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Recanalization therapies based on reopening of the occluded great vessel after ischemic stroke are the only treatment options available today and have made significant advances in improving clinical function. However, providing recanalization does not always result in tissue survival and positive functional recovery. One of the various reasons underlying this incompatibility is the "no-reflow" phenomenon. This term was first used in the cardiology literature to describe the situation in which parenchymal tissue reperfusion was not achieved despite recanalization. In the following period, the existence of a similar process in experimental ischemic stroke models, in which the blood flow did not improve at the microcirculation level despite the opening of the occluded great vessels, was proven. Some of the causes of this phenomenon, which has been known in experimental studies for many years but whose pathophysiology has not been fully elucidated, are the aggregation of blood elements, increase in blood viscosity, contraction of pericytes -a component of neurovascular unit, narrowing of microvessels, and activation of inflammatory processes. Since this phenomenon causes the success of recanalization treatments not to be at the desired level, its pathophysiology should be fully elucidated, especially through clinical studies. Cocktail therapies to improve reperfusion besides recanalization therapy in ischemic stroke can prevent the "no-reflow" phenomenon.

Background Deferred stenting, despite being successful in early studies, showed no benefit in recent trials. However, these trials were testing routine deferral; not in patients with heavy thrombus burden. Results This is a prospective, Randomized Clinical Trial that included 150 patients who presented with STEMI, patients were allocated into three equal groups after the coronary angiography ± primary intervention and before stenting of the culprit lesion; group (A) included 50 patients with early deferral of stenting, group (B) included 50 patients with late deferral and group (C) included 50 patients with immediate stenting. No-reflow was significantly higher in group C, while Final TIMI flow grade 3 and MBG grade 3 were significantly higher in group A and B than group C; p = 0.019 and p p = 0.029). Conclusions Stent deferral was proved to be better than immediate stenting after recanalization of IRA, in achieving TIMI III flow, reducing risk of 6 months MACE, and restoration of myocardial function in a subset of STEMI patients presenting with large thrombus burden. While, no significant difference was found between both deferral times in final TIMI flow, or clinical outcomes.

Introduction: No reflow phenomenon following primary percutaneous coronary intervention (PCI) is a strong predictor of mortality. Platelet/lymphocyte ratio (PLR) is an indicator of long-term outcome in ischemic heart disease patients. The aim of this study was to assess the relation between PLR measured on admission and the occurrence of no-reflow phenomenon in patients presenting with acute ST-segment elevation myocardial infarction (STEMI) managed by primary PCI. Methods: This was a prospective study including 100 patients with acute STEMI managed by primary PCI. Venous blood samples were obtained on admission to assess hemoglobin level, platelet count, and lymphocyte count. Thrombolysis in myocardial infarction (TIMI) flow grade, myocardial blush grade (MBG), and TIMI thrombus scale were assessed immediately following revascularization. During hospital stay, peak creatinine kinase MB fraction (CK-MB) was recorded, and transthoracic echocardiography was performed to assess left ventricular ejection fraction (LVEF). Results: Patients were divided into two groups based on the TIMI flow grade following PCI: Normal coronary flow group (TIMI 3 flow grade, n = 71) and reduced coronary flow (no-reflow) group (TIMI 0, 1, and 2, n = 29). There was a larger proportion of diabetic patients in the no-reflow group (P = 0.028). In addition, patients in the no-reflow group had a more advanced Killip class on presentation (P = 0.001), a lower LVEF (P < 0.0001), and a significantly higher PLR 213.66 ± 115.35 versus 122.81 ± 59.82 (P < 0.0001). PLR was significantly higher in patients with lower TIMI flow grade and lower MBG (P < 0.0001 for both). A significant correlation existed generally between PLR and peak CK-MB more in the no-reflow group (r = 0.471, P = 0.01). A PLR more than 108.08 predicted no-reflow with a sensitivity of 53%, a specificity of 86%, PPV of 80.%, and a NPV of 43.1% (AUC = 0.73). PLR was found to be an independent predictor of no-reflow multivariate regression analysis for predictors of no-reflow (ß = 0.0023, 9% CI = 0.0014–0.0032, P < 0.0001). Conclusions: PLR measured on admission is elevated in patients with STEMI who develop no-reflow during primary PCI. PLR is an independent predictor of no-reflow in such patients.

Objectives: The no-reflow phenomenon occurs in 25% of patients with ST elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PCI), and may be associated with adverse outcomes. The aim of our study was to detect novel predictors of no-reflow phenomenon and the resulting adverse long term outcomes. Methods: We enrolled 400 STEMI patients undergoing primary PCI; 228 patients had TIMI flow 3 after PCI (57%) and the remaining 172 patients had TIMI flow 5.6 ng/mL (OR = 1.040, 95% CI: 1.001–1.080, P = 0.04), diabetes mellitus (OR = 4.401, 95% CI: 1.081–17.923, P = 0.04) and heavy thrombus burden (OR = 16.915, 95% CI: 5.055–56.602, P 0.21, FAR >11.56, and AIP >0.52 could be considered as novel powerful independent predictors (OR = 3.357, 95% CI: 2.288–4.927, P

