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Background: Acute myocardial infarction (AMI) constitutes a major health problem with high mortality rates worldwide. In patients with ST-segment elevation myocardial infarction (STEMI), no-reflow phenomenon is a condition that adversely affects response to therapy. Previous studies have demonstrated that the CALLY index, calculated using C-reactive protein (CRP), albumin, and lymphocytes, is a reliable indicator of mortality in patients with non-cardiac diseases. The objective of this study is to investigate the potential utility of the CALLY index in detecting no-reflow patients and to determine the predictability of this phenomenon using machine learning (ML) methods. Methods: This study included 1785 STEMI patients admitted to the clinic between January 2020 and June 2024 who underwent percutaneous coronary intervention (PCI). Patients were in no-reflow status, and other clinical data were analyzed. The CALLY index was calculated using data on patients' inflammatory status. The Extreme Gradient Boosting (XGBoost) ML algorithm was used for no-reflow prediction. Results: No-reflow was detected in a proportion of patients participating in this study. The model obtained with the XGBoost algorithm showed high accuracy rates in predicting no-reflow status. The role of the CALLY index in predicting no-reflow status was clearly demonstrated. Conclusions: The CALLY index has emerged as a valuable tool for predicting no-reflow status in STEMI patients. This study demonstrates how machine learning methods can be effective in clinical applications and paves the way for innovative approaches for the management of no-reflow phenomenon. Future research needs to confirm and extend these findings with larger sample sizes. [ABSTRACT FROM AUTHOR]

Background and Aims Glycoprotein (GP) IIb/IIIa inhibitors are recommended in acute myocardial infarction (AMI) for bailout treatment in case of angiographic microvascular obstruction (MVO), also termed no-reflow phenomenon, after percutaneous coronary intervention (PCI) with, however, lacking evidence (class IIa, level C). Methods The investigator-initiated, international, multicentre REVERSE-FLOW trial randomized 120 patients with AMI and thrombolysis in myocardial infarction flow grade ≤ 2 after primary PCI to optimal medical therapy with or without GP IIb/IIIa inhibitor. The primary endpoint was infarct size [percentage of left ventricular (LV) mass assessed by cardiac magnetic resonance (CMR). Secondary endpoints included CMR-derived MVO and 30-day adverse clinical events. The trial is registered with ClinicalTrials.gov : NCT02739711. Results The population was predominantly male (76.7%) with a median age of 66 years and ST-elevation myocardial infarction in 73.3% of patients. Clinical and angiographic characteristics were well balanced between the cohorts. Patients in the treatment group (n = 62) received eptifibatide (n = 41) or tirofiban (n = 21). Infarct size assessed by CMR imaging was similar in both study groups [25.4% of LV mass (%LV) vs. 25.2%LV; P =.386]. However, the number of patients with evidence of CMR-derived MVO (74.5% vs. 92.2%; P =.017) and the extent of MVO (2.1%LV vs. 3.4%LV; P =.025) were significantly reduced in the GP IIb/IIIa inhibitor group compared with controls. Thirty-day outcome showed an increased bleeding risk after GP IIb/IIIa inhibitor administration restricted to non–life-threatening bleedings (22.6% vs. 6.9%; P =.016) without differences in all-cause mortality (4.8% vs. 3.4%; P =.703). Conclusions Bailout GP IIb/IIIa inhibition in AMI patients with angiographic MVO failed to reduce the primary endpoint infarct size but decreased CMR-derived MVO and led to an increase in non-fatal bleeding events. [ABSTRACT FROM AUTHOR]

Coronary heart disease (CHD), a prevalent cardiovascular disorder, poses a significant threat to human health.Particularly, ST-segment elevation myocardial infarction (STEMI) is associated with a higher mortality rate.Timely and effective revascularization of the culprit vessels is crucial.Percutaneous coronary intervention (PCI) is a preferred and critical treatment modality for STEMI patients, effectively addressing vascular obstruction.However, a subset of patients experiences coronary slow flow (CSF) or no-reflow (NR) postoperatively, which severely impacts their prognosis.This article provides a comprehensive review of the definition, diagnosis, epidemiology, predictive factors, mechanisms, and treatment of CSF/NR, aiming to offer guidance for the clinical management of these complications following PCI in CHD patients.

Objective: To investigate the relationship between systemic immune inflammatory index (SII), fibrinogen/albumin ratio (FAR), C-reactive protein/albumin ratio (CAR) and no-reflow during percutaneous coronary intervention (PCI) in patients with acute ST-elevation myocardial infarction (STEMI) and heart failure with preserved ejection fraction (HFpEF). Methods: 155 patients with STE- MI and HFpEF who underwent direct PCI in our hospital from May 2020 to May 2023 were prospectively selected, patients were divided into no-reflow group (n=35) and normal-reflow group (n=120) according to the blood flow during PCI. SII, FAR and CAR were calculated. The factors of no-reflow during PCI in patients with STEMI and HFpEF were analyzed by multivariate Logistic regression model, the predictive value of SII, FAR and CAR for no-reflow during PCI in patients with STEMI and HFpEF were analyzed by drawn receiver operating characteristic (ROC) curve. Results: The incidence of no-reflow during PCI in 155 patients with STEMI and HFpEF was 22.58% (35/155). Compared with normal-reflow group, SII, FAR and CAR increased in no-reflow group (P<0.05). The independent risk factors for no-reflow during PCI in patients with STEMI and HFpEF were increased age and increased SII, FAR and CAR (P<0.05). The area under the curve of SII, FAR, CAR alone and SII, FAR, CAR combined to predict no-reflow during PCI in patients with STEMI and HFpEF was 0.811, 0.800, 0.788, 0.940 respectively. Conclusion: The increase of SII, FAR and CAR in patients with STEMI and HFpEF is an independent risk factor for no-reflow during PCI, the combination of SII, FAR and CAR has a high predictive value for no-reflow during PCI in patients with STEMI and HFpEF. [ABSTRACT FROM AUTHOR]

Nutritional status and its index (Prognostic Nutritional Index, PNI) is an important prognostic factor for ST-segment elevation myocardial infarction (STEMI). The present study investigated whether PNI it is associated with no-reflow in patients with STEMI. In this retrospective study, 404 patients with STEMI and underwent primary percutaneous coronary intervention (pPCI) were consecutively included, between January 2016 and December 2018. No-reflow phenomenon (NRP) was detected in 103 (25.4%) patients. In multivariate logistic regression analysis C-reactive protein (CRP) (odds ratio (OR): 1.693, 95% confidence interval (CI): 1.126–2.547, P =.011), left ventricle ejection fraction (LVEF) (OR: 0.777, 95% CI: 0.678–0.891, P <.001), SYNTAX score (OR: 1.114, 95% CI: 1.050–1.183, P =.001), low density lipoprotein cholesterol (LDL-C) (OR: 1.033, 95% CI: 1.013–1.055, P =.002), hemoglobin level (OR: 0.572, 95% CI: 0.395–0.827, P =.003), PNI (OR: 0.554, 95% CI: 0.448–0.686, P <.001) were associated with NRP. The area under curve of PNI was significantly higher than albumin (z = 4.747, P <.001) and lymphocyte values (z = 3.481 P <.001). PNI was associated with no-reflow occurrence and mortality. So, PNI may be useful to predict NRP risk in patients with STEMI before pPCI. [ABSTRACT FROM AUTHOR]

Background: The occurrence of no-reflow in patients with STEMI means inadequate myocardial reperfusion despite patent coronary arteries and it accounts for as much as twenty percent of patients undergoing PPCI. Electrocardiogram (ECG) is a widely available non-invasive diagnostic tool in daily practice that is easy to use. So our study aimed to evaluate the corrected value of T wave peak interval to end terminal (cTPE) and corrected QT and assess the ratio of cTPE\c QT in predicting no-reflow. Methods: A total of 120 patients who fulfilled inclusion and exclusion criteria were subjected to 12 leads surface ECG, TPE interval was measured from the peak of the T wave to the end terminal of the T wave tangent to the baseline in the leads the least ST changes (defined as less than <0.055 mV from the isoelectric line. QT interval was assessed from the onset of the QRS complex to the T wave end, other clinical and angiographic data were compared in successful and no-reflow groups. Results: The population study was divided into no-reflow group I accounting for 33.3% and successful reperfusion group II accounting for 66.7%. Admission time cTPE\cQT was significantly more prolonged in group I 0.281±1.94 compared to 0.192±1.07 in group II. Multivariate analysis showed that admission time from symptoms onset to hospital admission (0.017), followed by Hs-troponin peak value pg\ml (0.007), then Admission time cTPE\cQT (0.001) were significant predictors of impaired flow TIMI <3 post PCI. Conclusions: Admission time cTPE\cQT at a cut-off value = 0.243 ms could accurately predict impaired flow TIMI <3 post PCI, with a sensitivity of 78.8% and, a specificity of 66.5 %. [ABSTRACT FROM AUTHOR]

