFGF) has been implicated in the pathogenesis of coronary atherosclerosis and in angiogenesis. We assessed the changes in serum bFGF before, immediately after, and 6 months after coronary angioplasty (PTCA). Using the ELISA methods we measured plasma bFGF in 28 patients who underwent PTCA, in 20 patients with coronary artery disease who underwent elective coronary angiography and in 28 healthy subjects. Before PTCA and coronary angiography, bFGF plasma levels were similar in both patient groups (4.4+/-1.0 vs. 3.3+/-0.5 pg/ml), but were significantly higher compared with those of the control group (0.8+/-0.1 pg/ml, P<0.05). By 24 h, 3 months and 6 months after PTCA, bFGF levels had decreased significantly in the PTCA group (3.2+/-0.6, 1.7+/-0.3 and 2.7+/-0.6 pg/ml, respectively, P<0.05). In conclusion, these findings show that bFGF levels are elevated in patients with coronary artery disease. Following PTCA, bFGF levels decreased significantly and remained stable for 6 months after the procedure. Thus, bFGF level may change in response to PTCA in patients with coronary artery disease and stable angina.     

Relation of plasma brain natriuretic peptide levels in non-ST-elevation coronary disease and preserved systolic function to number of narrowed coronary arteries

Elevated plasma brain natriuretic peptide (BNP) levels have been described in patients with acute myocardial infarction and left ventricular dysfunction. The aim of the present study was to evaluate circulating BNP levels in patients with coronary artery disease without ST-segment elevation acute myocardial infarction and preserved systolic function and to evaluate the BNP levels in relation to the number of involved coronary vessels. We studied 88 patients with coronary artery disease: group 1 had stable angina, group 2 had unstable angina (UA), group 3 had non-Q-wave myocardial infarction (NSTEMI), and group 0 consisted of 15 healthy subjects. All recruited subjects underwent angiographic examination and echocardiographic evaluation. No patients had heart failure, previous myocardial infarction, or electrocardiographic ST elevation. A significant increase in BNP levels was observed in the UA and NSTEMI groups compared with the stable angina group (stable angina 31.3 pg/ml, UA 147.3 pg/ml, NSTEMI, 165.8 pg/ml, p <0.01), and no differences were found between the UA and NSTEMI groups. Analysis of BNP in relation to the number of involved vessels showed significantly higher BNP levels in patients with 3- than in those with 1- or 2-vessel disease (1 to 45.2, 2 to 127.3, and 3 to 220.8 pg/ml, respectively, p <0.05 and p <0.0001, 3 vs 1- and 2-vessel disease, p = 0.01, respectively). Patients with left anterior descending stenosis had higher BNP levels than those with stenosis in other areas (150.8 vs 52.2 pg/ml, p <0.01). In conclusion, circulating BNP levels appeared elevated in patients with acute coronary syndromes with diffuse coronary involvement, even in the absence of systolic dysfunction or heart failure. BNP was also associated with multivessel disease and left anterior descending involvement.     

老年稳定型冠心病患者B型利钠肽分层随访5年结果

目的：探讨稳定型冠心病（SCHD）患者静脉血浆B型利钠肽（BNP）水平与中远期住院事件的关系。方法：入选88例老年SCHD患者,均经冠脉造影（CAG）证实。按所测定的静脉BNP浓度分为BNP≥108pg／ml组（44例）和BNP〈108pg／ml组（44例）。随访两组5年的死亡、非致死性ACS、再次PCI等心血管原因和非心血管原因住院事件,并进行比较。结果：平均随访62．7月,高水平BNP组的全因住院事件率显著高于低水平BNP组E62．1％（141／227）比37．9％（86／227）,P=0．041],非心血管原因住院率非常显著高于低水平BNP组E39．2％（89／227）比16．3％（37／227）,P=0．010]。结论：老年稳定型冠心病中基线B型利钠肽水平较高者的远期住院事件率较高。     

