Coronary Slow Flow Research Articles

Abstract 4137257: Hepatocyte growth factor -mediated Angiogenesis supersession in Hyperhomocysteinemia

Background: Homocysteine (Hcy) is a well-established cardiovascular risk factor. Elevated homocysteine, or hyperhomocysteinemia (HHcy), inhibit the growth of endothelial cells and stimulate vascular smooth muscle cell proliferation. However, the mechanisms of HHcy disrupts angiogenesis remain unclear. Here we examine the molecular pathways involved in HHcy-impaired angiogenesis. Method: We generated Tg-hCBS+ Cbs-/- mice by crossing Cbs knockout mice and Tg-hCBS mice where human CBS cDNA was regulated by a zinc-inducible metallothionein promoter. The model exhibited severe HHcy (＞115 μmol/L). We conducted both in vivo and in vitro experiments, including vasculogenesis assays of retinal and heart tissues, aortic ring assay, and tube formation. Retinas were stained with Isolectin B4 and imaged using a confocal microscope. The Human Angiogenesis RT 2 Profiler™ PCR Array was used to profile 84 key angiogenesis-related genes. Homocysteine metabolites in Cbs mice were measured by HPLC. ChIP-seq data were analyzed using Chip Atlas. Additionally, 91 patients went through coronary angiography were enrolled from the Second Affiliated Hospital of Nanchang University. Participants with CTFC, greater than 27 frames per second were identified as having slow coronary arteries flow (SCF). Results: HHcy caused SCF in patients and impaired vasculogenesis in the retinas of newborn and 12-week-old Tg-hCBS Cbs-/- mice. Capillary density in the hearts of adult Tg-hCBS Cbs-/- mice was reduced. HHcy suppressed tube formation and aortic ring microvessel growth in a concentration-dependent manner. The PCR array revealed significant gene expression changes in Hcy treated human aortic endothelial cells. Notably, genes encoding hepatocyte growth factor (HGF), collagen type IV alpha 3, epiregulin, interferons, and leukocyte cell-derived chemotaxin 1 were downregulated by at least four-fold. In an acute myocardial infarction model, HGF expression was further reduced, and HGF treatment rescued Hcy-inhibited tube formation and microvessel growth. Hcy and S-adenosylhomocysteine levels were negatively correlated with plasma HGF levels. ChIP-seq data identified homocysteine-responsive hypomethylation in ETF, TFII, FOXP3, RXRa, and c-Jun Hcy-hypomethylation Box (-2701/0). Conclusion: HHcy impair angiogenesis via HGF inhibition, which has a rescue effect. Hypomethylation caused by Hcy affects the methylation status of specific CpG sites within the Hcy-hypomethylation box of the HGF gene.

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.

Coronary slow flow as measured by corrected TIMI frame counts is associated with impaired microvascular resistance

Abstract Background The Coronary Slow Flow Phenomenon (CSFP) reflects an increased resting microvascular resistance and has been defined as a corrected thrombolysis in myocardial infarction frame count (cTFC) >27 in the in the absence of obstructive coronary artery disease (CAD). However, there is limited and conflicting data on the diagnostic utility of CTFC with respect to gold standard coronary haemodynamic parameters; namely coronary flow reserve (CFR) and hyperaemic microvascular resistance (hMR). Purpose To evaluate the relationship between angiography-derived cTFC and the coronary haemodynamic parameters (CFR and hMR). Methods Patients with angina and non-obstructive CAD (< 50% epicardial stenosis; ANOCA) underwent comprehensive functional coronary angiography utilising a dual sensor-tipped pressure-doppler flow wire during adenosine infusion for investigation of coronary microvascular impairment, and acetylcholine provocative testing for the diagnosis of coronary artery spasm. Results In 103 patients who underwent functional coronary angiography, 60 patients had CSFP and this was associated with low flow velocity and higher microvascular resistance at rest as compared with patients without CSFP (19.2 ± 7.3 versus 22.6 ± 6.7, p=0.024; and 5.9 ± 2.0 versus 4.6 ± 1.7, p=0.009, respectively). Whilst cTFC was poorly associated with CFR (r= 0.058, p= 0.564), there was a relatively strong, positive correlation with hMR (r=0.258, p=0.008). Furthermore, receiver operating characteristic analyses demonstrated that CTFC poorly predicts an impaired CFR <2.5 (AUC, 0.479 [0.36-0.59]) but does predict an impaired hMR >2.5 (AUC, 0.623 [0.51-0.74] p=0.037). Conclusion In patients with ANOCA, cTFC is associated with coronary microvascular dysfunction as measured by microvascular resistance during hyperaemia. This data suggests the cTFC may be a surrogate marker for impaired microvascular resistance.cTFC versus hMR