This study aimed to investigate the cardioprotective effect of quinacrine in an in vivo model of myocardial ischemia/reperfusion injury. A 30-min regional myocardial ischemia followed by a 2-h reperfusion was modeled in anesthetized Wistar rats. Starting at the last minute of ischemia and during the first 9 min of reperfusion the rats in the control (n=8) and experimental (n=9) groups were injected with 0.9% NaCl and quinacrine solution (5 mg/kg), respectively. The area at risk and infarct size were evaluated by "double staining" with Evans blue and triphenyltetrazolium chloride. To assess vascular permeability in the area at risk zone, indocyanine green (ICG) and thioflavin S (ThS) were injected intravenously at the 90th and 120th minutes of reperfusion, respectively, to assess the no-reflow zone. The images of ICG and ThS fluorescence in transverse sections of rat hearts were obtained using a FLUM multispectral fluorescence organoscope. HR tended to decrease by 13% after intravenous administration of quinacrine and then recovered within 50 min. Quinacrine reduced the size of the necrotic zone (p=0.01), vascular permeability in the necrosis region, and the no-reflow area (p=0.027); at the same time, the area at risk did not significantly differ between the groups. Intravenous administration of quinacrine at the beginning of reperfusion of the rat myocardium reduces no-reflow phenomenon and infarct size. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Aim. To evaluate the impact of chronic obstructive pulmonary disease (COPD) on hospital outcomes of percutaneous coronary interventions (PCI) in patients with acute coronary syndrome (ACS). Materials and methods. A cohort prospective study of the COPD effect on mortality and coronary microvascular obstruction (CMVO, no-reflow) development after PCI in ACS was carried out. 626 patients admitted in 2019–2020 were included, 418 (67%) – men, 208 (33%) – women. Median age – 63 [56; 70] years. Myocardial infarction with ST elevation identified in 308 patients (49%), CMVO – in 59 (9%) patients (criteria: blood flow 3 grade according to TIMI flow grade; perfusion 2 points according to Myocardial blush grade; ST segment resolution 70%). 13 (2.1%) patients died. Based on the questionnaire "Chronic Airways Diseases, A Guide for Primary Care Physicians, 2005", 2 groups of patients were identified: 197 (31%) with COPD (≥17 points) and 429 (69%) without COPD (17 points). Groups were compared on unbalanced data (÷2 Pearson, Fisher exact test). The propensity score was calculated, and a two-way logistic regression analysis was performed. The data were balanced by the Kernel “weighting” method, logistic regression analysis was carried out using “weighting” coefficients. Results as odds ratio (OR) and 95% confidence interval. Results. The conducted research allowed us to obtain the following results, depending on the type of analysis: 1) analysis of unbalanced data in patients with COPD: OR death 3.60 (1.16–11.12); p=0.03; OR CMVO 0.65 (0.35–1.22); p=0,18; 2) two-way analysis with propensity score: OR death 3.86 (1.09–13.74); p=0.04; OR CMVO 0.61 (0.31–1.19); p=0.15; 3) regression analysis with "weight" coefficients: OR death 12.49 (2.27–68.84); p=0.004; OR CMVO 0.63 (0.30–1.33); p=0.22. Conclusion. The presence of COPD in patients with ACS undergoing PCI increases mortality and does not affect the incidence of CMVO.

Abstract Objective Triglyceride glucose (TyG) index is considered as a new alternative marker of insulin resistance and a clinical predictor of type 2 diabetes mellitus (T2DM) combined with coronary artery disease. However, the prognostic value of TyG index on No-Reflow (NR) Phenomenon in T2DM patients with acute myocardial infarction (AMI) remains unclear. Methods In this retrospective study, 1683 patients with T2DM and AMI underwent primary percutaneous coronary intervention (PCI) were consecutively included between January 2014 and December 2019. The study population was divided into two groups as follows: Reflow (n = 1277) and No-reflow (n = 406) group. The TyG index was calculated as the ln [fasting triglycerides (mg/dL)×fasting plasma glucose (mg/dL)/2].Multivariable logistic regression models and receiver-operating characteristic curve analysis were conducted to predict the possible risk of no-reflow. Net Reclassification Improvement (NRI) and Integrated Discrimination Improvement (IDI) were calculated to determine the ability of the TyG index to contribute to the baseline risk model. Results Multivariable logistic regression models revealed that the TyG index was positively associated with NR[OR,95%CI:5.03,(2.72,9.28),p

Background: Primary percutaneous coronary intervention (PPCI) is the standard reperfusion treatment in ST-segment elevation myocardial infarction (STEMI). Intracoronary thrombolysis (ICT) may reduce thrombotic burden in the infarct-related artery, which is often responsible for microvascular obstruction and no-reflow. Methods: We conducted, according to the PRISMA statement, the largest meta-analysis to date of ICT as adjuvant therapy to PPCI. All relevant studies were identified by searching the PubMed, Scopus, Cochrane Library, and Web of Science. Results: Thirteen randomized controlled trials (RCTs) involving a total of 1876 patients were included. Compared to the control group, STEMI ICT-treated patients had fewer major adverse cardiac events (MACE) (OR 0.65, 95% CI, 0.48–0.86, P = 0.003) and an improved 6-month left ventricular ejection fraction (MD 3.78, 95% CI, 1.53–6.02, P = 0.0010). Indices of enhanced myocardial microcirculation were better with ICT (Post-PCI corrected thrombolysis in myocardial infarction (TIMI) frame count (MD − 3.57; 95% CI, − 5.00 to − 2.14, P < 0.00001); myocardial blush grade (MBG) 2/3 (OR 1.76; 95% CI, 1.16–2.69, P = 0.008), and complete ST-segment resolution (OR 1.97; 95% CI, 1.33–2.91, P = 0.0007)). The odds for major bleeding were comparable between the 2 groups (OR 1.27; 95% CI, 0.61–2.63, P = 0.53). Conclusions: The present meta-analysis suggests that ICT was associated with improved MACE and myocardial microcirculation in STEMI patients undergoing PPCI, without significant increase in major bleeding. However, these findings necessitate confirmation in a contemporary large RCT. [ABSTRACT FROM AUTHOR]

Objective: Triglyceride glucose (TyG) index is considered as a new alternative marker of insulin resistance and a clinical predictor of type 2 diabetes mellitus (T2DM) combined with coronary artery disease. However, the prognostic value of TyG index on No-Reflow (NR) Phenomenon in T2DM patients with acute myocardial infarction (AMI) remains unclear. Methods: In this retrospective study, 1683 patients with T2DM and AMI underwent primary percutaneous coronary intervention (PCI) were consecutively included between January 2014 and December 2019. The study population was divided into two groups as follows: Reflow (n = 1277) and No-reflow (n = 406) group. The TyG index was calculated as the ln [fasting triglycerides (mg/dL)×fasting plasma glucose (mg/dL)/2].Multivariable logistic regression models and receiver-operating characteristic curve analysis were conducted to predict the possible risk of no-reflow. Net Reclassification Improvement (NRI) and Integrated Discrimination Improvement (IDI) were calculated to determine the ability of the TyG index to contribute to the baseline risk model. Results: Multivariable logistic regression models revealed that the TyG index was positively associated with NR[OR,95%CI:5.03,(2.72,9.28),p<0.001] in patients with T2DM and AMI. The area under the curve (AUC) of the TyG index predicting the occurrence of NR was 0.645 (95% CI 0.615–0.673; p < 0.001)], with the cut-off value of 8.98. The addition of TyG index to a baseline risk model had an incremental effect on the predictive value for NR [net reclassification improvement (NRI): 0.077(0.043to 0.111), integrated discrimination improvement (IDI): 0.070 (0.031to 0.108), all p < 0.001]. Conclusions: High TyG index was associated with an increased risk of no-reflow after PCI in AMI patients with T2DM. The TyG index may be a valid predictor of NR phenomenon of patients with T2DM and AMI. Early recognition of NR is critical to improve outcomes with AMI and T2DM patients. [ABSTRACT FROM AUTHOR]

Incomplete reperfusion of the microvasculature ('no-reflow') after ischaemic stroke damages salvageable brain tissue. Previous ex vivo studies suggest pericytes are vulnerable to ischaemia and may exacerbate no-reflow, but the viability of pericytes and their association with no-reflow remains under-explored in vivo. Using longitudinal in vivo two-photon single-cell imaging over 7 days, we showed that 87% of pericytes constrict during cerebral ischaemia and remain constricted post reperfusion, and 50% of the pericyte population are acutely damaged. Moreover, we revealed ischaemic pericytes to be fundamentally implicated in capillary no-reflow by limiting and arresting blood flow within the first 24 h post stroke. Despite sustaining acute membrane damage, we observed that over half of all cortical pericytes survived ischaemia and responded to vasoactive stimuli, upregulated unique transcriptomic profiles and replicated. Finally, we demonstrated the delayed recovery of capillary diameter by ischaemic pericytes after reperfusion predicted vessel reconstriction in the subacute phase of stroke. Cumulatively, these findings demonstrate that surviving cortical pericytes remain both viable and promising therapeutic targets to counteract no-reflow after ischaemic stroke. [ABSTRACT FROM AUTHOR]

