Slow Coronary Flow Group Research Articles

Development and validation of a nomogram diagnostic model for coronary slow flow patients: A cross-sectional study.

In this study, risk factors for coronary slow flow (CSF) patients were examined, and a clinical prediction model was created. This study involved 573 patients who underwent coronary angiography at our hospital because of chest pain from January 2020 to April 2022. They were divided into CSF group (249 cases) and noncoronary slow flow (NCF) group (324 cases) according to the coronary blood flow results. According to a 7:3 ratio, the patients were categorized into a training group consisting of 402 cases and a validation group consisting of 171 cases. The outcome was assessed by employing multiple logistic regression analysis to examine the factors that influenced it. The model's recognizability was assessed by calculating the consistency index and plotting the receiver operating characteristic curve. Its consistency was assessed by calibration curve, decision curve, and Hosmer-Lemeshow testing goodness-of-fit. The multivariate model included factors such as male, BMI, smoking, diabetes, ursolic acid, and high-density lipoprotein cholesterol. The model validation showed that the consistency index was 0.714, and the external validation set had a consistency index of 0.741. The areas under the curve for the training and external validation sets were respectively 0.730 (95% CI: 0.681-0.779) and 0.770 (95%CI: 0.699-0.841). Nomogram calibration curves indicated intense calibration, and the results of the Hosmer-Lemeshow goodness-of-fit test indicated that χ² = 1.118, P = .572. The nomogram combining various risk factors can be used for individualized predictions of CSF patients and then facilitate prompt and specific treatment.

Comparison of the Effect of Non-HDL-C/HDL-C Ratio on Coronary Slow Flow with Other Non-Traditional Lipid Markers.

Coronary slow flow (CSF) is a microvascular disease characterized by delayed opacification of the epicardial coronary arteries during angiography. The main pathogenesis of CSF is endothelial dysfunction caused by diffuse atherosclerosis. Dyslipidemia is one of the primary factors raising the risk of atherosclerosis. Compared to conventional lipid profiles, non-traditional lipid profiles more accurately reflect dyslipidemic status. In this work, we compared the non-high density lipoprotein-cholesterol (HDL-C)/HDL-C ratio (NHHR) with other conventional and non-conventional lipid profiles in order to determine its impact on CSF. A total of 9112 subjects who underwent coronary angiography were screened retrospectively, of whom 130 subjects with CSF and 130 subjects with normal CF were included. Multivariate regression analysis was used to identify independent predictors of CSF. Additionally, in order to predict CSF, the diagnostic accuracies of NHHR and other non-traditional lipid profiles were examined. There were significantly higher non-traditional lipid profiles in the CSF group (all p < 0.001). Compared to other non-traditional lipid profiles, NHHR had a stronger association with thrombolysis in myocardial infarction frame count (r = 0.3593, p < 0.0001). In addition to NHHR, non-HDL-C, Castelli's risk index-II, atherogenic index of plasma, plasma glucose, dyslipidemia, smoking, and body mass index were identified as independent predictors of CSF. The ability of NHHR to detect CSF was superior to other non-traditional lipid profiles (area under the curve: 0.785; confidence interval: 0.730-0.840; p < 0.001). NHHR was found to be a potent and reliable predictor of CSF. This indicates that NHHR can be used as a reliable biomarker for risk stratification of CSF.

Coronary slow flow and its correlation with reduced left ventricle global longitudinal strain: a case–control study

BackgroundCoronary slow flow (CSF) often links to inflammation and endothelial function disturbance. While conventional ejection fraction measurements fall short in identifying myocardial dysfunction, left ventricular global longitudinal strain (LV GLS) has shown superior efficacy in this regard. Our study aimed to explore subclinical left ventricular systolic dysfunction by assessing LV GLS in patients diagnosed with coronary slow flow (CSF).MethodsThe study included sixty patients with CSF and sixty control individuals without CSF. Coronary angiography employed the Thrombolysis in Myocardial Infarction (TIMI) frame count (TFC) to identify CSF. LV GLS values were evaluated and compared between the two groups.ResultsSignificantly reduced LV GLS was evident in the CSF group compared to the control group (− 16.18 ± 1.25 vs. − 19.34 ± 1.33, p < 0.001). A notable correlation (r = 0.492, p < 0.001) between LV GLS and TFC was observed in the CSF group. Multivariate logistic regression analysis highlighted reduced LV-GLS (OR 2.2, 95% CI 1.57–3.09, p < 0.001) and smoking (OR 11.55, 95% CI 3.24–41.2, p < 0.001) as significant predictors for CSF presence. The receiver operating characteristic curve established that an LV GLS value of ≥ − 17.8% accurately predicted the presence of CSF (AUC: 0.958, 95% CI: 0.924–0.991, p < 0.001) with 90% specificity and 91.7% sensitivity.ConclusionOur study indicates that reduced LV GLS is associated with CSF presence, offering a valuable means to early detect subclinical left ventricular systolic dysfunction in high-risk patients susceptible to heart failure.Trial registration: ZU-IRB#7038/12-7-2021 Registered 12 July 2021, email: IRB_123@medicine.zu.edu.eg.

