Serum levels of IL-2, IL-4 and IL-6 were measured in 74 patients undergoing an elective cardiac catheterization due to angina pectoris and positive or equivocal non-invasive screening for cardiac ischaemia: 34 had CAE and non-obstructive CAD (Group A), 22 had obstructive CAD (Group B) and 18 had normal coronaries (Group C).
Patients with an EF ≥20% but ≤45%, multivessel coronary artery disease (CAD) not amenable to revascularization, inducible ischemia, and symptoms of either angina (CCS II-IV) or heart failure (NYHA Class II-III) on maximal medical therapy were enrolled.
Our study demonstrates a high incidence of the -174G>C polymorphism of the IL-6 gene in patients with angina pectoris compared with those carrying the G allele, reinforcing the contribution of genetic factors to the symptoms of angina pectoris.
MATERIAL AND METHODS To evaluate the effects of angina pectoris, the differences of scores of the Seattle angina questionnaire (SAQ), vascular endothelial function [endothelial progenitor cells (EPCs), nitric oxide (NO) and endothelin 1 (ET-1)], and inflammatory factors [tumor necrosis factor a (TNF-α), hypersensitive C-reactive protein (hs-CRP), interleukin-6 (IL-6)] in 2 groups were assessed before and after treatment.
We assessed the 4G/5G polymorphism of the PAI-I gene in 500 subjects including 148 normal controls, 23 subjects with normal coronary arteries, 28 subjects with a paradoxical acetylcholine response, 97 subjects with angina pectoris (AP) and 204 subjects with myocardial infarction (MI).
Prospective cohort studies of patients with previous myocardial infarction or angina pectoris have underlined the association between increased plasma PAI-1 levels and the risk of coronary events, but the predictive capacity of PAI-1 disappears after insulin resistance marker adjustments.
The number of percutaneous coronary interventions performed for stable angina in the NHS in 2015 was applied to a model based on SCOT-HEART (CTCA in patients with suspected angina due to coronary heart disease: an open-label, parallel-group, multicentre trial) data to estimate the requirement for CTCA, for full guideline implementation.
A 69-year-old male with multifocal recurrence of a hepatocellular carcinoma (HCC) presented with increasing ventricular arrhythmia and angina several weeks after posterior myocardial infarction and PCI of the RCA culprit lesion during which two further lesions present in the distal RCX and a posterolateral branch, and a chronically occluded LAD had not been addressed.
Two of them were identified; 14,158m/z peak was the double-charged form of Apolipoprotein A-I and its vasoprotective action accords with prominence in AP.
A 69-year-old male with multifocal recurrence of a hepatocellular carcinoma (HCC) presented with increasing ventricular arrhythmia and angina several weeks after posterior myocardial infarction and PCI of the RCA culprit lesion during which two further lesions present in the distal RCX and a posterolateral branch, and a chronically occluded LAD had not been addressed.
The prevalence of single-vessel disease (odd ratio [OR] = 2.490; 95% confidential interval [95% CI] = 1.376-4.506; P = .002), total LAD occlusion (OR = 1.897; 95% CI = 1.024-3.515; P = .041), absence of previous angina (OR = 1.930; 95% CI = 1.035-3.600; P = .037), time between myocardial infraction (MI) and coronary angiography more than 12 h (OR = 1.970; 95% CI = 1.044-3.719; P = .035), GFR less than 60 mL/min (OR = 2.933; 95% CI = 1.564-5.503; P = .001), and ferritin levels (P = .0003) were all higher in the aneurysm group compared with those in the control group.
In conclusion, the eNOST-786C mutation appears to be a reversible etiology of Prinzmetal's variant angina in white Americans whose angina might be ameliorated by l-arginine.
Following AMI, age-sex-adjusted rates of PCI/CABG were lower with higher levels of distress (test for trend: p = .037), as were rates of angiography and PCI/CABG (p < .01) following admission with angina.