Proximal coronary vasomotor reactivity after exercise training in dogs

The effects of exercise on large coronary vasoreactivity were determined in eight dogs trained by treadmill running for 8 weeks. Six nontrained dogs comprised the control group. The trained group showed a significant reduction in heart rate during graded submaximal exercise testing when compared with the controls, and resting plasma levels of norepinephrine (nontrained group, 331 +/- 99 pg/ml; trained group, 142 +/- 30 pg/ml; p less than .05) and epinephrine (nontrained, 424 +/- 105; trained, 258 +/- 45 pg/ml; p less than .05) were reduced significantly in the trained group. Epicardial coronary responses to intracoronary infusion of serotonin and phenylephrine were evaluated by quantitative coronary angiography, and myocardial blood flow was measured with 15 microns radioactive microspheres. Left ventricular/body weight ratio was similar in the trained (4.81 +/- 0.24 g/kg) and nontrained groups (4.79 +/- 0.17), and no differences were noted in resting myocardial oxygen consumption or coronary arteriovenous oxygen difference. The constriction of the proximal left anterior descending artery (LAD) in response to serotonin infusion was not different in the two groups, but the LAD and circumflex artery constrictor responses to phenylephrine were attenuated in the trained when compared with the nontrained dogs. The data indicate that endurance exercise diminishes the large epicardial coronary vasoconstrictor response to alpha-adrenergic stimulation, but not to serotonin. The blunted constrictor response in the trained animals suggests that exercise may be useful in reducing epicardial coronary vasoconstriction, which is thought to be important in some patients with coronary artery disease.     

Rise and fall of B-type natriuretic peptide levels in patients with coronary artery disease and normal left ventricular function after cardiac revascularization

BACKGROUND: Recently, it was shown that B-type natriuretic peptide levels are increased in patients with acute coronary syndromes. AIMS: To assess the relation between B-type natriuretic peptide and ischemia in patients with stable and unstable angina pectoris with normal left ventricular function in relation to the extent of ischemia and response to revascularization. METHODS: Fifty-nine consecutive patients were enrolled in the study, patients were divided into two groups: stable angina patients (group I, n=18), and unstable coronary patients (group II, n=41). Baseline characteristics were compared with 15 age-matched and sex-matched participants. B-type natriuretic peptide levels were measured at baseline and 3, 7 and 90 days after coronary revascularization in group I and II. RESULTS: Patients with unstable angina pectoris had increased B-type natriuretic peptide levels compared with stable angina pectoris patients (B-type natriuretic peptide levels: controls 15.5+/-13 pg/ml, stable angina pectoris group 28.4+/-19 pg/ml, unstable angina pectoris group 104+/-81 pg/ml; P<0.01). A relationship between the number of affected coronary vessels and B-type natriuretic peptide was assessed (one-vessel 29.9+/-21 pg/ml, two-vessel 93.8+/-87 pg/ml, three-vessel 119+/-88 pg/ml; P<0.01). After revascularization, B-type natriuretic peptide levels decreased in groups I and II (25+/-20 vs. 39+/-28 pg/ml) and were similar after 90 days in percutaneous transluminal coronary angiograghy and in coronary artery bypass grafting groups (percutaneous transluminal coronary angiography 26+/-22 pg/ml, coronary artery bypass grafting 36+/-26 pg/ml; NS). CONCLUSIONS: B-type natriuretic peptide levels increase in unstable angina pectoris patients and are linked to the extent of coronary disease in patients with normal left ventricular systolic function, and returned to baseline level after surgical or catheter revascularization.     

冠心病患者脑钠肽与冠状动脉病变程度的相关性研究

目的探讨脑钠肽与冠心病患者冠状动脉(冠脉)病变严重程度的相关性。方法入选行冠脉造影检查的冠心病患者173例,所有患者入院后均行冠脉造影检查及血浆脑钠肽(BNP)检查,分析不同冠脉病变支数、冠心病分型、冠脉病变程度(Gensini积分)与患者血清BNP水平之间的关系。结果随着冠脉病变支数增加,患者BNP水平呈显著增加趋势(P0.05)。稳定型心绞痛、不稳定型心绞痛、心肌梗死三组患者BNP水平呈显著增加趋势,三组BNP水平之间差异有统计学意义(P0.05)。BNP100pg/ml的患者Gensini积分显著高于BNP100 pg/ml的患者Gensini积分,分别为(53.7±15.9)分vs.(29.3±20.7)分,差异具有统计学意义(P0.05)。Gensini积分与BNP水平存在显著正相关(r=0.476,P0.05)。结论 BNP水平与冠心病患者冠脉病变严重程度正相关,BNP水平有可能作为冠心病患者冠脉病变严重程度的判断指标。     

