Related Articles

This study was designed to examine the relationship between pericardial fluid and plasma CRP levels, and to alterations in other biochemical parameters in patients undergoing Coronary Artery Bypass Grafting (CABG). The study group consisted of 96 Coronary Artery Disease (CAD) patients who were referred to our clinic for a CABG procedure and from whom sufficient amount of pericardial fluid could be collected. The patients were classified into 3 groups: Stable Angina Pectoris (SAP) (n = 27), Unstable Angina Pectoris (USAP) (n = 36), and Post-Myocardial Infarction (PMI) (n = 33). Levels of CRP, glucose, albumin, total protein, Creatine Kinase (CK), Creatine Kinase-MB (CK-MB), and Lactate Dehydrogenase (LDH) were determined in pericardial fluid samples and in simultaneously collected blood samples from radial artery. The pericardial CRP and LDH levels in the PMI group were higher than in the SAP (p = 0.015 and p = 0.000, respectively) and USAP (p = 0.011, p = 0.047) groups. Serum CRP levels in USAP (p = 0.014) and PMI (p = 0.000) groups were higher than those in the SAP group. Pericardial albumin levels in the PMI group were higher than in the USAP group (p = 0.038). In all groups, the pericardial fluid/serum protein ratio was > 0.5, the LDL ratio was > 0.6, and pericardial fluid LDH concentrations were > 300 mg/dl. CRP level of pericardial fluid was significantly higher in the PMI group than in other groups. However, pericardial fluid LDH levels were higher than blood LDH levels in this group and were also higher than pericardial fluid LDH levels of other groups.

BACKGROUND: The regions of ruptured atherosclerotic plaques have numerous macrophages. Osteopontin that modulates macrophage function has been shown in atherosclerotic plaques. We aimed to study the plasma levels of osteopontin in patients with unstable angina or non-ST-seg ment elevation myocardial infarction (NSTEMI) and the rela tionship between osteopontin and the extent of the coronary artery disease (CAD). METHODS: We studied 65 patients with unstable angina or NSTEMI, 25 patients with stable angina and 18 patients as the control group. The extent of coronary artery stenosis was determined by the number of vessels with >50% stenosis. Plasma osteopontin concentrations were measured from the blood samples that were drawn immediately after admission to the emergency department in unstable angina/NSTEMI patients and before the coronary angiograph in the stable angina and control groups. RESULTS: The plasma osteopontin concentration was (495 118 ng/ml) significantly higher in the patients with unstable angina/NSTEMI compared to the stable angina group (319 106 ng/ml) and control group (125+/-54 ng/ml) (p=0.0001 The plasma osteopontin levels were lower in the patients with stable angina pectoris who had one-vessel disease compared to those with two-vessel disease (p=0.01). How ever, in the unstable angina/NSTEMI group, the plasma osteopontin levels were statistically not different among the patients with one-vessel, and two-vessel and three-vessel disease (p=NS). There was no correlation between the plasma osteopontin levels and the extent of coronary stenosis. CONCLUSIONS: The plasma osteopontin levels are elevatedin patients with unstable angina/NSTEMI, but there appears to be no correlation with the extent of CAD. These results ma suggest that osteopontin may have a role in the pathobiology of ACS.

Background—Unstable angina is a heterogeneous clinical syndrome. The diverse clinical presentations of unstable angina may reflect different pathogenic mechanisms within the plaque.
Objective—To investigate the cellular constituents of culprit coronary atheromatous plaques in patients with stable angina pectoris and patients with diverse clinical presentations of unstable angina.
Methods—48 patients who underwent coronary atherectomy for management of ischaemic heart disease: 23 had stable angina and 25 had unstable angina. Of the latter, 11 patients were classified as Braunwald's IIB and 14 as Braunwald's IIIB unstable angina. The presence of thrombus, cholesterol clefts, and smooth muscle cell proliferation was assessed in atherectomy samples using standard histological techniques. Monoclonal antibodies were used to identify smooth muscle cells and macrophages within atherosclerotic plaque fragments.
Results—Fresh thrombus was more frequently found in patients with Braunwald's IIIB unstable angina (64%) than in patients with stable angina (22%) or IIB unstable angina (27%) (p < 0.0006). A pattern of smooth muscle cell proliferation ("accelerated progression pattern") was observed which was also associated with coronary thrombus. This pattern was present in 30% of patients with stable angina, 64% of patients with IIIB unstable angina, and in all patients (100%) with IIB unstable angina. Atherosclerotic plaques with thrombus, cholesterol clefts, and macrophages were more common in patients with unstable angina than in stable angina patients.
Conclusion—The presence of a specific smooth muscle cell proliferation (accelerated progression) pattern in patients with unstable angina, particularly in those with Braunwald's IIB unstable angina, suggests that episodic plaque disruption and subsequent healing may be an important mechanism underlying angina symptoms in these patients.