Apolipoprotein A-I was elevated (P<0.0001), as was high-density lipoprotein (P=0.098), and severity of angina was decreased (P=0.024) as a function of genotype.
MATERIAL AND METHODS To evaluate the effects of angina pectoris, the differences of scores of the Seattle angina questionnaire (SAQ), vascular endothelial function [endothelial progenitor cells (EPCs), nitric oxide (NO) and endothelin 1 (ET-1)], and inflammatory factors [tumor necrosis factor a (TNF-α), hypersensitive C-reactive protein (hs-CRP), interleukin-6 (IL-6)] in 2 groups were assessed before and after treatment.
Our main findings were: (i) patients with stable (n = 40) and unstable (n = 40) angina had elevated plasma levels of CXCL16 compared with controls (n = 20); (ii) low-dose simvastatin (20 mg qd, n = 15) and high-dose atorvastatin (80 mg qd, n = 9) down-regulated plasma levels of CXCL16 during 6 months of therapy; (iii) in vitro, atorvastatin significantly decreased the interleukin (IL)-1beta-mediated release of CXCL16 from PBMC and endothelial cells; (iv) attenuating effect of atorvastatin on the IL-1beta-mediated release of CXCL16 in PBMC seems to involve post-transcriptional modulation as well as down-regulation of CXCL16 release through inhibition of the protease a disintegrin and metalloproteinase 10 (ADAM10); (v) soluble CXCL16 increased the release of IL-8, monocyte chemoattractant peptide 1, and matrix metalloproteinases in vascular SMC and increased the release of IL-8 and monocyte chemoattractant peptide 1 in PBMC, with particularly enhancing effects in cells from CAD patients.
The prevalence of single-vessel disease (odd ratio [OR] = 2.490; 95% confidential interval [95% CI] = 1.376-4.506; P = .002), total LAD occlusion (OR = 1.897; 95% CI = 1.024-3.515; P = .041), absence of previous angina (OR = 1.930; 95% CI = 1.035-3.600; P = .037), time between myocardial infraction (MI) and coronary angiography more than 12 h (OR = 1.970; 95% CI = 1.044-3.719; P = .035), GFR less than 60 mL/min (OR = 2.933; 95% CI = 1.564-5.503; P = .001), and ferritin levels (P = .0003) were all higher in the aneurysm group compared with those in the control group.
We determined the frequency of the Pla2 allele in 589 prospectively recruited subjects aged <50 years presenting with symptomatic CAD with or without myocardial infarction and documented by coronary angiography (group I), 207 subjects investigated prospectively for restenosis 6 months after coronary balloon angioplasty (group II), and 570 control subjects without a history of angina or myocardial infarction, randomly selected from the community.
Plasma soluble (s) TNF-R2 was 5.1 +/- 0.1 ng/ml in CAD vs. 3.2 +/- 0.1 in control (P<0.0001), 5.2 +/- 0.1 in the presence vs. 4.6 +/- 0.2 in the absence of vessel disease (P=0.009), and rose with increasing severity of angina: 4.2 +/- 0.2 (no angina), 5.0 +/- 0.1 (stable angina), 5.4 +/- 0.2 (unstable angina; P=0.003). sTNF-R2 was correlated with age, cholesterol, creatinine, fibrinogen, transforming growth factor beta and homocysteine and was influenced by TNFRSF1B genotype.
A 69-year-old male with multifocal recurrence of a hepatocellular carcinoma (HCC) presented with increasing ventricular arrhythmia and angina several weeks after posterior myocardial infarction and PCI of the RCA culprit lesion during which two further lesions present in the distal RCX and a posterolateral branch, and a chronically occluded LAD had not been addressed.
Primary endpoint of the study was survival free of major adverse event individual, death, myocardial infarction (MI), repeat revascularisation (percutaneous coronary intervention [PCI], or coronary artery bypass grafting (CABG) and recurrent or continued angina.