The triglyceride-glucose index as a predictive marker for coronary slow flow phenomenon.

OBJECTIVE: The triglyceride-glucose index (TyG) has been proposed as a marker of insulin resistance (IR) and has shown associations with cardiovascular diseases. This study aimed to investigate the relationship between the TyG and the coronary slow flow phenomenon (CSFP) and explore the index's potential as a predictor of this condition. PATIENTS AND METHODS: A total of 187 patients who underwent coronary angiography were included; of these, 91 patients were diagnosed with CSFP, and 96 patients with normal coronary flow served as a control group. The TyG was calculated using fasting triglyceride and glucose levels. RESULTS: The results showed that the TyG was significantly higher in the CSFP group compared with the control group (p < 0.001). Additionally, the TyG exhibited a moderate positive correlation with the thrombolysis-in-myocardial-infarction frame count in coronary arteries (p < 0.001). A multivariate logistic regression analysis revealed that the TyG, along with gender, ejection fraction, and uric acid, remained significant predictors of CSFP (p < 0.05). CONCLUSIONS: This study's findings suggest that the TyG may serve as a useful marker for identifying individuals at risk of CSFP and provide insights into the potential role of IR in its pathophysiology.

No-Reflow Prediction in Acute Coronary Syndrome During Percutaneous Coronary Intervention: The NORPACS Risk Score.

BACKGROUND: Suboptimal coronary reperfusion (no reflow) is common in acute coronary syndrome percutaneous coronary intervention (PCI) and is associated with poor outcomes. We aimed to develop and externally validate a clinical risk score for angiographic no reflow for use following angiography and before PCI. METHODS: We developed and externally validated a logistic regression model for prediction of no reflow among adult patients undergoing PCI for acute coronary syndrome using data from the Melbourne Interventional Group PCI registry (2005-2020; development cohort) and the British Cardiovascular Interventional Society PCI registry (2006-2020; external validation cohort). RESULTS: A total of 30 561 patients (mean age, 64.1 years; 24% women) were included in the Melbourne Interventional Group development cohort and 440 256 patients (mean age, 64.9 years; 27% women) in the British Cardiovascular Interventional Society external validation cohort. The primary outcome (no reflow) occurred in 4.1% (1249 patients) and 9.4% (41 222 patients) of the development and validation cohorts, respectively. From 33 candidate predictor variables, 6 final variables were selected by an adaptive least absolute shrinkage and selection operator regression model for inclusion (cardiogenic shock, ST-segment-elevation myocardial infarction with symptom onset >195 minutes pre-PCI, estimated stent length ≥20 mm, vessel diameter <2.5 mm, pre-PCI Thrombolysis in Myocardial Infarction flow <3, and lesion location). Model discrimination was very good (development C statistic, 0.808; validation C statistic, 0.741) with excellent calibration. Patients with a score of ≥8 points had a 22% and 27% risk of no reflow in the development and validation cohorts, respectively. CONCLUSIONS: The no-reflow prediction in acute coronary syndrome risk score is a simple count-based scoring system based on 6 parameters available before PCI to predict the risk of no reflow. This score could be useful in guiding preventative treatment and future trials.

No-reflow after stroke reperfusion therapy: An emerging phenomenon to be explored.

In the field of stroke thrombectomy, ineffective clinical and angiographic reperfusion after successful recanalization has drawn attention. Partial or complete microcirculatory reperfusion failure after the achievement of full patency of a former obstructed large vessel, known as the "no-reflow phenomenon" or "microvascular obstruction," was first reported in the 1960s and was later detected in both experimental models and patients with stroke. The no-reflow phenomenon (NRP) was reported to result from intraluminal occlusions formed by blood components and extraluminal constriction exerted by the surrounding structures of the vessel wall. More recently, an emerging number of clinical studies have estimated the prevalence of the NRP in stroke patients following reperfusion therapy, ranging from 3.3% to 63% depending on its evaluation methods or study population. Studies also demonstrated its detrimental effects on infarction progress and neurological outcomes. In this review, we discuss the research advances, underlying pathogenesis, diagnostic techniques, and management approaches concerning the no-reflow phenomenon in the stroke population to provide a comprehensive understanding of this phenomenon and offer references for future investigations.