Association between inflammatory burden index and coronary slow flow phenomenon in patients with chest pain and no obstructive coronary arteries

BackgroundThe inflammatory burden index (IBI), a novel inflammation-based indicator, to is associated with the presence and prognosis of various diseases. However, few studies have focused on exploring the relationship between IBI and the coronary slow flow phenomenon (CSFP). In this study, we aimed to investigate the predictive value of IBI for CSFP in patients with chest pain and no obstructive coronary artery disease.MethodsA total of 1126 individuals with chest pain and no obstructive coronary arteries were consecutively included in this study. 71 patients developed CSFP were included in the CSFP group. A 1:2 age- and sex-matched patient with normal blood flow and angiographically proven normal coronary arteries was selected as the control group (n = 142). Plasma C-reactive protein (CRP), neutrophil, and lymphocyte counts were measured to determine the value of IBI.ResultsThe IBI were significantly higher in the CSFP group than in the controls (21.1 ± 6.5 vs. 14.5 ± 6.4, P < 0.001). The IBI increasedelevated with the increase of the numbers of vessels affected by CSFP. Multivariate logistic regression analysis revealed that IBI and body mass index (BMI) were independent predictors of CSFP. Receiver operating characteristic (ROC) curve analysis showed that when IBI was > 15.74, the sensitivity and specificity were 77.5% and 67.6%, respectively, and the area under the ROC curve (AUC) was 0.799 (95% CI: 0.737-0.862, P<0.001).ConclusionThe IBI may be an independent predictor of CSFP in patients with chest pain and normal coronary arteries. The IBI could improve the predictive value of CSFP compared with the indicators alone.

Association between sarcopenia index, intraoperative events and post-discharge mortality in patients undergoing percutaneous coronary intervention: a retrospective cohort study in a teaching hospital in Western China.

To examine the association between the sarcopenia index (SI) and the risk of intraprocedural events and post-discharge death during percutaneous coronary intervention (PCI). A retrospective cohort study. The study was conducted at a teaching hospital in Western China. The participants were patients aged 45 years and older who underwent PCI at the hospital and had an estimated glomerular filtration rate (eGFR) of ≥15 mL/min/1.73 m2. Patients who died during hospitalisation, as well as those with unknown death dates, those lost to follow-up and those with missing information for the SI calculation, were excluded. The SI was calculated as serum creatinine/cystatin C (Cr/CysC) × 100. The high-SI group was defined as the highest quartile, while the remaining participants were included in the low-SI group. Intraprocedural events included intraprocedural coronary slow flow (CSF)/coronary artery no-reflow (CNR) and malignant ventricular arrhythmia (MVA). In the event of death, the date of death was recorded. The study included 497 patients who underwent PCI in our hospital, of whom 369 (74.25%) were males. A total of 57 (11.47%) patients developed CSF, 100 (20.12%) developed CNR and 4 (0.8%) developed MVA. Forty-four (8.85%) patients died post-discharge. The proportion of patients in the low-SI group who developed CSF was higher than those who did not (16.94% vs 9.65%, p=0.027). In addition, the average SI was lower in patients who developed CSF than in those who did not (81.99 vs 87.11, p=0.043). After adjusting for possible confounding factors, logistic regression analysis showed that the risk of CSF in the low-SI group was higher than that in the high-SI group (OR = 2.01, 95% CI: 1.04 to 3.89). In addition, it was found that the lower the SI, the higher the risk of CSF (OR = 0.983, 95% CI: 0.967 to 0.999). Patients with lower SI had a greater risk of developing CSF, and the lower the SI, the higher the risk of CSF. However, these data suggest that SI is not associated with CNR and the risk of post-discharge death in patients after PCI.