Endocan may predict the presence of coronary slow flow and coronary artery disease.

Coronary artery disease (CAD) is frequent, but coronary slow flow (CSF) is a less common cardiovascular disease with a significant risk of mortality and morbidity. Endocan is a proinflammatory glycopeptide that has been investigated in cardiovascular diseases as well as some inflammatory diseases in recent years. We planned to compare the levels of endocan in both CAD and CSF in a similar population and examine the relationship of endocan with additional clinical variables. In the trial, we included 169 consecutive subjects having a coronary angiography indication. According to the results of coronary angiography, 58 people were included in the CAD group, 52 were in the CSF group, and 59 people were in the control group. The control group includes those who did not have any lesions in their epicardial coronary arteries. Thrombolysis in myocardial infarction (TIMI)-frame counts (TFC) were calculated for all patients. Notably, 2.6% of the population in our study had CSF. Both the CAD (555±223 pg/mL) and CSF (559±234 pg/mL) groups had higher endocan levels than the control group (331±252 pg/mL) (p<0.001). There were similar endocan levels between the CAD and CSF groups. Endocan levels were shown to be favorably associated with mean TFC (r=0.267; p0.001). Serum endocan levels (particularly those above 450 pg/mL) and the presence of hyperlipidemia were the most important predictors of both CAD and CSF. Endocan levels are higher in CAD and CSF patients than in those with normal coronary arteries.

Dysregulation of LncRNAs ANRIL, MALAT1, and LINC00305 in Coronary Slow Flow Patients: Implications for Inflammation and Endothelial Dysfunction.

Coronary Slow Flow (CSF) is observed in individuals who experience delayed blood supply in the coronary arteries. Inflammation and endothelial dysfunction may play a role in the etiology and development of CSF. The current investigation aimed to compare the expression of specific long noncoding RNAs (lncRNAs) associated with endothelial dysfunction and inflammation in CSF patients. This case‒control study enrolled 72 CSF patients and 71 healthy individuals. Blood samples were collected, and serum marker levels were measured. The expression levels of lncRNAs ANRIL, MALAT1, and LINC00305 in peripheral blood mononuclear cells (PBMCs) were assessed using real-time Polymerase Chain Reaction (PCR). All statistical analyses were performed using SPSS 22, with the significance level set at P < 0.05. The study revealed that the relative expression of MALAT1 and LINC00305 was significantly lower in the CSF group (p < 0.01), whereas ANRIL was expressed at higher levels (p < 0.0001). The areas under the ROC curves (AUCs) for MALAT1, LINC00305, and ANRIL were 0.64, 0.66, and 0.75, respectively. Notably, the expression level of LINC00305 exhibited an inverse correlation with CSF incidence (OR: 0.83, p: 0.008) in contrast to that of ANRIL (OR: 1.43, p < 0.0001). Additionally, compared to those in the control group, the average BMI, WBC, RBC, Hb, LDH, LDL, FBS, and percentage of neutrophils in the CSF group were significantly greater (p< 0.05). lncRNA ANRIL is upregulated in CSF patients, whereas MALAT1 and LINC00305 are downregulated. Dysregulation of ANRIL, MALAT1, and LINC00305 may serve as diagnostic and predictive factors for CSF leakage.