 Keywords: angina pectoris;  atherosclerosis;  unstable angina;  accelerated progression pattern

BACKGROUND—Raised plasma homocysteine is a risk factor for coronary artery disease. Patients with myocardial infarction or unstable angina show greater activation of coagulation, greater troponin release, and a worse outcome.
OBJECTIVE—To examine variations in plasma homocysteine concentration in relation to C reactive protein (CRP) in patients presenting with acute coronary syndromes.
METHODS—Consecutive patients presenting with acute myocardial infarction (22) and unstable angina pectoris (12) were studied. Plasma samples were obtained on admission (before clinical intervention), on days 2, 7, and 28, and again six months after admission. Plasma homocysteine, assayed by high performance liquid chromatography, and CRP were both determined at the same time points. Changes were assessed by analysis of variance.
RESULTS—CRP concentrations showed a classical rise on day 2, followed by a gradual decline to normal values taken at six months from admission in both myocardial infarction (p < 0.0001) and unstable angina (p = 0.02). Homocysteine concentrations in myocardial infarction (median, 25th to 75th interquartile range) were: 11.9 (10.7 to 12.6), 11.5 (9.1 to 13.4), 12.1 (11.4 to 14.1), 12.4 (11.1 to 14.4), and 12.1 (11.2 to 14.0) µmol/l, for days 1, 2, 7, 28, and 180, respectively (p = 0.02). Significant differences were observed only between day 2 and day 7 (p < 0.05). The final homocysteine measurement was not different from the admission level. Homocysteine concentrations in unstable angina did not differ between admission and convalescence (12.5 (9.1 to 14.5) µmol/l and 12.3 (7.7 to 14.9) µmol/l, respectively).
CONCLUSIONS—Plasma homocysteine concentrations are minimally influenced by acute phase variations with reliable measurements obtained on admission in patients with myocardial infarction and unstable angina.


Keywords: myocardial infarction; unstable angina; homocysteine; sample timing

Background:

Matrix metalloproteinases (MMPs) and Tissue Inhibitor of Matrix Metalloproteinases (TIMPs) may be associated with atherogenesis and plaque rupture. We evaluated the relationship between MMP-1, MMP-9, TIMP-1 and IL-6 levels and risk factors, presentation, extent and severity of atherosclerotic coronary artery disease (CAD).

Methods:

Consecutive patients who underwent coronary angiography were randomly included. The serum concentrations of MMP-1, MMP-9, TIMP-1 and IL-6 were analyzed with ELISA method in 134 patients. Participants were divided into 5 groups; stable angina pectoris (SAP; n= 34), unstable angina pectoris (USAP; n=29), non-ST elevation myocardial infarction (NSTEMI; n=16), acute ST elevation myocardial infarction (STEMI; n=25) and controls (n=30). Coronary angiographic Gensini score was calculated.

Results:

MMP-1 levels were higher in STEMI and NSTEMI groups compared with USAP, SAP and control groups (STEMI vs USAP p=0.005; STEMI vs SAP p=0.001; STEMI vs control p<0.001; NSTEMI vs USAP p=0.02; NSTEMI vs SAP p=0.027; NSTEMI vs control p<0.001). In STEMI group, MMP-9 levels were higher than USAP and control groups (p=0.002; p<0,001). TIMP-1 levels were not significantly different within all 5 groups. MMP-1 levels were found to be elevated in diabetic patients (p=0.020); whereas MMP-9 levels were higher in smokers (p=0.043). Higher MMP-1, MMP-9 and IL-6 levels were correlated with severe Left Anterior Descending artery (LAD) stenosis and higher angiographic Gensini Score (for severe LAD stenosis; r = 0.671, 0.363, 0.509 p<0.001; for Gensini score; r = 0.717, 0.371, 0.578 p<0.001).

Conclusions:

Serum levels of MMP-1, MMP-9, and IL-6 are elevated in patients with CAD; more so in acute coronary syndromes. MMP-1, MMP-9 and IL-6 are associated with more extensive and severe CAD (as represented by Gensini score).

Objective: To investigate the relationship between serum resistin level and acute coronary syndrome (ACS) or stable angina pectoris (SAP). Methods: Sixty-five patients, with coronary artery disease, were enrolled and divided into three subgroups: acute myocardial infarction (AMI), unstable angina pectoris (UAP) and SAP, and 26 healthy people were recruited as controls in the cross-sectional study. Serum resistin levels were determined by ELISA (enzyme-linked immunosorbent assay), and WBC (white blood cell count), hsCRP (high sensitive C-reaction protein), CKmax (maximum of creatinkinase), CK-MBmax (maximum of isozyme of creatinkinase) and cTnImax (maximum of troponin) were measured by standard laboratory methods. Results: The serum resistin levels were 4 folds higher in AMI patients, 2.43 folds in UAP patients and 1.12 folds in SAP patients than in the healthy controls (P<0.05). The resistin levels were also significantly different between AMI [(8.16±0.79) ng/ml], UAP [(5.59±0.75) ng/ml] and SAP [(3.45±0.56) ng/ml] groups (P<0.01); WBC, hsCRP, CKmax, CK-MBmax and cTnImax were significantly increased in AMI patients over UAP and SAP patients. Spearman analysis showed that serum resistin levels were positively correlated with WBC (r=0.412, P=0.046), hsCRP (r=0.427, P=0.037), CKmax, CK-MBmax and cTnImax (r=0.731, 0.678, 0.656; P<0.01). Conclusion: Serum resistin levels increased with inflammatory factors and myocardial impairment. The results suggest that human resistin might play an important role in the pathogenesis of atherosclerosis and AMI as an inflammatory factor.