Triglyceride glucose-body mass index as a novel predictor of slow coronary flow phenomenon in patients with ischemia and nonobstructive coronary arteries (INOCA).

BACKGROUND: The triglyceride glucose-body mass index (TyG-BMI index) has been suggested as a novel predictor of insulin resistance. However, its predictive value for slow coronary flow phenomenon (SCFP) in patients with ischemia and nonobstructive coronary arteries (INOCA) remains unclear. METHODS: We consecutively recruited 1625 patients with INOCA from February 2019 to February 2023 and divided them into two groups based on thrombolysis in myocardial infarction (TIMI) frame counts (TFCs): the SCFP group (n = 79) and the control group. A 1:2 age-matched case-control study was then performed. The TyG-BMI index was calculated as ln [plasma triglyceride (mg/dL) × fasting blood glucose (mg/dL)/2] × BMI. RESULTS: TyG-BMI index in the SCFP group (218.3 ± 25.2 vs 201.0 ± 26.5, P < .001) was significantly higher than in the normal controls. TyG-BMI index also increased with the number of coronary arteries involved in the SCFP. Multivariate logistic regression analysis showed that TyG-BMI, BMI, and TG were independent predictors for SCFP. Receiver operating characteristic (ROC) curve analysis showed that when the TyG-BMI index was above 206.7, the sensitivity and specificity were 88.6% and 68.5%, respectively, with an AUC of 0.809 (95% CI: 0.756-0.863, P = .027). Combined BMI with TG, the TyG-BMI index had a better predictive value for SCFP than BMI and TG (P < .001). CONCLUSION: The TyG-BMI index was an independent predictor for SCFP in INOCA patients, and it had a better predictive value than BMI and TG.

"No-reflow" phenomenon in acute ischemic stroke.

Acute ischemic stroke (AIS) afflicts millions of individuals worldwide. Despite the advancements in thrombolysis and thrombectomy facilitating proximal large artery recanalization, the resultant distal hypoperfusion, referred to "no-reflow" phenomenon, often impedes the neurological function restoration in patients. Over half a century of scientific inquiry has validated the existence of cerebral "no-reflow" in both animal models and human subjects. Furthermore, the correlation between "no-reflow" and adverse clinical outcomes underscores the necessity to address this phenomenon as a pivotal strategy for enhancing AIS prognoses. The underlying mechanisms of "no-reflow" are multifaceted, encompassing the formation of microemboli, microvascular compression and contraction. Moreover, a myriad of complex mechanisms warrant further investigation. Insights gleaned from mechanistic exploration have prompted advancements in "no-reflow" treatment, including microthrombosis therapy, which has demonstrated clinical efficacy in improving patient prognoses. The stagnation in current "no-reflow" diagnostic methods imposes limitations on the timely application of combined therapy on "no-reflow" post-recanalization. This narrative review will traverse the historical journey of the "no-reflow" phenomenon, delve into its underpinnings in AIS, and elucidate potential therapeutic and diagnostic strategies. Our aim is to equip readers with a swift comprehension of the "no-reflow" phenomenon and highlight critical points for future research endeavors.

Homocysteine levels in patients with coronary slow flow phenomenon: A meta-analysis.

BACKGROUND: With the development of coronary angiography, more and more attention has been paid to coronary slow flow phenomenon (CSFP). Recent studies have found that the correlation between homocysteine (Hcy) levels and CSFP was contradictory, so we conducted this meta-analysis to investigate the correlation. METHODS: By March 2022, studies that meet the research requirements were identified by searching multiple databases including Embase, Web of Science, and PubMed. We included studies evaluating the correlation between Hcy levels and CSFP. Random or fixed effect meta-analyses were performed according to heterogeneity among included studies. A leave-out method and subgroup analyses were conducted to determine the source of heterogeneity. RESULTS: Thirteen studies involving 625 CSFP and 550 subjects were included. After pooling data from each study, Hcy levels were higher in the CSFP groups (standard mean difference [SMD], 1.45; 95% CI, 0.94 to 1.96, P < .00001) than in the control group. In the meta-analysis, there was significant heterogeneity (I2 = 93%), which was further explored through leave-out method and and subgroup analyses. Specifically, pooling data from studies with a mean thrombolysis in myocardial infarction (TIMI) frame count ≥ 46 (SMD, 1.31; 95% CI, 1.00 to 1.63, P < .00001) resulted in no heterogeneity (0%), indicating that the TIMI frame count ≥ 46 was the source of heterogeneity. CONCLUSIONS: Our study found that elevated Hcy levels are strongly associated with CSFP. More importantly, the association was stronger in CSFP patients with mean TIMI frame count ≥ 46.