Objective: To determine the efficacy of intracoronary verapamil vs adenosine in restoration of coronary blood flow, post PCI in patients with No-Reflow. Study Design: Double blind (patient/operator blind) randomized control trial. Place and Duration of Study: Cath lab of AFIC & NIHD Rawalpindi, from Feb 2019 to Aug 2019. Methodology: A total of ninety (n=90) patients of either gender between age 25-80 years of age who underwent angioplasty for STEMI/NSTEMI demonstrating No-Reflow (thrombolysis in myocardial infarction 0,1,2) post PCI were enrolled and were randomized into two groups. Group A received verapamil 500 µg in 10 ml heparinized saline, given slowly over 1 minute and group B received adenosine 60 µg in 10 ml of heparinized saline, given quickly. After the administration of both drugs repeat angiogram was carried out and thrombolysis in Myocardial Infarction flow was assessed. Restoration of blood flow was defined as achievement of thrombolysis in myocardial infarction 3 grade. Results: Efficacy (restoration of thrombolysis in Myocardial Infarction grade 3) was better with intracoronary administration of verapamil when compared with intracoronary administration 2 of adenosine (84.4% vs 80%). The difference was, however, not statistically significant (p=0.581). Conclusion: Efficacy (restoration of thrombolysis in myocardial infarction grade 3) was not statistically significant between intracoronary administration of verapamil and adenosine in no-reflow cases after PCI in patients with STEMI/NSTEMI.

Recently, there has been a positive trend to reduce mortality from myocardial infarction. One of the reasons for such dynamics is the development of angiographic service in our country and the increase in the number of primary percutaneous coronary interventions. One of the most serious complications of endovascular interventions affecting the prognosis is the development of the phenomenon of slow or unrecoverable blood flow (≪slow/no-reflow≫ phenomenon). The reason for the development of this phenomenon is associated, first of all, with distal embolization by thrombotic masses and fragments of atherosclerotic plaque. In order to prevent this complication, manual thromboextraction was developed – the aspiration of thrombotic masses from the infarct-related artery. The manual thrombus aspiration has not been proven effective in a number of large randomized trials. In addition to the lack of influence on the prognosis, the method of manual thrombus aspiration significantly more often led to the development of ischemic strokes and currently should not be routinely carried out. Another method of preventing the phenomenon of delayed or unrecoverable blood flow is the use of glycoprotein IIb/IIIa receptor inhibitors which is, in contrast to the instrumental method, effective and relatively safe. According to a number of large randomized trials, drug treatment of this complication influences life expectancy in patients with ST-elevation myocardial infarction. At a time when there is already a meta-analysis on the routine use of glycoprotein IIb/IIIa receptor inhibitors during primary percutaneous coronary intervention and their positive impact on survival, in our country, unfortunately, the importance of these drugs is underestimated and according to the register they are used only in 3% of patients with ST-segment elevation myocardial infarction. This review presents studies and comparisons of glycoprotein IIb/IIIa receptor inhibitors existing on the market.

Aim: The aim of this study was to investigate the relationship between no-reflow (no-RF), reflow (RF), and the P-wave time index in patients undergoing percutaneous coronary intervention (PCI) with a diagnosis of acute myocardial infarction (AMI) due to total occlusion. Methods: This study included a total of 272 AMI patients with no-RF (110 patients) and RF (162 patients). Results: The no-RF group had higher values of mean maxPWTpostPCI(94.95 ± 15.61 vs. 117.86 ± 12.06, P < 0.001), minPWTpostPCI(54.21 ± 12.13 vs. 67.31 ± 11.79, P < 0.001), and PWDpostPCI(39.14 ± 12.55 vs. 50.91 ± 11.9, P < 0.001) during the post-PCI period. According to multivariate logistic regression analysis, maxPWTpostPCI(odds ratio [OR]: 1.103, 95% confidence interval [CI]: 1.049–1.160, P < 0.001), minPWTpostPCI(OR: 1.055, 95% CI: 1.011–1.101, P = 0.0014), and PWDpostPCI(OR: 1.107, 95% CI: 1.037–1.181, P = 0.002) were the independent predictors of RF after PCI. ROC curve analyses demonstrated that the optimal cutoff values for maxPWTpostPCI, minPWTpostPCI, and PWDpostPCIfor predicting no-RF were 112.95 ms (area under the curve [AUC]: 0.852, 95% CI: 0.807–0.898, P < 0.001, sensitivity 70%, specificity 85.2%), 62.66 ms (AUC: 0.650, 95% CI: 0.585–0.716, P < 0.001, sensitivity 54.5%, specificity 72.8%), and 43.43 ms (AUC: 0.782, 95% CI: 0.727–0.837, P < 0.001, sensitivity 75.5%, specificity 60.5%), respectively. Conclusions: Prolonged maxPWTpostPCI, maxPWTpostPCI,and PWDpostPCIare independent predictors that differentiate no-RF from RF in patients with AMI after PCI and can be used in the follow-up of no-RF patients during the post-PCI period.

Context: The possible pathophysiological mechanisms of no-reflow are ischemic injury, reperfusion injury, endothelial injury, distal thromboembolism, etc., Moreover, no-reflow can also remarkably increase the risks of acute myocardial infarction, heart failure, malignant arrhythmia, pericardial tamponade, and even death. Aims: The aim was to evaluate the efficacy of sodium nitroprusside combined with verapamil in the treatment of no-reflow. Settings and Design: From December 2016 to December 2017, 100 patients with no-reflow during coronary intervention in our hospital were selected and randomly divided into two groups: treatment group (50 cases) treated by sodium nitroprusside combined with verapamil and control group (50 cases) treated with sodium nitroprusside treatment alone. Subjects and Methods: The blood flow grading of the two groups according to a thrombolysis test in myocardial infarction (TIMI) was compared and analyzed, and the incidence of cardiovascular adverse events was compared in the 6-month period following the operation. Statistical Analysis Used: SPSS 17.0 (IBM, America) was employed in all calculations. Quantitative data were expressed as mean ± standard deviation, and intergroup comparison was calculated using a two-tailed t-test. Qualitative data were presented in percentages, and intergroup comparison was performed with Chi-square test.P < 0.05 was considered statistically significant. Results: The patients with TIMI Grade III blood flow in the treatment group were significantly more than those in the control group after medication, and the difference was statistically significant (P < 0.05). In the following 6-month period after the operation, the incidence of cardiovascular adverse events in the treatment group was 6.00% (3/50), which was lower than that in the control group 18.0% (9/50), with statistically significant difference (P < 0.05). Conclusions: Sodium nitroprusside combined with verapamil can significantly improve the no-reflow following coronary interventional therapy and reduce the incidence of adverse cardiovascular events.

