Efficiency and Safety of Intracoronary Epinephrine Administration in Patients With ST-Elevation Myocardial Infarction With Refractory Coronary No-Reflow.

Studies assessing the treatment of refractory no-reflow in patients with ST-elevation myocardial infarction (STEMI) are limited to clinical cases and pilot studies. This study aimed to evaluate the efficacy and safety of intracoronary adrenaline administration in such patients. Ninety consecutive patients with refractory coronary no-reflow during percutaneous coronary intervention (PCI) were prospectively included after the initial failure of conventional treatment. They were randomized into 2 groups: 45 patients in Group 1 received adrenaline, and 45 patients in Group 2 (control) received conventional treatments alone. After intracoronary drug administration, the adrenaline group demonstrated significantly higher rates of coronary flow restoration in the infarct-related artery to the level of thrombolysis in myocardial infarction grade 3 (56% vs 29% [p = 0.01]) and resolution of STEMI >50% after PCI (78% vs 36% [p <0.001]). Additionally, the adrenaline group showed a lower indexed microvascular obstruction (MVO) volume compared with the control group (0.9 [0.3; 3.1] % vs 1.9 [0.6; 7.9] % [p = 0.048]). A significant improvement in ejection fraction (EF) was observed in the adrenaline group (p = 0.025). Intracoronary adrenaline administration during PCI in patients with STEMI with refractory no-reflow is more effective compared with conventional treatments. This approach improves coronary flow in the infarct-related artery, facilitates a faster resolution of STEMI, enhances EF, and reduces MVO volume. Intracoronary adrenaline administration demonstrates a comparable safety profile to conventional treatment strategies in terms of life-threatening arrhythmias occurrence. The study suggests that intracoronary adrenaline administration during PCI could be an effective treatment strategy for patients with STEMI with refractory no-reflow.

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.

Intracoronary adenosine compared with adrenaline and verapamil in the treatment of no-reflow phenomenon following primary PCI in STEMI patients.

BACKGROUND: no-reflow can complicate up to 25% of pPCI and is associated with significant morbidity and mortality. We aimed to compare the outcomes of intracoronary epinephrine and verapamil with intracoronary adenosine in the treatment of no-reflow after primary percutaneous coronary intervention (pPCI). METHODS: 108 STEMI patients had no-reflow during pPCI were assigned into four groups. Group 1, in which epinephrine and verapamil were injected through a well-cannulated guiding catheter. Group 2, in which same drugs were injected in the distal coronary bed through a microcatheter or perfusion catheter. Group 3, in which adenosine was injected through a guiding catheter. Group 4, in which adenosine was injected in distal coronary bed. Primary end point was the achievement of TIMI III flow and MBG II or III. Secondary end point was major adverse cardiovascular and cerebrovascular events (MACCEs) during hospital stay. RESULTS: The study groups did not differ in their baseline characteristics. Primary end point was achieved in 15 (27.8%) patients in the guide-delivery arm compared with 34 (63%) patients in the local-delivery arm, p < 0.01. However, the primary end point did not differ between the epinephrine/verapamil group and the adenosine group (27 (50%) vs 22 (40.7%), p = 0.334). The secondary end points were similar between the study groups. CONCLUSION: Local delivery of epinephrine, verapamil and adenosine in the distal coronary bed is more effective in achieving TIMI III flow with MBG II or III compared with their guide-delivery in patients who suffered no-reflow during pPCI. There was no difference between epinephrine/verapamil Vs. adenosine.

Long-term outcome and prognostic value of angiographic slow/no-reflow phenomenon after emergency percutaneous coronary intervention for ST-elevation myocardial infarction.