An unusual no-reflow phenomenon due to neointimal tissue embolization during drug eluting balloon intervention in stent restenosis: A case report.

Acute coronary syndrome is one of the leading causes of death worldwide. Percutaneous coronary intervention (PCI), along with various devices, have been technically developed to dramatically improve mortality risk in patients with acute myocardial infarction. However, no-reflow phenomenon still remains a problematic complication during a PCI, even in the era of drug eluting stents. There are various hypotheses and mechanisms for no-reflow phenomenon, but none have been confirmed. Treatment for no-reflow phenomenon also depends on various underlying conditions, but have not yet shown effective improvement. We presented a case of no-reflow phenomenon caused by an unusual cause.

Techniques to Treat Slow-Flow/No-Reflow During Primary Percutaneous Coronary Intervention.

OBJECTIVE: The aim of this study was to compare TIMI flow after administering intracoronary (IC) medications through various routes for the treatment of slow flow/no-reflow during primary PCI. METHODS: Two independent parallel cohorts of the patients who underwent primary PCI for STEMI and developed slow/no-reflow were recruited. Selection of cohort was based on the route of administration of IC medications as proximal or distal. Post administration TIMI follow was compared between the two cohorts. RESULTS: A total of 100 patients were included in both, proximal and distal, cohort. Distribution of angiographic, clinical and demographic characteristics was not significant between the two cohorts except prevalence of hypertension, and diabetes mellitus. Frequency of hypertension, and diabetes mellitus were 45 % vs.70 %; p < 0.001 and 28 % vs. 44 %; p = 0.018 among patients in distal and proximal cohort respectively. Final TIMI III flow was achieved in significantly higher number of patients in distal cohort with the frequency of 88 % vs. 76 %; p = 0.027 as compared to proximal cohort. CONCLUSION: Administration of IC medication via distal route is observed to be more effective for the treatment of slow flow/no-reflow during primary PCI. Distal route via export catheter or perforated balloon technique should be preferred wherever feasible.

Relationship between increased systemic immune-inflammation index and coronary slow flow phenomenon.

BACKGROUND: Systemic immune-inflammation index (SII, platelet × neutrophil/lymphocyte ratio), a new marker of inflammation, is associated with adverse cardiovascular events, but its relationship with coronary slow flow phenomenon (CSFP) is unclear. Therefore, we aimed to investigate the relationship between SII and CSFP. METHODS: We enrolled consecutive patients who presented with chest pain, with normal/near-normal coronary angiography findings (n = 89 as CSFP group; n = 167 as control group). The baseline characteristics, laboratory parameters and angiographic characteristics of the two groups were compared. RESULTS: SII levels were significantly higher in the CSFP group than in the control group (409.7 ± 17.7 vs. 396.7 ± 12.7, p < 0.001). A significant positive correlation between SII and the mean thrombolysis in myocardial infarction frame count (mTFC) was found (r = 0.624, p < 0.001). SII increased with the number of coronary arteries involved in CSFP. In multivariate logistic regression analysis, SII/10 was an independent predictor of CSFP (odds ratio: 1.739, p < 0.001). In addition, the SII level > 404.29 was a predictor of CSFP with 67.4% sensitivity and 71.9% specificity. CONCLUSIONS: SII can predict the occurrence of CSFP.

Endothelial nitric oxide synthase Asp298Glu (894G/T) gene polymorphism as a possible risk factor for the coronary slow flow phenomenon among Iranians.