Reperfusion does not only salvage ischaemic myocardium but can also cause additional cell death which is called lethal reperfusion injury. The time of reperfusion is often accompanied by ventricular arrhythmias, i.e. reperfusion arrhythmias. While both conditions are seen as separate processes, recent research has shown that reperfusion arrhythmias are related to larger infarct size. The pathophysiology of fatal reperfusion injury revolves around intracellular calcium overload and reactive oxidative species inducing apoptosis by opening of the mitochondrial protein transition pore. The pathophysiological basis for reperfusion arrhythmias is the same intracellular calcium overload as that causing fatal reperfusion injury. Therefore both conditions should not be seen as separate entities but as one and the same process resulting in two different visible effects. Reperfusion arrhythmias could therefore be seen as a potential marker for fatal reperfusion injury.

Background Acute myocardial infarction is a leading cause of morbidity and mortality worldwide. It occurs when irreversible myocardial cell damage or death occurs. ST-segment elevation myocardial infarction (STEMI) is the most serious presentation of atherosclerotic coronary artery disease. STEMI results from the occlusion of a major coronary artery. Primary percutaneous coronary intervention (PCI) is the preferred reperfusion strategy. It should be performed by an experienced team within the shortest time possible from the first medical contact. Hypothesis Increased mortality risk and no-reflow in STEMI patients with epicardial adipose tissue thickness (EAT) more than 5 mm compared to STEMI patients with EAT less than 5 mm. Methods This study was conducted on 113 patients who presented to the cardiology department of Ain Shams university hospital with the first STEMI and underwent primary PCI. Medical treatment for STEMI was given to all subjects as per the guidelines. All patients underwent an echocardiographic evaluation of epicardial adipose tissue and left ventricular ejection fraction. Patients were divided into two groups using epicardial adipose tissue thickness of 5 mm as a cutoff point; this number was derived from the ROC curve. Group I: Included patients with EAT thickness less than 5 mm, including 44 patients (38.9%). Group II: Included patients with EAT thickness greater than 5 mm, including 69 patients (61.1%). Results The current study showed that epicardial fat thickness significantly correlated with the no-reflow phenomenon in the cath lab and overall prognosis in patients with STEMI. Conclusion Increased EAT thickness may be an independent predictor of the no-reflow phenomenon and mortality. Therefore, our study emphasizes that EAT thickness measured by echocardiography may provide additional and substantial information on the risk of no-reflow and mortality in STEMI patients.

Background: The coronary atherosclerotic burden in patients with ST-segment elevation myocardial infarction (STEMI) has been identified as the main predictor of prognosis. However, the association of lipoprotein(a) [Lp(a)], a well-established proatherogenic factor, with atherosclerotic burden in patients with STEMI is unclear.Methods: In total, 1,359 patients who underwent percutaneous coronary intervention (PCI) for STEMI were included in analyses. Three prespecified models with adjustment for demographic parameters and risk factors were evaluated. Generalized additive models and restricted cubic spline analyses were used to assess the relationships of Lp(a) with Gensini scores and the no-reflow phenomenon. Kaplan–Meier curves were generated to explore the predictive value of Lp(a) for long-term all-cause mortality. Furthermore, mRNA expression levels of LPA in different groups were compared using the GEO database.Results: Patients in the highest tertile according to Lp(a) levels had an increased incidence of heart failure during hospitalization. Furthermore, patients with high levels of Lp(a) (>19.1 mg/dL) had sharply increased risks for a higher Gensini score (Pfor trend = 0.03) and no-reflow (Pfor trend = 0.002) after adjustment for demographic parameters and risk factors. During a median follow-up of 930 days, 132 deaths (9.95%) were registered. Patients with high levels of Lp(a) (>19.1 mg/dL) had the worst long-term prognosis (Pfor trend < 0.0001). In a subgroup analysis, patients with higher Lp(a) still had the highest all-cause mortality. Additionally, the mRNA expression levels of LPA in patients with STEMI with lower cardiac function were higher than those in other groups (P = 0.003). A higher coronary atherosclerotic burden was correlated with higher LPA expression (P = 0.01).Conclusion: This study provides the first evidence that Lp(a) (at both the protein and mRNA levels) is independently associated with coronary atherosclerotic lesions and prognosis in patients with STEMI treated with PCI.Clinical Trial Registration:http://www.chictr.org.cn/index.aspx, identifier: ChiCTR1900028516.

