Chronic Stable Coronary Heart Disease Research Articles

Association of FoxP3<sup>+</sup> T regulatory lymphocytes with epicardial adipose tissue thickness in patients with coronary heart disease

Background. Increase ofthe epicardial adipose tissue (EAT) thickness isassociated with development of inflammation and cardiovascular complications, however, there is no data on the relationship between EAT thickening and the number of immunosuppressive regulatory T lymphocytes.The aim. To study the number of circulating T regulatory lymphocytes and nuclear translocation ofthe FoxP3 transcription factor in patients with stable coronary heart disease (CHD) depending on the epicardial adipose tissue thickness.Materials and methods. We examined 30 patients with chronic stable CHD. The EAT thickness was measured by echocardiography. Patients were divided into groups depending on the presence and absence of EAT thickening above 5 mm (groups 1 and 2, respectively). Imaging flow cytometry was used to determine the number of T regulatory lymphocytes and the level of FoxP3 nuclear translocation. The concentration of cytokines and high sensitivity C-reactive protein (hsCRP) was determined using enzyme-linked immunosorbent assay in blood serum.Results. Anthropometric indicators of obesity and the severity of atherosclerosis were comparable between groups. In group 2, there was an increase in low-density lipoprotein cholesterol concentration (p = 0.043), ratio of low-density lipoprotein cholesterol tohigh-density lipoprotein cholesterol (p = 0.017) and the concentration ofhsCRP (p = 0.044) andIL-1β (p = 0.005), adecrease in the number and relative count of Tregulatory lymphocytes (p = 0.020 andp = 0.026, respectively), aswellas thenumber of cells withFoxP3 nuclear translocation (p = 0.018) compared togroup1. According tomultiple logistic regression, the concentration ofhsCRP, IL-1β and T regulatory lymphocytes relative count in total were the predictors of EAT thickening (accuracy 80 %; sensitivity 75 %; specificity 84,6 %; AUC = 0.89).Conclusions. Thickening of epicardial adipose tissue inpatients withcoronary heart disease is associated with a decrease in the number of T regulatory lymphocytes andFoxP3 nuclear translocation inthem in presence of comparable anthropometric parameters of obesity and the severity of coronary atherosclerosis.

Exploring the "gene-protein-metabolite" network of coronary heart disease with phlegm and blood stasis syndrome by integrated multi-omics strategy.

Exploring the "gene-protein-metabolite" network of coronary heart disease with phlegm and blood stasis syndrome by integrated multi-omics strategy.

What’s New in the 2019 Esc Guidelines on Chronic Coronary Syndromes?

Abstract The European Guidelines for Diagnosis and Treatment of Chronic Coronary Syndromes (CCS) were published in 2019 with a different title than the previous 2013 Guidelines that referred to “chronic stable coronary heart disease”, underlining the dynamic nature of the atherosclerotic process. The main changes in these guidelines refer to the most frequent clinical presentations of CCS, to the assessment of the pretest probability of atherosclerotic coronary heart disease with the recommendation to include cardiovascular risk factors and other factors, as well as the choice of invasive anatomical and/or functional diagnostic tests, invasive and/or non-invasive, depending on the probability of the existence of the disease. Regarding the treatment, these guidelines underline the importance of a healthy lifestyle and the modalities for the implementation and the strategy of anti-ischemic drug treatment, antithrombotic therapy being more widely addressed. Recommendations for myocardial revascularization on top of drug treatment for symptoms control and for improving prognosis are less restrictive in these guidelines. The recommendations of the CCS guidelines are harmonized with the recommendations of the other European guidelines, especially with those on diabetes, prediabetes and cardiovascular diseases which were also published in 2019.