BACKGROUND: Mounting evidence indicates an association between endothelial dysfunction and the coronary slow flow phenomenon (CSFP). In the present study, we aimed to evaluate the possible role of endothelial nitric oxide synthase (eNOS) 894G/T and interleukin-1ß (IL-1ß) 315C/T polymorphisms as possible risk factors for CSFP. METHODS: This prospective study enrolled patients with CSFP and individuals with normal coronary arteries. Genotypes were assessed using regular polymerase chain reaction and direct Sanger-sequencing techniques. RESULTS: The study population consisted of 267 individuals: 180 patients with CSFP (49 women [27.2%]) at a median age of 55 (48-62) years and 87 controls with normal coronary arteries (56 women [64.4%]) at a median age of 47 (41-58) years. The allelic distribution of eNOS 894G/T was significantly associated with CSFP (odds ratio [OR], 1.58; 95% confidence interval (CI), 1.04-2.42; P = 0.03). This polymorphism increased the risk of CSFP under the dominant model (OR 1.73; 95% CI I.02-2.95; P = 0.04). However, the allelic frequencies (1.05; 95% CI 0.68-1.59; P = 0.83) and genotypic frequencies (0.88; 95% CI 0.52-1.49; P = 0.63) of the IL-1ß 315C/T polymorphism were not associated with the incidence of CSFP in the Iranian population. CONCLUSIONS: The CSFP and control groups were statistically different regarding the eNOS 894G/T polymorphism. Our findings also demonstrated that the IL-1ß 315C/T polymorphism was not a risk factor for CSFP.

The Relationship Between H2FPEF Score and Coronary Slow Flow Phenomenon.

OBJECTIVE: Diastolic dysfunction plays an important role in the pathophysiology of both coro- nary slow flow phenomenon and heart failure with preserved ejection fraction, which could be predicted by the H2FPEF score. We sought to investigate the association of H2FPEF score with coronary slow flow phenomenon in subjects undergoing coronary angiography for suspected stable ischemic heart disease. METHODS: The study included 228 consecutive individuals [60.5% male, mean age 52.6 (10.1)]. Subjects with non-obstructive coronary artery disease were classified as coronary nor- mal flow (n = 112) and coronary slow flow (n = 116) after confirmation of coronary angiography results. H2FPEF score of each participant was calculated. RESULTS: Subjects with coronary slow flow phenomenon were more likely to be male (75% vs. 45.5%, P < .001) and have a higher body mass index than that of normal flow group [30.5 (2.9) vs. 29.3 (2.8), P=.001]. H2FPEF score was significantly higher in the former group [2 (2-4) vs. 0 (0-1), P < .001]. H2FPEF score was also positively correlated with mean corrected thrombolysis in myocardial infarction frame count (r = 0.725, P < .001). On multivariate logistic regression analysis, male gender [odds ratio: 4.580, 95% CI: 1.700-12.336, P = .003], current smoker [OR: 2.398, 95% CI: 1.064-5.408, P=.035], total cholesterol [OR: 1.011, 95% CI: 1.001-1.021, P=.026], and H2FPEF score [OR: 3.111, 95% CI: 2.160-4.480, P < .001] were found to be the independent predictors of coronary slow flow phenomenon. CONCLUSION: We found that the H2FPEF score, which is useful in demonstrating diastolic dysfunction, is independently associated with coronary slow flow pattern in suspected ischemic heart disease.

Prolonged P Wave Peak Time May Be a Sign of LV Diastolic Dysfunction in the Coronary Slow Flow Phenomenon.

Background: The coronary slow flow phenomenon (CSFP) is an atherosclerotic process that causes ischemia at the microvascular level. The CSFP may affect P wave durations, especially P wave peak time (PWPT), by microvascular ischemia, left ventricular diastolic dysfunction, and changes in the left atrial dimension. Therefore, in the present study, we aimed to assess PWPT in the CSFP. Method: One hundred and ninety-five patients were included in this single-center, retrospective study. Ninety patients were enrolled in the CSFP group and 105 patients in the control group. PWPT was defined as the duration between the beginning and peak of the p wave and obtained from the leads Dii and V i. Results: The mean age of the study population was 48.5 ± 9.5, and 108 (55.3%) of the patients were female. We found PWPT was longer in the CSFP group than in the control group. Correlation analysis showed a positive correlation between PWPT in both leads (D II, V i) and left atrial anterior-posterior diameter, mean TIMI frame count (TFC), and E/e. A significant relationship was observed between mean TFC, E/e, EF, heart rate, and PWPT in lead D ii (ß coefficient = 0.33, 95% CI 0.44-1.33, p < 0.001, ß coefficient = 0.23, 95% CI 0.25-1.85, p=0.01, ß coefficient = -0.140, 95% CI -1.04--0.53, p=0.03, and ß coefficient = -0.13, 95% CI -0.29--0.014, p=0.03, respectively) in multivariable linear analysis. Conclusion: In the present study, we found prolonged PWPT in patients with the CSFP and found a relationship between PWPT and mean TFC.

