Glycosylated Haemoglobin A1c as An Independent Marker Predicting Coronary Artery Disease in Non-diabetic Patient Population in Primary Healthcare in Turkey: A crosssectional study

2020 ◽  
Author(s):  
Yildiz Kayali ◽  
Aclan Ozder

Abstract Background: In our role as a preventive physician, there is a need for cheap and accessible biochemical markers that will allow the determination of the risk of coronary artery disease. We aimed to research the value of glycosylated haemoglobin (HbA1c) in the prediction of coronary artery disease. Methods: Patients aged between thirty and ninety years who were admitted to outpatient clinic of Cardiology department in a university hospital between January 2016 and June 2018 for angiography for various reasons were retrospectively screened. Patients with known diabetes or patients with HbA1c of 6.5 or above were excluded from the study. Comparative HbA1c data were obtained according to the stenosis groups and statistical significance was sought. Logistic regression analysis was used to investigate the risk factors affecting stenosis positivity. Results: A total of 247 patients were identified, 120 patients without any stenosis in any coronary artery, 56 patients with> 50% stenosis in one coronary artery, and 71 patients with > 50% stenosis in more than one coronary artery. There was a statistically significant difference between HbA1c measurements according to the degree of stenosis (p = 0.001 and p <0.01, respectively). The odd ratio for HbA1c was 6.260 (95% CI: 3,160-12,401). According to the stenosis positivity, the cut off point for HbA1c was found to be 5.6 and above. In the regression analysis, HbA1c was an independent risk factor for coronary artery disease. One unit increase in HbA1c measurements increases the risk of stenosis positive to 12.424 times (95% CI: 5,990-25,767).Conclusions: The study showed HbA1c can be used as an independent marker in determining the probability and severity of coronary artery disease in non-diabetic individuals and as an useful marker in primary care predicting coronary artery disease (CAD).

2019 ◽  
Vol 34 (1) ◽  
Author(s):  
Efstathia Giannakopoulou ◽  
Fotios Konstantinou ◽  
Georgia Ragia ◽  
Zisis Gerontitis ◽  
Anna Tavridou ◽  
...  

Abstract Background Cystathionine γ-lyase enzyme, which is encoded by the CTH gene, is responsible for hydrogen sulfide (H2S) production in the endothelium. The CTH 1364 G>T polymorphism may alter the CTH expression and H2S bioavailability, thus leading to atherosclerosis and coronary artery disease (CAD). We examined the potential association of the CTH 1364 G>T polymorphism with CAD. Methods The CTH 1364 G>T polymorphism was determined in 178 coronary artery bypass grafting (CABG) patients and 156 non-atherosclerotic controls of Greek Caucasian origin using the PCR–RFLP method. Results No significant difference in the frequency of the CTH 1364 G>T genotypes (p = 0.281) and alleles (p = 0.265) was found between the CABG patients and controls. After conducting stratification according to sex, analysis showed a numerical difference in the CTH 1364 TT genotype frequency in female participants that did not reach statistical significance (16.3% and 8.5% in the CABG and controls, respectively, p = 0.26). The frequency of the CTH 1364 TT genotype between the male CABG patients and controls did not differ (p = 0.507). Conclusions The CTH 1364 G>T polymorphism was not associated with CAD in the studied population. However, interestingly, a higher – if not significantly so – CTH 1364 TT genotype frequency was present in female CABG patients compared with female controls. Larger studies are necessary to conclude on the potential overall or gender-driven association between CTH 1364 G>T gene polymorphism and CAD.


1994 ◽  
Vol 72 (05) ◽  
pp. 672-675 ◽  
Author(s):  
Nicolas W Shammas ◽  
Michael J Cunningham ◽  
Richard M Pomearntz ◽  
Charles W Francis

SummaryTo characterize the extent of early activation of the hemostatic system following angioplasty, we obtained blood samples from the involved coronary artery of 11 stable angina patients during the procedure and measured sensitive markers of thrombin formation (fibrino-peptide A, prothrombin fragment 1.2, and soluble fibrin) and of platelet activation ((3-thromboglobulin). Levels of hemostatic markers in venous blood obtained from 14 young individuals with low pretest probability for coronary artery disease were not significantly different from levels in venous blood or intracoronary samples obtained prior to angioplasty. Also, there was no translesional (proximal and distal to the lesion) gradient in any of the hemostatic markers before or after angioplasty in samples obtained between 18 and 21 min from the onset of the first balloon inflation. Furthermore, no significant difference was noted between angioplasty and postangioplasty intracoronary concentrations. We conclude that intracoronary hemostatic activation does not occur in the majority of patients during and immediately following coronary angioplasty when high doses of heparin and aspirin are administered.