Relationship between Circadian Blood Pressure Pattern and Coronary Slow Flow

Relationship between Circadian Blood Pressure Pattern and Coronary Slow Flow

Evaluation of changes in the global longitudinal strain for left ventricular function before and after eight weeks of taking high dose of atorvastatin in patients with coronary slow flow phenomenon

BackgroundCoronary Slow Flow Phenomenon (CSFP) is a well-recognized clinical entity characterized by delayed opacification of coronary arteries in the presence of a normal coronary angiogram. The objective of this study was determined and compared left ventricle (LV)strain in patients with CSFP before and after receiving a high-dose atorvastatin.Materials and methodsThis cross-sectional study was conducted on 51 patients with CSFP from the beginning of 2021 to the end of September 2022. Trans-thoracic Echocardiogram (TTE) was performed by an echocardiography specialist. Thereafter, the patient’s basic information was entered into the researcher’s checklist after treatment with atorvastatin 40 mg daily for eight consecutive weeks. After eight weeks, the patients were subjected again to TTE. The data were analyzed in SPSS statistical software.ResultsThe mean LV-GLS before taking atorvastatin was − 16.53%±3.63%. The mean LV-GLS after taking atorvastatin was 17.57%±3.53% (P.value = 0.01). The mean LV function before taking atorvastatin was 48.82%±9.19%. Meanwhile, the mean LV function after taking atorvastatin was 50.59%±7.91% (P = 0.01). There was no significantly change in left atrium volume (49.88 ± 0.68 vs. 49.9 + 0.67) after 8 weeks taking atorvastatin (P = 0.884).ConclusionThe plasma ET-1 levels are elevated in CSFP patients, and atorvastatin improves coronary flow and endothelial function. As evidenced by the results of this study, the daily intake of 40 mg of oral atorvastatin during eight consecutive weeks in patients with CSFP significantly improved LV strain and LV function, however atorvastatin does not have a significant effect on improving the right ventricular function and pulmonary artery systolic pressure.

Randomised Placebo-Controlled Pilot Trial Evaluating the Anti-Anginal Efficacy of Ticagrelor in Patients with Angina with Nonobstructive Coronary Arteries and Coronary Slow Flow Phenomenon.

Background: The coronary slow flow phenomenon (CSFP) is an angiographic finding characterised by the delayed passage of contrast through the coronary arteries, despite the absence of obstructive coronary artery disease (defined as less than 50% narrowing of the vessel lumen). Patients with the CSFP experience recurrent angina, for which there are limited evidence-based therapies. Ticagrelor may serve as an effective anti-anginal therapy for these patients by increasing adenosine levels, which could alleviate coronary microvascular dysfunction and its associated angina due to its vasodilatory properties. This study aimed to determine the anti-anginal efficacy of ticagrelor 90 mg taken twice daily on spontaneous angina episodes in patients with refractory angina (i.e., episodes ≥3/week despite two anti-anginals) and documented CSFP. Methods: In a randomised, double-blind, placebo-controlled, cross-over trial, the anti-anginal efficacy of a 4-week ticagrelor therapy regimen was evaluated in 20 patients with refractory angina (mean age 61.5 ± 10.5 years; 40% women) who had documented slow coronary flow. The primary endpoint was the frequency of angina episodes, recorded using an angina diary. Secondary endpoints included the duration and severity of angina episodes, consumption of short-acting nitrates, and health status evaluations using the Seattle Angina Questionnaire (SAQ) and the Short Form-36 (SF-36) indices. Results: During the four weeks of therapy, ticagrelor did not significantly improve angina symptoms compared to the placebo (placebo 25.7 (16.7)) vs. ticagrelor 19.8 (18.1), p > 0.05). Furthermore, it did not impact other patient-related outcome measures, including angina severity, duration, frequency of prolonged angina episodes, nitrate consumption, or the SAQ/SF-36 health outcome indices. No serious adverse events related to the study drug were observed. Conclusions: In patients with documented CSFP who were unresponsive to standard anti-anginal therapy, ticagrelor did not reduce the frequency of spontaneous angina episodes or the consumption of nitrates. Further confirmation of the potential benefits of this therapy may be obtained through a larger clinical trial.

Sildenafil’s effectiveness in the primary coronary slow flow phenomenon: a pilot randomised controlled clinical trial

BackgroundOn the one hand, the primary coronary slow flow phenomenon (CSFP) can cause recurrence of chest pain, prompting medical examinations and further healthcare costs, while on the other hand, it...