Relationship between quantitative epicardial adipose tissue based on coronary computed tomography angiography and coronary slow flow

BackgroundThe purpose of this study was to explore the relationship between quantitative epicardial adipose tissue (EAT) based on coronary computed tomography angiography (CCTA) and coronary slow flow (CSF).MethodsA total of 85 patients with < 40% coronary stenosis on diagnostic coronary angiography were included in this retrospective study between January 2020 and December 2021. A semi-automatic method was developed for EAT quantification on CCTA images. According to the thrombolysis in myocardial infarction flow grade, the patients were divided into CSF group (n = 39) and normal coronary flow group (n = 46). Multivariate logistic regression was used to explore the relationship between EAT and CSF. Receiver operating characteristic (ROC) curve was plotted to evaluate the diagnostic value of EAT in CSF.ResultsEAT volume in the CSF group was significantly higher than that of the normal coronary flow group (128.83± 21.59 mL vs. 101.87± 18.56 mL, P < 0.001). There was no significant difference in epicardial fat attenuation index between the two groups (P > 0.05). Multivariate logistic regression analysis showed that EAT volume was independently related to CSF [odds ratio (OR) = 4.82, 95% confidence interval (CI): 3.06–7.27, P < 0.001]. The area under ROC curve for EAT volume in identifying CSF was 0.86 (95% CI: 0.77–0.95). The optimal cutoff value of 118.46 mL yielded a sensitivity of 0.80 and a specificity of 0.94.ConclusionsIncreased EAT volume based on CCTA is strongly associated with CSF. This preliminary finding paves the way for future and larger studies aimed to definitively recognize the diagnostic value of EAT in CSF.

The expression levels of PPAR-α/γ and UCP1/2 on the slow coronary flow phenomenon; results from a case-control study.

The slow coronary flow (SCF) phenomenon is considered a coronary artery disorder. Because of the critical function of peroxisome proliferator-activated receptors (PPARs) in regulating the oxidative stress and inflammatory reactions in cardiovascular disease, The aim of the current study was to investigate the expression of the genes for uncoupling proteins 1 and 2 (UCP1 and UCP2), peroxisome proliferator-activated receptors and (PPAR- PPAR-), and PPAR- in SCF patients. In this case-control study, coronary angiography examination was used to analyze 35 individuals with SCF and 35 subjects with normal coronary flow (NCF). SCF was diagnosed using the TIMI (thrombolysis in myocardial infarction frame count) method. The SCF phenomenon is thought to be the TIMI > 27. In the peripheral blood mononuclear cells (PBMCs), the messenger ribonucleic acid (mRNA) expression levels of the PPAR-, PPAR-, UCP1, and UCP2 genes were evaluated. UCP1 and UCP2 expression levels were significantly higher in the SCF group compared to the NCF group (P = 0.034 and P0.001, respectively). The PPAR- and PPAR- levels were found to be significantly lower in the SCF group compared to the NCF group (P = 0.015, P0.001, respectively). According to the results of the logistic regression analysis, high UCP1 and UCP2 levels and low PPAR- and PPAR- levels are each independent predictors of the SCF phenomenon. This research provided evidence about the potential role of PPAR-α, PPAR-γ, UCP1, and UCP2 as biomarkers in SCF. More investigations are suggested to assess the functions of these factors in SCF patients mechanistically.

Investigation of the Relationship Between Triglycerides-Glucose İndex and Coronary Slow Flow: A Retrospective Case-Control Study.

Coronary slow flow (CSF) refers to delayed distal vessel opacification in the absence of epicardial coronary artery stenosis. The etiopathogenic mechanism of CSF is still unclear. This study investigates the relationship between CSF and the triglyceride-glucose (TyG) index. The study sample consisted of 118 CSF patients and 105 patients with normal coronary flow (NCF). The coronary flow rate was measured via the Thrombolysis in Myocardial Infarction (TIMI) frame count (TFC) method in all patients. The TyG index was calculated as the logarithm of the [fasting triglyceride (mg/dL)×fasting glucose (mg/dL)]/2 value. A significance level of < 0.05 was adopted as statistically significant. The TyG index, low-density lipoprotein (LDL), body mass index (BMI), neutrophil-to-lymphocyte ratio (NLR) and TFC values, male ratio, and the ratio of smokers were higher, whereas high-density lipoprotein (HDL) levels were significantly lower in the CSF group compared to the NCF group (p<0,05). The correlation analysis revealed that CSF was significantly correlated with TyG index, BMI, NLR, and HDL values. The strongest of these correlations was between CSF and TyG index (r= 0.57, p<0.001). Additionally, the multivariate analysis revealed that TyG index, BMI, NLR ratio, and male gender were independent predictors for CSF (p<0.05). Receiver operating characteristic (ROC) curve analysis indicated that a cut-off value of ≥ 9.28 for the TyG index predicted CSF with a sensitivity of 78% and a specificity of 78.1% [Area under the curve (AUC): 0.868 and 95% Confidence Interval (CI): 0.823-0.914]. The findings of this study revealed a very strong relationship between CSF and TyG index.