Author(s):  
P Han ◽  
A Turpie ◽  
E Genton ◽  
M Gent

Platelets play a role in the development and complications of coronary artery disease (CAD) and a number of abnormalities of platelet function which can be corrected by antiplatelet drugs have been described. Betathromboglobulin (BTG), a platelet-specific protein which is released from α-granules during platelet activation is significantly elevated in patients with angiographically demonstrated CAD (51.0 ± 31.0 ng/ml., n = 50) compared to normal (28.0 ± 8.0 ng/ml., n = 70) p < 0.001. The effect of sulphinpyrazone (800 mg.) or aspirin (1200 mg.)/dipyridamole (200 mg.) on plasma BTG in CAD was studied in a blind prospective crossover trial in 25 patients. Mean BTG concentration pre-treatment was 52.3 ng/ml. and after 1 month’s treatment with placebo, sulphinpyrazone or aspirin/dipyridamole mean plasma BTG concentrations were 53.5, 49.6 and 56.7 ng/ml. respectively. Analysis of variance showed no significant difference between the means (p > 0.1) . This study confirms increased plasma BTG concentrations in patients with CAD and indicates that therapeutic doses of these antiplatelet drugs do not significantly effect the BTG level and thus appear not to prevent α-granule release in CAD.


2020 ◽  
Vol 18 (5) ◽  
pp. 523-530 ◽  
Author(s):  
Konstantinos Maniatis ◽  
Gerasimos Siasos ◽  
Evangelos Oikonomou ◽  
Manolis Vavuranakis ◽  
Marina Zaromytidou ◽  
...  

Background: Osteoprotegerin and osteopontin have recently emerged as key factors in both vascular remodelling and atherosclerosis progression. Interleukin-6 (IL-6) is an inflammatory cytokine with a key role in atherosclerosis. The relationship of osteoprotegerin, osteopontin, and IL-6 serum levels with endothelial function and arterial stiffness was evaluated in patients with coronary artery disease (CAD). Methods: We enrolled 219 patients with stable CAD and 112 control subjects. Osteoprotegerin, osteopontin and IL-6 serum levels were measured using an ELISA assay. Endothelial function was evaluated by flow-mediated dilation (FMD) in the brachial artery and carotid-femoral pulse wave velocity (PWV) was measured as an index of aortic stiffness. Results: There was no significant difference between control subjects and CAD patients according to age and sex. Compared with control subjects, CAD patients had significantly impaired FMD (p<0.001) and increased PWV (p=0.009). CAD patients also had significantly higher levels of osteoprotegerin (p<0.001), osteopontin (p<0.001) and IL-6 (p=0.03), compared with control subjects. Moreover, IL-6 levels were correlated with osteoprotegerin (r=0.17, p=0.01) and osteopontin (r=0.30, p<0.001) levels. FMD was correlated with osteoprotegerin levels independent of possible confounders [b coefficient= - 0.79, 95% CI (-1.54, -0.05), p=0.04]. Conclusion: CAD patients have increased osteoprotegerin, osteopontin and IL-6 levels. Moreover, there is a consistent association between osteoprotegerin and osteopontin serum levels, vascular function and inflammation in CAD patients. These findings suggest another possible mechanism linking osteoprotegerin and osteopontin serum levels with CAD progression through arterial wall stiffening and inflammation.


2019 ◽  
Vol 2019 ◽  
pp. 1-6 ◽  
Author(s):  
Joanna Wojtasik-Bakalarz ◽  
Zoltan Ruzsa ◽  
Tomasz Rakowski ◽  
Andreas Nyerges ◽  
Krzysztof Bartuś ◽  
...  