The predictors of coronary slow flow in patients undergoing coronary angiography

BackgroundA new challenge in coronary artery disease treatment has emerged, where specific populations exhibit ischemic symptoms without any obstruction in the epicardial coronary artery. Instead, they exhibit slow coronary contrast flow, referred to as coronary slow flow (CSF). This study aims to identify several predictors of CSF.ResultsThis case–control study was conducted at the Regional General Hospital of West Nusa Tenggara Province in Indonesia from December 2016 to February 2024. The study involved sixty subjects, with 30 in each group of CSF and normal epicardial coronary artery angiogram (NECA). CSF is enforced by the TIMI frame count (TFC) greater than 27 frames. Among all the predictors studied, coronary artery diameter (p < 0.001) and random blood sugar (p = 0.049) were found to affect the CSF significantly. In the multivariate analysis, coronary artery diameter remained a significant predictor (adjusted OR 10.08, 95% CI 2.64–38.50, p < 0.001), with an optimal cut-off point of more than 3.56 mm, a sensitivity of 76.7%, and a specificity of 70.7% (AUC = 0.787, p < 0.001).ConclusionThe coronary artery diameter strongly predicts CSF in patients undergoing coronary angiography.

Neutrophil Percentage to Albumin Ratio as a Predictor for Coronary Slow Flow Phenomenon in Patients with Myocardial Ischemia with No Obstructive Coronary Arteries.

Accumulating evidences suggest that low-grade inflammatory response plays a key role in the pathophysiology of coronary slow flow phenomenon (CSFP). As a new hematological inflammatory indicator, the neutrophil percentage to albumin ratio (NPAR) and its role in the occurrence and development of CSFP remains unclear. In this study, we aimed to investigate the predictive value of NPAR in the presence of CSFP in patients with myocardial ischemia and no obstructive coronary arteries (INOCA). In total, 1323 individuals with INOCA were included in this study. 85 patients developed CSFP were included in the CSFP group. 1:2 age-and sex-matched patients were selected from the absence of CSFP, with normal blood flow, as the control group. Clinical characteristics, laboratory parameters, and angiographic findings were compared between groups. NPAR was also calculated to explore its relationship with CSFP. NPAR was significantly higher in the CSFP patients than in the controls (19.3±2.5 vs 16.7±1.8, p<0.001). The NPAR increased with the number of coronary arteries involved in CSFP. Multivariate logistic regression analysis showed that an elevated NPAR level was an independent predictor of CSFP (OR 1.915, 95% CI 1.612-2.275, P < 0.001). The ROC curve showed that when NPAR was > 17.39, the sensitivity and specificity were 90.6% and 78.8%, respectively, and the area under the ROC curve (AUC) was 0.860 (95% CI: 0.811-0.909, P < 0.001). The AUC of neutrophil percentage was 0.845 (95% CI: 0.794-0.897, p < 0.001), and that of albumin was 0.808 (95% CI: 0.753-0.864, p < 0.001). Elevated NPAR levels are an independent predictor of CSFP in patients with INOCA. NPAR could improve the predictive value of CSFP compared with neutrophil percentage or albumin ratio alone.

Effect of nano-curcumin supplementation on cardiometabolic risk factors, physical and psychological quality of life, and depression in patients with coronary slow flow phenomenon: a randomized double-blind clinical trial

BackgroundExtensive evidence has suggested the cardio-protective properties of the polyphenol curcumin. The aim of this study was to investigate the effects of a highly bioavailable curcumin supplement on cardiometabolic risk factors, health-related quality of life, and depression in patients with coronary slow flow phenomenon (CSFP).MethodsThis randomized double-blind placebo-controlled clinical trial was conducted in 42 patients with CSFP (age 35–70 years, 25 ≤ body mass index < 40 kg/m2). Patients received either 80 mg/day nano-curcumin or placebo for 12 weeks. Serum levels of visfatin, high-sensitivity C-reactive protein (hs-CRP), and glycemic indices were measured before and after the intervention. The short form 36-item quality of life (SF-36) and Beck’s Depression Inventory-II (BDI-II) questionnaires were assessed, as well.ResultsNo significant improvements were observed in circulating hs-CRP and visfatin following the intervention. A significant increase was observed in pre- to post-fasting blood glucose (− 0.9 ± 12.2 vs. 7.7 ± 12.4 mg/dl, p = 0.02) and hemoglobin A1C (− 0.1 ± 0.8 vs. 0.5 ± 0.8%, p = 0.04) levels, in the placebo compared with the intervention group. Physical (8.2 ± 8.1 vs. − 1.2 ± 6.5, p < 0.001) and mental (6.8 ± 11.8 vs. − 1.1 ± 10.4, p = 0.02) component summary scores were significantly improved in the nano-curcumin than the placebo group. Additionally, the number of patients with lower degrees of depression was significantly better in the intervention than the placebo group following the supplementation (p = 0.046).ConclusionCurcumin supplementation prevented deterioration of glycemic control and improved physical and psychological quality of life and depression in patients with CSFP.Trial registrationIranian Registry of Clinical Trials (IRCT20131125015536N8), June 19, 2019.