Circulating microRNA-92a level predicts acute coronary syndrome in diabetic patients with coronary heart disease

PurposeThis study was designed to explore the value of monitoring miR-92a in T2DM patients with coronary heart disease (CHD).Materials and methods40 ACS patients with prior history of CHD and diabetes while the onset time of diabetes preceded that of CHD by more than 2 years were enrolled as the DACS group(diabetic ACS group). 40 ACS subjects who had had a definite diagnosis of CHD for more than 2 years with no history of T2DM were recuited as the CACS group(chronic CHD with ACS group). All enrolled subjects from DACS and CACS group came from an emergency basis and diagnosed with ACS by coronary angiography. Another 68 age- and sex-matched volunteers with chronic stable CHD without diabetes history were assigned as the control group (CHD group). We examined the serum levels of miR-92a and analyzed their correlations with blood pressure, glucose level, and lipid level.ResultsThe levels of miR-92a were significantly elevated in the DACS group compared with those of the CACS and CHD groups. Multivariate analysis showed that miR-92a, systolic blood pressure (SBP), and glycosylated hemoglobin (HbA1c) were significantly related to ACS events in patients with T2DM. Forward stepwise binary logistic regression analysis identified miR-92a as an independent predictive factor for ACS events in the patients with T2DM.ConclusionAn elevated circulating miR-92a level was associated with an increased risk of ACS in CHD patients with T2DM. Thus the level of miR-92a, especially combined with elevated SBP and HbA1c, may be helpful in the detection of ACS in patients with T2DM.

P6412Prognostic impact of atrial fibrillation in patients with chronic stable coronary heart disease

P6412Prognostic impact of atrial fibrillation in patients with chronic stable coronary heart disease

Lipoprotein(a) as a predictor of poor collateral circulation in patients with chronic stable coronary heart disease.

As a mechanism compensating for obstructive coronary artery disease, coronary collateral circulation (CCC) has attracted cardiologists for a long time to explore its potential impact. In the present study, Chinese patients suffering from ≥95% coronary stenosis, as diagnosed by angiography, have been investigated for the correlation between CCC and lipoprotein(a) [Lp(a)] levels. A cohort of 654 patients was divided into four categories according to Rentrop grades 0, 1, 2, and 3. Lp(a) levels were divided into model 1, discretized with critical values of 33 and 66%, and model 2, discretized with a cutoff value of 30.0 mg/dL. Furthermore, we evaluated the correlation between CCC and serum Lp(a) levels. The four groups had significantly different Lp(a) levels (25.80±24.72, 18.99±17.83, 15.39±15.80, and 8.40±7.75 mg/dL; P<0.001). In model 1, concerning R0, the risk in the third Lp (a) tertile (OR=3.34, 95%CI=2.32-4.83) was greater than that in the first tertile. In model 2, concerning R0, the risk in Lp(a) >30.0 group (OR=6.77, 95%CI=4.44-10.4) was greater than that of Lp(a) <30.0 mg/dL. The worst condition of CCC can be predicted independently by Lp(a) levels. In addition to clinical usage, Lp(a) levels can also be utilized as biological markers.

National disease management guidelines (NVL) for chronic CAD : What is new, what is particularly important?

Coronary heart disease (CAD) is widespread and affects 1 in 10 of the population in the age group 40-79years in Germany. The German national management guidelines on chronic CAD comprise evidence and expert-based recommendations for the diagnostics of chronic stable CAD as well as for interdisciplinary/multidisciplinary therapy and care of patients with stable CAD. The focus is on the diagnostics, prevention, medication therapy, revascularization, rehabilitation, general practitioner care and coordination of care. Recommendations for optimizing cooperation between all medical specialties involved as well as the definition of mandatory and appropriate measures are essential aims of the guidelines both to improve the quality of care and to strengthen the position of the patient.

C-reactive protein as a predictor for poor collateral circulation in patients with chronic stable coronary heart disease

Aim To investigate the association between serum C-reactive protein (CRP) levels and coronary collateral circulation (CCC) in Chinese patients with angiography-proven ≥95% coronary stenosis.Methods In this study, 1158 patients with angiography-proven ≥95% occlusion in ≥1 major epicardial coronary artery were enrolled, and then classified into two groups: poor CCC (Rentrop grades 0–1) and good CCC (Rentrop grades 2–3). CRP levels were grouped using the following two models: Model 1 discretized CRP group with 33.33% and 66.66% as the critical values and Model 2 with 1.0 and 3.0 mg/L as the cut off values.Results There were significant differences in serum CRP levels between the two groups (5.76 ± 3.45 vs. 3.49 ± 2.44 mg/L, respectively; p < 0.001), and compared with the first CRP tertile, the risks of poor CCC were higher in the second and third CRP tertiles (OR 2.31, 95%CI [1.67–3.19], OR 6.25, 95%CI [4.52–8.62], respectively). The receiver operating characteristic curve analysis indicated that the optimal cutoff value of CRP to predict poor CCC was 4.21 mg/L with 59.6% sensitivity and 74.33% specificity.Conclusions CRP levels are an independent predictor for poor CCC and might supply a useful biomarker in clinical applications.Key messagesC-reactive protein (CRP) is a non-specific inflammatory marker that is regarded as an independent risk and prognostic factor for individuals who suffer from coronary artery disease (CAD) and cardiovascular disorders.In a Chinese cohort of patients with coronary artery occlusion or stenosis of ≥95% TIMI grade 1 anterograde-flow, the relationship between CRP concentrations and angiographically visible coronary collateral (CC) was assessed.Our data indicated that elevated CRP associated with a significant impairment in CC development, and might supply a useful biomarker in clinical applications.