ST-elevation myocardial infarction (STEMI) is a medical emergency demanding immediate intervention, and primary percutaneous coronary intervention (pPCI) is the standard of care for this condition. While PCI has proven highly effective, a subset of patients experience the devastating no-reflow phenomenon, and some face increased short-term mortality. The Hemoglobin, Albumin, Lymphocyte, and Platelet (HALP) score, a novel biomarker-based tool, has recently surfaced as an innovative predictor of these adverse outcomes. This study aims to investigate the groundbreaking findings that designate a low HALP score as a robust risk factor for no-reflow and short-term mortality in STEMI patients. 1817 consecutive STEMI patients who underwent pPCI were included in this retrospective study, and the patients were divided into two groups according to whether no-reflow developed or not, and the HALP scores of the groups were compared. In addition, short-term mortality was compared between the study groups according to their HALP score values. The predictive ability of the HALP score for no-reflow was evaluated using a receiver operating characteristic curve. No-reflow developed in 198 (10.1%) of the patients included in the study. HALP score value was found to be significantly lower in the no-reflow group (27 ± 13 vs 47 ± 24, p < 0.001). After multivariable adjustment, the HALP score was an independent predictor of no-reflow (OR, 0.923, 95% CI, 0.910–0.935, p < 0.001). Furthermore, the HALP score showed good discrimination for no-reflow (AUC, 0.771, 95% CI, 0.737–0.805, p < 0.001). In addition, HALP score was determined to be an independent predictor for short-term mortality (HR, 0.955, 95% CI, 0.945–0.966, p < 0.001). HALP score can independently predict the development of no-reflow and short-term mortality in STEMI patients undergoing pPCI. [ABSTRACT FROM AUTHOR]

Microvascular obstruction (MVO) of coronary arteries promotes an increase in mortality and major adverse cardiac events in patients with acute myocardial infarction (AMI) and percutaneous coronary intervention (PCI). Intramyocardial hemorrhage (IMH) is observed in 41-50% of patients with ST-segment elevation myocardial infarction and PCI. The occurrence of IMH is accompanied by inflammation. There is evidence that microthrombi are not involved in the development of MVO. The appearance of MVO is associated with infarct size, the duration of ischemia of the heart, and myocardial edema. However, there is no conclusive evidence that myocardial edema plays an important role in the development of MVO. There is evidence that platelets, inflammation, Ca2+ overload, neuropeptide Y, and endothelin-1 could be involved in the pathogenesis of MVO. The role of endothelial cell damage in MVO formation remains unclear in patients with AMI and PCI. It is unclear whether nitric oxide production is reduced in patients with MVO. Only indirect evidence on the involvement of inflammation in the development of MVO has been obtained. The role of reactive oxygen species (ROS) in the pathogenesis of MVO is not studied. The role of necroptosis and pyroptosis in the pathogenesis of MVO in patients with AMI and PCI is also not studied. The significance of the balance of thromboxane A2, vasopressin, angiotensin II, and prostacyclin in the formation of MVO is currently unknown. Conclusive evidence regarding the role of coronary artery spasm in the development of MVhasn’t been established. Correlation analysis of the neuropeptide Y, endothelin-1 levels and the MVO size in patients with AMI and PCI has not previously been performed. It is unclear whether epinephrine aggravates reperfusion necrosis of cardiomyocytes. Dual antiplatelet therapy improves the efficacy of PCI in prevention of MVO. It is unknown whether epinephrine or L-type Ca2+ channel blockers result in the long-term improvement of coronary blood flow in patients with MVO. [ABSTRACT FROM AUTHOR]

This systematic review, meta-analysis, and novel time course analysis examines microvascular failure in the treatment of acute ischemic stroke (AIS) patients undergoing endovascular therapy (EVT) and/or thrombolytic administration for stroke management. A systematic review and meta-analysis following PRIMSA-2020 guidelines was conducted along with a novel curve-of-best fit analysis to elucidate the time-course of microvascular failure. Scopus and PubMed were searched using relevant keywords to identify studies that examine recanalization and reperfusion assessment of AIS patients following large vessel occlusion. Meta-analysis was conducted using a random-effects model. Curve-of-best-fit analysis of microvascular failure rate was performed with a negative exponential model. Twenty-seven studies with 1151 patients were included. Fourteen studies evaluated patients within a standard stroke onset-to-treatment time window (≤6 hours after last known normal) and thirteen studies had an extended time window (>6 hours). Our analysis yields a 22% event rate of microvascular failure following successful recanalization (95% CI: 16–30%). A negative exponential curve modeled a microvascular failure rate asymptote of 28.5% for standard time window studies, with no convergence of the model for extended time window studies. Progressive microvascular failure is a phenomenon that is increasingly identified in clinical studies of AIS patients undergoing revascularization treatment. [ABSTRACT FROM AUTHOR]

Coronary artery ectasia or aneurysms are dilatation of an arterial segment to a diameter at least 1.5 times that of the adjacent normal. Blood flow through such arteries is disturbed and turbulent, which, with the activation of endothelium, leads to chronic thrombosis in the blood vessel wall. Percutaneous coronary interventions in ectatic / aneurysmal vessels carry a high risk of complications, primarily a “no-reflow” phenomenon. No-reflow is common in patients with acute coronary syndrome, especially ST elevation myocardial infarction (STEMI). In this article, we present the occurrence of the no-reflow phenomenon in a stable patient undergoing percutaneous intervention due to a significant stenosis of the aneurysmally altered right coronary artery. Despite the rapid placement and optimization of stents and the applied drug therapy combined with thromboaspiration periprocedurally, it was not possible to establish TIMI 3 flow. However, after the initial failure and development of periprocedural STEMI, the patient was successfully stabilized with unexpectedly good recovery of infarcted myocardial function. Control coronarography 6 weeks after the initial event confirmed a proper stent patency with normal TIMI 3 flow.

Objective: No-reflow phenomenon is one of well-known complications of percutaneous coronary intervention (PCI). The rate of no-reflow phenomenon was reported between 2-44% differing on the accompanying situations and more frequent in acute myocardial infarction. Predictive factors for no-reflow phenomenon have not been clearly defined. We aimed to define predictive factors for no-reflow development in patients who presented with ST-segment elevation MI (STEMI) and treated with primary (PPCI). Method: Patients who underwent PPCI between 2017 and 2021 in our clinic were included retrospectively. Demographic, clinical and laboratory findings were recorded. Two groups generated according to no-reflow development: no-reflow (+) and (-). Results: Six hundred eighty-nine patients were included. Mean age was 55.9±8.7 years and 71.8% were male. 107 patients (15.5%) were formed no-reflow (+) group and 582 patients were formed no-reflow (-) group. Left ventricular ejection fraction, troponin, fasting blood glucose, TIMI thrombus grade and TIMI thrombus category were determined as independent predictors of no-reflow development. Conclusion: Considering the relationship between no-reflow development and adverse outcomes such as in-hospital adverse cardiac events, left ventricular remodeling, malignant ventricular arrhythmia, or heart failure, it may help to identify the factors that predict the risk of no-reflow and take preventive measures to improve the long-term outcome.

