A Cautionary Tale of Hypertrophic Cardiomyopathy-From "Benign" Left Ventricular Hypertrophy to Stroke, Atrial Fibrillation, and Molecular Genetic Diagnostics: A Case Report and Review of Literature.

This case report concerns a 48-year-old man with a history of ischemic stroke at the age of 41 who reported cardiac hypertrophy, registered in his twenties when explained by increased physical activity. Family history was positive for a mother with permanent atrial fibrillation from her mid-thirties. At the age of 44, he had a first episode of persistent atrial fibrillation, accompanied by left atrial thrombosis while on a direct oral anticoagulant. He presented at our clinic at the age of 45 with another episode of persistent atrial fibrillation and decompensated heart failure. Echocardiography revealed a dilated left atrium, reduced left ventricular ejection fraction, and an asymmetric left ventricular hypertrophy. Cardiac magnetic resonance was positive for a cardiomyopathy with diffuse fibrosis, while slow-flow phenomenon was present on coronary angiography. Genetic testing by whole-exome sequencing revealed three variants in the patient, c.309C > A, p.His103Gln in the ACTC1 gene, c.116T > G, p.Leu39Ter in the PLN gene, and c.5827C > T, p.His1943Tyr in the SCN5A gene, the first two associated with hypertrophic cardiomyopathy and the latter possibly with familial atrial fibrillation. This case illustrates the need for advanced diagnostics in unexplained left ventricular hypertrophy, as hypertrophic cardiomyopathy is often overlooked, leading to potentially debilitating health consequences.

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.

The predictors of coronary slow flow in patients undergoing coronary angiography.

BACKGROUND: A 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. RESULTS: This 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). CONCLUSION: The 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.

Background: 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). Methods: 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. Results: 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). Conclusion: 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.

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.

BACKGROUND: The 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. METHODS: A 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. RESULTS: Patients 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. CONCLUSION: Combined uric acid with plasma albumin, UAR could serve as an independent predictor for CSFP.

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.

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

Background: 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. Methods: 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. Results: 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). Conclusions: 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.

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.

BACKGROUND: Extensive 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). METHODS: This 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. RESULTS: No 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). CONCLUSION: Curcumin supplementation prevented deterioration of glycemic control and improved physical and psychological quality of life and depression in patients with CSFP. TRIAL REGISTRATION: Iranian Registry of Clinical Trials (IRCT20131125015536N8), June 19, 2019.

Effect of nano-curcumin supplementation on angina status, and traditional and novel cardiovascular risk factors in overweight or obese patients with coronary slow flow phenomenon: a randomized double-blind placebo-controlled clinical trial.

BACKGROUND: Cardiovascular events and poor quality of life are frequently observed in patients with coronary slow flow phenomenon (CSFP). This trial evaluated the effect of nano-curcumin supplement containing curcuminoids, as multifunctional nutraceuticals, on angina status, and some traditional and novel cardiovascular risk factors in overweight or obese patients with CSFP. METHODS: In this double-blind, randomized, placebo-controlled clinical trial, 42 overweight or obese patients with CSFP received either 80 mg/day of nano-curcumin or placebo for 12 weeks. Seattle angina questionnaire (SAQ) as a clinical measure of angina status, circulating endocan, adropin, homocysteine, lipid profile, and the novel scores of visceral adiposity index (VAI) and waist-triglyceride index (WTI) were assessed before and after the intervention. The independent samples t-test, Mann-Whitney test, analysis of covariance, Chi-square, and Fisher's exact tests were used where appropriate. RESULTS: All domains of SAQ including physical limitation, angina stability, angina frequency-severity, treatment satisfaction, and disease perception and quality of life improved significantly in the nano-curcumin compared with the placebo group. No significant changes were observed in serum endocan, adropin, and homocysteine following the intervention. Triglycerides, triglyceride/high-density lipoprotein cholesterol ratio, WTI and VAI values improved significantly only within the nano-curcumin group. CONCLUSIONS: Supplementation with 80 mg/day nano-curcumin (containing curcuminoids) for 12 weeks significantly improved clinically important disease-specific aspects of health in patients with CSFP. Some traditional and novel cardiovascular risk factors improved significantly only compared with the baseline values, which need further investigation. TRIAL REGISTRATION: This study was approved by the Ethics Committee of Tehran University of Medical Sciences (IR.TUMS.VCR.REC.1398.794). The study protocol was registered at Iranian Registry of Clinical Trials by IRCT20131125015536N8 registration ID at 19.06.2019.