BACKGROUND: The coronary slow flow/no-reflow phenomenon (CSF/NRP) is a common complication of emergency percutaneous coronary intervention (PCI) for ST-elevated myocardial infarction (STEMI). Its long-term prognostic value, however, remains unclear. This study investigated the long-term outcome and prognostic value of CSF/NRP after emergency PCI for STEMI. METHODS: This retrospective, multicenter registry-based cohort study was conducted in STEMI patients who underwent emergency PCI between 2015 and 2016. Incidence of in-hospital mortality, major adverse cardiac and cerebrovascular events (MACCEs), and all-cause mortality during long-term follow-up were compared between CSF/NRP patients and the normal flow group. Cox proportional-hazards regression model was performed to identify the predictive impact of CSF/NRP in short- and long-term outcomes. RESULTS: A total of 649 STEMI patients were included in the study, of whom 193 (29.7%) developed CSF/NRP following emergency PCI. The CSF/NRP group had a higher incidence of in-hospital mortality than the non-CSF/NRP group (8.2 vs. 4.3%, P  = 0.04). All-cause mortality incidence was also higher in the CSF/NRP group during 5-year follow-up (22.2 vs. 16.2%, P  = 0.04). The Cox proportional hazards model adjusting for demographic and clinical variables identified the NRP as an independent predictor of 5-year cardiac mortality [hazard ratio: 1.89; 95% confidence interval (CI): 1.07-3.31; P  = 0.02]. In a landmark analysis, no difference was seen in overall mortality among the two study groups between 1 month and 5-year follow-up (hazard ratio: 1.33; 95% CI: 0.80-2.21, P -value: 0.23). Kaplan-Meier analysis showed lower 3-year cumulative MACCE-free survival in the CSF/NRP group compared with the normal flow group ( P  = 0.02). CONCLUSION: CSF/NRP in STEMI patients is associated with a worse short- and long-term prognosis. These results, however, are mostly related to the acute phase, and CSF/NRP had limited influence on clinical outcomes in early survivors of STEMI.

Intracoronary Near-Infrared Spectroscopy to Predict No-Reflow Phenomenon During Percutaneous Coronary Intervention in Acute Coronary Syndrome.

Near-infrared spectroscopy-intravascular ultrasound (NIRS-IVUS) can identify the lipid-rich lesions, described as high lipid-core burden index (LCBI). The aim of this study was to investigate the relation between lipid-core plaque (LCP) in the infarct-related lesion detected using NIRS-IVUS and no-reflow phenomenon during percutaneous coronary intervention (PCI) in patients with acute coronary syndrome (ACS). We investigated 371 patients with ACS who underwent NIRS-IVUS in the infarct-related lesions before PCI. The extent of LCP in the infarct-related lesion was calculated as the maximum LCBI for each of the 4-mm longitudinal segments (maxLCBI4mm) measured by NIRS-IVUS. The patients were divided into 2 groups using a maxLCBI4mm cut-off value of 400. The overall incidence of no-reflow phenomenon was 53 of 371 (14.3%). No-reflow phenomenon more frequently occurred in patients with maxLCBI4mm ≥400 compared with those with maxLCBI4mm<400 (17.5% vs 2.5%, p <0.001). After propensity score matching, multivariable logistic regression analysis demonstrated that maxLCBI4mm (odds ratio: 1.008; 95% confidence interval: 1.005 to 1.012, p <0.001) was independently associated with the no-reflow phenomenon. The maxLCBI4mm of 719 in the infarct-related lesion had the highest combined sensitivity (69.8%) and specificity (72.1%) for the identification of no-reflow phenomenon. In conclusion, in patients with ACS, maxLCBI4mm in the infarct-related lesion assessed by NIRS-IVUS was independently associated with the no-reflow phenomenon during PCI.

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 recanalization in ischemic stroke: From pathomechanisms to therapeutic strategies.

