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Objective: There is a huge uncertainty in the medical community regarding the significance of non-dominant right coronary artery (RCA) in patients with inferior wall ischemia on myocardial perfusion single-photon emission computed tomography (SPECT). The purpose of this study is to determine the effect of non-dominant RCA on myocardial perfusion SPECT (MPS) with respect to the misleading detection of ischemia in the inferior wall of the myocardium., Methods: This is a retrospective study of 155 patients, who had undergone elective coronary angiography owing to an indication of inferior wall ischemia by MPS between 2012 and 2017. Patients were divided into two groups based on the coronary dominance: group 1 (n = 107), if RCA is the dominant artery, and group 2 (n = 48), if there are dominance of left artery and codominance of both arteries. Obstructive CAD was diagnosed in the case of stenosis that had severity greater than 50%. The positive predictive value (PPV), which was calculated as per the correlation between the inferior wall ischemia in MPS and obstruction level in RCA, was compared in both groups., Results: Majority of patients were male (109, 70%) and the mean age was 59.5 ± 10.2. There were 45 patients with obstructive RCA disease (PPV: 42%) among 107 patients in group 1, whereas there were only 8 patients with obstructive coronary artery disease (CAD) in RCA among 48 patients in group 2, (PPV: 16% and p = 0.004)., Conclusions: The results demonstrated that non-dominant RCA is associated with false-positive detection of inferior wall ischemia via MPS., (© 2023. The Author(s), under exclusive licence to Springer Nature B.V.)

Objectives: Complex coronary lesions are more prone to complications; however, the relationship between complex coronary lesions and no-reflow phenomenon in patients undergoing primary percutaneous intervention (pPCI) is still not clarified. Previous studies reported the association of total coronary artery complexity with no-reflow; however, impact of culprit lesion complexity on no-reflow is not known. In this study, we aimed to investigate the impact of culprit lesion complexity on no-reflow phenomenon. Furthermore, we aimed to investigate the factors that are related to reversibility of no-reflow., Methods: We prospectively included 424 patients treated with pPCI. Patients' baseline characteristics and clinical variables were recorded. Reversibility of no-reflow was decided according to final angiography or ST resolution during the first hour following pPCI. There were 90 patients with a diagnosis of no-reflow constituted group 1 and patients without no-reflow constituted group 2. Complexity of coronary artery disease was assessed with SYNTAX score and culprit lesion complexity was assessed with both American College of Cardiology/Society of Cardiovascular Angiography and Interventions lesion classification and SYNTAX score., Results: Complexity of culprit lesion was significantly higher in group 1 patients (type C lesion 76.6 vs. 27.8%; P < 0.001 and SYNTAX score 8.7 ± 3.0 vs. 6.2 ± 2.6; P < 0.001, respectively, group 1 vs. 2). Multivariate analyses revealed that lesion complexity is independently associated with no-reflow. Among 90 patients of group 1, 43 patients were classified as reversible no-reflow. Logistic regression analysis revealed that only ischaemia duration is independently associated with reversibility of no-reflow., Conclusion: Our study demonstrated that culprit lesion complexity is independently associated with no-reflow phenomenon and short ischaemic duration is significantly associated with reversibility of no-reflow.

Objective: Since coronary artery disease (CAD) is a slow progressive disease, management and appropriate follow-up of patients with nonobstructive coronary artery disease (NOCAD) remains challenging, and there are no clear guidelines recommending a follow-up strategy and indications for repeat invasive coronary angiography (ICA). We investigated the predictors of the development of obstructive CAD in patients with previously diagnosed NOCAD., Methods: We prospectively included 186 patients who previously received a diagnosis of NOCAD with invasive coronary angiogram and underwent repeat ICA. Patients' demographics, clinical characteristics, biochemical analyses were recorded. Obstructive CAD is defined as >50% luminal narrowing in any epicardial coronary artery with a diameter of >2 mm., Results: A total of 186 patients (105 male) were assigned into our study. Mean age was 64.77 ± 10.31 in patients with obstructive CAD (n = 60) vs. 61.87 ± 9.94 in NOCAD patients (n = 126) (P value: 0.068). The median time interval between index and follow-up coronary angiograms was 8 (5-10) years. There was no significant difference between groups with respect to LDL and Hs-CRP levels (P value: 461 and 354, respectively). Although patients with obstructive CAD have more comorbidities, multivariate analyses revealed that there was no significant difference between groups. On the contrary, the total number of risk factors were significantly associated with the development of obstructive CAD during follow-up. Receiver operating characteristic analyses revealed with a cut-off value of 3.5 risk factors, the sensitivity of 71%, the specificity of 61% and the area under the curve was 0.71 for prediction of obstructive CAD., Conclusion: Our results indicate that no single risk factor alone is related with development of obstructive CAD; however, patients with high number of multiple risk factors are more prone to develop obstructive disease and require closer follow-up.