Coronary Slow Flow as Measured by Corrected TIMI Frame Counts is Associated With Impaired Microvascular Resistance

Coronary Slow Flow as Measured by Corrected TIMI Frame Counts is Associated With Impaired Microvascular Resistance

Uric acid to albumin ratio as a novel predictor for coronary slow flow phenomenon in patients with chronic coronary syndrome and non-obstructive coronary arteries

BackgroundThe plasma uric acid to albumin ratio (UAR) is considered as a novel indicator for Inflammation. However, the association between UAR and coronary slow flow phenomenon (CSFP) remains unclear.MethodsA total of 1328 individuals with chronic coronary syndrome (CCS) receiving coronary angiography (CAG) and found no obvious obstructive stenosis (< 40%) were included in this study. 79 individuals developed CSFP and were divided into CSFP group. The 1:2 age-matched patients with normal coronary blood flow were allocated to the control group (n = 158). The clinical characteristics, laboratory parameters including uric acid, albumin ratio, UAR and the angiographic characteristics were compared between the two groups.ResultsPatients with CSFP had a higher level of uric acid (392.3 ± 85.3 vs. 273.8 ± 71.5, P < 0.001), UAR (10.7 ± 2.2 vs. 7.2 ± 1.9, P < 0.001), but a lower level of plasma albumin (36.9 ± 4.2 vs. 38.5 ± 3.6, P = 0.003). Moreover, UAR increased as the numbers of vessels involved in CSFP increased. The logistic regression analysis demonstrated that UAR was independent predictors for CSFP. The Receiver operating characteristic (ROC) curve analysis showed that when UAR was more than 7.9, the AUC was 0.883 (95% CI: 0.840–0.927, p < 0.001), with the sensitivity and specificity were 78.2% and 88.2% respectively.ConclusionCombined uric acid with plasma albumin, UAR could serve as an independent predictor for CSFP.

Study of some components of the influence and formation of blood flow in patients with "slow flow".

"Slow flow" is one very important concept in modern fundamental and clinical biomedicine. Slow coronary flow is indicative of delayed filling of the terminal coronary artery vessels, occurring in the absence of significant coronary stenosis. This group patient of patients exhibits a high incidence of disability and represents a significant financial and material burden for the state and the healthcare system in general. The primary objective of our study was to examine patients with slow coronary flow. We studied the standard parameters recommended by the international health care system (electrocardiography (by Medica QRS-12, Germany), through the electrical activity of a patient's heart by the electrical impulses (beating) of the heart; HC1(Germany); coagulogramma by Coatron M1 (Germany), troponin by AQT 90 (Germany); general blood test we used automatic human counting device HC1(Germany). Also, we investigate the original parameters (non-standard parameters, which we use in this pilot study) that we were first studied for this diagnosis and non-standard parameters. A general blood test showed that patients with slow flow had a higher blood leukocyte count than the control group, but the amount of hemoglobin was normal, the hematocrit was much higher than in the control group, and the platelet count was close to the lower limit of clinical standards.We obtained details of blood flow by coagulation situation, such as prothrombin time, prothrombin index, international normalized ratio, activated partial thromboplastin time, thrombin time, fibrinogen, and rheological properties such as index of erythrocyte aggregability, index of erythrocyte deformability, plasma viscosity, in silico blood rheological index. Blood flow can be considered as a superposition of vortices with similar frequencies and wave vectors that change after bifurcations or other obstacles in the vascular network. These factors together determine the conditions for structuring the flow of moving blood. Disruption or alteration of these factors results in slow flow. It has been found that the speed of blood flow in the coronary arteries depends on changes in the number and function of red blood cells. Slow flow is directly influenced by the aggregation and deformation of red blood cells, their number, and plasma viscosity. Consequently, the rheological status plays a crucial role in determining blood flow and its velocity.

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.

Emerging Predictors by Non-HDL-C/HDL-C Ratio and Novel Biomarkers for Coronary Slow Flow Phenomenon.

