Active Coronary Artery Disease Research Articles

Non-invasive physiological assessment of coronary artery obstruction on coronary computed tomography angiography.

Computed tomography-derived fractional flow reserve (CT-FFR) enhances the specificity of coronary computed tomography angiography (CCTA) to that of the most specific non-invasive imaging techniques, while maintaining high sensitivity in stable coronary artery disease (CAD). As gatekeeper for invasive coronary angiography (ICA), use of CT-FFR results in asignificant reduction of negative ICA procedures and associated costs and complications, without increasing cardiovascular events. It is expected that CT-FFR algorithms will continue to improve, regarding accuracy and generalisability, and that introduction of new features will allow further treatment guidance and reduced invasive diagnostic testing. Advancements in CCTA quality and artificial intelligence (AI) are starting to unfold the incremental diagnostic and prognostic capabilities of CCTA's attenuation-based images in CAD, with future perspectives promising additional CCTA parameters which will enable non-invasive assessment of myocardial ischaemia as well as CAD activity and future cardiovascular risk. This review discusses practical application, interpretation and impact of CT-FFR on patient care, and how this ties into the CCTA 'one stop shop' for coronary assessment and patient prognosis. In this light, selective adoption of the most promising, objective and reproducible techniques and algorithms will yield maximal diagnostic value of CCTA without overcomplicating patient management and guideline recommendations.

Predicting coronary artery disease risk in firefighters – a cross-sectional study

Background: Firefighters are placed under severe cardiovascular load in performing active duty and, when carrying various coronary artery disease (CAD) risk factors, firefighters are predisposed to significant morbidity and mortality. Reducing the incidence of these risk factors is paramount. The purpose of this study is to determine the predictors of CAD risk. Methods: This study used a quantitative, cross-sectional and correlational design. The researchers conveniently sampled 124 full-time firefighters from the City of Cape Town Fire and Rescue Service. A researcher-generated questionnaire was used to collect sociodemographic and CAD risk factors information, such as age, gender, ethnicity, family history of CAD, cigarette smoking and physical activity levels, and all research procedures were conducted according to the American College of Sports Medicine guidelines. Data collection took place between September and November 2019. Linear and logistic regression were used to determine the relationship between the various CAD risk factors and the predictors of CAD risk. Results: Age was a significant predictor of hypertension (p <0.01), dyslipidemia (p <0.01), diabetes (p <0.01), obesity (p <0.01) and central obesity (p <0.01). Gender was a significant predictor of obesity, central obesity and cigarette smoking (p <0.05). Waist circumference was a significant predictor of hypertension (p <0.01), dyslipidemia (p <0.01) and diabetes (p <0.05). Conclusion: Age was a significant predictor of various modifiable CAD risk factors, including obesity, in both genders and all ethnicities. Attentive monitoring should be in place as firefighters age, along with behavioural modifications designed to reduce age-related increases in CAD risk factors.

Serum Complement C1q Activity Is Associated With Obstructive Coronary Artery Disease.

Background: Complement C1q plays a dual role in the atherosclerosis. Previous studies showed inconsistent results about the association of serum C1q levels and coronary artery disease (CAD). Here, we explored the associations of serum C1q activity with CAD, coronary stenosis severity, cardiovascular biomarkers, and 1-year restenosis after coronary artery revascularization.Methods: We enrolled 956 CAD patients and 677 controls to evaluate the associations of serum complement C1q activity to the presence and severity of obstructive CAD and non-obstructive CAD. Serum C1q activity and the concentrations of laboratory markers were measured in all subjects. All the data were analyzed using SPSS22.0 software.Results: Serum C1q activity in Obstructive CAD and Non-Obstructive CAD groups was significantly higher than the control group (195.52 ± 48.31 kU/L and 195.42 ± 51.25 kU/L vs. 183.44 ± 31.75 kU/L, P < 0.05). Greater C1q activity was significantly correlated with higher total cholesterol (TC) and triglyceride (TG) levels. C1q activity was associated with an increased Odds Ratio (OR) of CAD (OR = 1.322, 95% CI 1.168–1.496, P < 0.05) and 1-year restenosis after revascularization (the highest OR = 3.544, 95% CI 1.089–12.702, P < 0.05). Complement C1q activity was not correlated with Gensini score in the Obstructive CAD group after adjustment for confounders. C1q activity has low value in predicting the incidence of CAD.Conclusion: Serum complement C1q activity is associated with obstructive CAD.