Coronary artery disease (CAD), being a multifactorial disease process, has been suggested to be associated by the interaction of both environmental and genetic risk factors. Toll-like receptors (TLRs) are related to the receptors of the innate immune system which serves as the recognition of the conserved pathogen motifs and the activation of the signals that stimulate inflammatory genes. In this study, we investigated the relationship between the polymorphisms in the TLR2-Arg753Gly, TLR4-Asp299Gly and Thr399Ile gene and CAD. The study population consisted of 300 patients (149 men, 151 women) with angiographically documented CAD. The polymorphisms were genotyped by real time PCR. No association between TLR2-Arg677Trp or TLR4-Asp299Gly and -Thr399Ile gene polymorphisms and the presence or the severity of CAD was observed. On the other hand, the TLR2-Arg753Arg genotype seemed to have a protective effect against development of CAD (OR=0.17; 95% CI=0.04-0.83). Our findings suggest that TLR2-Arg753Gly polymorphism is associated with CAD susceptibility in Turkish patients., (Copyright © 2014 Elsevier B.V. All rights reserved.)

Increased levels of peripheral proinflammatory mediators can contribute to the development of coronary artery disease (CAD). Platelet activating factor (PAF) is an important proinflammatory mediator and plasma levels of PAF correlate with transmembrane transporter multidrug resistant 1 P-glycoprotein (MDR1 Pgp) expression and activity. MDR1 polymorphisms can affect the expression and activity of Pgp and plasma PAF levels. Therefore, we investigated the possible relationship between MDR1 C3435T and G2677T/A polymorphisms and plasma PAF levels and the risk of CAD. The study population consisted of 198 patients angiographically documented CAD, including 113 cases with at least 1 coronary artery with ≥50% luminal diameter stenosis and 85 control subjects with strictly normal coronary angiograms. Genotypes of the MDR1 C3435T and G2677T/A polymorphisms were determined by polymerase chain reaction (PCR) followed by restriction fragment length polymorphism (RFLP). Plasma PAF levels were detected by enzyme-linked immunosorbent assay (ELISA). There were no significant differences among plasma PAF levels in regard to MDR1 C3435T and G2677T polymorphisms in CAD patients and controls. No statistically significant difference was found for the genotypic and allelic distributions of the polymorphisms in the MDR1 gene between the patients and the control subjects. Furthermore, analysis of MDR1 haplotypes did not show any associations with increased plasma PAF levels and risk of CAD. Our results suggest that plasma PAF levels are not associated with MDR1 gene polymorphisms. There is no association between MDR1 C3435T and G2677T/A polymorphisms and the risk of CAD in Turkish patients., (© 2013.)

Background and Objective: Recent information has highlightened the impact of HA metabolism alterations in vascular permeability through its actions on endothelial glycocalyx and the importance of HA-cell interactions in cell behavior of arterial endothelial and smooth muscle cells. Therefore hyaluronan is thought to involve in pathophysiology of atherosclerosis. The aim of this study is to investigate the association of plasma hyaluronidase activity with atherosclerosis in non-diabetic patients with stable coronary artery disease., Methods: In the present study we used plasma hyaluronidase measurement as an indicator of hyaluronan metabolism and activity. A total of 162 subjects undergoing to coronary angiography were divided into two groups according to presence or absence of coronary artery disease, and their serum hyaluronidase activity were measured., Results: Serum hyaluronidase activities were 3797+/-670.62 mU/L and 2838+/-417.67 mU/L for patients with CAD (n:109) and control patients without CAD (n:53), respectively. Serum hyaluronidase activity in patients with coronary artery disease (CAD) were significantly higher than control subjects without CAD (p<0.001)., Conclusion: In the present study hyaluronidase activity was found to be associated with coronary artery disease reflecting the role of hyaluronan in atherosclerosis. We believe that the demonstration of relationship between serum hyaluronidase activity and atherosclerosis represents a remarkable finding highlighting the potential role of hyaluronan in pathophysiology of atherosclerosis (Tab. 2, Fig. 3, Ref. 28). Full Text (Free, PDF) www.bmj.sk.