Актуальность. Нет шкалы, объединяющей традиционные критерии коронарной микрососудистой обструкции (no-reflow) для эффективной оценки тяжести и прогноза данного осложнения. Цель. Разработать и изучить прогностическую ценность шкалы оценки тяжести коронарной микрососудистой обструкции в ходе чрескожных коронарных вмешательств при инфаркте миокарда. Методы. В когортное исследование включено 203 пациента с инфарк­том миокарда 1-го типа и коронарной микрососудистой обструкцией при чрескожном коронарном вмешательстве по критерию кровоток < 3 баллов по Thrombolysis in Myocardial Infarction (TIMI) flow grade. По предложенной шкале оценки тяжести коронарной микрососудистой обструкции (ШОТ-КМСО) выделены 3 группы. Коронарная микрососудистая обструкция 1-й степени (умеренная): TIMI flow grade 2 балла, Myocardial blush grade 2–3 балла, резолюция сегмента ST после чрескожного коронарного вмешательства > 70 %. Коронарная микрососудистая обструкция 2-й степени (средней тяжести): TIMI flow grade 2 балла, Myocardial blush grade 0–1 балл или резолюция сегмента ST < 70 %. Коронарная микрососудистая обструкция 3-й степени (тяжелая): TIMI flow grade 0–1 балл. Результаты. Распределение групп с коронарной микрососудистой обструкцией 1-й, 2-й и 3-й степеней: 65 (32 %) / 88 (43 %) / 50 (25 %) пациентов соответственно. Госпитальные исходы по группам: острая сердечная недостаточность III–IV класса — 2 (3 %) / 11 (13 %) / 14 (28 %), p < 0,001; фракция выброса — 48 [44; 53] % / 46 [40; 50] % / 42 [39; 49] %, p = 0,004; госпитальная смерть — 1 (1,5 %) / 12 (13,6 %) / 16 (32,0 %), p < 0,001; смерть в течение двух лет — 8 (12,3 %) / 19 (21,6 %) / 22 (44,0 %), p < 0,001. Многофакторный анализ: отношение шансов смерти в течение двух лет для ШОТ-КМСО — 2,40 [95% доверительный интервал 1,23–5,17], p = 0,009. Вероятность выжить за двухлетний период при КМСО 1-й степени по ШОТ-КМСО — 87,7 %, 2-й — 78,4 %, 3-й — 56,0 % (p < 0,001). Заключение. Степень тяжести коронарной микрососудистой обструкции, оцененная с помощью предложенной шкалы, ассоциирована с развитием неблагоприятных госпитальных исходов и является независимым предиктором смерти в течение двух лет. Поступила в редакцию 15 мая 2023 г. Исправлена 27 сентября 2023 г. Принята к печати 24 октября 2023 г. Финансирование Исследование выполнено в рамках программы стратегического академического лидерства «Приоритет-2030». Конфликт интересов Авторы заявляют об отсутствии конфликта интересов. Вклад авторов Концепция и дизайн работы: А.А. Фролов, Е.Г. Шарабрин, И.Г. Починка Сбор и анализ данных: А.А. Фролов, И.А. Фролов, К.В. Кузьмичев Статистическая обработка данных: А.А. Фролов, И.А. Фролов, К.В. Кузьмичев Написание статьи: А.А. Фролов, И.Г. Починка, И.А. Фролов Исправление статьи: И.Г. Починка, А.С. Мухин, Е.Г. Шарабрин, В.Н. Синютин Утверждение окончательного варианта статьи: все авторы

Coronary artery disease (CAD) involves a complex atherosclerotic process, and many factors play a role in this process. Although there are studies evaluating the development and severity of CAD with trace elements in the blood, there is no study evaluating coronary flow to our knowledge. This study aimed to evaluate the relationship between coronary flow and trace elements after percutaneous intervention in ST-elevation myocardial infarction (STEMI). This study included 126 consecutive patients who presented to the emergency department with STEMI between May 2023 and August 2023. Thrombolysis in myocardial infarction (TIMI) flow grades were calculated after primary percutaneous coronary intervention, and patients were categorized into two groups: low TIMI flow grade and normal TIMI flow grade. The diagnosis of STEMI was defined according to European acute coronary syndrome (ACS) guidelines. Demographic and clinical data were recorded. After coronary angiography, blood tests for trace elements were obtained in addition to routine laboratory parameters. All variables were compared between the two groups. There was no significant difference between low and normal TIMI flow grade groups regarding age and gender. Killip score (p=0.004) and tirofiban (p [Med-Science 2023; 12(4.000): 1050-5]

Abstract Objectives It is uncertain, if omitting post-dilatation and stent oversizing (stent optimization) is safe and may decrease the risk for distal thrombus embolization (DTE) in STEMI patients with large thrombus burden (LTB). Background In patients with ST-segment elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (pPCI) with stenting, (DTE) and flow deterioration are common and increase infarct size leading to worse outcomes. Methods From a prospective registry, 74 consecutive STEMI patients with LTB undergoing pPCI with stenting and intentionally deferred stent optimization were analyzed. Imaging data and outcomes up to 2 years follow-up were analyzed. Results Overall, 74 patients (18% females) underwent deferred stent optimization. Direct stenting was performed in 13 (18%) patients. No major complications occurred during pPCI. Staged stent optimization was performed after a median of 4 (interquartile range (IQR) 3; 7) days. On optical coherence tomography, under-expansion and residual thrombus were present in 59 (80%) and 27 (36%) cases, respectively. During deferred stent optimization, we encountered no case of flow deterioration (slow or no-reflow) or side branch occlusion. Minimal lumen area (mm2) and stent expansion (%) were corrected from 4.87±1.86mm to 6.82±2.36mm (p

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. [ABSTRACT FROM AUTHOR]

This study evaluated the association between no-reflow (NR) and serum uric acid/albumin ratio (UAR) in 360 consecutive patients with non-ST-elevation myocardial infarction (NSTEMI) undergoing primary percutaneous coronary intervention. The study population was divided into two groups as follows: reflow (n = 310) and NR (n = 50) group. The thrombolysis in myocardial infarction (TIMI) flow score was used to describe NR. High UAR (Odds Ratio: 3.495, 95% CI; 1.216–10.048; P <.001) was found to be an independent predictor of NR. Additionally, UAR was positively correlated with the SYNTAX score and neutrophil/lymphocyte ratio; UAR was negatively correlated with left ventricular ejection fraction. The highest cut-off ratio of UAR predicting NR was found to be 1.35 with 68% sensitivity and 66.8% specificity. The area under the curve (AUC) for UAR was.768 (95% CI:.690-.847) after receiver operating characteristic (ROC) curve assessment. The AUC for UAR was found to be higher than for its components: serum uric acid (AUC:.655) and albumin (AUC:.663) (P <.001 for each evaluation). [ABSTRACT FROM AUTHOR]

The reported incidence of persistent hypoperfusion despite complete recanalization as surrogate for impaired microvascular reperfusion (IMR) has varied widely among clinical studies, possibly due to differences in i) definition of complete recanalization, with only recent Thrombolysis in Cerebral Infarction (TICI) grading schemes allowing distinction between complete (TICI3) and partial recanalization with distal occlusions (TICI2c); ii) operational definition of IMR; and iii) consideration of potential alternative causes for hypoperfusion, notably carotid stenosis, re-occlusion and post-thrombectomy hemorrhage. We performed a systematic review to identify clinical studies that carried out brain perfusion imaging within 72 hrs post-thrombectomy for anterior circulation stroke and reported hypoperfusion rates separately for TICI3 and TICI2c grades. Authors were contacted if this data was missing. We identified eight eligible articles, altogether reporting 636 patients. The incidence of IMR after complete recanalization (i.e., TICI3) tended to decrease with the number of considered alternative causes of hypoperfusion: range 12.5–42.9%, 0–31.6% and 0–9.1% in articles that considered none, two or all three causes, respectively. No study reported the impact of IMR on functional outcome separately for TICI-3 patients. Based on this systematic review, IMR in true complete recanalization appears relatively rare, and reported incidence highly depends on definition used and consideration of confounding factors. [ABSTRACT FROM AUTHOR]

Copyright of Bagcilar Medical Bulletin / Bağcılar Tıp Bülteni is the property of Galenos Yayinevi Tic. LTD. STI and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Coronary artery disease (CAD) involves a complex atherosclerotic process, and many factors play a role in this process. Although there are studies evaluating the development and severity of CAD with trace elements in the blood, there is no study evaluating coronary flow to our knowledge. This study aimed to evaluate the relationship between coronary flow and trace elements after percutaneous intervention in ST-elevation myocardial infarction (STEMI). This study included 126 consecutive patients who presented to the emergency department with STEMI between May 2023 and August 2023. Thrombolysis in myocardial infarction (TIMI) flow grades were calculated after primary percutaneous coronary intervention, and patients were categorized into two groups: low TIMI flow grade and normal TIMI flow grade. The diagnosis of STEMI was defined according to European acute coronary syndrome (ACS) guidelines. Demographic and clinical data were recorded. After coronary angiography, blood tests for trace elements were obtained in addition to routine laboratory parameters. All variables were compared between the two groups. There was no significant difference between low and normal TIMI flow grade groups regarding age and gender. Killip score (p=0.004) and tirofiban (p<0.001) use were higher in the low TIMI flow grade group. Serum copper, high-density lipoprotein, low-density lipoprotein, diabetes mellitus, hypertension, and platelet variables were included in binary logistic regression analysis; low serum copper (p=0.014, OR=1.023, Cl=1.005-1.042) was found to be a risk factor for low TIMI flow grade. Regarding the outcomes of this research, we found that serum copper levels are an important risk factor for low TIMI flow grade in STEMI. [ABSTRACT FROM AUTHOR]