STUDY OF RISK FACTORS AND CLINICAL PROFILE OF ACUTE MYOCARDIAL INFARCTION IN FEMALES

Cardiovascular disease is the most important health issue facing mankind and continues to be major cause of morbidity and mortality.Women are disproportionately affected by coronary artery disease(CAD) compared with men.There are different clinical presentations of heart disease and acute myocardial infarction in women than in men.Also different studies shows that there is difference in the major cardiovascular risk factors amongst men and women at younger age.The present study was undertaken with a view to understand the clinical prole of acute myocardial infarction in women and observe the variations in acute myocardial infarction between men and women. Materials and methods-This observational and analytical study includes 118 female cases of acute myocardial infarction admitted to ICCU and randomly selected 118 male cases of acute myocardial infarction admitted to ICCU during the same tenure.Various necessary th investigations were carried out and risk factors of acute myocardial infarction were determined.All the cases were followed up on the 7 day of admission and one month after discharge from the hospital for various complications.Data thus collected was analysed at the end of study. Results-Maximum number of female cases were in age group 60-69 years(45.6%)while maximum number of male cases were in age group 50- 59 years(33.05%).Anterior wall myocardial infarction was the commonest type of acute myocardial infarction in both groups.ST elevation myocardial infarction was more common in males(94.9%)as compared to females(83.89%) whereas non ST elevation myocardial infarction was common in females(10%) as compared to males (5%).Atypical chest pain was more common in female cases(50.8%)whereas typical chest pain was more common with male cases(52.4%).Also dyspnoea as presenting symptom was signicantly more in female cases(51.6%)as compared to male cases(20.3%).Among the risk factors as Diabetes mellitus,signicant difference was observed in female(45.7%) vs male cases(30.5%).Other risk factors like lack of physical activity was signicantly more in female cases(84.7%) as compared to male cases(50%).Central obesity and family history of CAD were more common in female cases . 42(35.6%) female cases had arrthymias during hospital stay as compared to 50(42.4%) male cases.Post MI angina was present in 21 (20.38%) female cases and 12(11.11%) male cases during one month follow up.Mortality was more common in female cases(12.7%) compared with the male cases(8.47%)but it was not statistically signicant. Females suffer from coronary artery disease slightly at older age Conclusions- as compared to males.Atypical chest pain and dyspnoea are more common presenting symptoms in females compared to males.Diabetes mellitus,central obesity, lack of physical activity and family history of CAD are most common risk factors in female cases for acute myocardial infarction.ST elevation myocardial infarction is less common in females as compared to males.Complications like congestive cardiac failure ,arrthymias are more common in females as compared to males.The overall mortality with acute myocardial infarction are common in females than males.

Serum adenosine deaminase activity and coronary artery disease: a retrospective case-control study based on 9929 participants.

Background:Adenosine deaminase (ADA) regulates purine metabolism through the conversion of adenosine to uric acid (UA). Adenosine and UA are closely associated with cardiovascular events, but the correlation between serum ADA activity and coronary artery disease (CAD) has not been defined.Methods:We performed a hospital-based retrospective case-control study that included a total of 5212 patients with CAD and 4717 sex- and age-matched controls. The serum activity of ADA was determined by peroxidase assays in an automatic biochemistry analyzer.Results:Serum ADA activity in the CAD group (10.08 ± 3.57 U/l) was significantly lower than that of the control group (11.71 ± 4.20 U/l, p < 0.001). After adjusting for conventional factors, serum ADA activity negatively correlated with the presence of CAD (odds ratio = 0.852, 95% confidence interval: 0.839–0.865, p < 0.001). Among the patients with CAD, serum ADA activity was lowest in patients with myocardial infarction (MI; 9.77 ± 3.80 U/l). Diabetes mellitus and hypertension increased the serum ADA activity in CAD patients.Conclusions:Serum ADA activity is significantly attenuated in patients with CAD, particularly in MI. We propose a mechanism by which the body maintains adenosine levels to protect the cardiovascular system in the event of CAD.