The most relevant comorbidities in patients with peripheral artery disease (PAD) are coronary artery disease (CAD) and diabetes mellitus (DM). However, data of long-term follow-up of patients with chronic total occlusion (CTO) are scarce. The aim of the study was to assess the impact of CAD and DM on long-term follow-up patients after superficial femoral artery (SFA) CTO retrograde recanalization. In this study, eighty-six patients with PAD with diagnosed CTO in the femoropopliteal region and at least one unsuccessful attempt of antegrade recanalization were enrolled in 2 clinical centers. Mean time of follow-up in all patients was 47.5 months (±40 months). Patients were divided into two groups depending on the presence of CAD (CAD group: n=45 vs. non-CAD group: n=41) and DM (DM group: n=50 vs. non-DM group: n=36). In long-term follow-up, major adverse peripheral events (MAPE) occurred in 66.6% of patients with CAD vs. 36.5% of patients without CAD and in 50% of patients with DM vs. 55% of non-DM subjects. There were no statistical differences in peripheral endpoints in both groups. However, there was a statistically significant difference in all-cause mortality: in the DM group, there were 6 deaths (12%) (P value = 0.038). To conclude, patients after retrograde recanalization, with coexisting CTO and DM, are at higher risk of death in long-term follow-up.


2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
B Balcer ◽  
I Dykun ◽  
S Hendricks ◽  
F Al-Rashid ◽  
M Totzeck ◽  
...  

Abstract Background Anemia is a frequent comorbidity in patients with coronary artery disease (CAD). Besides a complemental effect on myocardial oxygen undersupply of CAD and anemia, available data suggests that it may independently impact the prognosis in CAD patients. We aimed to determine the association of anemia with long-term survival in a longitudinal registry of patients undergoing conventional coronary angiography. Methods The present analysis is based on the ECAD registry of patients undergoing conventional coronary angiography at the Department of Cardiology and Vascular Medicine at the University Clinic Essen between 2004 and 2019. For this analysis, we excluded all patients with missing hemoglobin levels at baseline admission or missing follow-up information. Anemia was defined as a hemoglobin level of &lt;13.0g/dl for male and &lt;12.0g/dl for female patients according to the world health organization's definition. Cox regression analysis was used to determine the association of anemia with morality, stratifying by clinical presentation of patients. Hazard ratio and 95% confidence interval are depicted for presence vs. absence of anemia. Results Overall, data from 28,917 patient admissions (mean age: 65.3±13.2 years, 69% male) were included in our analysis (22,570 patients without and 6,347 patients with anemia). Prevalence of anemia increased by age group (age &lt;50 years: 16.0%, age ≥80 years: 27.7%). During a mean follow-up of 3.2±3.4 years, 4,792 deaths of any cause occurred (16.6%). In patients with anemia, mortality was relevantly higher as compared to patients without anemia (13.4% vs. 28.0% for patients without and with anemia, respectively, p&lt;0.0001, figure 1). In univariate regression analysis, anemia was associated with 2.4-fold increased mortality risk (2.27–2.55, p&lt;0.0001). Effect sizes remained stable upon adjustment for traditional risk factors (2.38 [2.18–2.61], p&lt;0.0001). Mortality risk accountable to anemia was significantly higher for patients receiving coronary interventions (2.62 [2.35–2.92], p&lt;0.0001) as compared to purely diagnostic coronary angiography examinations (2.31 [2.15–2.47], p&lt;0.0001). Likewise, survival probability was slightly worse for patients with anemia in acute coronary syndrome (2.70 [2.29–3.12], p&lt;0.0001) compared to chronic coronary syndrome (2.60 [2.17–3.12], p&lt;0.0001). Interestingly, within the ACS entity, association of anemia with mortality was relevantly lower in STEMI patients (1.64 [1.10–2.44], p=0.014) as compared to NSTEMI and IAP (NSTEMI: 2.68 [2.09–3.44], p&lt;0.0001; IAP: 2.67 [2.06–3.47], p&lt;0.0001). Conclusion In this large registry of patients undergoing conventional coronary angiography, anemia was a frequent comorbidity. Anemia relevantly influences log-term survival, especially in patients receiving percutaneous coronary interventions. Our results confirm the important role of anemia for prognosis in patients with coronary artery disease, demonstrating the need for specific treatment options. Figure 1. Kaplan Meier analysis Funding Acknowledgement Type of funding source: None


2008 ◽  
Vol 24 (3) ◽  
pp. 175-179 ◽  
Author(s):  
Renato Scacchi ◽  
Giuseppe Gambina ◽  
Elisabetta Broggio ◽  
Maria Ruggeri ◽  
Rosa Maria Corbo