INTRODUCTION:

Adiponectin is a circulating hormone that is produced exclusively by adipocytes and has anti-inflammatory and anti-atherogenic properties. The hypothesis that there are differences in adiponectin levels between stable and unstable coronary-artery disease patients remains controversial. Furthermore, the potential relationships between the plasma adiponectin level and the inflammatory and non-inflammatory markers (oxidized low density lipoprotein and nitric oxide) in patients with stable and unstable coronary-artery disease relative to normal subjects have not been assessed.

OBJECTIVES:

To assess whether plasma adiponectin levels differ among patients with stable and unstable coronary-artery disease and among control subjects, and to correlate plasma adiponectin level with inflammatory and clinical risk factors (such as oxidized-LDL and nitric oxide) in these patients.

METHODS:

This study included 50 control subjects, 50 stable angina patients and 50 unstable angina patients with angiographically documented coronary-artery disease. Plasma adiponectin and oxidized-LDL levels were determined using an enzyme immunoassay. Plasma nitric oxide, high sensitivity C-reactive protein and lipid profile levels were also measured.

RESULTS:

Plasma adiponectin levels were lower in the unstable angina patients (4.9±1.30 µg/mL) than in the stable angina patients (6.34±1.0 µg/mL) or in the controls (9.25±1.8 µg/mL); these levels were also significantly lower in stable angina patients versus controls (p<0.001). Plasma adiponectin levels were negatively correlated with oxidized-LDL, high sensitivity C-reactive protein, lipid profile and other clinical risk factors but positively correlated with nitric oxide.

CONCLUSION:

Plasma adiponectin levels were found to be lower in both stable and unstable angina patients relative to control subjects, and the correlation between plasma adiponectin and cardiovascular markers is weakened in these patients.

In recent years, the indications for percutaneous transluminal coronary angioplasty have expanded to include multivessel disease, unstable angina pectoris, stenosis of coronary bypass grafts, and recent total coronary occlusion. To evaluate our experience in using percutaneous transluminal coronary angioplasty to treat unstable angina, we reviewed the records of the patients who underwent this procedure at our hospital between January 1983 and December 1986.

Of the 689 patients who underwent balloon angioplasty during the study period, 454 had stable angina and 235 had unstable angina; of the latter group, 34 (14.5%) required emergency coronary artery bypass grafting after balloon angioplasty failed. This outcome was associated with 2 risk factors: previous myocardial infarction and triple-vessel disease.

Our data suggest that, in cases of unstable angina pectoris, percutaneous transluminal coronary angioplasty should be reserved for patients with single-vessel disease and no evidence of previous myocardial infarction. They also lend credence to the conclusion that the disease process in unstable angina is different from that in stable angina, and that therapy should be directed towards reducing platelet aggregation and correcting global ischemia, rather than towards balloon angioplasty of “culprit lesions.” (Texas Heart Institute Journal 1988;15:152-154)

Background

Anaemia is an independent risk factor for cardiovascular (CV) events in patients with heart failure and patients with chronic kidney disease. The effect of anaemia on CV outcomes in patients with coronary artery disease (CAD) remains unclear. Therefore, we investigated the prognostic value of anaemia in this group of patients.

Methods

Patients with stable angina pectoris, referred for a first diagnostic coronary angiography, were eligible for this study. Only subjects with significant coronary artery disease (>50% luminal narrowing) were used for analysis (n=143). Cardiovascular events were defined as cardiovascular death, acute myocardial infarction and hospitalisation for unstable angina pectoris. Anaemia was defined according to WHO criteria as haemoglobin level ≤8 mmol/l in men and ≤7.5 mmol/l in women.

Results

The mean age of the population was 61.5±9.4 years. During follow-up (44±19 months), 19 CV events occurred. The diagnosis of anaemia predicted CV events, even when adjusted for other risk factors (hazard ratio 5.73, 95% confidence interval 1.49-22.13, p=0.01). In univariate analysis, serum erythropoietin levels predicted CV outcomes (p<0.05); however, this association was lost when adjusted for haemoglobin concentration.

Conclusion

Anaemia is associated with worse outcome in patients with established CAD and could be used as a prognostic indicator in this group of patients.