Soluble Vascular Cell Adhesion Molecule-1 as an Inflammation-Related Biomarker of Coronary Slow Flow.

Background: Coronary slow flow (CSF) is an angiographic entity characterized by delayed coronary opacification with no evident obstructive lesion in the epicardial coronary artery. Several studies have shown that the occurrence and development of CSF may be closely related to inflammation. Soluble vascular cell adhesion molecule-1 (sVCAM-1) is a biomarker related to inflammation. The aim of this study was to evaluate the correlation between plasma soluble VCAM-1 level and CSF occurrence and thus the predictive value of VCAM-1 for CSF. Methods: Forty-six CSF patients and thirty control subjects were enrolled. Corrected thrombolysis in myocardial infarction frame count (cTFC) was used to diagnose CSF. Functional status and quality of life were determined by the Seattle Angina Questionnaire (SAQ). Echocardiography was used to evaluate the systolic and diastolic function of the left ventricle (LV) and right ventricle (RV). The plasma levels of sVCAM-1, IL-6, and TNF-α were quantified by enzyme-linked immunosorbent assay. Results: Compared with the control group, the physical limitation score by the SAQ, the LV global longitudinal strain (GLS), mitral E, and mitral E/A decreased in patients with CSF, while the plasma IL-6 and TNF-α levels increased. The plasma sVCAM-1 level in the CSF group was significantly higher than that in the control group (186.03 ± 83.21 vs. 82.43 ± 42.12 ng/mL, p < 0.001), positively correlated with mean cTFC (r = 0.57, p < 0.001), and negatively correlated with the physical limitation score (r = −0.32, p = 0.004). Logistic regression analyses confirmed that plasma sVCAM-1 level (OR = 1.07, 95%CI: 1.03−1.11) is an independent predictor of CSF, and the receiver operating characteristic curve analysis showed that plasma sVCAM-1 levels had statistical significance in predicting CSF (area under curve = 0.88, p < 0.001). When the sVCAM-1 level was higher than 111.57 ng/mL, the sensitivity for predicting CSF was 87% and the specificity was 73%. Conclusions: Plasma sVCAM-1 level can be used to predict CSF and was associated with the clinical symptoms of patients. It may serve as a potential biomarker for CSF in the future.

Evaluation of Left Ventricular Function in Patients with Coronary Slow Flow by the Dobutamine Stress Echocardiography.

The study aims to assess the changes to left ventricular (LV) function of patients with the coronary slow flow (CSF) in response to stress induced by low dose dobutamine. Based on coronary angiography (CAG) results, a total of 186 patients undergoing CAG for chest pain and suspected coronary heart disease were assigned to the CSF group (n = 142) and control group (n = 44). Patients in the CSF group underwent two-dimensional speckle-tracking echocardiography (STE) during the dobutamine stress test to evaluate LV systolic and diastolic functions. At rest, there were no statistically significant differences in LV peak systolic longitudinal strain (LS), LV peak systolic longitudinal strain rate (LSRs), LV peak early diastolic longitudinal strain rate (LSRed), LV circumferential strain (CS), or LV circumferential strain rate (CSRed) between the CSF and control groups. In the CSF group, LS and LSRs first increased as the infusion rate was increased to 10 μg/kg/min (all, p < 0.05), before decreasing at infusion rates of 15 and 20 μg/kg/min (all, p < 0.05). CS and CSRed increased in the CSF group at infusion rates of 5, 10, and 15 μg/kg/min, (all, p < 0.05), but decreased significantly at 20 μg/kg/min (all, p < 0.05). At rest, LV systolic and diastolic functions were comparable between the CSF and control groups. However, when blood flow to the heart muscles was insufficient, LSRed decreased first, followed by LS. In terms of sensitivity to myocardial ischemia, LS is a better strain parameter than CS.

Predictive value of thrombolysis in myocardial infarction frame count for coronary microvascular dysfunction evaluated with an angiography-derived index of microcirculatory resistance in patients with coronary slow flow.