Background Vitamin D deficiency is a prevalent condition that is found in about 30–50% of the general population, and it is increasing as a new risk factor for coronary artery disease. Our study aimed to evaluate the relationship of serum vitamin D levels with coronary thrombus burden, Thrombolysis In Myocardial Infarction flow grade, and myocardial blush grade in patients managed by primary percutaneous coronary intervention for their first acute ST-segment elevation myocardial infarction. Results Eighty patients were included in the study with their first acute ST-segment elevation myocardial infarction and were managed by primary percutaneous coronary intervention. According to the serum concentrations of vitamin D, the study population was divided into 2 groups: group A with abnormal vitamin D levels less than 30 ng/ml (50 patients) and group B with normal vitamin D levels equal to or more than 30 ng/ml (30 patients). Angiographic data was recorded before and after coronary intervention. On comparing thrombus grade and initial and post-procedural Thrombolysis In Myocardial Infarction flow between both groups of patients, there was no significant difference (p = 0.327, p = 0.692, p = 0.397). However, myocardial blush grade was better in patients with normal vitamin D levels (p = 0.029) without a significant correlation between vitamin D concentration values and myocardial blush grade (r = 0.164, p = 0.146). Conclusions Patients with first acute ST-segment elevation myocardial infarction and normal vitamin D levels undergoing primary percutaneous coronary intervention had better myocardial blush grade and more successful microvascular reperfusion in comparison with patients with abnormal vitamin D levels. There was no significant difference between the normal and abnormal vitamin D groups regarding the coronary thrombus grade and Thrombolysis In Myocardial Infarction flow.

We describe the case of a middle-aged man undergoing three-vessel coronary angioplasty due to unstable angina. Attempt to predilate a calcified lesion in the left circumflex artery with a semi-compliant balloon, inflated above the rated burst pressure, resulted in balloon rupture. Subsequently, the patient developed ST elevations and became hemodynamically unstable; slow flow in the index vessel was noted. The complication was managed with vasopressor and respiratory support, plus forceful injections of warm saline. Thrombolysis in myocardial infarction (TIMI)-3 flow was eventually restored, and the rest of the procedure was completed uneventfully. Following retrieval of the device, a longitudinal tear in the balloon was observed. This mode of rupture is considered to be safer, when compared to circumferential or pin-hole rupture. Rupture can occur when a balloon is aggressively inflated above nominal pressures and against calcific lesions. The ensuing micro- and macrovascular complications, including slow-flow, no-reflow, vessel dissection or perforation, and intramural hematoma, may induce myocardial ischemia and ultimately cardiogenic shock, malignant arrhythmias, and cardiac arrest. Management should be swift, and relies on supportive measures, depending on the degree of complications caused by the rupture.

Background Despite evidence of a quite large beneficial effect of endovascular treatment (EVT) for ischemic stroke caused by anterior circulation large vessel occlusion, many patients do not recover even after complete recanalization. To some extent, this may be attributable to incomplete microvascular reperfusion, which can possibly be improved by antiplatelet agents and heparin. It is unknown whether periprocedural antithrombotic medication in patients treated with EVT improves functional outcome. The aim of this study is to assess the effect of acetylsalicylic acid (ASA) and unfractionated heparin (UFH), alone, or in combination, given to patients with an ischemic stroke caused by an intracranial large vessel occlusion in the anterior circulation during EVT. Methods MR CLEAN-MED is a multicenter phase III trial with a prospective, 2 × 3 factorial randomized, open label, blinded end-point (PROBE) design, which aims to enroll 1500 patients. The trial is designed to evaluate the effect of intravenous ASA (300 mg), UFH (low or moderate dose), both or neither as adjunctive therapy to EVT. We enroll adult patients with a clinical diagnosis of stroke (NIHSS ≥ 2) and with a confirmed intracranial large vessel occlusion in the anterior circulation on CTA or MRA, when EVT within 6 h from symptom onset is indicated and possible. The primary outcome is the score on the modified Rankin Scale (mRS) at 90 days. Treatment effect on the mRS will be estimated with ordinal logistic regression analysis, with adjustment for main prognostic variables. Secondary outcomes include stroke severity measured with the NIHSS at 24 h and at 5–7 days, follow-up infarct volume, symptomatic intracranial hemorrhage (sICH), and mortality. Discussion Clinical equipoise exists whether antithrombotic medication should be administered during EVT for a large vessel occlusion, as ASA and/or UFH may improve functional outcome, but might also lead to an increased risk of sICH. When one or both of the study treatments show the anticipated effect on outcome, we will be able to improve outcome of patients treated with EVT by 5%. This amounts to more than 50 patients annually in the Netherlands, more than 1800 in Europe, and more than 1300 in the USA. Trial registration ISRCT, ISRCTN76741621. Dec 6, 2017.

Background No-reflow occurs in 3–4% of all percutaneous coronary interventions (PCIs) and has a strong negative impact on clinical outcomes of acute coronary syndrome. (ACS). Therefore, the discovery of a biomarker that can early predict the occurrence of no-reflow has great clinical significance. Multiple factors including platelet activation are relevant to no-reflow. Calprotectin is found to be a biomarker of plaque instability and is identified to be a novel diagnostic and prognostic biomarker of cardiovascular diseases. But theThe association of plasma calprotectin with platelet activation and no-reflow phenomenon in acute coronary syndromeACS is not clear. Methods In this prospective study performed at Yantai Yuhuangding Hospital from 2017 to 2018, a total of 176 Chinese patients with acute coronary syndromeACS who had undergone percutaneous coronary interventionsPCIs were recruited consecutively, aged from 30 to 88 years. The coronary angiography and percutaneous coronary intervention procedures were performed and angiographicAngiographic no-reflow was defined as a thrombolysis in myocardial infarction scores grade less than 3. Blood samples were collected immediately at admission for the detection of plasma calprotectin and platelet–monocyte aggregates formation. Statistical analysis was performed for the variable’s comparisons between groups and for the prediction value of plasma calprotectin for no-reflow.Results In this study, we have demonstrated that acute coronary syndromeThe mean age of the 176 included ACS patients were 64(±11) years and acute ST-segment elevation myocardial infarction (STEMI) was present in 41.5 percent of patients. 22 patients had no-reflow during the PCI procedures and the prevalence was 12.5%. Patients with higher plasma calprotectin had an elevateda higher level of platelet activation–monocyte aggregates (PMA) and a higher incidenceprevalence of no-reflow. Plasma (p