Transient increase in plasma brain (B-type) natriuretic peptide after percutaneous transluminal coronary angioplasty

BACKGROUND: Brain (B-type) natriuretic peptide (BNP) is known to be secreted predominantly from the myocardium. Brain natriuretic peptide plasma concentrations have been shown to be markedly increased in patients with acute myocardial infarction; however, plasma BNP response during episodes of myocardial ischemia has not been established. HYPOTHESIS: This study was designed to examine plasma BNP in patients with transient myocardial ischemia induced by inflation of a percutaneous transluminal coronary angioplasty (PTCA) balloon. METHODS: Thirty consecutive patients (26 men and 4 women; mean age 61 years) who underwent PTCA, and another 49 patients (39 men and 10 women; mean age 63 years) who underwent diagnostic coronary angiography were enrolled in this study. Serum BNP concentrations were assayed in all patients. RESULTS: Plasma BNP was increased significantly with a peak concentration of 66.1 +/- 65.2 pg/ml 24 h after PTCA. Coronary angiography did not cause plasma BNP increase (immediately before 30.4 +/- 29.0 pg/ml, 24 h after 33.7 +/- 30.6 pg/ml). No significant differences were present in hemodynamic parameters measured immediately before and 24 h after PTCA. CONCLUSION: Plasma BNP is increased by transient myocardial ischemia induced by PTCA.     

Plasma and pericardial fluid natriuretic peptide levels in postinfarction ventricular dysfunction

AIMS: In the present study we examined plasma and pericardial fluid ANP and BNP concentrations in postinfarction ventricular dysfunction. The association of peptide levels to left ventricular (LV) dysfunction and to the localization of the myocardial infarction (MI) was studied. METHODS AND RESULTS: Plasma and pericardial fluid samples were obtained from 37 patients undergoing coronary bypass surgery. According to the ECG and preceding coronary angiography, the patients were divided into three groups: previous anterior myocardial infarction (MI) (n=12), previous inferior/posterior MI (n=15) and no history of MI (n=10). When compared to the control group with no MI, the patients with anterior MI had elevated plasma ANP and BNP (134+/-13 vs. 81+/-15 pg/ml, P<0.01 and 95+/-10 pg/ml vs. 26+/-8 pg/ml, P<0.01, respectively) and pericardial fluid BNP (473+/-60 pg/ml vs. 57+/-8 pg/ml, P<0.001) levels. The plasma natriuretic peptide concentrations were not increased in the patients with inferior/posterior MI, but the pericardial fluid BNP concentrations were greater than in the patients with no history of MI (129+/-35 pg/ml vs. 57+/-8 pg/ml, P<0.05). Six of the 12 patients with previous anterior MI had LVEF> or =45%. Despite their normal LV systolic function, these patients had increased plasma and pericardial fluid BNP levels when compared to the group with no history of MI (68+/-18 pg/ml vs. 26+/-8 pg/ml, P<0.05 and 534+/-258 pg/ml vs. 57+/-8 pg/ml, P<0.01, respectively). CONCLUSIONS: Previous anterior myocardial infarction was associated with increased cardiac BNP production even if the LV systolic function was normal (LVEF> or =45%). The high pericardial fluid BNP concentrations in postinfarction patients suggest that the BNP synthesis and release are augmented in the ventricular myocardium independent from the LVEF.     

The relationship between severity of coronary artery disease and plasma level of vascular endothelial growth factor.