BackgroundThe association between coronary slow flow (CSF) and coronary microvascular dysfunction (CMD) remains unclear. The objective of this study was to evaluate the correlation between the corrected thrombolysis in myocardial infarction (TIMI) frame count (CTFC) and the index of microcirculatory resistance (IMR).MethodsWe consecutively enrolled patients with CSF from January 2017 to March 2018. Concurrently, we randomly selected control participants with normal flow arteries at a ratio of 3:1. Two cardiologists performed the measurements of CTFC. Coronary angiography-derived IMR (caIMR) was used to assess CMD. The caIMR was analyzed by an independent agency, with CMD being defined as caIMR >40 U.ResultsA total of 111 patients with CSF and 39 patients without CSF were enrolled in this retrospective study. Compared with the non-CSF group, the CSF group had a greater proportion of males (65.8% vs. 23.1%; P<0.001) and a lower prevalence of hypertension (47.7% vs. 67.7%; P=0.042). Additionally, the CSF group had higher CTFC, coronary angiography–derived fractional flow reserve (caFFR), and caIMR regardless of left anterior descending artery (LAD), left circumflex artery (LCX), and right coronary artery (RCA) (all P values <0.001). A strong correlation between CTFC and caIMR was observed for all arteries (all P values <0.001). In the univariate analysis, male sex [hazard ratio (HR) =2.63, 95% CI: 1.30–5.31], E/e’ (HR =0.88, 95% CI: 0.78–0.99), CTFC (HR =1.12, 95% CI: 1.09–1.16), and caFFR (HR =1.81, 95% CI: 1.50–2.17) were significantly correlated with CMD. After adjusting for covariates, male sex (HR =2.72, 95% CI: 1.22–6.06), CTFC (HR =1.10, 95% CI: 1.07–1.14), and caFFR (HR =1.22, 95% CI: 1.00–1.50) were independent predictors for CMD. Additionally, the best cutoff value of CTFC of all arteries for predicting CMD was 38 frames, with an area under the curve of 0.873, a sensitivity of 92.8%, and a specificity of 63.8% (P<0.001). Moreover, the best cutoff value of CTFC of LAD, LCX, and RCA to identify CMD was 35 frames, 52 frames, and 50 frames, respectively (all P values <0.001).ConclusionsCTFC correlated well with caIMR and had a strong predictive power to identify CMD.

Evaluation of the relationship between aspartate aminotransferase/alanine aminotransferase ratio and coronary slow-flow phenomenon.

Aim: To assess the correlation between the ratio of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) and slow coronary flow (SCF). Methods: A total of 119 patients with SCF and 121 age- and sex-matched patients with normal coronary flow were included in this retrospective cross-sectional study. Thrombolysis in myocardial infarction frame count of angiography images was marked by two interventionalists. In addition to AST and ALT levels, complete blood count; kidney, liver and thyroid function tests; age; sex; medication and medical history were recorded. Results: Significant spikes in AST/ALT ratio were discovered in the SCF group compared with the normal coronary flow group (p < 0.001). Thrombolysis in myocardial infarction frame count values were significantly higher in all coronaries for the SCF group compared with the normal coronary flow group (p<0.001). Thrombolysis in myocardial infarction frame count values of the left anterior descending artery (r=0.258; p<0.001), left circumflex artery (r=0.297; p<0.001) and right coronary artery (r=0.195; p=0.002) were positively correlated with AST/ALT ratio. Conclusion: AST/ALT ratio is significantly correlated with SCF; therefore, this ratio may have predictive value.

Elevated levels of sIL-2R, TNF-α and hs-CRP are independent risk factors for post percutaneous coronary intervention coronary slow flow in patients with non-ST segment elevation acute coronary syndrome

To evaluate the association between circulating levels of inflammatory cytokines and the occurrence of post-percutaneous coronary intervention (PCI) coronary slow flow (CSF) in patients with non-ST segment elevation acute coronary syndrome (NSTE-ACS). CSF after PCI commonly occurs and implies poor outcomes, while the determinants of post-PCI CSF in patients with NSTE-ACS remain controversial. In this multicenter case control study, 176 patients diagnosed with NSTE-ACS and with post-PCI CSF occurred composed of CSF group, while 352 matched NSTE-ACS patients composed control group. Corrected thrombolysis in myocardial infarction frame count (cTFC), circulating levels of inflammatory cytokines and PCI related parameters were analyzed using Logistic regression models. Among 528 patients with median age of 67 (59–76) and male proportion of 65.5%, 176 (35.0%) patients had occurrence of post-PCI CSF defined as cTFC ≥ 24. Patients with CSF presented more intense inflammatory activity revealed by higher levels of white blood cell, high-sensitivity C-reactive protein (hs-CRP), interleukin-1ß (IL-1ß), soluble IL-2 receptor (sIL-2R), IL-6, IL-8, IL-10 and tumor necrosis factor-α (TNF-α), while PCI related parameters were comparable. Correlation analysis showed cTFC was positively correlated with those inflammatory cytokines. Logistic regression model indicates that hs-CRP (odds ratio (OR) = 3.038, 95% confidence interval (CI) 1.545–5.975), sIL-2R (OR = 2.103, 95% CI 1.959–4.026) and TNF-α (OR = 3.708, 95% CI 1.426–9.641) were valuable predictors for CSF occurrence. Elevated circulating levels of inflammatory cytokine including hs-CRP, sIL-2R and TNF-α rather than PCI related parameters could predict post-PCI CSF in patients with NSTE-ACS.