Study on Correlation between Type 2 Diabetes and No-Reflow after PCI.

Diabetes, a serious chronic disease globally, is often complicated with cardiovascular diseases for which percutaneous coronary intervention (PCI) is the mainstay. The no-reflow rate of diabetic patients after PCI is 2-4 times higher than that of nondiabetic patients, yet the specific mechanism is still unclear. This study was designed to investigate the correlation between the duration of diabetes, preoperative blood glucose level, coronary angiographic blood flow, coronary artery stenosis level, and no-reflow after PCI. A total of 131 patients with type 2 diabetes who underwent PCI in our hospital from 2019 to 2020 were divided into control group and observation group. The disease duration, preoperative blood glucose level, coronary angiographic blood flow, and coronary artery stenosis level of the two groups were calculated. There were differences in the duration of diabetes between the two groups; the blood glucose level of the control group was about 3.8%, which was lower than 5.8% of the observation group; the thrombolysis in myocardial infarction (TIMI) value of the control group was 18.46 ± 4.6, which was lower than 20.67 ± 3.9 of the observation group; The degree of coronary stenosis in the control was 63% ± 2%, which was lower than 76% + 3% in the observation group. Binary logistic stepwise regression analysis was performed on these indicators and no-reflow after PCI to explore the correlation between these indicators and no-reflow after PCI in diabetic patients. The study found that the diabetes duration, higher preoperative blood glucose level, coronary angiography blood flow, and coronary artery were positively associated with no-reflow after PCI.

Usefulness of intravascular ultrasound assessment after development of the slow flow phenomenon during percutaneous coronary intervention.

The slow flow phenomenon is a critical complication during percutaneous coronary intervention (PCI) that leads to poor outcomes. We aimed to evaluate the mechanisms underlying the slow flow phenomenon using intravascular ultrasound (IVUS). We retrospectively analyzed IVUS data from 62 lesions in 58 consecutive patients who experienced the slow flow phenomenon during PCI. IVUS was performed immediately after the development of the slow flow phenomenon to assess its cause. No IVUS-based evidence of mechanical obstruction was categorized as distal embolization. Distal embolization was observed in 46 lesions (74%). The slow flow phenomenon occurred in all these lesions after stent implantation. In addition to distal embolization, three different mechanisms underlying the induction of the slow flow phenomenon due to mechanical obstructions (16 lesions, 26%) were detected on IVUS, namely, medial dissection/hematoma (6 lesions), intimal flap (6 lesions), and thrombus obstruction (4 lesions). Most mechanical obstructions (13 lesions, 81%) could not be identified by angiography alone. In 15/16 lesions (94%) with mechanical obstruction, deteriorated flow improved immediately after balloon dilatation or bail-out stent implantation, although intracoronary vasodilator administration could not reestablish coronary flow. The frequency of mechanical obstruction as the cause of the slow flow phenomenon was relatively high. Given the difficulty in angiographical differentiation, IVUS-guided management of slow flow may be a useful strategy.

Luteolin alleviates ischemia/reperfusion injury-induced no-reflow by regulating Wnt/ß-catenin signaling in rats.

The no-reflow phenomenon induced by ischemia-reperfusion (I/R) injury seriously limits the therapeutic value of coronary recanalization and leads to a poor prognosis. Previous studies have shown that luteolin (LUT) is a vasoprotective factor. However, whether LUT can be used to prevent the no-reflow phenomenon remains unknown. Positron emission tomography perfusion imaging, performed to detect the effects of LUT on the no-reflow phenomenon in vivo, revealed that LUT treatment was able to reduce the no-reflow area in rat I/R models. In vitro, LUT was shown to reduce the hypoxia-reoxygenation injury-induced endothelial permeability and apoptosis. The levels of malondialdehyde, reactive oxygen species and NADPH were also measured and the results indicated that LUT could inhibit the oxidative stress. Western blot analysis revealed that LUT protected endothelial cells from I/R injury by regulating the Wnt/ß-catenin pathway. Overall, we concluded that the use of LUT to minimize I/R induced microvascular damage is a feasible strategy to prevent the no-reflow phenomenon.