OBJECTIVE: It has been known that ischemia or occlusion of coronary arteries in animal models increases the production of vascular endothelial growth factor (VEGF); however, little is known about the relationship between coronary artery disease and VEGF in humans. In this study, our aim was to evaluate the relationships between the degree of coronary occlusion and plasma VEGF level as well as other risk factors, including age, weight, arterial blood pressure, cholesterol, triglyceride, blood glucose, and high-sensitive C-reactive protein (hsCRP) in patients with established coronary artery disease. MATERIALS AND METHODS: Our study group consisted of 77 patients. Of these, 38 patients had normal coronary angiography (control group; group C) and 39 had abnormal angiography (17 critical lesion; group CL, 22 noncritical lesion; non-CL group). RESULTS: Plasma VEGF level was 116.95+/-30.12 pg/ml in the control group, 212.47+/-75.28 pg/ml in group CL, and 138.89+/-45.18 pg/ml in the non-CL group. Plasma VEGF level of group C was found to be lower than that of group CL (P<.05), but the difference between groups C and non-CL was insignificant (P>.05). However, logistic regression analysis showed that VEGF level of group CL was significantly higher (P<.001). There was a negative correlation between VEGF and haemoglobin (r=-0.58, P<.01), and positive correlation between VEGF and age (r=0.29, P<.04). There was no relationship between plasma VEGF level and other cardiac risk parameters. Group CL had a higher level of total and LDL-cholesterol levels. CONCLUSION: Increased plasma VEGF levels in patients with coronary artery disease may point that the coronary lesion is critical, and VEGF increase in patients with established coronary artery disease may be used as an indicator of the need for revascularization.     

Usefulness of serum N-terminal pro-brain natriuretic peptide to predict in-stent restenosis in patients with preserved left ventricular function and normal troponin I levels

The level of N-terminal pro-B-type natriuretic peptide (NT-pro-BNP) is a strong predictor of mortality in patients with acute coronary syndrome and may be a strong prognostic marker in patients with chronic coronary artery disease. We investigated whether NT-pro-BNP could predict in-stent restenosis (ISR) in asymptomatic patients with preserved left ventricular (LV) systolic function who underwent percutaneous coronary intervention. We measured serum NT-pro-BNP levels in 249 patients (61 +/- 9 years of age; 73% men) with preserved LV systolic function (ejection fraction >50%) who underwent follow-up coronary angiography. Initial diagnoses were stable angina in 50 (20%), unstable angina in 133 (53%), and myocardial infarction in 66 (27%). Baseline characteristics between groups with ISR (n = 92) and without ISR (n = 157) were similar. The level of NT-pro-BNP was higher in patients with ISR than in those without ISR (222 +/- 327 vs 94 +/- 136 pg/ml, p = 0.001). In the ISR group, NT-pro-BNP level was higher in patients with left anterior descending coronary artery ISR (n = 53, 312 +/- 479 pg/ml) than in those with left circumflex coronary artery ISR (n = 19, 115 +/- 98 pg/ml, p = 0.018). At the standard cutoff of >200 pg/ml, a high NT-pro-BNP level indicated a high probability of ISR (odds ratio 2.18, 95% confidence interval 1.0 to 4.5, p = 0.038). In multivariate analysis, NT-pro-BNP level was an independent predictor for ISR. In conclusion, NT-pro-BNP could be a predictor of ISR in asymptomatic patients with preserved LV systolic function.     

Relationship between brain natriuretic peptide and coronary stenosis: influence of aging