Background: Various experimental and clinical studies have reported on coronary microcirculatory dysfunction ( "no-reflow" phenomenon). Nevertheless, pathogenesis and effective treatment are yet to be fully elucidated. This study aimed to measure the intracoronary pressure gradient in the no-reflow artery during emergent percutaneous coronary intervention and explore the potential mechanism of no-reflow. Methods: From September 1st, 2018 to June 30th, 2019, intracoronary pressure in acute myocardial infarction patient was continuously measured by aspiration catheter from distal to proximal segment in the Department of Coronary Care Unit, Tianjin Chest Hospital, respectively in no-reflow arteries (no-reflow group) and arteries with thrombolysis in myocardial infarction-3 flow (control group). At least 12 cardiac cycles were consecutively recorded when the catheter was pulled back. The forward systolic pressure gradient was calculated as proximal systolic pressure minus distal systolic pressure. Comparison between groups was made using the Student t test, Mann-Whitney U-test or Chi-square test, as appropriate. Results: Intracoronary pressure in 33 no-reflow group and 26 in control group were measured. The intracoronary forward systolic pressure gradient was －1.3 (－4.8, 0.7) and 3.8 (0.8, 8.8) mmHg in no-reflow group and control group (Z = －3.989, P < 0.001), respectively, while the forward diastolic pressure gradient was －1.0 (－3.2, 0) and 4.6 (0, 16.5) mmHg in respective groups (Z = －3.851, P < 0.001). Moreover, the intracoronary forward pressure gradient showed significant difference between that before and after nicorandil medication (Z=－3.668, P < 0.001 in systolic pressure gradient and Z =－3.530, P < 0.001 in diastolic pressure gradient). Conclusions: No reflow during emergent coronary revascularization is significantly associated with local hemodynamic abnormalities in the coronary arteries. Intracoronary nicorandil administration at the distal segment of a coronary artery with an aspiration catheter could improve the microcirculatory dysfunction and resume normal coronary pressure gradient. Clinical trial registration: www.ClinicalTrials.gov (No. NCT 03600259). Key words: Acute myocardial infarction; Coronary hemodynamics; Intracoronary pressure gradient; No-reflow; Primary percutaneous coronary intervention

Background: Coronary no-reflow (NR) is a dreadful complication of primary percutaneous coronary intervention (pPCI) that is seen in nearly 50% of cases. A great effort is being done to discover simple tools that could predict such a complication. We aimed primarily to study the predictive power of R-wave peak time (RWPT) on NR. Methods: From October 2017 to March 2018, we enrolled 123 patients with STEMI treated with pPCI at Benha University Hospital and National Heart Institute. We measured RWPT from infarct-related artery (IRA) leads and assessed the development of NR in all finally included 100 patients (after exclusions). Results: Based on occurrence of NR, patients were divided into 2 groups; Group I (n = 39) with NR and group II (n = 61) without NR. Smoking, DM, HTN, longer reperfusion times and higher thrombus burden were significantly associated with NR. Both pre- and postprocedural RWPT were significantly higher in group I than Group II. Preprocedural RWPT > 46 ms predicted NR with a sensitivity and specificity of 79.5% and 86.9% respectively (AUC 0.891, 95% CI 0.82–0.962, P

Timely delivered coronary revascularization with no residual anatomical stenosis does not always lead to prompt restoration of anterograde coronary flow and complete myocardial reperfusion. This condition is known as coronary no-reflow and is associated with major clinical adverse events and poor prognosis. The pathophysiology of no-reflow phenomenon is still poorly understood. Proposed mechanisms include distal microembolization of thrombus and plaque debris, ischemic injury, endothelial dysfunction and individual susceptibility to microvascular dysfunction/obstruction. Older age, diabetes, hypercholesterolemia, prolonged ischemic time, hemodynamic instability, high thrombus burden, complex angiographic lesions and multivessel disease are frequently reported to be associated with the no-reflow phenomenon. There is no general consensus on the correct prevention and management of no-reflow. Non-pharmacological measures such as distal embolic protection devices and manual thrombus aspiration did not result in improved flow or reduction of infarct size. Current preventive measures include reduction of time from symptoms onset to reperfusion therapy, and intracoronary administration of vasodilators such as adenosine, verapamil or nitroprusside.