Objective To investigate the predictive value of preoperative plasma soluble suppression of tumorigenicity 2 protein (sST2) combined with atherogenic index of plasma (AIP) on the development of slow flow/non-reflow (SRF/ NRF) during percutaneous coronary intervention (PCI) in patients with acute ST-segment elevation myocardial infarction (STEMI). Methods Totally 120 STEMI patients were selected as the STEMI group, and they were classified into the SRF/NRF group of 47 cases and the non-SRF/NRF group of 73 cases according to the occurrence of SRF/NRF during PCI; another 57 volunteers for physical examination were selected as the control group during the same period. Plasma sST2 was detected by enzyme-linked immunosorbent assay. Plasma TG and HDL-C were detected, and AIP was calculated by fully automated biochemistry analyzer. The medical records of patients with STEMI were collected. Multifactorial Logistic regression was used to analyze the factors affecting the occurrence of SRF/NRF during PCI in STEMI patients; the predictive value of plasma sST2 and AIP for the occurrence of SRF/NRF during PCI in STEMI patients was analyzed by using the receiver operating characteristic (ROC) curve. Results Plasma sST2 and AIP were higher in the STEMI group than in the control group (both P<0. 05). Multifactorial Logistic regression analysis showed that increased age, diabetes mellitus, and elevated plasma sST2 and AIP were independent risk factors for the development of SRF/NRF during PCI in STEMI patients (all P<0. 05). ROC curve analysis showed that the area under the curve of plasma sST2, AIP, and the combination of the two in predicting the development of SRF/NRF during PCI in patients with STEMI was 0. 780, 0. 777, and 0. 877, respectively, and the area under the curve of the combination of the two with AIP was greater than that of either alone (all P<0. 05). Conclusion Elevated preoperative plasma sST2 and AIP are risk factors for the development of SRF/NRF during PCI in STEMI patients, and the combination of the two has a high predictive value for the development of SRF/NRF during PCI. [ABSTRACT FROM AUTHOR]

Objective: To evaluate the association of admission blood glucose levels with no-reflow or slow flow in patients with STElevation Myocardial Infarction (STEMI) undergoing Primary Percutaneous Coronary Intervention (PPCI). Study Design: Analytic Cross-sectional study. Place & Duration of Study: Armed Forces Institute of Cardiology/National Institute of Heart Diseases, Rawalpindi, Pakistan, from Jan 2023 till Jun 2023 Methodology: Total 141 STEMI patients (regardless of age and gender) presented in the emergency department with the time duration of 12 hours after onset of chest pain were included in the study by using non-probability Consecutive Sampling technique. Admission glucose levels were measured, and the occurrence of no-reflow or slow flow was assessed using the Thrombolysis in Myocardial Infarction (TIMI) flow score. Statistical analysis, including t-test and Chi-square tests were applied to evaluate the association between glucose levels and no-reflow or slow flow. Level of significance taken was ≤0.05. Results: Out of total 141 patients, mean age of the patients was 61.74+10.87 years and majority were males, 118(83.7%). 101(71.6%) were hypertensive and 69(48.9%) were diabetic. The average admission glucose level was 181.13+112.16mg/dl. Patients with no-reflow or slow flow had significantly higher admission glucose levels compared to those with normal flow (p=0.031). Additionally, a significantly higher number of patients developed no-reflow 4(9.3%) or slow flow 24(55.8%) in the group with admission glucose levels >200 mg/dl (p=0.01). Conclusion: Admission glucose levels may serve as a simple predictor of no-reflow or slow flow in STEMI patients undergoing PPCI, emphasizing the importance of adequate glucose management in these patients.

Objectives: It is uncertain, if omitting post-dilatation and stent oversizing (stent optimization) is safe and may decrease the risk for distal thrombus embolization (DTE) in STEMI patients with large thrombus burden (LTB). Background: In patients with ST-segment elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (pPCI) with stenting, (DTE) and flow deterioration are common and increase infarct size leading to worse outcomes. Methods: From a prospective registry, 74 consecutive STEMI patients with LTB undergoing pPCI with stenting and intentionally deferred stent optimization were analyzed. Imaging data and outcomes up to 2 years follow-up were analyzed. Results: Overall, 74 patients (18% females) underwent deferred stent optimization. Direct stenting was performed in 13 (18%) patients. No major complications occurred during pPCI. Staged stent optimization was performed after a median of 4 (interquartile range (IQR) 3; 7) days. On optical coherence tomography, under-expansion and residual thrombus were present in 59 (80%) and 27 (36%) cases, respectively. During deferred stent optimization, we encountered no case of flow deterioration (slow or no-reflow) or side branch occlusion. Minimal lumen area (mm2) and stent expansion (%) were corrected from 4.87±1.86mm to 6.82±2.36mm (p<0.05) and from 69±18% to 91±12% (p<0.001), respectively. During follow-up, 1 patient (1.4%) required target lesion revascularization and 1 (1.4%) patient succumbed from cardiovascular death. Conclusions: Among STEMI patients with LTB, deferring stent optimization in the setting of pPCI appears safe and potentially mitigates the risk of DTE. The impact of this approach on infarct size and clinical outcomes warrants further investigation in a dedicated trial. [ABSTRACT FROM AUTHOR]

Aims: Despite successful vascular recanalization in stroke, one‐fourth of patients have an unfavorable outcome due to no‐reflow. The pathogenesis of no‐reflow is fully unclear, and therapeutic strategies are lacking. Upon traditional Chinese medicine, Tongxinluo capsule (TXL) is a potential therapeutic agent for no‐reflow. Thus, this study is aimed to investigate the pathogenesis of no‐reflow in stroke, and whether TXL could alleviate no‐reflow as well as its potential mechanisms of action. Methods: Mice were orally administered with TXL (3.0 g/kg/d) after transient middle cerebral artery occlusion. We examined the following parameters: neurological function, no‐reflow, leukocyte‐endothelial cell interactions, HE staining, leukocyte subtypes, adhesion molecules, and chemokines. Results: Our results showed stroke caused neurological deficits, neuron death, and no‐reflow. Adherent and aggregated leukocytes obstructed microvessels as well as leukocyte infiltration in ischemic brain. Leukocyte subtypes changed after stroke mainly including neutrophils, lymphocytes, regulatory T cells, suppressor T cells, helper T type 1 (Th1) cells, Th2 cells, B cells, macrophages, natural killer cells, and dendritic cells. Stroke resulted in upregulated expression of adhesion molecules (P‐selectin, E‐selectin, and ICAM‐1) and chemokines (CC‐chemokine ligand (CCL)‐2, CCL‐3, CCL‐4, CCL‐5, and chemokine C‐X‐C ligand 1 (CXCL‐1)). Notably, TXL improved neurological deficits, protected neurons, alleviated no‐reflow and leukocyte‐endothelial cell interactions, regulated multiple leukocyte subtypes, and inhibited the expression of various inflammatory mediators. Conclusion: Leukocyte‐endothelial cell interactions mediated by multiple inflammatory factors are an important cause of no‐reflow in stroke. Accordingly, TXL could alleviate no‐reflow via suppressing the interactions through modulating various leukocyte subtypes and inhibiting the expression of multiple inflammatory mediators. [ABSTRACT FROM AUTHOR]

Calcified atheroma has been viewed conventionally as stable lesion which less likely increases no-reflow phenomenon. Given that lipidic materials triggers the formation of calcification, lipidic materials could exist within calcified lesion, which may cause no-reflow phenomenon after PCI. The REASSURE-NIRS registry (NCT04864171) employed near-infrared spectroscopy and intravascular ultrasound imaging to evaluate maximum 4-mm lipid-core burden index (maxLCBI4mm) at target lesions containing small (maximum calcification arc < 180°: n = 272) and large calcification (maximum calcification arc ≥ 180°: n = 189) in stable CAD patients. The associations of maxLCBI4mm with corrected TIMI frame count (CTFC) and no-reflow phenomenon after PCI were analyzed in patients with target lesions containing small and large calcification, respectively. No-reflow phenomenon occurred in 8.0% of study population. Receiver-operating characteristics curve analyses revealed that optimal cut-off values of maxLCBI4mm for predicting no-reflow phenomenon were 585 at small calcification (AUC = 0.72, p < 0.001) and 679 at large calcification (AUC = 0.76, p = 0.001). Target lesions containing small calcification with maxLCBI4mm ≥ 585 more likely exhibited a greater CTFC (p < 0.001). In those with large calcification, 55.6% of them had maxLCBI4mm ≥ 400 [vs. 56.2% (small calcification), p = 0.82]. Furthermore, a higher CTFC (p < 0.001) was observed in association with maxLCBI4mm ≥ 679 at large calcification. On multivariable analysis, maxLCBI4mm at large calcification still independently predicted no-reflow phenomenon (OR = 1.60, 95%CI = 1.32–1.94, p < 0.001). MaxLCBI4mm at target lesions exhibiting large calcification elevated a risk of no-reflow phenomenon after PCI. Calcified plaque containing lipidic materials is not necessarily stable lesion, but could be active and high-risk one causing no-reflow phenomenon. [ABSTRACT FROM AUTHOR]