OBJECTIVES: The relationship between brain natriuretic peptide (BNP) and coronary stenosis, and the utility of BNP for the prediction of coronary stenosis were investigated. METHODS: This study included 100 consecutive patients (48 men, 52 women, mean age 65.8 +/- 9.9 years) who underwent elective cardiac catheterization for the diagnosis of coronary stenosis without other heart diseases (heart failure, valvular heart disease, cardiomyopathy, sick sinus syndrome), and E/A was recorded by echocardiography. The relationship between coronary stenosis, left ventricular ejection fraction by left ventriculography, left ventricular end-diastolic pressure, E/A, left ventricular stroke volume index by echocardiography and BNP were investigated. RESULTS: Thirty-nine patients revealed coronary stenosis > or = 75% (CS), and 6 patients had chronic total occlusion. In the CS(+) group, BNP and left ventricular end-diastolic pressure were elevated significantly (50.7 +/- 48.5 vs 22.1 +/- 21.6 pg/ml, p < 0.05; 9.2 +/- 5.3 vs 6.4 +/- 3.4 mmHg, p < 0.05). In logistic regression analysis, BNP and left ventricular end-diastolic pressure had significant correlations with CS(+), independent of age, systolic blood pressure, E/A and left ventricular ejection fraction (p = 0.007, p = 0.05, respectively). Prognostic values of BNP (> 20 pg/ml) for the diagnosis of CS(+) were sensitivity of 79%, and specificity of 61% (p < 0.005). In the CS(-) group, the patients showing BNP > 20 pg/ml were older than the patients showing BNP < or = 20 pg/ml (68.4 +/- 8.5 vs 60.0 +/- 9.4, p < 0.05). Therefore, the prognostic values were reduced (sensitivity 78%, specificity 82%, p < 0.005) in the younger group (age < 65, n = 42). Even in patients with coronary stenosis but without chronic total occlusion, both BNP and left ventricular end-diastolic pressure were elevated significantly compared with the patients without coronary stenosis (22.1 +/- 21.6 vs 44.0 +/- 43.2 pg/ml, p < 0.01; 6.4 +/- 3.4 vs 9.1 +/- 5.2 mmHg, p < 0.01). CONCLUSIONS: Plasma BNP levels are useful markers for detecting coronary stenosis, especially in younger patients.     

Association of elevated B-type natriuretic peptide levels with angiographic findings among patients with unstable angina and non-ST-segment elevation myocardial infarction

OBJECTIVES: We hypothesized that elevated B-type natriuretic peptide (BNP) levels would be associated with a greater severity of angiographic disease and a greater extent of myocardium at risk. BACKGROUND: Elevations of BNP have been associated with increased risk of adverse outcomes in patients with unstable angina and non-ST-segment elevation myocardial infarction (UA/NSTEMI). METHODS: Of the 2,220 patients with UA/NSTEMI enrolled in the Treat Angina with Aggrastat and Determine Cost of Therapy with an Invasive or Conservative Strategy-Thrombolysis In Myocardial Infarction-18 (TACTICS-TIMI-18) trial, 276 randomized to the invasive arm had both baseline BNP levels and angiographic core laboratory data. Patients were categorized according to their baseline BNP levels as < or =80 or >80 pg/ml. RESULTS: A total of 233 patients (84%) had BNP levels >80 pg/ml, and 43 (16%) had admission BNP levels >80 pg/ml. Patients with BNP >80 pg/ml had tighter culprit vessel stenosis on quantitative coronary angiography (median stenosis 76% vs. 67%, p = 0.004) and a higher (slower) corrected TIMI frame count (median CTFC 43 vs. 30, p = 0.018) in the culprit vessel. The median BNP level was higher in patients with a left anterior descending coronary artery (LAD) versus non-LAD culprit lesion location (median BNP level 40 vs. 24 pg/ml, p = 0.005), and the culprit artery was more often the LAD in patients with BNP >80 pg/ml compared with < or =80 pg/ml (44% vs. 30%, p = 0.06). CONCLUSIONS: Among patients with UA/NSTEMI, elevated BNP levels are associated with tighter culprit stenosis, higher CTFC, and LAD involvement. These findings suggest that elevated BNP may be associated with a greater severity and extent of myocardial ischemic territory during the index event and may partly explain the association between elevated BNP and adverse outcomes.     

Increased plasma levels of soluble vascular cellular adhesion molecule-1 in patients with chest pain and angiographically normal coronary arteries