We evaluated leukocyte counts and levels of CRP, fibrinogen, MPO, and PAPP-A in patients with stable and unstable angina pectoris, acute myocardial infarction, and healthy controls. All biomarkers were analyzed again after 6 months. Leukocyte counts and concentrations of fibrinogen, CRP, MPO, and PAPP-A were significantly increased in patients with acute myocardial infarction. Leukocyte counts and concentrations of MPO were significantly increased in patients with unstable angina pectoris compared with controls. After 6 months, leukocyte counts and MPO concentrations were still increased in patients with acute myocardial infarction when compared to controls. Discriminant analysis showed that leukocyte counts, MPO, and PAPP-A concentrations classified study group designation for acute coronary events correctly in 83% of the cases. In conclusion, combined assessment of leukocyte counts, MPO, and PAPP-A was able to correctly classify acute coronary events, suggesting that this could be a promising panel for a multibiomarker approach to assess cardiovascular risk.

Background

Atherosclerosis is an inflammatory condition and increased blood levels of inflammatory biomarkers have been observed in acute coronary syndromes. In addition, high expression of inflammatory markers is associated with worse prognosis of coronary artery disease. The presence and extent of inducible ischemia in patients with stable angina has previously been shown to have strong prognostic value. We hypothesized that evidence of inducible myocardial ischemia by local lesions, as measured by fractional flow reserve (FFR), is associated with increased levels of blood based inflammatory biomarkers.

Methods

Whole blood samples of 89 patients with stable angina pectoris and 16 healthy controls were analyzed. The patients with stable angina pectoris underwent coronary angiography and FFR of all coronary lesions.

We analyzed plasma levels of cytokines IL-6, IL-8 and TNF-α and membrane expression of Toll-like receptor 2 and 4, CD11b, CD62L and CD14 on monocytes and granulocytes as markers of inflammation.

Furthermore, we quantified the severity of hemodynamically significant coronary artery disease by calculating Functional Syntax Score (FSS), an extension of the Syntax Score.

Results

For the majority of biomarkers, we observed lower levels in the healthy control group compared with patients with stable angina who underwent coronary catheterization.

We found no difference for any of the selected biomarkers between patients with a positive FFR (≤0.75) and negative FFR (>0.80). We observed no relationship between the investigated biomarkers and FSS.

Conclusion

The presence of local atherosclerotic lesions that result in inducible myocardial ischemia as measured by FFR in patients with stable coronary artery disease is not associated with increased plasma levels of IL-6, IL-8 and TNF-α or increased expression of TLR2 and TLR4, CD11b, CD62L and CD14 on circulating leukocytes.

OBJECTIVE—To investigate the hypothesis that in coronary artery disease large plaques in compensatorily enlarged segments are associated with acute coronary syndromes, whereas smaller plaques in shrunken segments are associated with stable angina pectoris.
METHODS—Patients selected for percutaneous transluminal coronary angioplasty (PTCA) were divided into two groups, one with stable angina pectoris (stable group, n = 37) and one with unstable angina or postmyocardial infarction angina of the infarct related artery (unstable group, n = 32). In both groups, remodelling at the culprit lesion site was determined by intravascular ultrasound before the intervention. Remodelling was calculated as relative vessel area: [vessel area culprit lesion site ÷ mean vessel area of both proximal and distal reference sites] × 100%. Compensatory enlargement was defined as remodelling of ⩾ 105%, whereas shrinkage was defined as remodelling of ⩽ 95%.
RESULTS—In the unstable group, the vessel area at the culprit lesion site was larger than in the stable group, at mean (SD) 18.1 (5.3) v 14.6 (5.4) mm2 (p = 0.008). Lumen areas were similar. Consequently, plaque area and percentage remodelling were larger in the unstable group than in the stable group: mean (SD) 14.8 (4.8) v 11.6 (4.9) mm2 (p = 0.009) and 112 (31)% v 95 (17)% (p = 0.005), respectively. Significantly more culprit lesion sites were classified as shrunken in the stable group (21/37) than in the unstable group (8/32; p = 0.014). On the other hand, more lesion sites were classified as enlarged in the unstable group (16/23) than in the stable group (8/37; p = 0.022).
CONCLUSIONS—In patients selected for PTCA, the mode of remodelling is related to clinical presentation.


Keywords: atherosclerosis; coronary disease; remodelling; intravascular ultrasound

Background

Accumulating evidence shows that the novel anti-inflammatory cytokine IL-35 can efficiently suppress effector T cell activity and alter the progression of inflammatory and autoimmune diseases. The two subunits of IL-35, EBI3 and p35, are strongly expressed in human advanced plaque, suggesting a potential role of IL-35 in atherosclerosis and coronary artery disease (CAD). However, the plasma levels of IL-35 in patients with CAD have yet to be investigated.

Methods

Plasma IL-35, IL-10, TGF-β1, IL-12 and IL-27 levels were measured using an ELISA in 43 stable angina pectoris (SAP) patients, 62 unstable angina pectoris (UAP) patients, 56 acute myocardial infarction (AMI) patients and 47 chest pain syndrome patients as a control group.