Tendency to Angry Rumination Predicts Stress-Provoked Endothelin-1 Increase in Patients With Coronary Artery Disease

To determine whether a tendency to angry rumination predicts anger recall (AR) stress-provoked increase in endothelin (ET)-1 among patients with coronary heart disease (CHD). Patients with chronic stable CHD (n = 105) completed a five-item measure of tendency to angry rumination (DAB-VR) and underwent a laboratory AR stress protocol (15-minute resting baseline [BL], 8-minute AR). Blood samples drawn at end of BL and AR were assayed for ET-1. Change in ET-1 from BL to AR (increase versus decrease/no change) was treated dichotomously in multivariate logistic regression models, including DAB-VR score and potential confounders, to evaluate the contribution of DAB-VR to the prediction of change in ET-1. In the multivariate model, DAB-VR score significantly predicted ET-1 increase (odds ratio, 1.34; 95% confidence interval, 1.10-1.1.63; p = .004), controlling for age, history of diabetes, hypercholesterolemia, rate pressure product, use of beta blockers, and statins. A tendency to angry rumination independently predicted AR stress-provoked ET-1 increase among patients with CHD. Given the involvement of ET-1 in plaque rupture, anger rumination tendency may identify vulnerability to anger-triggered acute coronary syndrome through prolongation of initial anger mobilization. The contribution of ruminative thinking to sustained poststress ET-1 elevation and the synergistic relationship of ET-1 during emotional stress with norepinephrine and nitric oxide remain to be explored.

Impact of genetic polymorphisms on platelet function and aspirin resistance

Genetic polymorphisms may affect platelets' responses to the antiplatelet therapy. Our aim was to determine the role of genetic polymorphisms on aspirin resistance in patients with coronary heart disease (CHD). A total of 126 consecutive patients (35-85 years old, 32% women) with chronic stable CHD was enrolled in the study. Platelet function assays were realized by the platelet function analyzer (PFA)-100 with collagen and epinephrine (Col/Epi) and collagen and adenosine diphosphate (Col/ADP) cartridges. Aspirin resistance was defined as having a closure time of less than 186 s with Col/Epi cartridges despite regular aspirin therapy. Factor V, prothrombin, factor XIII, beta-fibrinogen, plasminogen activator inhibitor I (PAI-1), glycoprotein IIIa, methylene tetrahydrofolate reductase, ACE and ApoB gene polymorphisms were determined by three consecutive steps: isolation and amplification of DNA and reverse hybridization. We determined that 30 patients (23.8%) had aspirin resistance by the PFA-100. Mean closure time measured with the Col/ADP cartridges was 74 +/- 12 s (51-104 s). Ten of the 30 patients with aspirin resistance were women (33.3%). Genetic polymorphisms were determined in 30 aspirin-resistant and 17 aspirin-sensitive patients. No statistically significant relationship was determined between aspirin resistance and the genetic panel. In our study we did not determine a significant relationship between the aspirin resistance and factor V, prothrombin, factor XIII, beta-fibrinogen, PAI-1, glycoprotein IIIa, methylene tetrahydrofolate reductase, ACE and ApoB gene polymorphisms.