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

BACKGROUND: Primary 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. METHODS: Between 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. RESULTS: Thirty-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). CONCLUSION: Primary CSF was independently associated with increased EFT volume. Further studies are needed to validate this finding and elucidate whether a causal relationship exists.

Could Pan-Immune-Inflammation Value be a Marker for the Diagnosis of Coronary Slow Flow Phenomenon?

Inflammation plays a key role in the pathogenesis of the coronary slow flow phenomenon (CSFP). The newly developed inflammatory marker, pan-immune-inflammation value (PIV), is associated with adverse cardiovascular events. This study investigated the predictive value of PIV for diagnosing CSFP in comparison to other inflammation-based markers. A total of 214 patients, 109 in the CSFP group and 105 in the normal coronary flow (NCF) group, were retrospectively included in the study. Coronary flow was calculated using the Thrombolysis in Myocardial Infarction frame count method. In addition to PIV, other inflammatory markers such as neutrophil-lymphocyte ratio, platelet-lymphocyte ratio (PLR), and systemic immune-inflammation index (SII) were calculated for the patients. The average age of patients was 50.3 ± 8.4, with a male ratio of 55.1%. Compared to the NCF group, patients in the CSFP group had higher levels of hyperlipidemia, glucose, triglyceride, NLR, PLR, SII, and PIV, while their high-density lipoprotein cholesterol (HDL-C), was lower (p < 0.05). Logistic regression analysis demonstrated that HDL-C, glucose, triglyceride, and PIV were independent predictor factors for CSFP (p < 0.05). PIV is a strong and independent predictor factor for CSFP and superior in predicting CSFP compared to other inflammatory markers.

Coronary slow flow and angiography-derived index of microcirculatory resistance as prognostic predictors in patients with angina and normal coronary arteries: a retrospective cohort study.

BACKGROUND: This study aims to investigate prognostic implications of coronary slow flow (CSF) and angiography-derived index of microcirculatory resistance (caIMR) in patients with angina and normal coronary arteries. METHODS: A total of 582 patients were enrolled with angiographically normal coronary arteries. caIMR was calculated using a commercial software. Patients were followed up for a median of 45 months. The primary endpoint was defined as major adverse cardiovascular events (MACEs) comprising death, myocardial infarction and readmission for angina or heart failure. RESULTS: CSF was diagnosed when TIMI grade 2 flow presented in at least one coronary artery. Multivariate analysis indicated TIMI-flow-based determination of CSF was not significantly associated with MACEs [hazard ratio (HR): 2.14; 95% confidence interval (CI): 0.87-5.31; p = 0.099), while caIMR >42 (HR: 2.53; 95% CI: 1.02-6.32; p = 0.047) were independent predictors of MACEs. Incorporation of caIMR improved the area under the curve from 0.587 to 0.642. CONCLUSIONS: caIMR was an independent prognostic factor of long-term cardiovascular events in patients with CSF. Evaluation of caIMR improved the risk stratification of patients with angiographically-normal coronary arteries.

Anti-Anginal Efficacy of Zibotentan in the Coronary Slow-Flow Phenomenon.