Introduction:Althoughit has been established that high-degree atrioventricular block (HAVB) isassociated with mortality in the course of ST segment elevation myocardialinfarction (STEMI), the mechanisms by which this AV block cause mortality arenot yet fully understood. In this study we aimed: (i) to investigate therelationship between HAVB and no-reflow, which has been repeatedly shown to beassociated with both short- and long-term mortality; (ii) to determine theeffect of both HAVB and no-reflow on in-hospital and long-term mortality.Patientsand Methods: A total of 1.217 patients who underwent primarypercutaneous coronary intervention (pPCI) were divided into two groups,according to HAVB development, and were further divided according to no-reflowdevelopment. Independent predictors of no-reflow were investigated.Furthermore, patients were compared in terms of in-hospital and long-termmortality. Results: In thepresent study, 47 patients (3.8%) suffered from HAVB and 150 patients (12.3%)had no-reflow. HAVB was an independent predictor of no-reflow [odds ratio (OR):3.127, 95% confidence interval (CI): 1.215-9.056; p= 0.006]. In survivalanalysis, both HAVB and no-reflow were associated with in-hospital (19.1% vs.3.2%; p< 0.001 and 10.7% vs. 2.9%; p< 0.001, respectively) and long-term(15.7% vs. 6.2%; p= 0.037 and 14.1% vs. 5.5%; p< 0.001, respectively)mortality.Conclusion: To our knowledge, this isthe first study in the literature to examine the effect of HAVB on reperfusionsuccess. In this study, we found that HAVB emerged with STEMI isassociated with long-term mortality and to short-term mortality. Also HAVB wasan independent predictor of no-reflow, and patients who had no-reflow had aworse prognosis both in short- and long-term follow-up., Giriş: ST segment yükselmeli miyokart infarktüsü (STEMİ) seyrinde yüksek dereceliatriyoventriküler bloğun (HAVB) mortalite ile ilişkili olduğu tespit edilmişolsa da AV bloğunun mortaliteye hangi mekanizmalarla neden olduğu, net olarakortaya konulmamıştır. Bu çalışmada, (i) HAVB ile hem kısa hem de uzun dönemmortalite ile ilişkili olduğu defalarca gösterilen no-reflow arasındakiilişkiyi (ii) hem HAVB hem de no-reflow’un hastane içi ve uzun dönemmortaliteye etkisini araştırmayı amaçladık.Hastalar veYöntem: Primer perkütan koroner girişim (pPCI) yapılan toplam1217 hasta, HAVB gelişip gelişmemesine, daha sonra da no-reflow gelişipgelişmemesine göre iki gruba ayrıldı. No-reflow’un bağımsız prediktörleriaraştırıldı. Son olarak da hastalar, hastane içi ve uzun dönem mortaliteaçısından karşılaştırıldı.Bulgular: Bu çalışmada, 47 (%3.8) hastada HAVB, 150 (%12.3) hastada no-reflowizlendi. HAVB, no-reflow’un bağımsız bir prediktörü olarak saptandı (OR: 3.127,%95 CI: 1.215-9.056; p= 0.006). Sağkalım analizinde HAVB ve no-reflow’dahastane içi mortalite (sırasıyla %19.1’e karşı %3.2; p< 0.001 ve %10.7’yekarşı %2.9; p< 0.001) ve uzun dönem mortalite (sırasıyla %15.7’ye karşı%6.2; p= 0.037 ve %14.1’e karşı %5.5; p< 0.001) daha yüksek olarak izlendi.Sonuç: Bu çalışmada, STEMİ ileortaya çıkan HAVB’nin, kısa döneme ek olarak, uzun dönem mortalite ile deilişkili olduğu tespit edildi. HAVB ile sağkalımla ileri derecede korelasyonuolan reperfüzyon başarısının ilişkisini gösteren bu ilk çalışmada, HAVB’ninno-reflow için bağımsız bir prediktör olduğunu ve no-reflow’u olan hastalarınhem kısa hem de uzun dönem izlemlerinde kötü prognoza sahip olduğunu ortayakoyduk.

Aims: Ventricular arrhythmia (VA) bursts following recanalisation in acute ST-elevation myocardial infarction (STEMI) are related to larger infarct size (IS). Inadequate microvascular reperfusion, as determined by microvascular obstruction (MVO) using cardiac magnetic resonance imaging (CMR), is also known to be associated with larger IS. This study aimed to test the hypothesis that VA bursts identify larger infarct size in spite of optimal microvascular reperfusion. Methods: All 65 STEMI patients from the Maastricht ST elevation (MAST) study with brisk epicardial flow (TIMI 3), complete ST recovery post-percutaneous coronary intervention and early CMR were included. Using 24-hour Holter registrations from the time of admission, VA bursts were identified against subject-specific Holter background VA rates using a statistical outlier method. MVO and final IS were determined using delayed enhancement CMR. Results: MVO was present in 37/65 (57%) of patients. IS was significantly smaller in the group without MVO (median 9.4% vs. 20.5%; p < 0.001). IS in the group with MVO did not differ depending on VA burst ( n = 28/37; median 20.8% vs. 19.7%; p = 0.64). However, in the group without MVO, VA burst was associated with significantly larger IS ( n = 17/28; median 10.5% vs. 4.1%; p = 0.037). In multivariable analyses, VA burst as well as anterior infarct location remained independent predictors of larger infarct size. Conclusion: In the presence of suboptimal reperfusion with MVO by CMR, VA burst does not further define MI size. However, with optimal TIMI 3 reperfusion and optimal microvascular perfusion (i.e. no MVO), VA burst is associated with larger IS, indicating that VA burst is a marker of additional cell death.

Introduction Prevention of the no-reflow phenomenon has a crucial role in primary percutaneous coronary intervention (P-PCI) procedures. Aim To assess the effects of early intracoronary administration of nicorandil (NIC) during P-PCI on myocardial microcirculation in patients with acute myocardial infarction (AMI). Material and methods A total of 120 patients with first acute anterior wall ST segment elevation myocardial infarction who underwent P-PCI were randomly divided into two groups: the NIC group (A, n = 60) and the placebo group (B, n = 60). Before stent placement, NIC or normal saline was injected using a guiding catheter. The thrombolysis in myocardial infarction (TIMI) grade, TIMI myocardial perfusion grade (TMPG), resolution of ST segment elevation (defined as > 50% decrease in ST elevation) 1 h after surgery, and 99Tcm-methoxyisobutyl isocyanide (MIBI) rest myocardial perfusion imaging (MPI) via single-photon emission computed tomography (99Tcm-MIBI SPECT) findings 10 days after surgery were compared between the two groups. Results The number of patients who achieved TIMI grade 3 (96.67% vs. 86.67%; p = 0.047) and TMPG 3 (95% vs. 83.33%; p = 0.040) was higher in the NIC group than in the placebo group. Resolution of ST segment elevation occurred in 95% and 81.67% of the patients in the NIC and placebo groups, respectively (p = 0.023); the MPI score of the two groups was 4.1 ±1.89 and 7.3 ±2.65, respectively (p = 0.014). Conclusions Early coronary administration of NIC can significantly reduce the damage in the myocardial microcirculation caused by P-PCI and the myocardial infarct size in patients with AMI.