No current treatments target microvascular reperfusion after stroke, which can contribute to poor outcomes even after successful clot retrieval. The G protein–coupled receptor GPR39 is expressed in brain peri-capillary pericytes, and has been implicated in microvascular regulation, but its role in stroke is unknown. We tested the hypothesis that GPR39 plays a protective role after stroke, in part due to preservation of microvascular perfusion. We generated GPR39 knockout (KO) mice and tested whether GPR39 gene deletion worsens capillary blood flow and exacerbates brain injury and functional deficit after focal cerebral ischemia. Stroke was induced in male and female GPR39 KO and WT littermates by 60-min middle cerebral artery occlusion (MCAO). Microvascular perfusion was assessed via capillary red blood cell (RBC) flux in deep cortical layers in vivo using optical microangiography (OMAG). Brain injury was assessed by measuring infarct size by 2,3,5-triphenyltetrazolium chloride staining at 24 h or brain atrophy at 3 weeks after ischemia. Pole and cylinder behavior tests were conducted to assess neurological function deficit at 1 and 3 weeks post-stroke. Male but not female GPR39 KO mice exhibited larger infarcts and lower capillary RBC flux than WT controls after stroke. Male GPR39 KO mice also exhibited worse neurologic deficit at 1 week post-stroke, though functional deficit disappeared in both groups by 3 weeks. GPR39 deletion worsens brain injury, microvascular perfusion, and neurological function after experimental stroke. Results indicate that GPR39 plays a sex-dependent role in re-establishing microvascular flow and limiting ischemic brain damage after stroke. [ABSTRACT FROM AUTHOR]

Intracoronary administration of drugs allows to achieve the fastest possible effect in interventional cardiology. This allows to avoid all the biological filters of the body and achieve the required concentration of the active substance at the injection site. Also, given the local action, systemic side effects are nearly absent. The aim. To study the literature data of the leading countries of the world in the field of intracoronary drug administration. To analyze the experience of different centers on the use of various medications in the treatment of the phenomenon of distal microembolization. Results. One of the first drugs administered intracoronary was streptokinase for the treatment of acute myocardial infarction. After that, it became clear that this method of delivering drugs is possible and can be used. With the beginning of the treatment of acute coronary syndromes by stenting, one of the possible complications arose in the form of no-reflow. At the same time, realizing that this is a local problem, they began to use the possibility of intracoronary administration of drugs to treat this phenomenon. The main advantage of this method is quick response to drug administration. Today, the drugs of choice in the treatment of no-reflow are verapamil, adenosine, nitroprusside, adrenaline. On the other hand, probably the most common drug that is administered intracoronary is nitroglycerin. It is used as a vasodilator in the event of spasm of the coronary arteries. Subsequently, it has been recommended to deliver drugs via a microcatheter or aspiration catheter to achieve even more selective effect in the area of the affected vessel, and this also minimizes drug loss due to coronary reflux into the aortic sinuses while usinga guiding catheter. Work is also underway on the use of intracoronary insulin in acute coronary syndrome in order to reduce the area of damage in myocardial infarction. It is also very promising to study the introduction of stem cells directlyinto the myocardium through a microcatheter in order to regenerate the myocardium after a heart attack. Conclusions. Intracoronary administration of drugs allows to achieve the maximum effect in the shortest possible time. Today, many drugs can be used in this way, starting from the treatment of the phenomenon of distal microembolization and ending with myocardial regeneration after myocardial infarction.

Introduction: The focus of this research was to explore the link between CRP (C-reactive protein) /albumin ratio (CAR), a novel inflammatory response marker, and no-reflow (NR) phenomena in non-ST elevation myocardial infarction (non-STEMI) patients during percutaneous coronary intervention (PCI). Methods: The current study recruited 209 non-STEMI participants who underwent PCI. The patients were divided into two groups based on their post-intervention Thrombolysis in Myocardial Infarction (TIMI) flow grade; those with and without NR. Results: In all, 30 non-STEMI patients (6.9%) had NR after PCI. CAR values were substantially greater in the NR group. The CAR was identified to be a determinant of the NR (OR: 1.250, 95% CI: 1.033-1.513, P=0.02), although CRP and albumin were not independently related with NR in the multivariate analysis. In our investigation, low density lipoprotein-cholesterol levels and high thrombus burden were also predictors of the occurrence of NR. According to receiver operating characteristic curve evaluation, the optimal value of CAR was>1.4 with 60% sensitivity and 47% specificity in detecting NR in non-STEMI patients following PCI. Conclusion: To the best of knowledge, this is the first investigation to demonstrate that the CAR, a new and useful inflammatory marker, can be utilized as a predictor of NR in patients with non-STEMI prior to PCI.

Background: In patients with ST-segment elevation myocardial infarction (STEMI), primary percutaneous coronary intervention (PCI) tries to reestablish coronary flow and ensure effective cardiac reperfusion. An independent predictor of no-reflow is a large thrombus load. Objective: This investigation sought to determine if the red cell distribution width (RDW) and neutrophil-lymphocyte ratio (NLR) were reliable indicators of excessive thrombus load on coronary angiography. Patients and methods: Two-hundred patients, with STEMI managed by primary PCI within 12 hours from chest pain onset, were divided into group A with high thrombus burden (Thrombolysis in myocardial infarction (TIMI) thrombus grade 4-5) and group B with low thrombus burden (TIMI thrombus grade 1-3). Results: One-hundred and seventeen patients (58.5%) had a high thrombus burden (group A). They had more mean number of cardiovascular disease (CVD) risk factors (2.4 ±0.99 versus 2.06 ±1.06, p=0.02), longer pain to balloon time (PTB) (151.28 ±42.05 versus116.99 ±43.16 minutes, p<0.001), higher mean Killip class (1.49±0.73 versus 1.28±0.6, p=0.03), higher RDW (18.99±1.55 versus 14.03±1.52, p<0.001), and higher NLR (5.93±1.39 versus 4.08±0.93 p<0.001) compared to group B. Independent predictors of high thrombus burden were RDW (OR: 4.06, p<0.001), NLR (OR: 1.35, p= 0.04), number of CVD risk factors (OR: 1.62, p= 0.01), and PTB time (OR: 1.02, p<0.001). Cut-off values to predict high thrombus burden were 16% for RDW and 4.55 for NLR. Conclusions: Rapid identification of RDW more than 16% or NLR more than 4.55, could predict a high thrombus burden. [ABSTRACT FROM AUTHOR]

Background: Stress hyperglycemia (SHG) is related to an increased risk of mortality in diabetic patients with ST elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PPCI). However, data are limited in non-diabetic patients especially in patients with multivessel disease (MVD). Methods and Results: In this retrospective study, 742 non-diabetic patients with STEMI and MVD were divided into SHG group and non-SHG group. The overall incidence of SHG was 24.9%. The incidence of no-reflow (NR) phenomenon (18.4% vs 11.8%; P =.024) and in-hospital mortality (1.6% vs.2%; P =.020) in SHG group were significantly higher than those in non-SHG group. SHG was associated with 30-day MACE (hazard ratio, 4.265; 95% confidence interval (CI), 1.354–13.439; P =.013), but not 1-year. Multivariate logistic analysis showed that SHG (odds ratio: 1.691, 95% CI: 1.072–2.667, P =.024) was an independent predictor of NR. If complete revascularization (CR) was performed during PPCI, the incidence of NR would be significantly higher. Conclusion: In non-diabetic patients with STEMI and MVD, SHG is associated with increased SF-NR and short-term adverse events, and CR during PPCI further increases the risk of NR. [ABSTRACT FROM AUTHOR]

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Objective To investigate the predictive value of serum plasminogen activator inhibitor-1(PAI-1) and retinol-binding protein 4(RBP4) levels for patients with acute ST-segment elevation myocardial infarction (STEMI) with‐ out reflow after percutaneous coronary intervention (PCI). Methods Totally 129 STEMI patients were selected as the STEMI group. According to the blood flow grading of thrombolysis therapy after PCI, they were divided into the no-reflow group (38 cases) and the reflow group (91 cases), and 55 healthy subjects were selected as the control group during the same period. Clinical data of STEMI patients were collected, and serum levels of PAI-1 and RBP4 were detected by en‐ zyme-linked immunosorbent assay. The predictive value of serum PAI-1 and RBP4 levels in patients with STEMI without reflow after PCI was analyzed by receiver operating characteristic (ROC) curve. Results Compared with the control group, the serum levels of PAI-1 and RBP4 in STEMI group increased (all P<0. 05). Compared with the reflow group, the serum levels of PAI-1 and RBP4 in no-reflow group increased (all P<0. 05). Multivariate Logistic regression analysis showed that the increase of age and the increase of LDL cholesterol, PAI-1 and RBP4 were independent risk factors for noreflow after PCI in STEMI patients (all P<0. 05), and the increase of left ventricular ejection fraction was a protective fac‐ tor (P<0. 05). ROC curve analysis showed that the area under the curve of serum PAI-1 and RBP4 levels was greater than that of PAI-1 and RBP4 alone in predicting no-reflow of STEMI patients after PCI (both P<0. 05). Conclusion The in‐ creased serum levels of PAI-1 and RBP4 in STEMI patients are associated with no-reflow after PCI, and the serum PAI-1 combined with RBP4 has a high value in predicting no-reflow after PCI. [ABSTRACT FROM AUTHOR]

