Stable Coronary Artery Disease Group Research Articles

The Importance of Gamma‐Glutamyltransferase Activity in Patients with Coronary Artery Disease

In this study, we sought to investigate the relation of gamma-glutamyltransferase (GGT) levels with the significance of coronary artery disease (CAD), clinical presentation, left ventricular (LV) function, and inflammatory activity. A total of 235 patients (mean age: 60.1 +/- 10.5 years, 166 [70%] males) who had coronary angiography were included in the study. Patients who had CAD constituted the study group (Group 1, n=189) and patients who had insignificant coronary disease or normal coronary activity constituted the control group (Group 2, n=46). GGT levels were higher in Group 1 than Group 2 (38.7 +/- 30.9 U/L versus 27.5 +/- 17.5 U/L, p =0.025). Left ventricular ejection fraction (LVEF) was lower in Group 1 than Group 2 (52.6% +/- 11.7% versus 58.8% +/- 11.3%, p < 0.002). GGT activity (40.2 +/- 32.5 U/L versus 29.1 +/- 18.3 U/L, p < 0.002) and c-reactive protein (CRP) levels (33.9 +/- 43.6 mg/dl versus 17.8 +/- 29.8 mg/dl, p < 0.002) were higher, LVEF (52.6% +/- 12.1% versus 56.5% +/- 11.0%, p =0.021) was lower in patients with acute coronary syndrome compared with stable CAD group. In regression analysis, CRP levels (p < 0.0001, odds ratio [OR]=3.77, 95% confidence interval [CI] 0.10 < OR < 0.32), LVEF (p =0.016, OR=- 2.44, 95% CI - 0.95 < OR < - 0.10) and LV end-diastolic pressure (p =0.015, OR=4.31, 95% CI - 1.19 < OR < - 0.13) were independent predictors of GGT activity. The increased GGT activity is related to LV function, clinical stability, and inflammatory activity rather than the severity of CAD. Measurement of GGT activity may be useful in predicting cardiovascular risk.

Comparison of coronary plaque composition among patients with acute coronary syndrome and stable coronary artery disease

The identification of vulnerable plaques before rupture is an important clinical goal. The purpose of the present study was to assess the difference in plaque composition among patients with acute coronary syndrome (ACS) and stable coronary artery disease (SCAD) by intravascular ultrasound virtual histologic analysis. One hundred and thirty-nine patients were divided into ACS group and SCAD group according to clinical presentation. A total of 229 de novo lesions with >50% stenosis in native coronary arteries with diameters >2.5 mm were studied with intravascular ultrasonography. Geometric and compositional data were obtained using intravascular ultrasound virtual histology software. There were no significant differences in overall lesions for fibrous ((52.0+/-11.9)% vs (54.3+/-8.5)%, P>0.05), fibrolipidic ((12.3+/-10.1)% vs (13.8+/-9.5)%, P > 0.05), calcium ((14.0+/-9.1)% vs (19.3+/-13.1)%, P>0.05), or necrotic core ((22.0+/-11.1)% vs (19.7 +/- 5.4)%, P > 0.05) percentages in ACS and SCAD patients, respectively. There were also no significant differences in culprit lesions for fibrous ((46.4+/-12.0)% vs (53.6+/-8.8)%, P>0.05), fibrolipidic ((9.1+/-9.0)% vs (12.9+/-9.7)%, P>0.05), calcium ((16.6+/-9.7)% vs (21.8+/-26.3)%, P>0.05), or necrotic core ((28.0+/-12.6)% vs (20.6+/-5.2)%, P>0.05) percentages in ACS and SCAD patients, respectively. High density lipoprotein-cholesterol levels >1.04 mmol/L were associated with more fibrolipidic ((14.5+/-10.4)% vs (7.1+/-6.5)%, P<0.05) and less necrotic core ((20.6+/-9.7)% vs (27.9+/-12.6)%, P<0.05) percentages in the cohort with ACS. In this study, coronary plaque composition assessed by intravascular ultrasound virtual histologic analysis was not significantly different between ACS and SCAD patients. The anatomic relationship of the specific plaque components to the lumen of the vessel was more important than the quantitative information of plaque composition for plaque stability.