Results

The results showed that plasma IL-35 levels were significantly decreased in the SAP group (90.74±34.22 pg/ml), the UAP group (72.20±26.63 pg/ml), and the AMI group (50.21±24.69 pg/ml) compared with chest pain syndrome group (115.06±32.27 pg/ml). Similar results were also demonstrated with IL-10 and TGF-β1. Plasma IL-12 and IL-27 levels were significantly increased in the UAP group (349.72±85.22 pg/ml, 101.75±51.42 pg/ml, respectively) and the AMI group (318.05±86.82 pg/ml, 148.88±68.45 pg/ml, respectively) compared with chest pain syndrome group (138.68±34.37 pg/ml, 63.60±22.75 pg/ml, respectively) and the SAP group (153.84±53.86 pg/ml, 70.84±38.77 pg/ml, respectively). Furthermore, lower IL-35 levels were moderately positively correlated with left ventricular ejection fraction (LVEF) in CAD patients (R = 0.416, P<0.01), whereas higher IL-27 levels were weakly negatively correlated with LVEF in CAD patients(R = −0.205, P<0.01).

Conclusions

The results of the present study show that circulating IL-35 is a potentially novel biomarker for coronary artery disease. Regulating the expression of IL-35 also provides a new possible target for the treatment of atherosclerosis and CAD.

OBJECTIVE—To assess whether neopterin concentrations in women with unstable angina differ from those in women with chronic stable angina.
DESIGN—Prospective cohort study.
SETTING—University hospital in south west London.
PATIENTS—114 consecutive women with angina were studied: 82 had chronic stable angina (typical exertional chest pain, positive exercise ECG testing, and/or abnormal myocardial scintigraphy; symptoms stable for at least three months), and 32 had unstable angina (Braunwald class III). All patients with chronic stable angina (100%) and 18 with unstable angina (56.3%) underwent digital coronary angiography; neopterin concentrations were determined using a commercially available immunoassay.
MAIN OUTCOME MEASURES—Major clinical events during one year follow up were readmission with Braunwald's class IIIb unstable angina, non-fatal myocardial infarction, and cardiac death.
RESULTS—Major events occurred in 12 women with chronic stable angina (14.6%) and nine women with unstable angina (28.1%). Mean (range) neopterin concentrations were significantly higher in women with unstable angina than in those with chronic stable angina (7.6 (5.1-11.5) nmol/l v 5.9 (4.4-7.5) nmol/l; p = 0.003), even after adjustment for variables which were significantly different on univariate analysis. In women with chronic stable angina, baseline neopterin concentrations were higher in those with cardiac events than in those without events (7.1 (5.9-9.1) nmol/l v 5.7 (3.9-7.3 nmol/l); p = 0.010), even after adjustment for variables with significant differences between both groups on univariate analysis.
CONCLUSIONS—On average, women with unstable angina had significantly higher neopterin concentrations than women with chronic stable angina. Women with chronic stable angina with events during follow up had higher neopterin concentrations than those without events. Neopterin concentrations were similar in patients with unstable angina and women with chronic stable angina who developed events. Neopterin concentrations may therefore be a marker of risk in women with coronary artery disease.


Keywords: neopterin; women; coronary artery disease

BACKGROUND

Leptin and adiponectin are two adipose tissue hormones and their association with the incidence of cardiovascular diseases is under evaluation. The aim of this study was to determine the relationship of leptin and adiponectin with coronary artery diseases.

METHODS

One hundred and seventy patients with angina pectoris and indications of coronary angiography underwent angiography. Serum levels of blood lipids, leptin, and adiponectin were measured. The gathered data was evaluated using SPSS15 software, by multivariate variance analysis.

RESULTS

Analysis of the data demonstrated that 45.1% of the patients had positive angiographic findings. The serum levels of leptin and adiponectin were significantly lower than the minimum levels specified by the kit. However, the two groups, i.e., patients with positive angiographic findings and those with negative findings were not significantly different according to the serum levels of the hormones. Moreover, no significant correlation between the serum levels of the hormones and serum lipids was observed.

CONCLUSION

Various studies have demonstrated that high serum level of leptin and the incidence of coronary artery diseases are correlated. On the other hand, they have reported that adiponectin has cardioprotective role. Confirmation of these findings requires more detailed studies.

Blood samples were taken for haemostatic analysis from 225 patients with angina pectoris who were admitted to hospital for coronary angiography. beta thromboglobulin, platelet factor 3, platelet factor 4, factor VII:C, factor VIII:C, von Willebrand factor antigen, activated partial thromboplastin time, fibrinogen, antithrombin III, protein C:Ag, plasminogen, and antiplasmin were measured before angiography. Patients who had had a myocardial infarction in the two months before the investigation were excluded from the study. Multiple linear regression analysis showed that none of the haemostatic variables contributed independently to the prediction of an angiographic score that indicated the extent of coronary atherosclerosis. History of myocardial infarction, male sex, worsening of angina pectoris, serum triglycerides, and ejection fraction were independently associated with the angiographic score. There were some significant correlations between haemostatic variables and conventional risk factors for coronary heart disease. Thus data obtained from haemostatic analyses of peripheral venous blood do not permit the presence or the extent of atherosclerosis in coronary arteries to be predicted.