Assessment of triglyceride/glucose index with respect to coronary slow flow.

Coronary slow flow (CSF) is determined by delayed opacification of the epicardial coronary arteries without obstructive disease. The triglyceride glucose index (TGI) has been suggested as a useful marker of insulin resistance. Previous studies have shown that TGI is associated with cardiovascular disease, but no study has examined the relationship between TGI and CSF. Therefore, the primary objective of the present study was to investigate the relationship between TGI and CSF. This study retrospectively evaluated patients who were admitted to our clinic with complaints of chest pain and underwent coronary angiography between January and December 2018. A total of 1100 coronary angiography images were assessed, and 72 patients with CSF were detected. Coronary flow was quantified objectively using the TIMI (thrombolysis in myocardial infarction) frame count (TFC) method as described by Gibson et al. TGI was calculated as follows: ln [fasting triglycerides (mg/dL) × fasting glucose (mg/dL)/2]. The CSF group had significantly higher glucose levels (mg/dl) [ (114.92±30.92), (125.61±33.22), than the control and CSF groups, respectively, p=0.0001], TGI [ (9.02±0.56), (9.26±0.54), p=0.0001], and triglyceride levels (mg/dl) [ (170.67±110.81), (201.19±136.93), p=0.002]. There was no statistically significant correlation between TGI and left anterior descending artery TFC, circumflex artery TFC, right coronary artery TFC (r/p values; 0.24/0.06; 0.32/0.08; 0.18/0.36, respectively). TGI, HDL, HT, age, and sex were examined with a multiple logistic model, and TGI was found to be statistically significant for the risk of CSF (p=0.0001; O.R:7.459). TGI was statistically significantly higher in the CSF group than the control group. According to the multivariate logistic regression analysis, only TGI was independently associated with the risk of CSF, but higher TGI did not predict more slow coronary flow. Prospective studies are needed to clarify the prognostic relationship of TGI and CSF in terms of future cardiovascular events (Tab. 2, Fig. 1, Ref. 19).

Evaluation of index of cardio-electrophysiological balance in patients with coronary slow flow

Background Coronary slow flow (CSF) is defined as the late progression of applied contrast through coronary arteries. The cardiac electrophysiological balance index (iCEB) reflects the balance between ventricular depolarisation and repolarisation and provides more information about ventricular arrhythmogenesis (VA) than other electrocardiography (ECG) parameters (QT, corrected QT [QTc], etc.). Aim We aimed to evaluate iCEB in patients with CSF. Methods We divided the study population into two groups as CSF and control. The CSF group consisted of 100 patients (33 female, 67 male, mean age 52.2 ± 2.6), while the control group consisted of the same number of age and sex-matched patients (35 female, 65 male, mean age 51.7 ± 1.4). ECG parameters of the study population (QRS duration, QT, T wave peak-to-end (Tp-e) intervals, iCEB (QT/QRS), and iCEBc (heart rate QTc/QRS) rates were calculated and compared between CSF and control groups. Results Intervals (QT and QTc intervals) and Tp-e/QTc ratio were greater in the CSF group compared with controls [422.1 ± 12.8 vs. 349.4 ± 14.3 bpm, respectively, p < .001; 457.0 ± 12.2 vs. 378.1 ± 12.3 bpm, respectively, p < .001, and 0.19 vs. 0.12, respectively, p < .001]. ICEB and iCEBc were significantly greater than controls [(4.9 ± 0.4 vs. 4.2 ± 0.4, respectively, p < .001), (5.7 ± 0.3 vs. 4.4 ± 0.3, respectively, p < .001)]. Conclusions ICEB and iCEBc were significantly increased in patients with CSF. This may suggest that CSF may predispose to malign arrhythmias.