Return of blood flow after periodic ischemia is often accompanied by myocardial injury, commonly known as lethal reperfusion injury (RI). Experimental studies have shown that 50% of muscle die of ischemia and another 50% die because of reperfusion. It is characterized by myocardial, vascular, or electrophysiological dysfunction that is induced by the restoration of blood flow to previously ischemic tissue. This phenomenon reduces the efficiency of the present modalities used to combat the ischemic myocardium. Moreover, despite an improved understanding of the pathophysiology of this process and encouraging preclinical trials of multiple agents, most of the clinical trials to prevent RI have been disappointing and leaves us at ground zero to explore newer approaches. Keywords: Microvascular obstruction, No-reflow, Myocardial stunning, Aspiration thrombectomy, Ischemic conditioning, Pharmacological conditioning

PubMed: 28623012 Objectives Coronary no-reflow (NR) following primary percutaneous coronary intervention (pPCI) is associated with worsened prognosis in patients with ST segment elevation myocardial infarction (STEMI). Despite rapid developments in cardiovascular area; there are limited data regarding prediction of NR before pPCI. P wave duration and dispersion (PWD, PWDIS respectively) have been studied in STEMI patients and found to be associated with reperfusion success; however none of them has been found to predict NR before PCI. In our study we aimed to evaluate whether PWD, PWDIS and a novel parameter P wave peak time (PWPT) could predict NR development in STEMI patients. Method Fifty six patients who were admitted with anterior STEMI constituted study populations. The diagnosis and treatment of STEMI was made on the basis of current guidelines. P wave parameters including PWD, PWDIS and PWPT were calculated from electrocardiograms that were obtained on admission and 60 min after pPCI. Results Patients were divided into two groups according to the development of NR. We observed that PWPT that were obtained from D2 (PWPTD2) and V1 (PWPTV1) leads were longer in NR group than reflow group. There were significant correlations between PWPT and reperfusion parameters regarding percent of ST segment resolution, peak CKMB level and TIMI frame count of infarct related artery. Preprocedural PWPTD2 was found to be an independent predictor of NR development. Conclusion In our study we observed that PWPT could be a useful parameter in the assessment of reperfusion success and prediction of NR development. © 2017 Elsevier Inc.

Reciprocal ST-segment downsloping on electrocardiogram is a frequent finding during ST-elevated myocardial infarction (STEMI), but its etiology is still disputed. We sought to evaluate the relation between reciprocal ST-segment downsloping during STEMI and major cardiac perfusion and functional parameters. One hundred eighty-five patients with STEMI underwent emergency coronary angiography. The presence of reciprocal ST-segment downsloping was assessed. At coronary angiography, the corrected TIMI frame count (cTFC) was computed both on culprit and remote vessels and the occurrence of "no/slow reflow" phenomenon after percutaneous coronary intervention (PCI) identified. The left ventricular wall motion score index ratio (discharge/admission values) at echocardiography and the slope of high-sensitivity troponin elimination were computed as measures of effective myocardial reperfusion. Reciprocal ST-segment downsloping was revealed in 91 patients (49%). They presented higher cTFC values on remote vessels than patients without reciprocal electrocardiographic abnormalities (44 ± 18 vs 37 ± 15 cineframes × second −1 , p = 0.004). The presence of remote ST-segment downsloping was also associated with a higher prevalence of "no/slow reflow" phenomenon (59% vs 40%, p = 0.013) as well as more abnormal values of wall motion score index ratio (p = 0.042) and high-sensitivity troponin slope (p = 0.012). At multivariate analyses, a higher cTFC on remote vessels predicted the occurrence of reciprocal ST-segment changes (p = 0.018) and the development of "no/slow reflow" phenomenon after PCI (p = 0.005). In conclusion, the presence of reciprocal ST-segment downsloping during STEMI clusters with significant perfusion and cardiac functional abnormalities, predicting the development of "no reflow" phenomenon after PCI.

MicroRNA-208a is a cardiac specific oligo-nucleotide. We aimed at investigating the ability of microRNA-208a to diagnose myocardial infarction and predict the outcome of primary percutaneuos coronary angiography (PCI). Patients (n = 75) presented by chest pain were recruited into two groups. Group 1 (n = 40) had ST elevation myocardial infarction (STEMI) and underwent primary PCI: 21 patients had sufficient reperfusion and 19 had no-reflow. Group 2 (n = 35) had negative cardiac troponins (cTns). Plasma microRNA-208a expression was assessed using quantitative polymerase chain reaction and patients were followed for occurrence of in-hospital major adverse cardiac events (MACE). MicroRNA-208a could diagnose of MI (AUC of 0.926). After primary PCI, it was superior to cTnT in prediction of no-reflow (AUC difference of 0.231, P = 0.0233) and MACE (AUC difference of 0.367, P = 0.0053). Accordingly, circulating levels of miR-208a can be used as a diagnostic marker of MI and a predictor of no-reflow and in-hospital MACE. Graphical abstract Receiver operating curve analysis of no-reflow prediction of miRNA208a, CK-MB and hs-Troponin T. MicroRNA-208a shows significantly higher prediction of no-reflow as compared to routine cardiac biomarkers.