Endovascular reperfusion therapy is the primary strategy for acute ischemic stroke. No-reflow is a common phenomenon, which is defined as the failure of microcirculatory reperfusion despite clot removal by thrombolysis or mechanical embolization. It has been reported that up to 25% of ischemic strokes suffer from no-reflow, which strongly contributes to an increased risk of poor clinical outcomes. No-reflow is associated with functional and structural alterations of cerebrovascular microcirculation, and the injury to the microcirculation seriously hinders the neural functional recovery following macrovascular reperfusion. Accumulated evidence indicates that pathology of no-reflow is linked to adhesion, aggregation, and rolling of blood components along the endothelium, capillary stagnation with neutrophils, astrocytes end-feet, and endothelial cell edema, pericyte contraction, and vasoconstriction. Prevention or treatment strategies aim to alleviate or reverse these pathological changes, including targeted therapies such as cilostazol, adhesion molecule blocking antibodies, peroxisome proliferator-activated receptors (PPARs) activator, adenosine, pericyte regulators, as well as adjunctive therapies, such as extracorporeal counterpulsation, ischemic preconditioning, and alternative or complementary therapies. Herein, we provide an overview of pathomechanisms, predictive factors, diagnosis, and intervention strategies for no-reflow, and attempt to convey a new perspective on the clinical management of no-reflow post-ischemic stroke.

The predictive value of laboratory parameters for no-reflow phenomenon in patients with ST-elevation myocardial infarction following primary percutaneous coronary intervention: A meta-analysis.

To date, the predictive role of laboratory indicators for the phenomenon of no flow is unclear. Hence, our objective was to conduct a meta-analysis to investigate the association between laboratory parameters and the risk of the no-reflow phenomenon in patients with ST-elevation myocardial infarction (STEMI) following primary percutaneous coronary intervention (PCI). This, in turn, aims to offer valuable insights for early clinical prediction of no-reflow. We searched Pubmed, Embase, and Cochrane Library from the establishment of the database to October 2023. We included case-control or cohort study that patients with STEMI following primary PCI. We excluded repeated publication, research without full text, incomplete information or inability to conduct data extraction and animal experiments, reviews, and systematic reviews. STATA 15.1 was used to analyze the data. The pooled results indicated that elevated white blood cell (WBC) count (odds ratio [OR] = 1.061, 95% confidence interval [CI]: 1.013-1.112), neutrophil count (OR = 1.324, 95% CI: 1.128-1.553), platelet (PLT) (OR = 1.002, 95% CI: 1.000-1.005), blood glucose (OR = 1.005, 95% CI: 1.002-1.009), creatinine (OR = 1.290, 95% CI: 1.070-1.555), total cholesterol (TC) (OR = 1.022, 95% CI: 1.012-1.032), d-dimer (OR = 1.002, 95% CI: 1.001-1.004), and fibrinogen (OR = 1.010, 95% CI: 1.005-1.015) were significantly associated with increased risk of no-reflow. However, elevated hemoglobin was significantly associated with decreased risk of no-reflow. In conclusion, our comprehensive analysis highlights the predictive potential of various parameters in assessing the risk of no-reflow among STEMI patients undergoing PCI. Specifically, WBC count, neutrophil count, PLT, blood glucose, hemoglobin, creatinine, TC,  d-dimer, and fibrinogen emerged as significant predictors. This refined risk prediction may guide clinical decision-making, allowing for more targeted and effective preventive measures to mitigate the occurrence of no-reflow in this patient population.

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.

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.

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.

The non-HDL-C/HDL-C ratio is a strong and independent predictor of the no-reflow phenomenon in patients with ST-elevation myocardial infarction.