Paraoxonase 1 Gene Polymorphisms (Q192R and L55M) Are Associated with Coronary Artery Disease Susceptibility in Asian Indians

Background: Coronary artery disease (CAD) is a complex metabolic disorder in which lifestyle and genetic factors are known to play key roles in pathogenesis. The paraoxonase 1 (PON1) enzyme has a defensive effect against CAD progression, as it safeguards low-density lipoproteins (LDLs) from oxidative modifications. The most extensively studied genetic variants in the PON1 gene are Q192R and L55M, which have been related with LDL antioxidative activity and risk of CAD. Objective: The present case-control study intended to examine the Q192R and L55M polymorphisms and their association with the risk of CAD patients in north Indians. Methods: A total of 872 subjects (412 CAD patients and 460 controls) were recruited from north India. The PON1 gene was amplified and genotypes were studies using PCR-RFLP. χ² analysis was performed to compare genotype/allele frequencies in patients and controls. Results: The present study indicated abdominal obesity, elevated body mass index, and dyslipidemia with increased levels of total cholesterol and triglycerides as well as reduced high-density lipoprotein cholesterol in CAD subjects compared to healthy controls (p < 0.05). Logistic regression analysis of the data revealed an association of the RR genotype of the Q192R polymorphism with an about 2-fold elevated risk of CAD (OR = 2.23, 95% CI = 1.47–3.37, p = 0.0001). Contrariwise, the L55M polymorphism did not show significant association with CAD (OR = 1.81, 95% CI = 0.66–4.95, p = 0.326). Conclusions: The Q192R polymorphism in the PON1 gene may be a susceptibility gene associated with increased risk of CAD in an Asian Indian population.

PP.24.27] RELATIONSHIP BETWEEN MATRIX METALLOPROTEINASES MMP-9,MMP-7, THEIR INHIBITORS, HS CRP AND SEVERITY OF ATHEROSCLEROTIC CORONARY ARTERY DISEASE

Objective: To describe the enzymatic profile of matrix metalloproteinases (MMP-7 and -9) and tissue inhibitors of metalloproteinases (TIMP-1 and -2) and the relationship with hs-CRP serum levels in different categories of patients with coronary artery disease (CAD) Design and method: Consecutive patients who underwent coronary angiography were randomly included. Serum concentrations of MMP-9,MMP-7 TIMP-1,2 and hs CRP were determined in 112 patients divided into 5 groups:stable angina pectoris(SAP) n = 47,unstable angina pectoris(UAP) n = 32,acute myocardial infarction(AMI), n = 16 and Conrols(C), n = 17 with ELISA method using Quantikine Human MMP-9 and MMP7 (total) ELISA (R&D Systems) and Quantikine Human TIMP-1,2 (R&D Systems;for hs CRP determination was used hs CRP ELISA assays(DRG Int.INC.USA), Results: High levels of MMP-9, TIMP-1 and hs-CRP were obtained in SAP, UAP and AMI groups versus controls probably because acute coronary syndromes are associated with an important inflammatory status. Levels of MMP-9 and TIMP-1 tend to have a parallel evolution, and are associated with the evolution of SAP into an UAP and AMI. Total lMMP-7 and its ratio with TIMPcorrelated with parameters of LV systolic even in patients with normal LVEF. Baseline serum MMP-9, TIMP-1 and hs-CRP concentrations increased significantly in patients with CAD, compared to healthy controls. MMP-9, MMP-7,TIMP-1,2 and hs-CRP reflects the presence of inflammation and the evolution of stable atherosclerotic plaques into unstable ones and developing of acute coronary syndromes Conclusions: Inflammatory mechanisms play a significant role in atheromatous plaque vulnerability and rapid CAD progression. hs-CRP levels predict future cardiovascular events independently of CAD severity. Therefore, hs-CRP levels may be considered as marker of atheromatous plaque vulnerability and CAD activity.

Echocardiographic epicardial fat thickness is a predictor for target vessel revascularization in patients with ST-elevation myocardial infarction.