Pregnancy-Associated Plasma Protein-A Elevation in Patients With Acute Coronary Syndrome and Subsequent Atorvastatin Therapy

Pregnancy-associated plasma protein-A (PAPP-A) was associated with atherosclerotic plaque vulnerability, whereas statin therapy was associated with increased plaque stability. Eighty-six patients presenting with clinical indications (non-ST-elevation myocardial infarction, unstable angina, and stable angina) for invasive coronary angiography and subsequent verified coronary artery disease (CAD) were randomly assigned in a double-blind manner to atorvastatin 10 or 80 mg/day. PAPP-A, high-sensitivity C-reactive protein (hs-CRP), and lipids were measured at baseline (before statin therapy) and at 1 and 6 months. PAPP-A was significantly increased in 35 patients with acute coronary syndrome (ACS) compared with 51 patients with stable CAD (p <0.001). Patients randomly assigned to atorvastatin 10 mg did not show a significant decrease in PAPP-A from baseline at 1 or 6 months. Patients treated with atorvastatin 80 mg showed a significant decrease at 1 month compared with baseline, but not at 6 months. hs-CRP was not significantly different between the ACS and stable CAD groups. Patients receiving atorvastatin 10 mg showed no hs-CRP decrease at 1 or 6 months, whereas it significantly decreased in the 80-mg group at 6 months, but not at 1 month. In conclusion, PAPP-A significantly increased in patients with ACS compared with those with stable coronary disease. High-dose atorvastatin significantly decreased PAPP-A at 1 month and hs-CRP at 6 months in patients with verified CAD. Low-dose atorvastatin did not produce this effect.

Plasminogen activator inhibitor-1 4G4G genotype is associated with myocardial infarction but not with stable coronary artery disease

A case control study was conducted to test the hypothesis that plasminogen activator inhibitor type-1 (PAI-1) 4G/5G gene polymorphism confers an increased risk for myocardial infarction (MI) in patients with known coronary atherosclerosis. One hundred fifty-six consecutive patients who presented with acute MI and 111 stable coronary artery disease (SCAD) patients with documented critical coronary artery stenoses were prospectively enrolled. PAI-1 4G/5G gene polymorphism and conventional atherosclerotic risk factors were studied in all patients. PAI-1 4G/5G gene polymorphism was studied in another 281 healthy blood bank donors. The frequency 4G4G genotype was significantly higher in the MI group as compared to SCAD group (32.7% vs. 15.3%, P = 0.001) while it was not statistically significant between MI and healthy control groups (32.7% vs. 26.0%, P = 0.136). Comparing with healthy controls SCAD group had significantly lower frequency of 4G4G genotype (P = 0.024). In comparison with SCAD group PAI-1 4G/4G genotype, male sex and smoking habits favored to MI in univariate analysis with a P value of less than 0.2. These variables were included in multivariate regression model to estimate the associated risk for MI. PAI-1 4G/4G genotype was the only independent variable (OR 2.67, 95%CI 1.43-4.96, P = 0.002) associated with MI in this regression model. Comparing with healthy control group 4G4G genotype was not associated with MI (OR 1.38, 95%CI 0.90-2.12). However, presence of 4G4G genotype had a protective effect against development of SCAD (OR 0.52, 96%CI 0.29-0.92). Compared to patients with critical coronary stenoses, PAI-1 4G/4G genotype was found to be an independent predictor for development of MI in this population. PAI-1 4G4G genotype have a protective effect against development of high grade stable coronary stenoses.

Echolucent Carotid Plaques as a Feature in Patients With Acute Coronary Syndrome

Carotid arterial ultrasound examination may be helpful for screening populations at high risk for acute coronary syndrome (ACS), so the present study was designed to identify the carotid arterial characteristics of patients with ACS. Carotid ultrasound examinations were performed in 172 patients with ACS, 166 patients with stable coronary artery disease (CAD), and 96 control subjects. Common carotid arterial structures were assessed by the intima - media thickness (IMT), interadventitial diameter (IAD), lumen diameter (LD), the IMT to LD ratio (IMT/LD), and the plaque burden based on the plaque score. Plaque morphology was assessed by the echogenecity based on the gray-scale median (GSM). IMT, IAD, IMT/LD, and plaque score did not differ between the ACS and stable CAD groups. The GSM in the ACS group was lower (47.5+/-25.3, p<0.001) than in the control (70.1+/-22.5) and stable CAD (73.7+/-23.4) groups. Multiple logistic regression analysis showed that the presence of carotid echolucent plaques (GSM <or=60) was an independent predictor of ACS. Echolucent carotid plaques were strongly associated with ACS and may be a surrogate marker of high-risk patients.