BACKGROUND: No-reflow (NR) is the inability to achieve adequate myocardial perfusion despite successful restoration of attegrade blood flow in the infarct-related artery after primary percutaneous coronary intervention. The non-HDL-C/HDL-C ratio has been shown to be superior to conventional lipid markers in predicting most cardiovascular diseases. In this study, we wanted to reveal the predictive value of the NR by comparing the Non-HDL-C/HDL-C ratio with traditional and non-traditional lipid markers in patients who underwent primary percutaneous coronary intervention (pPCI) due to ST-elevation myocardial infarction (STEMI). METHODS: A total of 1284 consecutive patients who underwent pPCI for STEMI were included in this study. Traditional lipid profiles were detected and non-traditional lipid indices were calculated. Patients were classified as groups with and without NR and compared in terms of lipid profiles. RESULTS: No-reflow was seen in 18.8% of the patients. SYNTAX score, maximal stent length, high thrombus burden, atherogenic index of plasma and non-HDL-C/HDL-C ratio were determined as independent predictors for NR (p < 0.05, for all). The non-HDL-C/HDL-C ratio predicts the development of NR in STEMI patients with 71% sensitivity and 67% specificity at the best cut-off value. In ROC curve analysis, the non-HDL-C/HDL-C ratio was superior to traditional and non-traditional lipid markers in predicting NR (p < 0.05, for all). CONCLUSION: The non-HDL-C/HDL-C ratio can be a strong and independent predictor of NR in STEMI patients and and therefore non-HDL-C/HDL-C ratio may be a useful lipid-based biomarker that can be used in clinical practice to improve the accuracy of risk assessment in patients with STEMI.

The stress hyperglycemic ratio can predict the no-reflow phenomenon following saphenous vein graft intervention in patients with acute coronary syndrome.

AIMS: The no-reflow phenomenon (NRP) is a common complication of saphenous vein graft (SVG) interventions. The aim of this study was to investigate the effect of the stress hyperglycemia ratio (SHR) on the development of NRP in patients with acute coronary syndrome (ACS) undergoing percutaneous SVG intervention. METHODS: The study included 223 patients who presented at our center with ACS, had a history of coronary artery bypass graft and underwent a saphenous graft procedure. The relationship between SHR calculated at the time of presentation from glucose and HbA1c values, and the development of NRP evaluated after the procedure with angiography was determined with univariate and multivariate binary regression analysis. RESULT: The study population was separated into two groups as those who developed and did not develop NRP. Mean age was determined to be significantly higher in the group that did not develop NRP compared to the group with NRP (p: 0.004). Angiographically, the thrombus burden was determined to be significantly higher in the group that developed NRP (p < 0.001). Patients were separated into 3 tertiles according to the SHR level (T1, T2, T3), and the rate of NRP development was determined at a significantly higher rate in the T3 group (p < 0.001). CONCLUSIONS: This study showed that SHR, a parameter that can be easily calculated noninvasively, is an independent predictor of NRP development in ACS patients undergoing saphenous interventions. In addition, high thrombus burden and predilatation before stenting were also found to be factors that increase the likelihood of developing NRP.

Pan-Immune-Inflammation Value Is Independently Correlated to Impaired Coronary Flow After Primary Percutaneous Coronary Intervention in Patients With ST-Segment Elevation Myocardial Infarction.

Immune-inflammatory biomarkers have been shown to be correlated with impaired coronary flow (ICF) in ST-segment elevation myocardial infarction. In this study, we assessed the relation between a novel comprehensive biomarker, pan-immune-inflammation value (PIV), and ICF after primary percutaneous coronary intervention (pPCI) in ST-segment elevation myocardial infarction. A total of 687 patients who underwent pPCI between 2019 and 2023 were retrospectively analyzed. Blood samples were collected at admission. PIV and other inflammation parameters were compared. PIV was calculated as (neutrophil count × platelet count × monocyte count)/lymphocyte count. Postprocedural coronary flow was assessed by thrombolysis in myocardial infarction (TIMI) classification. Patients were divided into 2 groups: a group with ICF defined as postprocedural TIMI 0 to 2 and a group with normal coronary flow defined as postprocedural TIMI flow grade of 3. The mean age was 61 ± 12 years, and 22.4% of the patients were women. Compared with the normal coronary flow group (median 492, interquartile range 275 to 931), the ICF group (median 1,540, interquartile range 834 to 2,909) showed significantly increased PIV (p <0.001). The optimal cutoff for the PIV was 804, as determined by receiver operating characteristic curve. The incidence of ICF was 17.0% in all patients, 6.4% in low-PIV group (<804), and 34.2% in high-PIV group (≥804). Multivariate analyses revealed that a baseline PIV ≥804 was independently associated with post-pPCI ICF (odds ratio 5.226, p <0.001). PIV was superior to neutrophil/lymphocyte ratio and platelet/lymphocyte ratio in determining ICF. In conclusion, a high-PIV was significantly associated with an increased risk of ICF after pPCI. Moreover, PIV was a better indicator of ICF than were other inflammatory markers.