BACKGROUND: Patients with coronary microvascular disorders often experience recurrent angina for which there are limited evidence-based therapies. These patients have been found to exhibit increased plasma levels of endothelin; thus, selective endothelin-A (Et-A) receptor blockers such as zibotentan may be an effective anti-anginal therapy in these patients. The study evaluated the impact of a 10 mg daily dose of zibotentan on spontaneous angina episodes in patients with the coronary slow-flow phenomenon who had refractory angina (i.e., experiencing angina at least three times/week despite current anti-anginal therapy). METHODS: Using a randomized, double-blind, placebo-controlled, crossover trial design with 4-week treatment periods, 18 patients (63.2 ± 9.9 years, 33% females) were recruited. The primary endpoint was angina frequency as measured by an angina diary, with secondary endpoints including nitrate consumption, angina duration/severity and the Seattle Angina Questionnaire (SAQ) domains. RESULTS: During the 4 weeks of therapy, angina frequency significantly improved with zibotentan therapy (placebo 41.4 (58.5) vs. zibotentan 29.2 (31.6), p < 0.05), and sublingual nitrate consumption significantly reduced (placebo 11.8 (15.2) vs. zibotentan 8.8 (12.9), p < 0.05. CONCLUSIONS: Zibotentan improved the frequency of spontaneous angina episodes and reduced sublingual nitrate consumption in patients unresponsive to standard anti-anginal therapy.

Differential gene expression and miRNA regulatory network in coronary slow flow.

Coronary slow flow (CSF) is characterized by slow progression of coronary angiography without epicardial stenosis. The aim of this study was to explore the potential biomarkers and regulatory mechanism for CSF. Peripheral blood mononuclear cells from 3 cases of CSF and 3 healthy controls were collected for high-throughput sequencing of mRNA and miRNA, respectively. The differentially expressed mRNAs (DE-mRNAs) and miRNAs (DE-miRNAs) was identified. A total of 117 DE-mRNAs and 32 DE-miRNAs were obtained and they were mainly enriched in immune and inflammatory responses. Twenty-six DE-mRNAs were the predicted target genes for miRNAs by RAID, and then the regulatory network of 15 miRNAs were constructed. In addition, through the PPI network, we identified the three genes (FPR1, FPR2 and CXCR4) with larger degrees as hub genes. Among them, FPR1 was regulated by hsa-miR-342-3p, hsa-let-7c-5p and hsa-miR-197-3p and participated in the immune response. Finally, we validated the differential expression of hub genes and key miRNAs between 20 CSF and 20 control. Moreover, we found that miR-342-3p has a targeted regulatory relationship with FPR1, and their expression is negatively correlated. Then we established a hypoxia/reoxygenation (H/R) HUVEC model and detected FPR1, cell proliferation and apoptosis. Transfection with miR-342-3p mimics can significantly promote the proliferation of HUVEC under H/R conditions. FPR1 were associated with CSF as a biomarker and may be regulated by miR-342-3p potential biomarkers.

Establishment and verification of a nomogram that predicts the risk for coronary slow flow.

Background: Coronary slow flow (CSF) has gained significance as a chronic coronary artery disease, but few studies have integrated both biological and anatomical factors for CSF assessment. This study aimed to develop and validate a simple-to-use nomogram for predicting CSF risk by combining biological and anatomical factors. Methods: In this retrospective case-control study, 1042 patients (614 CSF cases and 428 controls) were randomly assigned to the development and validation cohorts at a 7:3 ratio. Potential predictive factors were identified using least absolute shrinkage and selection operator regression and subsequently utilized in multivariate logistic regression to construct the nomogram. Validation of the nomogram was assessed by discrimination and calibration. Results: N-terminal pro brain natriuretic peptide, high density lipoprotein cholesterol, hemoglobin, left anterior descending artery diameter, left circumflex artery diameter, and right coronary artery diameter were independent predictors of CSF. The model displayed high discrimination in the development and validation cohorts (C-index 0.771, 95% CI: 0.737-0.805 and 0.805, 95% CI: 0.757-0.853, respectively). The calibration curves for both cohorts showed close alignment between predicted and actual risk estimates, demonstrating improved model calibration. Decision curve analysis suggested high clinical utility for the predictive nomogram. Conclusion: The constructed nomogram accurately and individually predicts the risk of CSF for patients with suspected CSF and may be considered for use in clinical care.