A novel inflammatory signaling pathway in patients with slow coronary flow: NF-κB/IL-1β/nitric oxide

PurposeThe slow coronary flow (SCF) was identified as delayed opacification of epicardial coronary arteries in the absence of stenotic lesion. Metabolic syndrome (MetS), oxidative stress, and inflammation may be possible known insulting factors for the pathogenesis of SCF. This investigation aimed to assess the relationship between some inflammatory markers, oxidative stress parameters and MetS components with SCF phenomenon. MethodsA total of 35 patients with SCF and 35 subjects with normal coronary flow (NCF) were included in the study. We assessed some inflammatory markers (IL-1β, IL-18, TNF-α, and NF-κB mRNA expression in peripheral blood mononuclear cells (PBMCs)). Moreover, blood samples of the participants were tested for total antioxidant capacity (TAC), glutathione peroxidase (GPX) and nitric oxide (NO) levels using enzyme-linked immunosorbent assay (ELISA). Diagnosis of MetS was based on the National Cholesterol Education Program’s Adult Treatment Panel III report (ATPIII) criteria, 2005. Diagnostic criteria for coronary flow rates of all subjects were documented by thrombolysis in myocardial infarction (TIMI) frame count method. ResultsSCF patients had significantly higher prevalence of MetS (46%, p = 0.048).We found that the level of TAC was significantly higher in the NCF group (p = 0.006). Furthermore, the NO concentration was significantly lower in SCF groups (p = 0.001). A significant incremental difference was detected in IL-1β (fold change 2.82 ± 0.31, p < 0.05) and NF-κB (fold change 4.62 ± 0.32, p < 0.05) mRNA expression in the SCF group when compared with its level in the NCF group. Furthermore, according to logistic regression analysis, there were significant associations between IL-1β, NF-κB expression levels and the incidence of SCF (p < 0.05). ConclusionBased on the findings of this study, the pathogenesis of the SCF phenomenon may be closely associated with metabolic syndrome and inflammation. The NF-κB/IL-1β/nitric oxide & MetS signaling pathway might be considered as potential therapeutic targets in the management of SCF patients but further researches is required to guarantee these findings.

Association of the lymphocyte-to-monocyte ratio, mean diameter of coronary arteries, and uric acid level with coronary slow flow in isolated coronary artery ectasia

BackgroundThe pathophysiology of isolated coronary artery ectasia (CAE) with the coronary slow flow (CSF) phenomenon is still unclear. The purpose of this study was to investigate the risk factors for isolated CAE complicated with CSF.MethodsA total of 126 patients with isolated CAE were selected retrospectively. The patients were grouped into the no CSF (NCSF) group (n = 55) and the CSF group (n = 71) according to the corrected thrombolysis in myocardial infarction (TIMI) frame count (CTFC). Data on demographics, laboratory measurements, left ventricular ejection fraction (LVEF), left ventricular end-diastolic diameter (LVEDd), CTFC and diameters of three coronary arteries were collected.ResultsThe proportions of males (84.5% vs. 61.8%, p = 0.004) and patients with a smoking history (63.4% vs. 43.6%, p = 0.021) were higher in the CSF group than in the NCSF group. The neutrophil-to-lymphocyte ratio (NLR) (2.08(1.68–3.21) vs. 1.89 ± 0.58, p = 0.001), mean diameter of coronary arteries (mean D) (5.50 ± 0.85 vs. 5.18 ± 0.91, p < 0.001), and uric acid (URIC) level (370.78 ± 109.79 vs. 329.15 ± 79.71, p = 0.019) were significantly higher in the CSF group, while the lymphocyte-to-monocyte ratio (LMR) (4.81 ± 1.66 vs. 5.96 ± 1.75, p < 0.001) and albumin (ALB) level (44.13 ± 4.10 vs. 45.69 ± 4.11, p = 0.036) were lower. Multivariable logistic analysis showed that the LMR (odds ratio: 0.614, 95% CI: 0.464–0.814, p = 0.001), mean D (odds ratio: 2.643, 95% CI: 1.54–4.51, p < 0.001) and URIC level (odds ratio: 1.006, 95% CI: 1.001–1.012, p = 0.018) were independent predictors of CSF in CAE.ConclusionsThe LMR was a negative independent predictor of CSF in isolated CAE, while URIC level and mean D were positive independent predictors.