No-reflow phenomenon in stroke patients: A systematic literature review and meta-analysis of clinical data.

BACKGROUND: The no-reflow phenomenon refers to the absence of microvascular reperfusion despite macrovascular reperfusion. AIM: The aim of this analysis was to summarize the available clinical evidence on no-reflow in patients with acute ischemic stroke. METHODS: A systematic literature review and a meta-analysis of clinical data on definition, rates, and impact of the no-reflow phenomenon after reperfusion therapy was carried out. A predefined research strategy was formulated according to the Population, Intervention, Comparison, and Outcome (PICO) model and was used to screen for articles in PubMed, MEDLINE, and Embase up to 8 September 2022. Whenever possible, quantitative data were summarized using a random-effects model. RESULTS: Thirteen studies with a total of 719 patients were included in the final analysis. Most studies (n = 10/13) used variations of the Thrombolysis in Cerebral Infarction scale to evaluate macrovascular reperfusion, whereas microvascular reperfusion and no-reflow were mostly assessed on perfusion maps (n = 9/13). In one-third of stroke patients with successful macrovascular reperfusion (29%, 95% confidence interval (CI), 21-37%), the no-reflow phenomenon was observed. Pooled analysis showed that no-reflow was consistently associated with reduced rates of functional independence (odds ratio (OR), 0.21, 95% CI, 0.15-0.31). CONCLUSION: The definition of no-reflow varied substantially across studies, but it appears to be a common phenomenon. Some of the no-reflow cases may simply represent remaining vessel occlusions, and it remains unclear whether no-reflow is an epiphenomenon of the infarcted parenchyma or causes infarction. Future studies should focus on standardizing the definition of no-reflow with more consistent definitions of successful macrovascular reperfusion and experimental set-ups that could detect the causality of the observed findings.

Secondary rotational atherectomy is associated with reduced occurrence of prolonged ST-segment elevation following ablation.

Elevation of the ST segment after percutaneous coronary intervention (PCI) using rotational atherectomy (RA) for severely calcified lesions often persists after disappearance of the slow-flow phenomenon on angiography. We investigated clinical factors relevant to prolonged ST-segment elevation following RA among 152 patients with stable angina undergoing elective PCI. PCI procedures were divided into two strategies, RA without (primary RA strategy) or with (secondary RA strategy) balloon dilatation before RA. Incidence of prolonged ST-segment elevation after disappearance of slow-flow phenomenon was higher in the 56 patients with primary RA strategy (13%) than in the 96 patients with secondary RA strategy (3%, p = 0.039). Univariate logistic regression analysis showed levels of low-density lipoprotein cholesterol (LDL-C) (odds ratio [OR] 0.95, 95% confidence interval [CI] 0.93-0.99; p = 0.013), levels of triglycerides (OR 0.97, 95%CI 0.94-0.99; p = 0.040), and secondary RA strategy (OR 0.23, 95% CI 0.05-0.85; p = 0.028) were inversely associated with occurrence of prolonged ST-segment elevation following ablation. However, hemodialysis, diabetes mellitus, left-ventricular ejection fraction, lesion length ≥ 20 mm, and burr size did not show significant associations. Multivariate logistic regression analysis modeling revealed that secondary RA strategy was significantly associated with the occurrence of prolonged ST-segment elevation (Model 1: OR 0.24, 95% CI 0.05-0.95, p = 0.042; Model 2: OR 0.17, 95% CI 0.03-0.68, p = 0.018; Model 3: OR 0.21, 95% CI 0.03-0.87, p = 0.041) even after adjusting for levels of LDL-C and triglycerides. Secondary RA strategy may be useful to reduce the occurrence of prolonged ST-segment elevation following RA.