The human endothelin-converting enzyme (ECE) is involved inβ-amyloid synthesis and regulation of the endothelin-1 (ET-1) vasoconstricting peptide. We investigated the distribution of the C-338A polymorphism of the ECE-1b gene in sporadic late-onset Alzheimer’s disease (LOAD) and in coronary artery disease (CAD) to verify its role in the onset of these two complex diseases. Two cohorts of 458 Italian Caucasian LOAD patients and 165 CAD patients were examined for the C-338A polymorphism and compared with respective control samples (260 and 106 subjects, respectively). The A allele was less present in LOAD patients than in controls, but an at limits statistically significant difference was achieved only in subjects aged less than 80 years, where only the AA genotypes appeared to have a protective role against the onset of the sporadic LOAD. For the overall CAD sample the pattern was similar and significant differences were observed only in subjects non carrying the apolipoprotein E (APOE) e*4 allele, where the A allele carrying genotypes had a protective role against the onset of the disease.


2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Tien-Hung Huang ◽  
Cheuk-Kwan Sun ◽  
Yi-Ling Chen ◽  
Pei-Hsun Sung ◽  
Chi-Hsiang Chu ◽  
...  

Background. This study was aimed at testing the association between the therapeutic efficacy of CD34+ cell treatment in patients with end-stage diffuse coronary artery disease as reflected in angiographic grading and results of directed in vivo angiogenesis assay (DIVAA) on their isolated peripheral blood mononuclear cell- (PBMC-) derived endothelial progenitor cells (EPCs). Methods. Angiographic grades (0: <5%; 1: 5–35%; 2: 35–75%; 3: >75%) which presented the improvement of vessel density pre- and post-CD34+ treatment were given to 30 patients with end-stage diffuse coronary artery disease having received CD34+ cell treatment. The patients were categorized into low-score group (angiographic grade 0 or 1, n=12) and high-score group (angiographic grade 2 or 3, n=18). The percentages of circulating EPCs with KDR+/CD34+/CD45−, CD133+/CD34+/CD45−, and CD34+ were determined in each patient using flow cytometry. PBMC-derived EPCs from all patients were subjected to DIVAA through a 14-day implantation in nude mice. The DIVAA ratio (i.e., mean fluorescent units in angioreactors with EPCs/mean fluorescent units in angioreactors without EPCs) was obtained for each animal with implanted EPCs from each patient. Results and Conclusions. The number of EPCs showed no significant difference among the two groups. The DIVAA ratio in the high-score group was significantly higher than that in the low-score group (p=0.0178). Logistic regression revealed a significant association between the DIVAA ratio and angiographic grading (OR 3.12, 95% CI: 1.14–8.55, p=0.027). The area under the ROC curve (AUC) was 0.8519 (p=0.0013). We proposed that DIVAA may be a reliable tool for assessing coronary vascularization after CD34+ cell treatment.


2017 ◽  
Vol 2017 ◽  
pp. 1-8
Author(s):  
Bingjie Wu ◽  
Jingjing Jiang ◽  
Minghui Gui ◽  
Lin Liu ◽  
Qiqige Aleteng ◽  
...  

The aim of this study was to evaluate the association between thyroid hormone levels, pulmonary hypertension (PH), and pulmonary artery systolic pressure (PASP) in euthyroid patients with coronary artery disease (CAD). A cross-sectional study was conducted in individuals who underwent coronary angiography and were diagnosed as CAD from March 2013 to November 2013. 811 subjects (185 women and 626 men) were included in this study. PASP was measured by transthoracic Doppler echocardiography. 86 patients were diagnosed as PH and had significantly higher free thyroxine (FT4) levels than those without PH. Multiple logistic regression analysis demonstrated an independent association of FT4 levels with PH after adjustment of gender, age, body mass index, systolic blood pressure, left ventricular ejection fraction, hypertension, and medication use of calcium channel blockers, ACE inhibitors, angiotensin II receptor antagonists, and nitrates. Serum-free triiodothyronine (FT3) and thyroid-stimulating hormone (TSH) were not associated with PH. Furthermore, multivariate linear regression analysis showed that FT4 levels emerged as an independent predictor for PASP, while FT3 and TSH levels were not associated with PASP. Our study demonstrated that, in euthyroid patients with CAD, FT4 was an independent risk factor for PH, and FT4 levels were independently associated with PASP.


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