AIMS: To assess plasma levels of vascular cellular adhesion molecule-1, a marker of endothelial dysfunction, in patients presenting with coronary syndromes submitted to coronary angiography. METHODS AND RESULTS: Plasma levels of soluble vascular cellular adhesion molecule-1 were measured by enzymatic immunoabsorbent assay in eight patients with angina-like chest pain and angiographically normal coronary arteries; in 14 patients with stable angina and in 18 patients with unstable angina, both with coronary lesions by angiography, and in 10 healthy volunteers. Levels of soluble vascular cellular adhesion molecule-1 were higher in unstable angina patients (1777+/-161 SE pg ml(-1)) compared to patients with stable angina (1178+/-206 SE pg ml(-1), P<0.05). Moreover, patients with angina-like chest pain and normal coronary arteries had significantly higher soluble vascular cellular adhesion molecule-1 levels (2307+/-295 SE pg ml(-1)) compared to stable angina patients (P<0.05), but similar levels compared to unstable angina patients. Patient groups had higher values of soluble vascular cellular adhesion molecule-1 compared to the control group (734+/-97 SE pg ml(-1)). CONCLUSIONS: Increased levels of soluble vascular cellular adhesion molecule-1 are associated with coronary artery disease in patients with anatomically established lesions. In patients free of flow-limiting lesions and angina-like chest pain, high levels of this marker may indicate endothelial dysfunction.     

Effect of atrial natriuretic factor on coronary vascular tone

To test whether atrial natriuretic factor (ANF) may be involved in the modulation of coronary vasomotor tone, ANF was injected into angiographically normal left coronary arteries. Measurement of epicardial diameters of the circumflex (Cx) and left anterior descending artery (LAD) were made from biplane angiograms by an automatic contour-detection system. Bolus injection of ANF (0.07 micrograms/kg, diluted in 1 ml 0.9% NaCl, n = 7) increased diameter of proximal segments of LAD (11 +/- 4%) and Cx (10 +/- 4%) (p less than 0.02 each vs control) without altering heart rate and mean arterial pressure (MAP). Intracoronary nitroglycerin (NTG, 0.3 mg) increased diameters of identical LAD and Cx segments by 18 +/- 3% and 20 +/- 4%. Intracoronary ANF infusion (0.02 micrograms/kg/min over 5 min, followed by 0.1 micrograms/kg/min, n = 10) exerted dose-dependent increases in diameters of LAD and Cx (low dose: + 5 +/- 2%, p less than 0.05 vs control; high dose: + 13 +/- 3%, p less than 0.01 vs control). ANF-infusion increased arterial plasma ANF levels from 280 +/- 80 pg/ml during control to 894 +/- 82 pg/ml (low dose; + 614 pg/ml vs control) and to 2290 +/- 228 pg/ml (high dose). Severe ischemia in four patients undergoing angioplasty exerted substantial increase in arterial ANF levels (160 +/- 60 to 608 +/- 111 pg/ml; + 448 pg/ml vs control), similar to the increase elicited by low dose ANF infusion in man.(ABSTRACT TRUNCATED AT 250 WORDS)     

Chemokines in patients with ischaemic heart disease and the effect of coronary angioplasty

Percutaneous coronary transluminal angioplasty (PTCA) may release inflammatory mediators such as chemokines. Monocyte chemoattractant protein-1 (MCP-1) and eotaxin (EOX) are monocyte- and eosinophil-specific chemokines involved in the inflammation and pathogenesis of coronary atherosclerosis. A total of 28 patients undergoing elective PTCA, 20 coronary artery disease (CAD) patients undergoing coronary angiography and 28 healthy controls were studied. In PTCA patients before the procedure, MCP-1 plasma levels (441+/-64 pg/ml) were similar to those of CAD patients (430+/-24 pg/ml), and significantly higher compared with controls (145+/-17 pg/ml, P<0.01). MCP-1 rose significantly after 3 and 6 months following PTCA (696+/-89 and 876+/-86 pg/ml, respectively, P<0.01 vs. before PTCA). EOX plasma levels (155+/-14 pg/ml) were similar to those of CAD patients (157+/-14 pg/ml), but significantly higher compared with controls (83.2+/-10 pg/ml, P<0.05). EOX rose significantly 24 h (273+/-41 pg/ml, P<0.05) but not 3 months after PTCA (160+/-20 and 158+/-19 pg/ml, respectively). These findings indicate that chemokine-induced monocyte- and eosinophil-specific chemoattraction is stimulated in patients with coronary artery disease. MCP-1 levels remain significantly elevated for at least 6 months following elective PTCA, suggesting an inflammatory stimulation.     

