Both sOX40L and PAPP-A in patients with UA (15.7±4.9ng/mL, 25.4±6.8μg/mL, respectively) and AMI (17.1±5.3ng/mL, 26.3±5.6μg/mL, respectively) were significantly higher than those in patients with SA (3.4±1.4ng/mL, 9.6±2.1μg/mL, respectively) and controls (3.9±1.3ng/mL, 8.5±2.8μg/mL, respectively) (P<0.001).
The protein and mRNA levels of CRP were determined in lipopolysaccharide (LPS)-induced peripheral blood mononuclear cells of patients with unstable angina pectoris.
The meta-analysis indicated that the combined use of STS and Western medicine (WM) in the treatment of UAP can obviously improve the total effective rate [risk ratio (RR)=1.31, 95% confidence interval (CI) (1.24,1.39), P<0.0001], and the total effective rate of electrocardiogram [RR=1.43, 95% CI (1.30,1.56), P<0.0001], decrease the level of CRP [mean difference (MD)=-3.06, 95%CI (-3.85,-2.27), P<0.00001], fibrinogen [MD=-1.03, 95% CI (-1.16,-0.89), P<0.00001], and whole blood high shear viscosity [MD=-0.70, 95% CI (-0.92,-0.49), P<0.00001].
In the recently completed JUPITER trial, men and women without prior cardiovascular disease or diabetes who had baseline low-density lipoprotein cholesterol <130 mg/dL and high-sensitivity C-reactive protein ≥ 2 mg/L were randomly allocated to rosuvastatin 20 mg daily or to placebo and followed for first major vascular events (nonfatal myocardial infarction, nonfatal stroke, hospitalization for unstable angina, arterial revascularization, or vascular death) and for all-cause mortality.
Thus, CRP within coronary plaque might contribute to increased plasma CRP levels across coronary circulation, particularly among patients with unstable angina pectoris.
PBMC from 35 patients with stable angina (SA) in study 1, 10 male patients with SA, 10 with unstable angina (UA) and 10 matched controls in study 2, and 25 patients with inflammatory disorders (ID) and 24 normal controls in study 3 were stimulated with CRP, interferon-gamma (IFN) or lipopolysaccharide (LPS), or their combination.
ST-segment elevation myocardial infarction exhibited a higher CRP concentration than without elevation (non-ST-segment elevation myocardial infarction) and patients with unstable angina (21.81, 17.10, and 5.91 mg/L; p < 0.01).
We assessed the IL-6 -174 G>C polymorphism and TNF-alpha -308 G>A polymorphism in 139 consecutive elderly male patients affected by an ACS, such as ST-Elevation (STEMI), No ST-Elevation (NSTEMI) Myocardial Infarction and Unstable Angina.
Serum levels of soluble TRAIL but not TNF-alpha or Fas-ligand were reduced significantly in patients with unstable angina as compared with patients with stable atherosclerotic disease and healthy subjects.
These results suggest the crucial role of TNF-alpha in the mechanisms responsible for unstable angina in accordance with the concept of vulnerable plaque.
We looked for the presence of activated DR+ inflammatory cells and the expression patterns, localization, and immunostaining identification of genes for cytokines (IL-1beta, TNF-alpha, IL-6, and IFN-gamma), MCP-1, and iNOS in the left ventricle biopsies from 2-vessel disease anginal patients, 24 with UA and 12 with stable angina (SA), who underwent coronary bypass surgery.
PARP activity and PARP-1 expression in circulating MNCs were increased and positively correlated with plasma TNF-alpha and IL-6, respectively, in UA patients.
We assessed the IL-6 -174 G>C polymorphism and TNF-alpha -308 G>A polymorphism in 139 consecutive elderly male patients affected by an ACS, such as ST-Elevation (STEMI), No ST-Elevation (NSTEMI) Myocardial Infarction and Unstable Angina.
Compared with those allocated to placebo, CANTOS participants receiving canakinumab who achieved on-treatment IL-6 levels below the study median value of 1.65 ng/L experienced a 32% reduction in major adverse cardiovascular events [MACE, multivariable adjusted hazard ratio (HRadj) 0.68, 95% confidence interval (CI) 0.56-0.82; P < 0.0001], a 30% reduction in MACE plus the additional endpoint of hospitalization for unstable angina requiring urgent revascularization (MACE+, HRadj 0.70, 95% CI 0.59-0.84; P < 0.0001), a 52% reduction in cardiovascular mortality (HRadj 0.48, 95% CI 0.34-0.68; P < 0.0001), and a 48% reduction in all-cause mortality (HRadj 0.52, 95% CI 0.40-0.68; P < 0.0001) with prolonged treatment.
The present study was performed to investigate the correlation between ACE genetic polymorphism and acute coronary syndrome by comparing the distribution of ACE genotypes and ACE activities in patients with acute MI and unstable angina with those in control group.
Large-scale studies have indicated that treatment with angiotensin converting enzyme (ACE) inhibitors reduces the incidence of myocardial infarction and unstable angina pectoris among patients with recent myocardial infarction and moderate left ventricular dysfunction.
Serum levels of IL-27 in patients with AMI and UA were significantly lower than those in SA and control groups, while serum levels of IL-17 and IFN-γ in AMI and UA groups were dramatically increased compared to those in SA and healthy control groups.
The levels of miRNA-155 (0.49 ± 0.08 <i>vs.</i> 0.23 ± 0.09) and IFN-γ (227.58 ± 26.01 <i>vs.</i> 141.23 ± 17.89) in the UAP group were significantly higher than that of the control group, the difference was statistically significant.
The upregulation of miR-155 expression was positively correlated with the percentage of Th1 cells and interferon-gamma (IFN-γ) levels in patients with UA.
Predictors of a triggered ACS were age <65 years, previous angina, no previous angiotensin-converting enzyme inhibitors/angiotensin 2 receptor blockers, impaired functional class, not having typical chest pain on admission, and a final diagnosis of unstable angina.