Coronary microembolization is one of the main causes of the "no-reflow" phenomenon, which commonly occurs after reperfusion of an occluded coronary artery. Given its high incidence and the fact that it has been proven to be an independent predictor of cardiac morbidity and mortality, there is an imperative need to study its underlying mechanisms and pathophysiology. Large animal models are essential to perform translational studies. Currently there is no animal model that recapitulates a clinical scenario of thrombogenic microembolism with preceding myocardial ischemia. Therefore, the goal of this study was to develop and characterize a novel pig model of coronary microembolization using autologous thrombus injection (CMET). Twenty-three pigs underwent myocardial infarction through percutaneous balloon occlusion of the left anterior descending artery (LAD). Each animal was enrolled in one of two groups: (1) the CMET group, in which the LAD occlusion was followed by delivery of autologous clotted blood in the LAD (distal to the balloon occlusion) and reperfusion; (2) the ischemic reperfusion (I/R) group, in which the LAD ischemia was followed by reperfusion. Surviving animals underwent functional and morphological characterization at 1-week post-procedure. Three sham operated animals were used as a control. CMET resulted in impaired left ventricular function compared to I/R pigs at 1 week. Three-dimensional echocardiography demonstrated reduced ejection fraction in the CMET group (CMET vs. I/R: 35.6 ± 4.2% vs. 47.6 ± 2.4%, p = 0.028). Invasive hemodynamic measurements by Swan-Ganz and left ventricular pressure-volume catheters revealed that CMET impaired left ventricular contractility and diastolic function. This was confirmed by both load-dependent indices including cardiac output (CMET vs. I/R: 2.7 ± 0.2 l/min, vs. 4.0 ± 0.1 l/min, p = 0.002) and load independent indices including preload-recruitable stroke work (CMET vs. I/R: 25.8 ± 4.0 vs. 47.5 ± 6.5 mmHg, p = 0.05) and end-diastolic pressure-volume relationship (slope, 0.68 ± 0.07 vs. 0.40 ± 0.11 mmHg/ml, p = 0.01). Our unique closed-chest model of coronary microembolization using autologous thrombus injection resembles the clinical condition of thrombogenic coronary microembolization in I/R injury. This model offers opportunities to conduct translational studies for understanding and treating coronary microembolization in myocardial infarction.

The ability of platelets to activate and aggregate to form blood clots in response to endothelial injury is well established. They are therefore critical contributors to ischaemia in atherothrombosis [1]. However, their role in cardiovascular disease is not limited to end-stage thrombosis in large vessels [2]. Abundant experimental evidence has established that activated platelets are also important mediators of microvascular thrombosis and promote the inflammatory response during ischaemia-reperfusion (IR) injury [3–5]. While platelets do not physically interact with the healthy endothelium, they can bind to the wall of hypoxic microvessels and release a plethora of inflammatory mediators that further enhance the activation of the endothelial monolayer and the recruitment of circulating leukocytes (monocytes, neutrophils, T-cells) [2]. In addition, deposition of platelets to the dysfunctional endothelium can lead to vasoconstriction which accelerates microvascular occlusion, thereby impairing tissue perfusion [3]. In this chapter, we discuss the role of platelets in promoting microvascular dysfunction and inflammation during IR injury. Focus is placed on the cross-talk between platelets and other cell types (endothelial cells [ECs] and leukocytes) via platelet adhesion receptors and platelet-derived proinflammatory mediators. We also consider new paradoxical functionalities of platelets promoting cardiac recovery after myocardial infarction (MI).

Association between CD69 and EGR1 levels and coronary heart disease (CHD) patients without reflow after percutaneous coronary intervention (PCI) was investigated. Data of 156 patients undergoing PCI from September 2014 to December 2016 in People's Hospital of Hunan Province were analyzed, and they were divided into 72 cases in reflow group (group A) and 84 cases in no-reflow group (group B) according to the patient's postoperative blood flow. Another 70 volunteers undergoing normal physical examination in the same period were selected as control group (group C). The venous blood was extracted from patients before operation, at 5 min, 2 h and 6 months after operation, the serum CD69 and EGR1 levels were detected with flow cytometry and RT-qPCR methods, and association between CD69 and EGR1 levels and postoperative blood flow recovery was analyzed. CD69 expression before and 2 h after operation in group A was significant (P

Background and objectives: We aimed to demonstrate the clinical utility of CHA2DS2-VASc score in risk assessment of patients with STEMI regarding adverse clinical outcomes particularly no-reflow phenomenon. Materials and Methods: We designed a retrospective cohort study using the data of Tehran Heart Center registry for acute coronary syndrome. The study included 1331 consecutive patients with STEMI who underwent primary angioplasty. Patients were divided into two groups according to low and high CHA2DS2-VASc score. Angiographic results of reperfusion were inspected to evaluate the association of high CHA2DS2-VASc score and the likelihood of suboptimal TIMI flow. The secondary endpoint of the study was short-term in-hospital mortality of all cause. Results: The present study confirmed that CHA2DS2-VASc model enables us to determine the risk of no-reflow and all-cause in-hospital mortality independently. Odds ratios were 1.59 (1.30–2.25) and 1.60 (1.17–2.19), respectively. Moreover, BMI, high thrombus grade, and cardiogenic shock were predictors of failed reperfusion (odds were 1.07 (1.01–1.35), 1.59 (1.28–1.76), and 8.65 (3.76–24.46), respectively). We showed that using a cut off value of ≥ two in CHA2DS2-VASc model provides a sensitivity of 69.7% and specificity of 64.4% for discrimination of increased mortality hazards. Area under the curve: 0.72 with 95% CI (0.62–0.81). Conclusions: Calculation of CHA2DS2-VASc score applied as a simple risk stratification tool before primary PCI affords great predictive power. Furthermore, incremental values are obtained by using both CHA2DS2-VASc and no-reflow regarding mortality risk assessment.