BACKGROUND

Atherosclerosis is the commonest cause of vascular disease which can involve peripheral and/or cardiac vessels. This study was conducted to evaluate the possible link between Ankle-Brachial Index (ABI) and coronary vessel involvement in patients with stable angina.

METHODS

This cross-sectional study was conducted in 2008 on 120 individuals who were hospitalized in Chamran Heart Center and underwent coronary angiography. A questionnaire was completed to obtain demographic information, history of previous heart disease and smoking. Body height and weight, as blood pressure on hand and foot were measured. The patients underwent angiography and the extent of coronary involvement (> 75%) was determined. After12-14-hour of fasting, blood sugar was obtained to measure total cholesterol, triglyceride, low-density lipoprotein cholesterol (LDL-C) and high-density lipoprotein cholesterol (HDL-C). The Ankle Brachial Pressure Index (ABI) was calculated as the ratio of the blood pressure in the ankles to the blood pressure in the arms. The data were analyzed by SPSS-15 using ANOVA, T-Student test, Spearman's rank correlation coefficient, and discriminant analysis.

RESULTS

Samples were 46 women (38.33%) and 74 men (61.67%) with a mean age of 55.50 ± 10.49. Mean and SD of ABI in men and women was 0.72 ± 0.20 and 0.80 ± 0.19 with no significant difference (P=0.012). The correlation between ABI and extent of coronary involvement was 0.47 (P < 0.0001). The group with lower ABI had the highest levels of coronary involvement (triple vessel, P < 0.05).

CONCLUSION

ABI had a significant relationship with the degree of coronary involvement and a significant predictive value. Therefore ABI seems to be a reliable indicator of high coronary risk.

OBJECTIVE—To measure plasma interferon γ, monocyte chemotactic protein-1 (MCP-1), and interleukin 6 and to assess their correlation with cardiac troponin T in unstable angina.
DESIGN—Blood sampling in patients undergoing coronary arteriography for known or suspected ischaemic heart disease.
PATIENTS—76 patients divided in three groups: 29 with unstable angina (group 1), 28 with stable angina (group 2), and 19 without ischaemic heart disease and with angiographically normal coronary arteries (group 3).
MAIN OUTCOME MEASURES—Plasma interleukin 6, interferon γ, MCP-1, and troponin T in the three groups of patients.
RESULTS—Interleukin 6 was increased in group 1 (median 2.19 (range 0.53-50.84) pg/ml) compared with the control group (1.62 (0.79-3.98) pg/ml) (p < 0.005), whereas interferon γ was higher in group 1 (range 0-5.51 pg/ml) than in the other two groups (range 0-0.74 pg/ml and 0-0.37 pg/ml; p < 0.005 and p < 0.001, respectively). Patients with unstable angina (group 1) and positive troponin T had higher concentrations of interferon γ than those with negative troponin T (0-5.51 pg/ml v 0-0.60 pg/ml, p < 0.001). Plasma MCP-1 was also higher in group 1 (median 267 (range 6-8670) pg/ml) than in the other two groups (134 (19-890) pg/ml and 84.5 (5-325) pg/ml; p < 0.005 and p < 0.001, respectively), and among group 1 patients with a positive troponin T assay than in those with normal troponin T (531 (14.5-8670) pg/ml v 69 (6-3333) pg/ml; p < 0.01). There was no difference in plasma interleukin 6 in group 1 patients between those with and without raised troponin T.
CONCLUSIONS—The inflammatory cytokines interferon γ and MCP-1 are increased in patients with unstable angina, particularly in those with raised concentrations of troponin T, suggesting that they are probably related to myocardial cell damage or to plaque rupture and thrombus formation.


Keywords: inflammatory cytokines; troponin T; unstable angina

OBJECTIVE: To assess sex-related differences in coronary revascularization practices in a Canadian setting. DESIGN: Prospective analytic cohort study. SETTING: Regional referral office in Toronto. PATIENTS: A selected but consecutive group of 131 women and 440 men referred by cardiologists for revascularization procedures between Jan. 3, 1989, and June 30, 1991. INTERVENTIONS: Coronary artery bypass grafting (CABG) or percutaneous transluminal coronary angioplasty (PTCA). Nurse-coordinators placed the referral with a surgeon or interventional cardiologist at one of three hospitals, who then communicated directly with the referring cardiologist. MAIN OUTCOME MEASURES: Symptom status at referral, procedures requested and performed, and time from referral to procedure. RESULTS: Although the women were more likely than the men to have unstable angina at the time of referral (odds ratio [OR] 2.28, 95% confidence interval [CI] 1.38 to 3.79, p = 0.0006), more women than men (16.8% v. 12.1%) were turned down for a procedure. Significant sex-related differences in practice patterns (p < 0.001) persisted after controlling for age or for the referring cardiologists' perception of expected procedural risk. A stepwise multivariate model showed that anatomy was the main determinant of case management; sex was the only other significant variable (p = 0.016). The referring physicians requested CABG more often for men than for women (p = 0.009), and the men accepted for a procedure were much more likely to undergo CABG than the women (OR 2.40, CI 1.47 to 3.93, p = 0.0002). Although the women undergoing CABG waited shorter periods than the men (p = 0.0035), this difference was attributable to their more severe symptoms. CONCLUSIONS: In this selected group women had more serious symptoms before referral but were turned down for revascularization more often than men. Reduced use of CABG rather than PTCA largely accounted for the sex-related differences in revascularization. Once accepted for a procedure women had shorter waiting times, which was appropriate given their more severe symptoms.