Analysis of Risk Factors and Construction of a Predictive Model for Readmission in Patients with Coronary Slow Flow Phenomenon.

Background: Coronary slow flow phenomenon (CSFP) is a phenomenon in which distal vascular perfusion is delayed on angiography, but coronary arteries are not significantly narrowed and there is no other organic cardiac disease. Patients with CSFP may be repeatedly readmitted to the hospital because of chest pain or other symptoms of precordial discomfort, and there is a risk of adverse events. In order to investigate the risk factors affecting the readmission of CSFP patients, a prediction model was constructed with the aim of identifying patients at risk of readmission at an early stage and providing a reference for further clinical intervention. Methods: In this study, we collected clinical data from 397 CSFP patients between June 2021 and January 2023 in Xinjiang Medical University Hospital. Telephone follow-up clarified whether the patients were readmitted to the hospital. A predictive model for readmission of CSFP patients was constructed using multifactorial logistic regression. Nomogram was used to visualize the model and bootstrap was used to internally validate the model. ROC, DCA and Calibration curve were plotted to evaluate the calibration and discriminative ability of the column line graphs, respectively. Calibration and resolution of the column line graphs, respectively. Results: A total of 34 of 397 CSFP patients experienced readmission. Smoking history, creatine kinase isoenzyme-MB, total cholesterol, and left ventricular ejection fraction were the predictors of readmission in patients with CSFP. The area under the curve of the Nomogram model was 0.87, which indicated that the model had good predictive ability and differentiation, and the DCA and Calibration curves also indicated that the model had good consistency and was clinically useful. Conclusion: A readmission prediction model for patients with CSFP may facilitate early identification of patients at potential risk for readmission and timely interventional therapy to improve patient prognosis.

Ranolazine as a First-Choice Anti-anginal Medication for Patients With Coronary Artery Ectasia: A Case Series.

Coronary artery ectasia (CAE) is characterized by the abnormal dilation of coronary arteries, resulting in disturbed or slow blood flow, which causes angina pectoris-the most prevalent symptom of CAE. To date, there is no consensus on the therapeutic management of CAE due to its rarity and the scarcity of research. We present a case series of five patients with different ethnicities, including both men and women, whose CAE was successfully managed by the administration of ranolazine. All five patients were found to have CAE by coronary angiography, which was also associated with slow blood flow. Clinically, the patients had accelerating angina. They were prescribed an initial dose of 500 mg of ranolazine twice daily, which led to the resolution of their anginal symptoms. They have been clinically and hemodynamically stable for the last several years. In light of these results, we propose that ranolazine be considered as a first-choice anti-anginal medication for patients with CAE.

Comparison of the effect of uric acid/albumin ratio on coronary slow flow with other inflammation-based markers.

Background: Many inflammation-based markers (IBMs) have been shown to be closely related to coronary slow flow (CSF), but the effect of the uric acid/albumin ratio (UAR) on CSF and its relationship with other IBMs are not clearly known. In this study, we aimed to compare the effects of UAR and other IBMs on CSF. Methods: After the exclusion criteria, 126 patients with CSF detected on coronary angiography and 126 subjects with normal coronary flow as the control group were included in the study. Results: UAR was determined as an independent predictor for CSF. In addition, the UAR was superior to other IBMs in detecting CSF (p < 0.05 for all). Conclusion: This study is the first to investigate the effect of UAR on CSF in comparison with other IBMs.

Predictors of non-obstructive coronary slow flow in poorly controlled type 2 diabetes mellitus: a cross-sectional study.