BackgroundThe amount of epicardial adipose tissue (EAT) has been demonstrated to correlate with the severity of coronary artery disease (CAD) and the CAD activity.The aim of this study is to assess the impact of EAT on long term clinical outcomes in patients with ST elevation myocardial infarction (STEMI) after percutaneous coronary intervention (PCI).MethodsWe analyzed the data and clinical outcomes of 761 patients (614 males, 57 ± 12 year-old) with STEMI who underwent successful primary PCI from 2003 to 2009. All patients were divided into two groups: thick EAT group, EAT ≥ 3.5 mm and thin EAT group, EAT < 3.5 mm. The primary end points were all-cause death, recurrent MI, target vessel revascularization (TVR) and major cardiac adverse events (MACEs), composite of all-cause death, recurrent MI and TVR, within 5 years.ResultsMedian and mean EAT of 761 patients were 3.3 mm and 3.6 ± 1.7 mm, respectively. Mean follow up period was 46 ± 18 months. MACE-free survival rate in the thick EAT group was significantly lower than in the thin EAT group (log-rank P = 0.001). The event-free survival rate of all-cause death of the thick EAT group was significantly lower than that of the thin EAT group (log-rank P = 0.005). The TVR-free survival rate in the thick EAT group was significantly lower than in the thin EAT group (log-rank P = 0.007). The event-free survival rate of recurrent MI were not significantly different between the groups (log-rank P = 0.206). In the Cox’s proportional hazard model, the adjusted hazard ratio of thick EAT thickness for TVR was 1.868 (95% confidence interval 1.181–2.953, P = 0.008).ConclusionThis study demonstrates that the EAT thickness is related with long term clinical outcome in patients with STEMI. The EAT thickness might provide additional information for future clinical outcome, especially TVR.

Prevalence of coronary artery disease and its risk factors in Kerala, South India: a community-based cross-sectional study.

BackgroundThere are no recent data on prevalence of coronary artery disease (CAD) in Indians. The last community based study from Kerala, the most advanced Indian state in epidemiological transition, was in 1993 that reported 1.4 % definite CAD prevalence. We studied the prevalence of CAD and its risk factors among adults in Kerala.MethodsIn a community-based cross sectional study, we selected 5167 adults (mean age 51 years, men 40.1 %) using a multistage cluster sampling method. Information on socio-demographics, smoking, alcohol use, physical activity, dietary habits and personal history of hypertension, diabetes, and CAD was collected using a structured interview schedule. Anthropometry, blood pressure, electrocardiogram, and biochemical investigations were done using standard protocols. CAD and its risk factors were defined using standard criteria. Comparisons of age adjusted prevalence were done using two tailed proportion tests.ResultsThe overall age-adjusted prevalence of definite CAD was 3.5 %: men 4.8 %, women 2.6 % (p < 0.001). Prevalence of any CAD was 12.5 %: men 9.8 %, women 14.3 % (p < 0.001). There was no difference in definite CAD between urban and rural population. Physical inactivity was reported by 17.5 and 18 % reported family history of CAD. Other CAD risk factors detected in the study were: overweight or obese 59 %, abdominal obesity 57 %, hypertension 28 %, diabetes 15 %, high total cholesterol 52 % and low level of high density lipoprotein cholesterol 39 %. Current smoking was reported only be men (28 %).ConclusionThe prevalence of definite CAD in Kerala increased nearly three times since 1993 without any difference in urban and rural areas. Most risk factors of CAD were highly prevalent in the state. Both population and individual level approaches are warranted to address the high level of CAD risk factors to reduce the increasing prevalence of CAD in this population.

Obstructive sleep apnea is associated with increased inflammatory activity in non-obese patients with coronary artery disease; a cross sectional study

Background: Inflammation has a crucial role in the development of coronary artery disease (CAD). Obstructive sleep apnea (OSA) is a common condition in CAD patients and associated with increased inflammation. The impact of OSA on inflammatory activity in CAD is unknown. Methods and results: Inflammatory markers, High-sensitive (Hs)-CRP, Interleukin (IL)-6, IL-8 and Tumor Necrosis Factor (TNF)-α, were studied in a non-obese cohort of revascularized CAD patients with OSA (Apnea Hypopnea-Index [AHI] ≥15 events/h; n=267) and non-OSA (AHI<5 events/h; n=104), respectively. CAD patients with OSA had higher levels of Hs-CRP (3.52 vs 2.41 mg/ml; p=0.011), IL-6 (11.66 vs 6.27 pg/ml; p<0.001), IL-8 (1.81 vs 1.52 pg/ml; p=0.075) and TNFα (6.06 vs 5.41 pg/mL; p=0.019) compared to the levels seen in non-OSA. In a univariate regression analysis, OSA, based on AHI≥15 events/h was significantly correlated with all four biomarkers but only with IL-6 in the multivariate model (Odds Ratio [OR] 1.33, 95% Confidence Interval [CI] 1.08; 1.65). Applying Oxygen Desaturation Index (ODI) ≥5 events/h as a marker of the severity of intermittent hypoxemia in OSA, we found a significant relationship between ODI≥5 events/h and Hs-CRP (OR 1.28; 95% CI 1.02; 1.62) as well as between ODI≥5 and IL-6 (OR 1.35; 95% CI 1.11; 1.64). Conclusion: OSA is independently related with increased inflammatory activity in this non-obese CAD cohort. The inflammatory activity seems to be triggered by intermittent hypoxemia more than the degree of the apneic events per se in OSA. ClinicaTrials.gov; NCT 00519597.