The coronary slow-flow (CSF) phenomenon is a condition characterized by delayed coronary opacification during diagnostic angiography without the presence of epicardial coronary artery disease. This mini-review explores various emerging predictors and biomarkers associated with CSF, aiming to address the potential diagnostic tools. A comprehensive analysis of recent studies has investigated different biomarkers, including growth differentiation factor 15, galectin 3, microRNA (miRNA)-22, miRNA-155, interleukin 34, soluble vascular cell adhesion molecule-1, long non-coding RNA, plasma choline, adropin, and lipid markers non-high-density lipoprotein cholesterol (HDL-C)/HDL-C ratio to enhance understanding and predict CSF. Additionally, we have summarizes the major findings and significant limitations observed in various studies on CSF biomarkers. The implications of these findings suggest significant advancements in personalized treatment strategies and improved prognostic outcomes for patients exhibiting CSF.

Adiponectin and Paraoxonase-1 Correlation With Thrombolysis in Myocardial Infarction Frame Count With Coronary Slow Flow Phenomenon

Objectives: Coronary slow flow phenomenon (CSFP) is an important angiographic entity, with no clear-cut etiology. The effects of adiponectin (APN) and paraoxonase-1 (PON-1) have been proven in microvascular disease pathophysiology, endothelial dysfunction and atherosclerosis. The present study aimed to determine the correlation between APN and PON-1 and CSFP. Methods: Subjects who were undergone coronary angiography and met the inclusion and exclusion criteria were included in this study. The study subjects were divided into the following groups: 40 subjects without coronary artery disease (CAD) and CSFP, 22 patients without CAD but with CSFP, 29 patients with CAD &lt; 50% and without CSFP, 22 patients with CAD (50-90%) but without CSFP and 16 patients with CAD and CSFP. Coronary flow rates of the participants with slow flow diagnosis were determined by thrombolysis in myocardial infarction (TIMI) frame count method. The serum levels of APN and PON-1 were measured by ELISA kit. Results: There were no significant differences between groups in serum levels of APN. No significant correlation was observed between APN serum concentration and corrected TIMI frame count (TFC) (r=0.17, P=0.29). The PON-1 serum concentration in patients with CAD (50-90%) and without CSFP was significantly lower than the other groups (P&lt;0.01). There was a near significant correlation between PON-1 serum levels and corrected TFC in left anterior descending coronary artery (r=0.32, P=0.08). Discussion: The present study has demonstrated no significant correlation between the serum concentration of APN and PON-1 and corrected TFC, so we need more extensive studies in this regard with larger sample size.

A Comprehensive Analysis of Clinical, Demographic, Risk Factor, and Echocardiography Profiles of Coronary Slow Flow Phenomenon from Somalia’s Largest PCI Center

A Comprehensive Analysis of Clinical, Demographic, Risk Factor, and Echocardiography Profiles of Coronary Slow Flow Phenomenon from Somalia’s Largest PCI Center

Epicardial fat volume is associated with primary coronary slow-flow phenomenon in patients with severe aortic stenosis undergoing transcatheter valve implantation

BackgroundPrimary coronary slow flow (CSF) is defined as delayed opacification of the distal epicardial vasculature during coronary angiography in the absence of relevant coronary artery stenoses. Microvascular disease is thought to be the underlying cause of this pathology. Epicardial fat tissue (EFT) is an active endocrine organ directly surrounding the coronary arteries that provides pro-inflammatory factors to the adjacent tissue by paracrine and vasocrine mechanisms. The aim of the present study was to investigate a potential association between EFT and primary CSF and whether EFT can predict the presence of primary CSF.MethodsBetween 2016 and 2017, n = 88 patients with high-grade aortic stenosis who were planned for transcatheter aortic valve implantation (TAVI) were included in this retrospective study. EFT volume was measured by pre-TAVI computed tomography (CT) using dedicated software. The presence of primary CSF was defined based on the TIMI frame count from the pre-TAVI coronary angiograms.ResultsThirty-nine of 88 TAVI patients had CSF (44.3%). EFT volume was markedly higher in patients with CSF (142 ml [IQR 107–180] vs. 113 ml [IQR 89–147]; p = 0.009) and was strongly associated with the presence of CSF (OR 1.012 [95%CI 1.002–1.021]; p = 0.014). After adjustment, EFT volume was still an independent predictor of CSF (OR 1.016 [95%CI 1.004–1.026]; p = 0.009).ConclusionPrimary CSF was independently associated with increased EFT volume. Further studies are needed to validate this finding and elucidate whether a causal relationship exists.