BACKGROUND: Coronary slow flow (CSF) can occur due to various factors, such as inflammation, small vessel disease, endothelial dysfunction, and inadequate glucose control. However, the exact pathological mechanisms behind CSF remain incompletely understood. The objective of this study was to identify the risk factors associated with slow coronary flow in individuals with Type 2 Diabetes Mellitus (T2DM) who have non-obstructive coronary artery disease (CAD) and experience CSF. METHODS: We conducted a prospective cohort study involving 120 patients with T2DM who were referred for invasive coronary angiography due to typical chest pain or inconclusive results from non-invasive tests for myocardial ischemia. Using a 2 × 2 design, we categorized patients into groups based on their glycemic control (adequate or poor) and the presence of CSF (yes or no), defined by a TIMI frame count > 27. All patients had non-obstructive CAD, characterized by diameter stenosis of less than 40%. We identified many variables associated with CSF. RESULTS: Our investigation revealed no significant differences in age, sex, family history of coronary artery disease, ECG ischemia abnormalities, or echocardiographic (ECHO) data between the groups. In patients with adequate glycemic control, hypertension increased the risk of CSF by 5.33 times, smoking by 3.2 times, while dyslipidemia decreased the risk by 0.142. Additionally, hematocrit increased the risk by 2.3, and the platelet-to-lymphocyte ratio (PLR) increased the risk by 1.053. Among patients with poor glycemic control, hematocrit increased the risk by 2.63, and the Neutrophil-to-Lymphocyte Ratio (NLR) by 24.6. Notably, NLR was positively correlated with glycemic control parameters in T2DM patients with CSF. CONCLUSIONS: In T2DM patients with CSF, various factors strongly correlate with glycemic control parameters and can be employed to predict the likelihood of CSF. These factors encompass hypertension, smoking, increased body mass index (BMI), elevated platelet count, hematocrit, NLR, PLR, and C-reactive protein (CRP). TRIAL REGISTRATION: Registry: ZU-IRB (ZU-IRB#9419-3-4-2022), Registered on: 3 April 2022, Email: IRB_123@medicine.zu.edu.eg.

Asymmetric Dimethylarginine Is Associated with the Phenomenon of Coronary Slow Flow in Patients with Nonvalvular Atrial Fibrillation.

INTRODUCTION: Coronary slow flow phenomena (CSFP) are associated with endothelial and blood component abnormalities in coronary arteries. Asymmetric dimethylarginine (ADMA) can damage the endothelium of the heart or blood vessels in patients with non-valvular atrial fibrillation (NVAF), causing changes in levels of biological indicators. Our aim was to analyze the relationship between ADMA and CSFP in NVAF patients. METHODS: We consecutively enrolled 134 patients diagnosed with NVAF and underwent coronary angiography, 50 control patients without a history of atrial fibrillation and with normal coronary angiographic flow were included at the same time. Based on the corrected TIMI frame count (CTFC), the NVAF patients were categorized into two groups, CTFC ≤27 frames and CTFC >27 frames. Plasma ADMA, P-selectin (p-sel), von Willebrand factor (vWF), D-dimer (D-Di), plasminogen activator inhibitor 1 (PAI-1), and nitric oxide (NO) were detected by ELISA in the different groups. RESULTS: We found that plasma ADMA levels were significantly higher among NVAF patients in the CTFC >27 grade group compared with the control or CTFC ≤27 group. In addition, the levels of blood cells and endothelium-related biomarkers (NO, P-selectin, vWF, D-Di, and PAI-1) were significantly altered and correlated with ADMA levels. Multifactorial analysis showed that plasma ADMA (odd ratio [OR; 95% CI]: 1.65 [1.21-2.43], p < 0.001) and left atrial internal diameter (OR [95% CI]: 1.04 [1.02, 1.1], p < 0.001) could be used as independent risk factors for the development of CSFP in patients with NVAF. The ROC curves of ADMA can predict the development of CSFP in NVAF patients. The minimum diagnostic concentration for the development of CSFP in patients was 2.31 µmol/L. CONCLUSION: Our study demonstrated that CSFP in NVAF patients was associated with high levels of ADMA and left atrial internal diameter. Therefore, aggressive preoperative detection and evaluation of ADMA and left atrial internal diameter can help deal with the intraoperative presence of CSFP.