Usefulness of Self-Reported Leisure-Time Physical Activity to Predict Long-Term Survival in Patients With Coronary Heart Disease

Self-reported leisure-time physical activity level correlates well with both cardiovascular (CV) and non-CV mortality in subjects without coronary heart disease (CHD). The impact of leisure-time physical activity on long-term outcomes has not been well studied in patients with preexisting CHD, who are often physically limited because of symptoms, medications, and co-morbid conditions. The aim was to determine the long-term prognostic value of self-reported leisure-time physical activity in a large CHD cohort. Leisure-time physical activity was evaluated using a self-administered questionnaire and categorized using a 4-level scale (sedentary, mild, moderate, and strenuous) in 14,021 of 24,958 subjects from the Coronary Artery Surgery Study Registry with suspected or proven CHD who underwent cardiac catheterization from 1974 to 1979. Median long-term follow-up was 14.7 years (interquartile range 9.8 to 16.2). Clinical outcomes were evaluated according to physical activity level and adjusted for potential confounders. Long-term all-cause and CV mortality progressively increased from most to least active subjects, with sedentary patients showing a 1.6-fold increase in mortality for both these outcomes (hazard ratio [HR] 1.63, 95% confidence interval [CI] 1.34 to 1.97, p <0.0001 for all-cause mortality). Similar trends were noted for men and women and in adjusted models, although HRs were attenuated after adjusting for age, gender, smoking, hypertension, diabetes mellitus, total cholesterol, body mass index, and ejection fraction (adjusted HR 1.23, 95% CI 1.01 to 1.49, p = 0.03 for all-cause mortality; adjusted HR 1.25, 95% CI 0.99 to 1.57, p = 0.05 for CV mortality). In conclusion, leisure-time physical activity independently predicted long-term survival in men and women with chronic stable CHD.

Role of Novel Biomarkers of Inflammation in Patients With Stable Coronary Heart Disease

Atherosclerosis is a dynamic chronic inflammatory process, and some inflammatory biomarkers have roles in this process. The levels of C-reactive protein (CRP) in patients with chronic stable coronary heart disease (CHD) have not been investigated well, and the levels of macrophage colony-stimulating factor (M-CSF) and interleukin-3 (IL-3) in patients with chronic stable CHD and the effects of these cytokines on atherogenesis are not known. To determine whether new inflammatory biomarkers have roles in atherosclerosis, the authors measured the levels of CRP, M-CSF, and IL-3 in patients with chronic stable CHD and in healthy controls. They measured plasma CRP concentrations by using a highly sensitive CRP reagent with immunonephelometric method, and plasma M-CSF and IL-3 concentrations with the help of a commercial enzyme-linked immunoassay test in 31 patients with chronic stable CHD documented by coronary angiography and in 22 age-matched healthy control subjects documented by coronary angiography. Mean plasma CRP, M-CSF, and IL-3 concentrations in patients with chronic stable CHD were significantly higher than those in controls (8.2 vs 4.6 mg/L, 195.3 vs 28.9 pg/mL, 173 vs 118 ng/mL, respectively, ppi.05). CRP, M-CSF, and IL-3 were all increased in patients with chronic stable CHD relative to controls. These findings suggest that these are new inflammatory biomarkers that may have important roles in the development of atherosclerotic lesions.

Role of novel markers of inflammation in patients with stable coronary heart disease

The role of novel markers of inflammation in patients with coronary heart disease (CHD) is still unclear. We conducted a case-control study to assess the association between various markers of inflammation and the presence and severity of chronic stable CHD. We included 312 clinically stable patients with angiographically documented CHD, aged 40 to 68 years. Voluntary blood donors (n = 479) matched for age and gender served as controls. High-sensitivity C-reactive protein, serum amyloid A, plasminogen activator inhibitor-1 activity, von Willebrand factor, fibrinogen, plasma viscosity, albumin, and neutrophils were determined. The severity of CHD was evaluated by 3 coronary scoring systems: the clinical 1- to 3-vessel disease score, the American Heart Association extension score (1 to 15 segments), and the Gensini score. All markers of inflammation were highly significantly elevated (all p <0.005) in patients with stable CHD compared with controls. After multivariable adjustment by means of logistic regression analysis, the association between CHD and fibrinogen, plasma viscosity, von Willebrand factor, and plasminogen activator inhibitor-1 activity remained substantial, whereas it decreased in high-sensitivity C-reactive protein, serum amyloid A, and neutrophils. The combination of ≥2 markers of inflammation was associated with a strongly increased risk of CHD. No association between markers of inflammation and any of the coronary scores applied was found. These results document an independent association between most of the markers of inflammation and chronic CHD, even in clinically stable patients. The combination of several of these biochemical markers, i.e., the determination of an “inflammatory risk profile,” may be useful to further stratify cardiovascular risk.

