MB is significantly associated with epicardial and microvascular endothelial dysfunction in patients with non-obstructive CAD supporting its potential role as amechanism for angina in symptomatic patients with MB.
Stratified medical therapy, including an IDP with linked medical therapy, is routinely feasible and improves angina in patients with no obstructive CAD.
Observation outcomes include age, sex, C-reaction protein (CRP), medical history including major risk factors for CAD, ferritin and GFR, previous angina, time between MI and coronary angiography or time to rescue (TTR), and prior treatment.Around 60 patients were included in the case group (AMI with LVA) and 133 matched patients (AMI without LVA) in the control group.
Inclusion criteria were hospitalization for MI, Thrombolysis In Myocardial Infarction flow 0 at coronary angiography, reperfusion within 12 h from the onset of chest pain, cardiac MRI within the first month, and a 5-days' biological follow-up with at least hs-T-Troponin and C-reactive protein (CRP).
CRP-induced monocyte TF activity correlated with serum CRP levels in controls (P = 0.005) and ID (P = 0.007) in study 3, but not in patients with angina (P =0.84) in study 2.
In summary, the II genotype of the ACE gene was associated with a longer period of time between the first anginal pain and the onset of myocardial infarction than the ID and DD genotypes of the ACE gene.
The relation of the ACE and AT1R gene polymorphisms to coronary heart disease and the severity of coronary artery stenosis has now been investigated in 133 patients with myocardial infarction (MI) or angina pectoris who underwent coronary angiography and in 258 control subjects.
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.
Thirty-one patients (63.0 ± 6.4 years, 70% male) with recurrent CCS II-IV angina, despite optimal medical therapy, enrolled in the REGENT-VSEL single center, randomized, double-blinded, and placebo-controlled trial.
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.
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).
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.
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.
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.
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.
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.
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.