Shenlian (SL) extract has been proven to be effective in the prevention and treatment of atherosclerosis and myocardial ischemia. However, the function and molecular mechanisms of SL on coronary artery no‐reflow have not been fully elucidated. This study was designed to investigate the contribution of SL extract in repressing excessive mitochondrial autophagy to protect the mitochondrial function and prevent coronary artery no‐reflow. The improvement of SL on coronary artery no‐reflow was observed in vivo experiments and the molecular mechanisms were further explored through vitro experiments. First, a coronary artery no‐reflow rat model was built by ligating the left anterior descending coronary artery for 2 hr of ischemia, followed by 24 hr of reperfusion. Thioflavin S (6%, 1 ml/kg) was injected into the inferior vena cava to mark the no‐reflow area. Transmission electron microscopy was performed to observe the cellular structure, mitochondrial structure, and mitochondrial autophagy of the endothelial cells. Immunofluorescence was used to observe the microvascular barrier function and microvascular inflammation. Cardiac microvascular endothelial cells (CMECs) were isolated from rats. The CMECs were deprived of oxygen–glucose deprivation (OGD) for 2 hr and reoxygenated for 4 hr to mimic the Myocardial ischemia‐reperfusion (MI/R) injury‐induced coronary artery no‐reflow in vitro. Mitochondrial membrane potential was assessed using JC‐1 dye. Intracellular adenosine triphosphate (ATP) levels were determined using an ATP assay kit. The cell total reactive oxygen species (ROS) levels and cell apoptosis rate were analyzed by flow cytometry. Colocalization of mitochondria and lysosomes indirectly indicated mitophagy. The representative ultrastructural morphologies of the autophagosomes and autolysosomes were also observed under transmission electron microscopy. The mitochondrial autophagy‐related proteins (LC3II/I, P62, PINK, and Parkin) were analyzed using Western blot analysis. In vivo, results showed that, compared with the model group, SL could reduce the no‐reflow area from 37.04 ± 9.67% to 18.31 ± 4.01% (1.08 g·kg−1 SL), 13.79 ± 4.77% (2.16 g·kg−1 SL), and 12.67 ± 2.47% (4.32 g·kg−1 SL). The extract also significantly increased the left ventricular ejection fraction (EF) and left ventricular fractional shortening (FS) (p < 0.05 or p < 0.01). The fluorescence intensities of VE‐cadherin, which is a junctional protein that preserves the microvascular barrier function, decreased to ~74.05% of the baseline levels in the no‐reflow rats and increased to 89.87%(1.08 g·kg−1SL), 82.23% (2.16 g·kg−1 SL), and 89.69% (4.32 g·kg−1 SL) of the baseline levels by SL treatment. SL administration repressed the neutrophil migration into the myocardium. The oxygen–glucose deprivation/reoxygenation (OGD/R) model was induced in vitro to mimic microvascular ischemia–reperfusion injury. The impaired mitochondrial function after OGD/R injury led to decreased ATP production, calcium overload, the excessive opening of the Mitochondrial Permeability Transition Pore, decreased mitochondrial membrane potential, and reduced ROS scavenging ability (p < 0.05 or p < 0.01). The normal autophagosomes (double‐membrane vacuoles with autophagic content) in the sham group were rarely found. The large morphology and autophagosomes were frequently observed in the model group. By contrast, SL inhibited the excessive activation of mitochondrial autophagy. The mitochondrial autophagy regulated by the PINK/Parkin pathway was excessively activated. However, administration of SL prevented the activation of the PINK/Parkin pathway and inhibited excessive mitochondrial autophagy to regulate mitochondrial dysfunction. Results also demonstrated that mitochondrial dysfunction stimulated endothelial cell barrier dysfunction, but Evans blue transmission was significantly decreased and transmembrane resistance was increased significantly by SL treatment (p < 0.05 or p < 0.01). Carbonylcyanide‐3‐chlorophenylhydrazone (CCCP) could activate the PINK/Parkin pathway. CCCP reversed the regulation of SL on mitochondrial autophagy and mitochondrial function. SL could alleviate coronary artery no‐reflow by protecting the microvasculature by regulating mitochondrial function. The underlying mechanism was related to decreased mitochondrial autophagy by the PINK/Parkin pathway. [ABSTRACT FROM AUTHOR]

Summary: Background: Coronary microvascular obstruction also known as no-reflow phenomenon is a major issue during myocardial infarction that bears important prognostic implications. Alterations of the microvascular network remains however challenging to assess as there is no imaging modality in the clinics that can image directly the coronary microvascular vessels. Ultrasound Localization Microscopy (ULM) imaging was recently introduced to map microvascular flows at high spatial resolution (∼10 μm). In this study, we developed an approach to image alterations of the microvascular coronary flow in ex vivo perfused swine hearts. Methods: A porcine model of myocardial ischemia-reperfusion was used to obtain microvascular coronary alterations and no-reflow. Four female hearts with myocardial infarction in addition to 6 controls were explanted and placed immediately in a dedicated preservation and perfusion box manufactured for ultrasound imaging. Microbubbles (MB) were injected into the vasculature to perform Ultrasound Localization Microscopy (ULM) imaging and a linear ultrasound probe mounted on a motorized device was used to scan the heart on multiple slices. The coronary microvascular anatomy and flow velocity was reconstructed using dedicated ULM algorithms and analyzed quantitatively. Findings: We were able to image the coronary microcirculation of ex vivo swine hearts at a resolution of tens of microns and measure flow velocities ranging from 10 mm/s in arterioles up to more than 200 mm/s in epicardial arteries. Under different aortic perfusion pressures, we measured in large arteries of a subset of control hearts an increase of flow velocity from 31 ± 11 mm/s at 87 mmHg to 47 ± 17 mm/s at 132 mmHg (N = 3 hearts, P

Microvascular obstruction (MVO) of coronary arteries promotes an increase in mortality and major adverse cardiac events in patients with acute myocardial infarction (AMI) and percutaneous coronary intervention (PCI). Intramyocardial hemorrhage (IMH) is observed in 41–50% of patients with ST-segment elevation myocardial infarction and PCI. The occurrence of IMH is accompanied by inflammation. There is evidence that microthrombi are not involved in the development of MVO. The appearance of MVO is associated with infarct size, the duration of ischemia of the heart, and myocardial edema. However, there is no conclusive evidence that myocardial edema plays an important role in the development of MVO. There is evidence that platelets, inflammation, Ca2+overload, neuropeptide Y, and endothelin-1 could be involved in the pathogenesis of MVO. The role of endothelial cell damage in MVO formation remains unclear in patients with AMI and PCI. It is unclear whether nitric oxide production is reduced in patients with MVO. Only indirect evidence on the involvement of inflammation in the development of MVO has been obtained. The role of reactive oxygen species (ROS) in the pathogenesis of MVO is not studied. The role of necroptosis and pyroptosis in the pathogenesis of MVO in patients with AMI and PCI is also not studied. The significance of the balance of thromboxane A2, vasopressin, angiotensin II, and prostacyclin in the formation of MVO is currently unknown. Conclusive evidence regarding the role of coronary artery spasm in the development of MVhasn’t been established. Correlation analysis of the neuropeptide Y, endothelin-1 levels and the MVO size in patients with AMI and PCI has not previously been performed. It is unclear whether epinephrine aggravates reperfusion necrosis of cardiomyocytes. Dual antiplatelet therapy improves the efficacy of PCI in prevention of MVO. It is unknown whether epinephrine or L-type Ca2+ channel blockers result in the long-term improvement of coronary blood flow in patients with MVO.

Aim and Objectives: The aim of the study was to compare the effectiveness of pre-procedural Statin therapy and Statin/Ezetimibe in reducing the no-reflow phenomenon in patients undergoing primary PCI. Patients and Methods: The study was carried out on 200 patients (age 55.86 6 11.32) presenting to Ain Shams university hospitals with ST-segment elevation Myocardial Infarction and received the standard of care management which is Primary PCI. The patients were assessed regarding the demographic data, risk factors, symptoms including characterization of chest pain, physical examination, 12 lead ECG, labs, Coronary angiography to identify the coronary anatomy, culprit vessel, TIMI flow score and MBG. Results: Our study compared 100 patients who received high intensity Statin/Ezetimibe combination before primary PCI and 100 patients who received high intensity statin only. Among the case group, 72% were smokers, 33% were diabetic and 24% were hypertensive, 94% presented with killip 1, 5 with killip 2, 1% with killip 3, 70% were anterior STEMI, 2% Lateral, 18% inferior and 10% posterior. Among the control group 75% were smokers, 18% were diabetic and 24% were hypertensive, 95 % presented with killip 1, 3% with killip 2, 2% with killip 3, 49% were anterior STEMI, 6% Lateral, 34% inferior and 11% posterior. The study revealed that there was no statistically significant difference between the two groups, group A (case group) and group B (control group) regarding the occurrence of no reflow, 7 no reflow patients in group A versus 8 in group B, with a P-value of 0.788. There was no significant difference between the two groups in the tissue perfusion post primary PCI as being assessed by TIMI flow classification and myocardial blush grade. Conclusion: Statin/Ezetimibe combination did not result in a significant reduction in the incidence of no-reflow in STEMI patients in comparison to Statins alone. Although the occurrence of MACE was less in the case group, the exact effect on inhospital MACE could not be detected due to the small number of total MACE in the study. Larger additional randomized studies are needed to establish the effect of preprocedural high-dose Statin/Ezetimibe combination therapy on angiographic results in patients who undergo primary PCI. [ABSTRACT FROM AUTHOR]