Usefulness of an elevated B-type natriuretic peptide to predict allograft failure, cardiac allograft vasculopathy, and survival after heart transplantation

B-type natriuretic peptide (BNP) has emerged as an important marker of ventricular wall stress and is predictive of hemodynamic abnormalities in heart transplantation despite "preserved" systolic function. We evaluated the capacity of BNP to predict deaths due to allograft failure in 62 patients long after heart transplantation (mean 5 +/- 2.5 years). Based on the median tendency of measurement of BNP in the absence of rejection during stable surveillance, 2 distinct patient groups were identified as having low BNP (n = 39, < 250 pg/ml; median BNP 70 pg/ml) and high BNP (n = 23, > or =250 pg/ml; median BNP 592 pg/ml). No differences between the 2 BNP groups were noted with regard to age, gender, race, time after transplantation, diabetes mellitus, hypertension, and hyperlipidemia with measurement of BNP. Multivariable analysis showed that decreased left ventricular ejection fraction, angiographic coronary artery disease, and increased serum creatinine were independent predictors of elevated BNP. Cardiac deaths were significantly greater in those with high BNP levels (35%) than in those with low BNP (2.5%, p = 0.01). Absence of significant angiographic coronary artery disease coupled with a BNP of < 250 pg/ml was associated with the lowest event rate (0%), whereas patients with coronary artery disease and BNP > or =250 pg/ml exhibited a 50% cardiac death rate (p <0.01 for trend). Cox's model confirmed that increased BNP and decreased left ventricular ejection fraction are independent predictors of poor survival. Survival analysis associated lower BNP levels with an excellent long-term survival rate (95%) and higher BNP levels with a markedly decreased survival rate (60%, p = 0.002). Higher BNP levels in patients long after heart transplantation are associated with allograft dysfunction and cardiac allograft vasculopathy and are strongly and independently predictive of cardiovascular death.     

冠心病患者动静脉血浆B型利钠肽浓度变化及其意义

目的：初步探讨稳定型冠心病（CAD）患者动静脉血浆B型利钠肽（BNP）浓度的变化及其与冠脉病变的关系。方法：所有患者均经心脏超声和冠脉造影检查,应用化学发光法测定43例经冠脉造影（CAG）证实的稳定型CAD、22例急性冠脉综合征（ACS）和22例CAG正常患者动、静脉（冠状动脉窦和贵要静脉）BNP浓度,收集临床资料,进行统计分析和比较。结果：（1）各组动、静脉血浆BNP浓度无显著差异（P〉0．05）;（2）ACS组动静脉血浆BNP浓度均显著高于CAG正常组和稳定型CAD组（P〈0．01）;（3）稳定型CAD组的动脉血浆BNP浓度显著高于CAG正常组（P〈0．05）,但静脉血浆浓度比较无显著差异（P〉0．05）;（4）冠脉病变狭窄程度越严重,BNP浓度越高（P〈0．05）。结论：血浆BNP浓度可能是反映稳定型CAD患者冠脉病变严重程度的一个预测因子。     

Increased plasma level of endothelin-1-like immunoreactivity during coronary spasm in patients with coronary spastic angina

To examine the role of endothelin in coronary spasm, the plasma endothelin-1-like immunoreactivity in the coronary sinus and the aortic root was measured before and during spasm of the left coronary artery induced by injection of acetylcholine (20 to 100 micrograms) into the left coronary artery in 26 patients with coronary spastic angina. The plasma level of endothelin-1-like immunoreactivity was measured by the radioimmunoassay with a monoclonal antibody against endothelin-1. Plasma lactate levels in the coronary sinus and the aortic root were also measured to evaluate myocardial lactate metabolism during spasm. In 13 patients who had myocardial lactate production during spasm, the plasma level of endothelin-1-like immunoreactivity in the coronary sinus increased from 19.8 +/- 3.0 to 25.7 +/- 6.4 pg/ml (p less than 0.01), while that in the aortic root remained unchanged (from 20.2 +/- 5.9 to 21.3 +/- 5.8 pg/ml). No significant changes in the plasma levels of endothelin-1-like immunoreactivity in the coronary sinus (from 21.1 +/- 7.3 to 19.7 +/- 5.2 pg/ml) and the aortic root (from 21.1 +/- 5.7 to 19.7 +/- 5.6 pg/ml) were observed in 13 patients who did not show myocardial lactate production during spasm. On the other hand, 16 patients without ischemic heart disease showed no significant changes in the plasma levels of endothelin-1-like immunoreactivity in the coronary sinus (from 24.4 +/- 9.7 to 25.8 +/- 6.9 pg/ml) and the aortic root (from 23.0 +/- 7.1 to 23.4 +/- 5.8 pg/ml) by acetylcholine injection (100 micrograms).(ABSTRACT TRUNCATED AT 250 WORDS)     