Serum γ-Glutamyltransferase Levels Correlate With Epicardial Adipose Tissue Thickness in Patients With Coronary Artery Disease

Epicardial adipose tissue (EAT) is related to the presence of coronary artery disease (CAD). Increased γ-glutamyltransferase (GGT) activity is associated with atherosclerosis. We assessed the relationship between EAT and serum GGT activity in addition to cardiovascular risk factors in patients with stable anginal symptoms. Consecutive patients (n = 120) who underwent coronary angiography were included. Epicardial adipose tissue thickness was measured by echocardiography. Serum GGT activity was measured by enzymatic colorimetric assay. Epicardial adipose tissue thickness and serum GGT activity were higher in patients with CAD (n = 83). Patients with metabolic syndrome (n = 83) were found to have higher EAT thickness. Serum GGT activity was independently associated with EAT values. In conclusion, echocardiographic EAT was significantly higher in patients with CAD and serum GGT activity correlated with EAT thickness.

Potential Use of Coronary Artery Calcium Progression to Guide the Management of Patients at Risk for Coronary Artery Disease Events

Subclinical coronary artery disease (CAD) is widespread and under-diagnosed. Preventive efforts are required to reduce the burden of this disease and its complications. Imaging of coronary artery calcium (CAC) with cardiac computed tomography is highly specific for the diagnosis of subclinical CAD and can also facilitate treatment decisions in preventive cardiology. Indeed, CAC testing has been recommended by the American Heart Association for asymptomatic patients at intermediate risk for future cardiac events (as defined by clinical risk factors) to refine existing risk estimates. However, the optimal follow-up of those patients who have already undergone CAC testing remains unclear, particularly with regards to repeat CAC testing. The existing literature points to two major considerations for the use of CAC progression in the management of subclinical CAD. On one hand, CAC progression has been used as a surrogate marker to test the efficacy of cardiac preventive medications in halting or regressing CAD. To date, study results have been mostly disappointing and CAC progression appears resistant to medications such as statins. On the other hand, however, CAC progression has potential as a clinical indicator of underlying CAD activity. This may facilitate optimization or up-titration of preventive medications by using CAC progression as a marker of subclinical disease activity. We believe that the data, thus far, argues against the use of a CAC progression as a clinical surrogate marker of preventive therapy efficacy. Further studies with non-statin medications and with concomitant outcome data are needed. However, CAC progression has potential for monitoring subclinical CAD in some patients and may facilitate treatment decisions. In this review we will provide recommendations for repeat CAC testing and discuss when repeat CAC testing may be helpful to assess coronary artery disease progression.

Genotype-phenotype relationship of F7 R353Q polymorphism and plasma factor VII coagulant activity in Asian Indian families predisposed to coronary artery disease

Elevated factor VII (FVII) level is a risk factor for coronary artery disease (CAD). We investigated the role of R353Q polymorphism in the F7 gene in 139 Indian families with CAD, comprising of 222 affected subjects, 105 unaffected subjects and 126 affected sibling pairs. Plasma per cent FVIIc activity (FVII.c activity) differed ignificantly across R353Q genotype (P < 0.0001). Frequency of subjects with RR and QQ genotypes were higher in 4th quartile and 1st quartile of FVII.c activity, respectively (P < 0.0001). F7 R353Q SNP was able to explain up to 7% of variation in FVII.c activity by regression analysis and an additive genetic component of variance of 28.04% by heritability analysis. Quantitative trait loci analysis showed suggestive linkage evidence of F7 SNP with per cent FVII.c activity (LOD score -1.82; P = 0.002). Individuals with RR and RQ genotypes carried an OR of 2.071 (95% c.i. = 1.506-2.850) and 2.472 (95% c.i. = 1.679-3.641), espectively, towards CAD risk. There was significant correlation of FVII.c activity with lipid markers, particularly among those with RR and RQ genotype after covariate adjustment. In conclusion, the F7 R353Q SNP appears to moderately influence plasma FVII.c activity and risk of CAD in Indians.