OBJECTIVE—To assess prospectively the prognostic value of soluble cellular adhesion molecules (CAMs) in patients with unstable angina and non-Q wave myocardial infarction and to compare their prognostic accuracy with that of C reactive protein (CRP).
DESIGN AND SETTING—Prospective observational study of patients presenting acutely with unstable angina and non-Q wave myocardial infarction to a single south Dublin hospital.
METHODS—Patients with Braunwald IIIA unstable angina and non-Q wave myocardial infarction had serum samples taken at presentation before initiation of antithrombotic treatment and were followed for six months. The primary end point was the occurrence of major adverse cardiovascular events (recurrent unstable angina, non-fatal myocardial infarction, and cardiovascular death) at six months. Concentrations of soluble intercellular adhesion molecule-1 (sICAM-1), soluble vascular cell adhesion molecule-1 (sVCAM-1), soluble endothelial selectin, and soluble platelet selectin were measured using an enzyme linked immunosorbent assay technique. CRP was measured with an immunophelometric assay.
RESULTS—91 patients (73 men and 18 women, mean (SD) age 61 (11) years) were studied; 27 patients (30%) had major adverse cardiac events during the six months of follow up. Concentration of CRP were significantly raised in patients who had an ischaemic event (mean (SEM) 11.5 (6.4) mg/l v 5.4 (2.5) mg/l, p < 0.001). Concentrations of sVCAM-1 were also significantly raised in the ischaemic event group (979 (30) ng/ml v 729 (22) ng/ml, p < 0.001). Both sVCAM-1 and CRP concentrations correlated strongly with the occurrence of an adverse event. The sensitivity of CRP > 3 mg/l and sVCAM-1 > 780 ng/ml for predicting future events was > 90%. There was no difference in concentrations of sICAM-1, soluble endothelin selectin, or soluble platelet selectin between event and non-event groups.
CONCLUSION—Raised concentrations of sVCAM-1 and CRP are predictive of an increased risk of major adverse cardiovascular events six months after presentation with unstable angina and non-Q wave myocardial infarction. These findings suggest that the intensity of the vascular inflammatory process at the time of presentation is a determinant of clinical outcome in unstable coronary artery disease. 


Keywords: cell adhesion molecules; risk stratification; unstable angina

One hundred and five patients with unstable angina and 175 with chronic stable angina were treated by primary percutaneous transluminal coronary angioplasty. Patients with unstable angina had had symptoms for a shorter time and were more likely to have angiographically complex lesions and lesions less than 10 mm in length than patients with chronic stable angina. Other baseline variables were not significantly different in the two groups. The overall primary success rate was similar in both groups (87% v 86%). Nine of the 14 unsuccessful procedures in those with unstable angina and nine of the 24 unsuccessful procedures in those with stable angina were the result of acute occlusion. These results led to a 9% frequency of procedure related myocardial infarction in patients with unstable angina and a 5% rate in those with stable angina (NS). The procedure related infarct rate tended to be higher in patients with unstable angina who had coronary angioplasty soon after an episode of unstable angina (mean 10 days) than in those in whom it was delayed (mean 35 days) (12% v 3%) (NS). In patients with unstable angina who had had a previous myocardial infarction procedure related infarction was significantly more common (18%) than in patients with no previous myocardial infarction (3%). The difference between those with and without previous infarction was also significant in patients with stable angina (10% v 3%).

Background

The current understanding of the pathophysiology of coronary artery disease is based largely on postmortem studies. Optical coherence tomography (OCT) is a high-resolution (≈ 10 µm), catheter-based imaging modality capable of investigating detailed coronary plaque morphology in vivo.