Coffee and coronary heart disease

Background: The role of coffee consumption in the onset of myocardial infarction remains uncertain. A review of published reports showed that although cohort data suggest very little excess risk of coronary heart disease among habitual coffee drinkers, case-control data suggest an excess risk of the order of 60% for people drinking five or more cups per day. Methods: We obtained as much information as possible on the lifestyle and habits, including coffee consumption, of people admitted with chest pain to the Coronary Care Unit at the Royal Perth Hospital, Australia. A questionnaire was given to them by the attending nursing staff. Details were recorded by the patient, often with help from the nursing staff. A similar questionnaire was completed by patients attending the Cardiology Outpatient Clinic. Results: One of the outstanding differences between the 182 patients with myocardial infarction or unstable angina and 185 patients with chronic stable coronary heart disease who filled in forms while waiting in the Cardiology Outpatient Clinic was that more people with acute coronary syndromes were drinking in excess of five cups of coffee per day (18 vs 7.5%; P = 0.003). In logistic regression analysis adjusted for age, smoking status (past and current), hypertension, dyslipidaemia and diabetes, the odds ratio was 2.51 (95% CI 1.43,4.43; P = 0.021). Conclusion: The present case-control study provides evidence for an increased risk of myocardial infarction or unstable angina among individuals drinking more than five cups of coffee per day.

Pacemaker-induced ventricular tachycardia in normally functioning ventricular demand pacemakers

Pacemaker-induced ventricular tachycardia (VT) or fibrillation is a rare event. 1–5 These episodes were mostly found to be initiated by stimulation during the vulnerable period of the myocardium in asynchronous pacemakers (WO), 1–3 in malfunctioning ventricular demand pacemakers (VVI), in an atrioventricular sequential demand pacemaker (DVI) 4 and in an atrial synchronous ventricular inhibited pacemaker (VDD). Pacemaker-induced VT has also been reported during the acute phase of myocardial infarction, during the first 2 days after implantation of the electrode or during hypoxia or electrolyte imbalance. To the best of our knowledge, initiation of VT by a normally functioning pacemaker in the setting of chronic stable coronary heart disease has not yet been described.

Noninvasive assessment of segmental left ventricular wall motion: Its clinical relevance in detection of ischemia

AbstractNewly developed noninvasive techniques, using fluoroscopic, electromagnetic, ultrasonic and nuclear medical devices, now make evaluation of segmental wall motion (SWM) widely applicable to man. Experiments in open chest animal preparations have demonstrated that SWM abnormalities (SWMA) are sensitive and specific markers of ischemia. Following coronary occlusion in closed chest dogs, using various techniques, we observed the same sequence of SWMA over a similar time course.In 122 angiographically documented patients, SWMA assessed by stress cardiokymography (CKG) revealed a sensitivity of 74% and a specificity of 94% in detecting coronary heart disease (CHD). The combined predictive power of stress ECG/CKG was superior to either test alone. Using radionuclide equilibrium scintigraphy and sitting bicycle exercise, stress induced SWMA revealed a sensitivity of 84% in detecting CHD.SWMA were detected in nearly all patients 24 h after acute transmural myocardial infarction (MI). These abnormalities extended beyond the location predicted by ST segment elevation and Q waves in the ECG, significantly more in anterior (15/16) than inferior (9/16) MI (p &lt; 0.05). In inferior MI, precordial ST segment depression was frequently (8/10) associated with anterior SWMA, indicative of ischemia rather than of a reciprocal electrical phenomenon. Scintigraphic assessment of left ventricular SWM correlated poorly with calculated CK‐MB infarct size (r = 0.64), suggesting that left ventricular function is determined not only by the necrotic zone but is also related to dysfunction of ischemic segments. SWM of the infarcted as well as the remote zone of the left ventricle showed no consistent directional changes within 10 days after infarction.In conclusion, noninvasive analysis of SWM is of clinical relevance 1. during diagnostic stress testing to detect ischemia, 2. in chronic stable CHD to assess the extent of mechanical dysfunction, 3. in acute MI to localize and assess extent and severity of regional myocardial dysfunction.