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Can mean platelet component be used as an index of platelet activity in stable coronary artery disease?

Acute coronary syndrome is associated with intracoronary thrombosis secondary to platelet activation. Previous groups have investigated platelet activation in both stable and unstable vascular disease. Most measures of platelet activation are not routinely available or easily adaptable to large scale clinical use. Recently, measurement of the mean platelet component (MPC) has become part of the routine data provided by an automated full blood count analyser, the Advia 120. MPC measures platelet density which changes on platelet activation. Our objectives were to determine if platelet activation, as measured by MPC, is increased in patients with stable coronary artery disease (CAD) and to determine if MPC could be useful in differentiating people with stable CAD from controls on an everyday clinical basis. Three hundred and forty-five consecutive patients attending for elective coronary angiography had full blood count analysis and MPC measurement performed using an ADVIA-120 analyser. Three hundred and twenty-four were analysed in our final dataset. Two hundred and fifty-three (78%) had CAD. Patients with CAD were significantly (p<0·001) older than those without (63·8 versus 56·0 years). Results failed to demonstrate a difference (p=0·467) in MPC between patients with CAD and those with normal coronary arteries (25·8 versus 26·0). Likewise, there was no correlation between MPC and the severity of CAD (Kendall's tau b=−0·086, p=0·04). MPC is not a useful index of platelet activity in stable CAD when used in everyday clinical practice.

Neopterin: Marker of coronary artery disease activity, severity and/or extent in patients with clinically stable angina?

We read with great interest the comments of Avanzas et al. on our recent article. In acute coronary syndromes, inflammatory markers such as neopterin – a macrophage-specific activation marker – reflect plaque instability, i.e. disease activity. In stable coronary artery disease (CAD) patients, inflammatory markers such as C-reactive protein (CRP) not only predict the incidence of future events, but are also associated with disease prevalence and severity.In our study population including male, non-diabetic patients with stable CAD, neopterin serum concentrations also correlated with angiographically evaluated CAD. In contrast to our study, Avanzas et al. did not find such an association in 297 stable CAD patients, but neopterin serum levels were predictive for the incidence of a combined clinical endpoint. Different patient populations, e.g. the inclusion of diabetic patients and women, the higher event rate as well as the correction for age in the multivariate analyses in the latter study might explain the divergent results.In light of these observations, the association of neopterin or of other inflammatory markers with CAD activity, severity and/or extent should probably not be separated from each other and might be interpreted in the context of the broad spectrum of clinically stable CAD.

NK cell apoptosis in coronary artery disease: Relation to oxidative stress

Objective Natural killer (NK) cells, key elements in initiation and modulation of immune responses, were recently found to be reduced in coronary artery disease (CAD). To clarify mechanisms behind this reduction, we here investigated NK cell apoptosis in CAD patients. Since oxidative stress has been linked to NK cell apoptosis, we related the findings to oxidative stress in vivo and evaluated the ex vivo susceptibility of NK cells to oxidized lipids. Methods and results The number of apoptotic NK cells in peripheral blood was significantly increased in CAD patients compared to controls. Purified NK cells from CAD patients also showed a higher rate of spontaneous apoptosis ex vivo. Dose- and time-dependent effects of oxidized LDL and 7β-hydroxycholesterol (7βOH) on apoptosis and ROS production were determined in NK cells from blood donors. Thereafter, purified NK cells from CAD patients and healthy controls were exposed to the oxidized lipids in a paired design. NK cells from patients were more susceptible to apoptosis induced by oxidized LDL, in particular 7βOH, compared to cells from controls. Plasma measurements of LDL protein oxidation and lipid peroxidation did not show any differences between patients and controls. On the other hand, plasma carotenoids were significantly decreased in patients and inversely correlated to NK cell apoptosis rate. Conclusion The rate of spontaneous NK cell apoptosis was increased in CAD patients. Although NK cells in CAD patients were more sensitive to oxidized lipids ex vivo, indicating a mechanism contributing to the reduced NK cell activity in CAD, the data could not verify an obvious link between NK cell apoptosis and increased oxidative stress in vivo.

Relationship of epicardial adipose tissue by echocardiography to coronary artery disease

Objective:To study the relationship of echocardiographic epicardial adipose tissue (EAT) with coronary artery disease (CAD) risk factors and the extent of coronary atherosclerosis.Methods:EAT thickness was measured in 527 patients undergoing...