Methods and Results

Patients undergoing cardiac catheterization were enrolled and categorized according to their clinical presentation: recent acute myocardial infarction (AMI), acute coronary syndromes (ACS) constituting non–ST-segment elevation AMI and unstable angina, or stable angina pectoris (SAP). OCT imaging was performed with a 3.2F catheter. Two observers independently analyzed the images using the previously validated criteria for plaque characterization. Of 69 patients enrolled, 57 patients (20 with AMI, 20 with ACS, and 17 with SAP) had analyzable images. In the AMI, ACS, and SAP groups, lipid-rich plaque (defined by lipid occupying ≥2 quadrants of the cross-sectional area) was observed in 90%, 75%, and 59%, respectively (P = 0.09). The median value of the minimum thickness of the fibrous cap was 47.0, 53.8, and 102.6 µm, respectively (P = 0.034). The frequency of thin-cap fibroatheroma (defined by lipid-rich plaque with cap thickness ≤65 µm) was 72% in the AMI group, 50% in the ACS group, and 20% in the SAP group (P = 0.012). No procedure-related complications occurred.

Conclusions

OCT is a safe and effective modality for characterizing coronary atherosclerotic plaques in vivo. Thin-cap fibroatheroma was more frequently observed in patients with AMI or ACS than SAP. This is the first study to compare detailed in vivo plaque morphology in patients with different clinical presentations.

Background

C reactive protein (CRP), an important serum marker of atherosclerotic vascular disease, has recently been reported to be active inside human atherosclerotic plaques.

Aims

To investigate the simultaneous presence of macrophages, CRP, membrane attack complex C5b–9 (MAC), and oxidised low density lipoprotein (oxLDL) in atherectomy specimens from patients with different coronary syndromes.

Methods

In total, 54 patients with stable angina (SA; n = 21), unstable angina (UA; n = 15), and myocardial infarction (MI; n = 18) underwent directional coronary atherectomy for coronary lesions. Cryostat sections of atherosclerotic plaques were immunohistochemically stained with monoclonal antibodies: anti‐CD68 (macrophages), anti‐5G4 (CRP), aE11 (MAC), and 12E7 (oxLDL). Immunopositive areas were evaluated in relation to fibrous and neointima tissues, atheroma, and media. Quantitative analysis was performed using image cytometry with systematic random sampling (percentage immunopositive/total tissue area).

Results

Macrophages, CRP, MAC, and oxLDL were simultaneously present in a higher proportion of fibrous tissue and atheroma of atherectomy specimens from patients with UA and MI compared with SA (p<0.05). Quantitative analysis showed significantly higher mean percentages of macrophages in plaques from patients with MI (44%) than UA (30%; p<0.01) and SA (20%; p<0.001). Significantly higher mean percentages of CRP were also seen in MI (25%) and UA (25%) compared with SA (12%; p<0.05).

Conclusions

The presence of CRP, complement, and oxLDL in a high proportion of plaque tissue from patients with unstable coronary artery disease implies that these surrogate markers have important proinflammatory effects inside atherosclerotic plaques. This may increase vulnerability to plaque rupture and thrombosis, with subsequent clinical sequelae.

A 38-year-old black woman with thyrotoxicosis, whose first symptom was angina pectoris, is described. Chest pain became progressively more frequent, and an unstable angina pattern developed. Angina attacks were associated with transient ischemic electrocardiographic changes and recurrent ventricular tachycardia was documented. Coronary angiography revealed no significant obstructive lesions. The patient became free of pain with antithyroid treatment and angina has not recurred.

It is important to recognize that angina pectoris may be the major presenting symptom of thyrotoxicosis; unstable angina requires careful work-up and management including the performance of coronary angiography.

Images

Background

Since cardiovascular diseases are associated with high mortality and generally undiagnosed before the onset of clinical findings, there is a need for a reliable tool for early diagnosis. Carotid intima-media thickness (CIMT) is a non-invasive marker of coronary artery disease (CAD) and is widely used in practice as an inexpensive, reliable, and reproducible method. In the current study, we aimed to investigate prospectively the relationship of CIMT with the presence and extent of significant coronary artery narrowing in patients evaluated by coronary angiography for stable angina pectoris.

Methods

One hundred consecutive patients with stable angina pectoris and documented ischemia on a stress test were included in the study. The patients were divided into two groups according to the result of the coronary angiography: group 1 (39 patients) without a noncritical coronary lesion, and group 2 (61 patients) having at least one lesion more than 50% within the main branches of the coronary arteries. All of the patients underwent carotid Doppler ultrasound examination for measurement of the CIMT by a radiologist blinded to the angiographic data.

Results

The mean CIMT was 0.78 ± 0.21 mm in Group 1, while it was 1.48 ± 0.28 mm in Group 2 (p = 0.001). The mean CIMT in patients with single vessel disease, multi-vessel disease, and left main coronary artery disease were significantly higher compared to Group 1 (1.2 ± 0.34 mm, p = 0.02; 1.6 ± 0.32 mm, p = 0.001; and 1.8 ± 0.31 mm, p = 0.0001, respectively). Logistic regression analysis identified CIMT (OR 4.3, p < 0.001) and hypertension (OR 2.4, p = 0.04) as the most important factors for predicting CAD.

Conclusions

The findings of this study show that increase in CIMT is associated with the presence and extent of CAD. In conclusion, we demonstrated the usefulness of carotid intima-media thickness in predicting coronary artery disease but large-scale studies are required to define its role in clinical practice.