冠心病患者内皮素水平的变化及其与冠脉病变的关系

目的：探讨冠心病患者血浆内皮素（ET）水平变化与冠状动脉病变的关系.方法：选择2012年12月至2013年12月在我院心内科住院确诊的冠心病患者130例,其中稳定型心绞痛（SAP）、不稳定型心绞痛（UAP）各40例,非ST段抬高型心肌梗死（NSTEMI）、ST段抬高型心肌梗死（STEMI）各25例;多支血管病变58例,单支病变72例.冠状动脉造影正常者50名为非冠心病正常对照组.检测各组ET浓度并进行比较分析.结果：（1）冠心病各组血浆ET水平均显著高于非冠心病对照组（P均＜0.01）;STEMI组、NSTEMI组血浆ET水平显著高于UAP组和SAP组[（95.6±14.7） pg/ml、（89.6±11.2） pg/ml比（67.2±8.5） pg/ml比（35.7±5.8） pg/m门,且UAP组显著高于SAP组（P均＜0.01）,STEMI组和NSTEMI两组间比较无显著差异（P＞0.05）;（2）冠心病组中多支血管病变组血浆ET水平显著高于单支血管病变组[（81.3±12.6） pg/ml比（64.5±10.3） pg/ml],P＜0.01.结论：冠心病患者血内皮素水平显著升高,其检测对于观察病情、判断预后有重要临床意义.     

Increased plasma endothelin levels in angina patients with rapid coronary artery disease progression.

AIMS: To investigate the association between plasma endothelin levels and rapid coronary artery disease progression, as assessed by quantitative angiography. METHODS AND RESULTS: Changes in diameter were assessed in 224 coronary stenoses of 92 consecutive patients (62 men) with chronic stable angina pectoris who were on a waiting list for routine coronary angioplasty and underwent coronary angiography on two occasions: the first (diagnostic) angiogram was carried out at study entry and the second 5.5+/-3.0 months later, immediately prior to coronary angioplasty. A digital quantitative angiographic analysis system was used to assess differences in stenosis diameter between the first and second angiogram. Plasma immunoreactive endothelin levels were estimated by radioimmunoassay at study entry. Rapid coronary artery disease progression occurred in 29 (31.5%) patients according to pre-established criteria: 12 (41%) had a > or =10% diameter reduction of at least one pre-existing stenosis > or =50%, 10 (34%) had a > or =30% diameter reduction of a pre-existing stenosis <50%, 5 (17%) patients developed a new stenosis and 2 (7%) had progression of a lesion to total occlusion by the second angiogram. Baseline demographic, clinical and angiographic data were similar in patients with and without stenosis progression. Plasma endothelin levels were significantly higher in patients with rapid disease progression than in those without (5.7+/-2.0 pg. ml(-1)vs 3.9+/-1.6 pg. ml(-1), P<0.001). Multiple logistic regression analysis revealed that endothelin was an independent predictor of disease progression (P=0.001). Moreover, endothelin levels above 4.26 pg. ml(-1)(the median of the total endothelin concentrations) were associated with a sixfold increase in the risk of developing rapid stenosis progression. CONCLUSIONS: Plasma endothelin is raised in patients with coronary artery disease progression and may be a marker of risk of rapid stenosis progression. Endothelin may also play a pathogenic role in this process.