Th1/Th2 Imbalance, Measured by Circulating and Intracytoplasmic Inflammatory Cytokines – Immunological Alterations in Acute Coronary Syndrome and Stable Coronary Artery Disease

To describe how peripheral immune-parameters reflect the inflammatory alterations of the atherosclerotic plaques in coronary atherosclerosis. We measured general inflammatory markers C-reactive protein (CRP) and granulocyte activity, lymphocyte subpopulations and their state of activation, evaluated circulating Th1/Th2-type cytokines, and specific intracytoplasmic cytokines. We investigated the association of immune-parameters with disease outcome and mortality. Thirty-three patients with acute coronary syndrome (ACS), 62 with stable coronary artery disease (CAD) and 58 healthy controls were studied. Peripheral blood lymphocyte subgroups were quantified by flow cytometry, soluble cytokines and autoantibodies were assessed using enzyme-linked immunosorbent assay (ELISA), while intracellular cytokine levels were measured by flow cytometry after intracellular staining. We found elevated levels of CRP and granulocyte activity in ACS versus CAD (P < 0.001, P = 0.017, respectively). Natural killer (NK) cell percentages were elevated, while percentage of T cells to the total lymphocyte count was slightly decreased in ACS compared to controls (P < 0.0001, P = 0.012, respectively). Both forms of coronary atherosclerosis showed significantly higher percentages of activated T cells than controls when stained for the activation markers HLA-DR3 and CD69(+) (ACS: P < 0.0001, P = 0.002, CAD: P < 0.0001, P = 0.018, respectively). IL-1, IL-4 and IL-10 proved significantly higher in ACS versus controls (P = 0.036, P = 0.01, P < 0.0001 respectively). Th1 to Th2 ratio shifted towards a Th1 dominance in both diseases. Both general proinflammatory markers and activated T cells signify CAD. The orchestrated proinflammatory cascade eventually leads to the development of the disease.

C-reactive protein elevation and disease activity in patients with coronary artery disease

Aims We sought to assess (1) whether C-reactive protein (CRP) is an independent predictor of future cardiovascular events after adjustment for coronary artery disease (CAD) severity and (2) whether CRP levels correlate with number of angiographically complex coronary artery stenosis. Methods and results We studied 825 consecutive angina patients (mean age 63±10 years, 74% men), 700 with chronic stable angina (CSA) and 125 with acute coronary syndromes without ST-segment elevation (ACS). The composite endpoint of non-fatal acute myocardial infarction, hospital admission with class IIIb unstable angina and cardiac death was assessed at one year follow-up. Hs-CRP level was higher in CSA patients with the combined end-point (\batchmode \documentclass[fleqn,10pt,legalpaper]{article} \usepackage{amssymb} \usepackage{amsfonts} \usepackage{amsmath} \pagestyle{empty} \begin{document} \(P=0.03\) \end{document}) after adjustment for number of diseased coronary arteries. Hs-CRP was also significantly higher in patients with ACS compared to CSA (\batchmode \documentclass[fleqn,10pt,legalpaper]{article} \usepackage{amssymb} \usepackage{amsfonts} \usepackage{amsmath} \pagestyle{empty} \begin{document} \(P=0.004\) \end{document}) and correlated with number of complex angiographic stenoses (\batchmode \documentclass[fleqn,10pt,legalpaper]{article} \usepackage{amssymb} \usepackage{amsfonts} \usepackage{amsmath} \pagestyle{empty} \begin{document} \(r=0.36\) \end{document}, \batchmode \documentclass[fleqn,10pt,legalpaper]{article} \usepackage{amssymb} \usepackage{amsfonts} \usepackage{amsmath} \pagestyle{empty} \begin{document} \(P=0.01\) \end{document}). Hs-CRP was also increased in patients with NYHA functional class III or IV compared to those in class I or II (\batchmode \documentclass[fleqn,10pt,legalpaper]{article} \usepackage{amssymb} \usepackage{amsfonts} \usepackage{amsmath} \pagestyle{empty} \begin{document} \(P{<}0.0001\) \end{document}). Conclusions CRP levels predict future cardiovascular events independently of CAD severity and correlate with number of angiographically complex coronary artery stenosis in patients with ACS. Thus, CRP levels are a marker of atheromatous plaque vulnerability and CAD activity.