The goal of this investigation was to explore the relationship between serum uric acid/albumin ratio (UAR) and no-reflow (NR) in ST elevation myocardial infarction (STEMI) patients (n = 838) who underwent primary percutaneous coronary intervention (pPCI). Angiographic NR was defined as thrombolysis in myocardial infarction (TIMI) flows 0, 1, and 2 in the absence of coronary spasm or dissection. NR developed in 91 (10.9%) STEMI patients. Patients with NR had higher UAR and according to multivariable logistic regression models, a high UAR was an independent risk factor for NR. The area under the curve (AUC) value of the UAR was.760 (95%CI:.720-.801) in a receiver-operating characteristics curve (ROC) assessment. Notably, the UAR AUC value was greater than that of its components: albumin (AUC:.642) and serum uric acid (AUC:.637) (P <.05 for both comparisons). The optimum UAR value in detecting NR in STEMI patients was >1.21 with a sensitivity of 82% and a specificity of 67%. This was the first study to report that the UAR was independently associated with NR in STEMI patients who underwent pPCI. [ABSTRACT FROM AUTHOR]

Background: Primary percutaneous coronary intervention (pPCI) performed for STEMI may be complicated by the "no-reflow" phenomenon. Aims: A super-selective intracoronary injection of saline solution through a thrombus aspiration catheter (SALINE technique), was investigated for the treatment of no-reflow as compared with the standard care of therapy (SCT). Methods: Among the 1471 patients with STEMI undergoing pPCI between May 2015 and June 2020, 168 patients developed no-reflow. Primary endpoints were the incidence of ST-segment resolution (STR) ≥ 70% at 90 min after PCI and the rate of flow restoration (TIMI flow grade 3 with an MBG > 1). The secondary endpoint was the incidence of major adverse cardiac and cerebrovascular events at 3 years follow-up. Results: After propensity score matching analysis, patients treated with SALINE showed STR ≥ 70% in twelve out of the sixteen patients (75.0%), compared to only three patients out of the sixteen in the SCT control group (19.0%), (p < 0.004). SALINE was associated with a higher probability of final TIMI flow grade 3 with an MBG > 1, as shown in fourteen out of sixteen patients (87.5%), as compared to only seven out of sixteen patients in the SCT group (43.8%), (p < 0.03). MACCE at 3 years follow-up occurred in only one patient (6.3%) in the SALINE group, as compared to eight patients (50%) in the SCT group (p = 0.047). Conclusions: The SALINE technique showed to be a safe and effective strategy to reduce "no-reflow" in STEMI patients as assessed by significant STR, improvement of TIMI flow grade, and better 3-year outcomes. [ABSTRACT FROM AUTHOR]

Objective Coronary no-reflow during percutaneous conranary intervention (PCI) often results in the failure of ischemic myocardial reperfusion and major adverse cardiovascular events (MACE). The present study sought to evaluate whether the GRACE risk score can predict coronary no-reflow in STEMI patients undergoing PCI. Methods We consecutively recruited 1 118 patients with STEMI who were admitted to Gansu Provincial People’s Hospital and The First Affiliated Hospital of Xi’an Jiaotong University from January 2009 to December 2011. Main demographic data, cardiovascular risk factors, blood lipid and other biochemical indicators were recorded. Coronary angiography was performed by a radial artery approach using the standard Judkins technique. Coronary no-reflow was evaluated by at least two independent experienced cardiologists. The GRACE risk score was calculated with a computer program. All the cases were followed up by medical records, face-to-face interviews or telephone calls. Finally, we analyzed the predictive value of the GRACE risk score for coronary non-reflow and MACE in STEMI patients undergoing PCI. Results During a median period of 36 months, 58 of the 1 118 patients (5.2%) were lost to follow-up. Of the remaining 1 060 patients, 118 (11.1%) had no-reflow and 147 (13.9%) hadMACE. The GRACE score was higher in patients with no-reflow than those without no-reflow. Multivariate logistic regression established that the GRACE score was an independent predictor for coronary no-reflow (OR=1.034; P=0.002). And multivariate Cox analysis showed the GRACE score was an independent predictor of MACE. The area under the ROC curve for coronary no-reflow and MACE was 0.719 and 0.697, respectively. Kaplan-Meier analysis showed that the probability of rehospitalization for heart failure, reinfarction, all-cause death and cumulative cardiovascular events increased with the increase of the GRACE risk score. Conclusion The GRACE risk score is a readily available predictive scoring system for coronary no-reflow and MACE in STEMI patients. [ABSTRACT FROM AUTHOR]

Background: The no-reflow phenomenon refers to a failure to restore normal cerebral microcirculation despite brain large artery recanalization after acute ischemic stroke, which was observed over 50 years ago. Summary: Different mechanisms contributing to no-reflow extend across the endovascular, vascular wall, and extravascular factors. There are some clinical tools to evaluate cerebral microvascular hemodynamics and represent biomarkers of the no-reflow phenomenon. As substantial experimental and clinical data showed that clinical outcome was better correlated with reperfusion status rather than recanalization in patients with ischemic stroke, how to address the no-reflow phenomenon is critical. But effective treatments for restoring cerebral microcirculation have not been well established until now, so there is an urgent need for novel therapeutic perspectives to improve outcomes after recanalization therapies. Conclusion: Here, we review the occurrence of the no-reflow phenomenon after ischemic stroke and discuss its impact, detection method, and therapeutic strategies on the course of ischemic stroke, from basic science to clinical findings. [ABSTRACT FROM AUTHOR]

Background: There have been a big number of studies assessing the efficacy of delayed coronary artery stenting (DCAS) in the prevention of no-reflow microvasculature injury compared to the standard immediate coronary artery stenting (ICAS) in ST-segment elevation myocardial infarction (STEMI). However, the results of these studies are contradictory in a lot of ways. Aim: To summarize studies on the assessment of DCAS in the prevention of no-reflow compared to the standard ICAS. Materials and methods: We performed a systematic literature search in PubMed, Google Scholar, and eLIBRARY.RU databases. The analysis included 17 studies with a total sample of 3505 patients. The comparative analysis included angiography-based endpoints prevalence of no-reflow (thrombolysis in myocardial infarction, TIMI 3 and myocardial blush grade, MBG 2, corrected TIMI frame count, CTFC) and clinical endpoints of all-cause mortality, cardiovascular mortality, major adverse cardiac events (MACE), recurrent myocardial infarction and recurrent revascularization. In addition, the analysis included the assessment of ST-elevation resolution, left ventricular ejection fraction values in the delayed post-intervention period and between-group differences. Results: The no-reflow phenomenon was significantly less frequent in the DCAS groups for the following parameters: epicardial flow TIMI 3 (odds ratio (OR) 2.00; 95% confidence interval (CI) 1.492.69; p 0.00001; I = 16%), myocardial perfusion MBG 2 (OR 4.69; 95% CI 1.9811.14; p = 0.0005; I = 59%), CTFC (mean difference (MD) 10.29; 95% CI 0.9619.62; p = 0.03; I = 96%). The analysis of secondary endpoints showed that MACE were less frequent in the DCAS groups (OR 1.29; 95% CI 1.041.60; p = 0.02; I = 42%), the difference becoming more significant in the studies with high initial thrombotic burden (TTG 3) (OR 1.83; 95% CI 1.282.62; p = 0.0009; I = 41%). The most clinically significant decrease of the MACE rate was found in 5 studies (n = 656) with high initial thrombotic burden (TTG 3) and mean time to repeated intervention from 4 to 7 days (OR 3.15; 95% CI 1.865.32; p 0.0001; I = 0%). The reverse trend for a benefit in the ICAS group was observed in the studies with a high initial thrombotic burden (TTG 3) and mean time to recurrent intervention of 48 hours (OR 0.60; 95% CI 0.301.19; p = 0.14; I = 20%). The ICAS and DCAS groups did not differ in overall mortality (p = 0.31), cardiovascular mortality (p = 0.49), repeated revascularization (p = 0.66), and ST resolution of 70% (p = 0.65). In the DCAS groups, there was an obvious trend to lower incidence of recurrent myocardial infarction (OR 1.28; 95% CI 0.951.73; p = 0.10; I = 0%), as well as to higher myocardial mass during the deferred analysis of left ventricular ejection fraction (OR -0.79; 95% CI -1.61 -0.04; p = 0.06; I = 36%). Conclusion: Deferred coronary artery stenting is an effective method for prevention of no-reflow. In patients with extended coronary thrombosis (TTG 3) and STEMI, the DCAS technique with time to recurrent intervention of 4 to 7 days decreases the probability of MACE compared to that with immediate stenting of the index coronary artery.