The relationship between coronary slow-flow and frontal QRS-T angle

ObjectiveIt is known that increased frontal QRS-T angle, which is a new ventricular repolarization marker is associated with adverse cardiac outcomes. It has been observed that the coronary slow-flow (CSF) phenomenon can cause arrhythmias and sudden cardiac death. The aim of our study is to investigate the relationship between CSF in patients and the frontal QRS-T angle. Material and methodA total of 200 patients, 97 of who had CSF and 103 with the normal coronary flow (NCF), were included in our study. The CSF group was divided into two groups; single-vessel CSF and multi-vessel CSF. The TIMI-frame count was calculated from the coronary angiography images of each patient. 12-lead electrocardiography (ECG) records were examined. The frontal QRS-T angle was obtained from the automated reports of the ECG device. ResultsThe mean age of the study population was 50.7 ± 9.5 and 102 (51%) of patients were female. The frontal QRS-T angle was significantly higher in patients with CSF compared to the NCF group [48(31-64) vs 37(25-46), p = 0.001]. A positive correlation was observed between the frontal QRS-T angle and TIMI-frame count in the correlation analysis performed separately for LAD, Cx, RCA patients with CSF (respectively; r = 0.340 and p < 0.001, r = 0.262 and p = 0.002, r = 0.247 and p = 0.003). The frontal QRS-T angle was higher in patients with multi-vessel CSF than in patients with single-vessel CSF [53.5(41.5-76.5) vs 43.0(23.5-60.5), p = 0.039]. ConclusionThere is a positive correlation between frontal QRS-T angle and TIMI-frame count. The frontal QRS-T angle is higher in patients with CSF. Also, frontal QRS-T angle was higher in the multi-vessel CSF group.

Eosinophil cationic protein: A new diagnostic biomarker in coronary slow flow phenomenon.

This study has investigated the role of eosinophil cationic protein (ECP), released by eosinophils, in the coronary slow flow phenomenon. This study included sixty patients with coronary slow flow (CSF) and sixty patients with normal coronary flow. The coronary flow rate was evaluated with TIMI frame count (TFC). ECP level, blood count and biochemical parameters were assessed. The ECP levels (18.9±7.5 vs 13.1±6.4 ng/ml, p<0.001) and eosinophil counts (0.25±0.14 vs 0.18±0.09 10³/mm³, p=0.001) were higher in the CSF group. Multivariable regression analysis showed that ECP level and eosinophil counts were independent predictors the presence of CSF (p=0.003 and p=0.006). There was a weak but important correlation among the ECP level, eosinophil count and mean TFC (p=0.001, p=0.003, respectively). The ROC analysis showed a cut off value of 14.05 ng/ml for ECP level to diagnose CSF with 73.3 % sensitivity and 66.7 % specificity, and area under the ROC curve was 0.745 (95% CI: 0.657-0.833, p<0.001). ECP levels were increased in CSF patients and this increasing correlated with coronary artery flow rates. The ECP level was independent predictor for the presence of SCF and it may be use as suitable diagnostic biomarker for CSF (Tab. 3, Fig. 3, Ref. 30).

Aortic flow propagation velocity and neutrophil-to-lymphocyte ratio in coronary slow flow.

A useful tool for determining the presence of systemic inflammation is the neutrophil-to-lymphocyte ratio (NLR). Chronic inflammation causes more microvascular resistance, which is known to be involved with coronary slow flow (CSF). Aortic flow propagation velocity (APV) can be used to evaluate the aorta's rigidity. We hypothesized that NLR and APV might be related to CSF. Therefore, we aimed to evaluate the NLR and APV in CSF patients. Eighty-six CSF patients and 43 subjects with normal coronary flow were enrolled in this study. We utilized the Thrombolysis in Myocardial Infarction (TIMI) frame count (TFC) method for determining each enrolled patient's coronary flow rate. APV values were determined via color M-mode Doppler echocardiography. Differences in NLR and APV values were determined in CSF and control groups. Patients with CSF had lower APV values and higher NLR values than the normal controls (39.9±11.4 vs 48.0±10.6, p<0.01; 3.3±2.8 vs 2.3±1.2, p=0.03). TFC was significantly higher in CSF patients compared to controls (29.8±5.0 vs 12.9±2.6; p<0.01). TFC and APV were negatively correlated in CSF patients (r=-0.338 p=0.001). APV was independently associated with CSF (OR: 1.164, CI: 1.078-1.257, p=0.001). APV was significantly associated with TFC, and it is independently associated with CSF (Tab. 4, Fig. 3, Ref. 30). Text in PDF www.elis.sk Keywords: coronary slow flow, neutrophil-to-lymphocyte ratio, aortic flow propagation velocity, atherosclerosis, inflammation.