Background: Atherosclerosis is considered to be an inflammatory disease in which the initial process is augmented infiltration of monocytes into the vessel wall and their subsequent differentiation from macrophages into lipid-laden foam cells. Chitotriosidase is one of the most quantitative proteins secreted by activated macrophages, so the aim of this study was to investigate the association of the level of serum chitotriosidase activity with atherosclerotic coronary artery disease (CAD)., Methods and Results: A total of 200 subjects undergoing coronary angiography were divided into 4 subgroups according to the number of diseased vessels and their serum chitotriosidase activity levels were measured. Serum chitotriosidase activity in patients with CAD was significantly higher than in normal control subjects (p<0.001). Serum chitotriosidase activity was also significantly associated with the extent of CAD as defined by the number of stenosed vessels (p<0.001)., Conclusion: Serum chitotriosidase activity can be considered a strong inflammatory marker of CAD. Moreover, plasma chitotriosidase activity may be also regarded as a quantitative indicator of disease extent, as well as being a marker of disease presence.

We describe the case of a 39-year-old human immunodeficiency virus (HIV)-infected man with angiographically documented rapid progression of coronary artery disease. Over a time course of only 2 months, he developed high-grade stenosis of the left anterior descending coronary artery. The risk of myocardial infarction is increased in patients with HIV infection receiving antiretroviral therapy. However, the absolute risk is small and the marked overall benefits of antiretroviral therapy are evident. Patients receiving HIV protease inhibitors should be screened for hyperlipidemia, hyperglycemia, and hypertension. They may be candidates for lipid-lowering therapies depending on their long-term prognosis and individual risk of cardiovascular disease. Care is need because of possible drug interactions between lipid-lowering drugs and antiretroviral therapy. Invasive treatment of acute myocardial infarction does not differ from that in patients not infected with HIV. The rate of progression of coronary artery disease and the restenosis rate, however, are often unexpectedly high in these patients.

Objective: Coronary artery disease (CAD), which develops from complex interactions between genetic and enviromental factors, is a leading cause of death worldwide. Based on genome-wide association studies (GWAS), the chromosomal region 9p21 has been identified as the most relevant locus presenting a strong association with CAD in different populations. The aim of the present study was to investigate the association of two SNPs on chromosome 9p21 on susceptibility to CAD and the effect of these SNPs along with cardiovascular risk factors on the severity of CAD in the Turkish population. Methods: This study had an observational case-control design. We genotyped 460 subjects, aged 30-65 years, to investigate the association of 2 SNPs (rs1333049, rs2383207) on chromosome 9p21 and CAD risk in Turkish population. Real-time polymerase chain reaction (RT-PCR) was used to analyze the 2 SNPs in CAD patients and healthy controls. The genotype and allelic variations of these SNPs with the severity of CAD was also assessed using semi-quantitative methods such as the Gensini score. Student's t test and multiple regression analysis were used for statistical analysis. Results: The SNPs rs1333049 and rs2383207 were found to be associated with CAD with an adjusted OR of 1.81 (95% Cl 1.05-3.12) and 2.12 (95% CI 1.19-4.10) respectively. After adjustment of CAD risk factors such as smoking, family history of CAD and diabetes, the homozygous AA genotype for rs2383207 increased the CAD risk with an OR 3.69. Also a very strong association was found between rs1333049 and rs2383207 and Gensini scores representing the severity of CAD (p<0.001). Conclusion: The rs2383207 and rs1333049 SNPs on 9p21 chromosome were significantly associated with the risk and severity of CAD in the Turkish population. [ABSTRACT FROM AUTHOR]