The psychometric properties of four quality of life instruments used in cardiovascular populations.

The psychometric properties of four quality of life instruments used in cardiovascular populations.

Increased C-reactive protein level after coronary stent implantation in patients with stable coronary artery disease

Background Elevation of C-reactive protein (CRP), among other markers of inflammation, is associated with an increased risk for cardiac events in patients with known coronary diseases and in apparently healthy individuals. Moreover, in patients with acute coronary syndromes, elevated serum levels of CRP are strongly predictive of the risk for death from cardiac causes. The purpose of this study was to investigate whether mechanical rupture of an atherosclerotic coronary plaque during elective stent implantation in patients with stable coronary artery disease (CAD) at low risk will cause a significant increase in serum levels of CRP. Methods and Results We measured serum CRP levels in 40 patients. Group 1 consisted of 12 consecutive patients with stable coronary disease who were at low risk, before and after elective coronary stent implantation. We compared the results in these patients to those of patients in 2 control groups: group 2 consisted of 12 consecutive patients with non-ST-segment elevation acute coronary syndrome (NSTSE ACS) who were undergoing coronary stent implantation, and group 3 included 16 consecutive patients with stable or unstable CAD who were undergoing diagnostic coronary angiography only without PCI. Peripheral blood samples for CRP level testing were withdrawn before percutaneous coronary intervention or angiography at the completion of the procedure, and 6, 20, and 48 hours thereafter. All patients with stable CAD (group 1) had a significant and uniform increase in serum CRP levels after elective stent implantation. The low mean baseline serum CRP levels increased 4.9 ± 4.1-fold 20 hours after coronary intervention (2.1 ± 1.2 before, 7.9 ± 3.4 after, P <.002). The baseline CRP level was much higher in the patients with unstable coronary syndromes (group 2). In this group, only a 2.1-fold increase in mean CRP level was observed after stent implantation (7.4 ± 5.5 before, 14.1 ± 9.6 after, P <.004). Also, the response in this group was less uniform when compared with that in the stable CAD group. By contrast, in patients undergoing diagnostic coronary angiography, the mean baseline CRP level was higher than in the patients in the group with stable CAD; however, the mean CRP after the procedure was not significantly elevated in this group (4.5 ± 3.6 before, 5.5 ± 3.7 20 hours after, P = not significant). Conclusions Mechanical disruption of an atherosclerotic coronary plaque during elective coronary stent implantation in patients with stable CAD who are at low risk causes a systemic inflammatory response expressed by marked elevation in CRP concentration. (Am Heart J 2003;145:248-53.)

Blood histamine is associated with coronary artery disease, cardiac events and severity of inflammation and atherosclerosis.

Mast cells are prevalent in the shoulder of unstable atheromas; cardiac mast cells secrete proteases capable of activating matrix metalloproteinases. Histamine is essential in the inflammatory cascade of the unstable plaque. Ascorbate depletion has been correlated with histaminemia which has been shown to impair endothelial-dependent vasodilation. This study evaluates whether oxidative stress as measured by isoprostanes (PGF(2alpha)) coupled with an inflammatory state characterized by histaminemia predisposes patients to acute coronary syndrome (ACS). Whole blood histamine, serum vitamin C, and serum PGF(2alpha) levels were drawn on 50 patients with ACS as determined by standard diagnostic criteria, 50 patients with stable coronary artery disease (SCAD), and 50 age and sex matched normal controls (C). Data were analyzed by stepwise discriminant and Spearman's rank correlation coefficient. A significant relationship exists between histamine and PGF(2alpha). As PGF(2alpha) rises above 60 pg/mL, an increase in histamine occurs in both the ACS and SCAD groups. A significant inverse relationship exists between ascorbate and histamine in the ACS versus C groups (P < 0.01) and the SCAD versus C groups (P < 0.01). Histamine and isoprostane levels increase in SCAD and ACS patients. Mast cell activation and lipid oxidation generated during atherosclerosis manifest this inflammatory response. Accelerated isoprostane formation and depleted ascorbate paired with histaminemia is active in CAD and predispose patients to acute coronary syndrome. Blood histamine alone may be a better risk factor for coronary events, and a better prognostic indicator than CRP even when combined with lipid indexes.