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.

Treatment of Slow-Flow After Primary Percutaneous Coronary Intervention With Flow-Mediated Hyperemia: The Randomized RAIN-FLOW Study.

Background ST-segment-elevation myocardial infarction complicated with no reflow after primary percutaneous coronary intervention is associated with adverse outcomes. Although several hyperemic drugs have been shown to improve the Thrombolysis in Myocardial Infarction flow, optimal treatment of no reflow remains unsettled. Saline infusion at 20 mL/min via a dedicated microcatheter causes (flow-mediated) hyperemia. The objective is to compare the efficacy of pharmacologic versus flow-mediated hyperemia in patients with ST-segment-elevation myocardial infarction complicated with no reflow. Methods and Results In the RAIN-FLOW (Treatment of Slow-Flow After Primary Percutaneous Coronary Intervention With Flow-Mediated Hyperemia) study, 67 patients with ST-segment-elevation myocardial infarction and no reflow were randomized to receive either pharmacologic-mediated hyperemia with intracoronary adenosine or nitroprusside (n=30) versus flow-mediated hyperemia (n=37). The angiographic corrected Thrombolysis in Myocardial Infarction frame count and the minimal microcirculatory resistance, as assessed with intracoronary pressure-thermistor wire, dedicated microcatheter, and thermodilution techniques, were compared after study interventions. Both Thrombolysis in Myocardial Infarction frame count(40.2±23.1 versus 39.2±20.7; P=0.858) and minimal microcirculatory resistance (753.6±661.5 versus 993.3±740.8 Wood units; P=0.174) were similar between groups. Thrombolysis in Myocardial Infarction 3 flow was observed in 26.7% versus 27.0% (P=0.899). Flow-mediated hyperemia showed 2 different thermodilution patterns during saline infusion indicative of the severity of the no reflow phenomenon. In-hospital death and nonfatal heart failure were observed in 10.4% and 26.9%, respectively. Conclusions Both treatments showed similar (and limited) efficacy restoring coronary flow. Flow-mediated hyperemia with thermodilution pattern assessment allowed the simultaneous characterization of the no reflow degree and response to hyperemia. No reflow was associated with a high rate of adverse outcomes. Further research is warranted to prevent and to treat no reflow in patients with ST-segment-elevation myocardial infarction. Registration URL: https://www.clinicaltrials.gov; Unique identifier: NCT04685941.

Effects of atorvastatin and rosuvastatin on dysfunctional coronary circulation in patients with ST-segment elevation myocardial infarction.

OBJECTIVE: Evidence of therapy for dysfunctional coronary circulation in patients with ST-segment elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (pPCI) is limited. This study was performed to compare the effects of atorvastatin and rosuvastatin on dysfunctional coronary circulation. METHODS: This retrospective study enrolled 597 consecutive patients with STEMI who underwent pPCI in 3 centers from June 2016 to December 2019. Dysfunctional coronary circulation was defined by the thrombolysis in myocardial infarction (TIMI) grade and the TIMI myocardial perfusion grade (TMPG). Logistic regression analysis was used to evaluate the impact of different statin types on dysfunctional coronary circulation. RESULTS: The incidence of TIMI no/slow reflow did not differ between the two groups, but the incidence of TMPG no/slow reflow was significantly lower in the atorvastatin than rosuvastatin group (44.58% vs. 57.69%, respectively). After multivariate adjustment, the odds ratio with 95% confidence interval of rosuvastatin was 1.72 (1.17-2.52) for after pretreatment TMPG no/slow reflow and 1.73 (1.16-2.58) for after stenting TMPG no/slow reflow. Atorvastatin and rosuvastatin showed no significant differences in clinical outcomes during hospitalization. CONCLUSIONS: Compared with rosuvastatin, atorvastatin was associated with better coronary microcirculatory perfusion in patients with STEMI who underwent pPCI.