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no-reflow can complicate up to 25% of pPCI and is associated with significant morbidity and mortality. We aimed to compare the outcomes of intracoronary epinephrine and verapamil with intracoronary adenosine in the treatment of no-reflow after primary percutaneous coronary intervention (pPCI). 108 STEMI patients had no-reflow during pPCI were assigned into four groups. Group 1, in which epinephrine and verapamil were injected through a well-cannulated guiding catheter. Group 2, in which same drugs were injected in the distal coronary bed through a microcatheter or perfusion catheter. Group 3, in which adenosine was injected through a guiding catheter. Group 4, in which adenosine was injected in distal coronary bed. Primary end point was the achievement of TIMI III flow and MBG II or III. Secondary end point was major adverse cardiovascular and cerebrovascular events (MACCEs) during hospital stay. The study groups did not differ in their baseline characteristics. Primary end point was achieved in 15 (27.8%) patients in the guide-delivery arm compared with 34 (63%) patients in the local-delivery arm, p < 0.01. However, the primary end point did not differ between the epinephrine/verapamil group and the adenosine group (27 (50%) vs 22 (40.7%), p = 0.334). The secondary end points were similar between the study groups. Local delivery of epinephrine, verapamil and adenosine in the distal coronary bed is more effective in achieving TIMI III flow with MBG II or III compared with their guide-delivery in patients who suffered no-reflow during pPCI. There was no difference between epinephrine/verapamil Vs. adenosine. • No-reflow complicates almost 25% of STEMI patients treated by primary PCI and has major consequences on morbidity and mortality. • Prevention of No-reflow is of utmost importance but its treatment is a major challenge and, indeed, there is no definitive treatment for such a problem till now. • This study compared most evident drugs in treatment of no-reflow comparing 2 routes of administration. • Local delivery of epinephrine/verapamil or adenosine in the distal coronary bed is more effective in treatment of No-reflow compared to their guide-delivery with no difference between epinephrine/verapamil and adenosine. [ABSTRACT FROM AUTHOR]

The no-reflow phenomenon increases mortality and morbidity in patients with ST-segment elevation myocardial infarction (STEMI). Inflammation, endothelial dysfunction, and oxidative stress play important role in its pathophysiology. We aim to evaluate the relationship between the no-reflow phenomenon and C-reactive protein (CRP) and uric acid (UA) to albumin ratio (CUAR), which is a new marker indicating all these pathophysiological mechanisms. Study population were divided into two groups as no-reflow and reflow; according to the post-procedural thrombolysis in myocardial infarction flows and myocardial blush grade. A1:4 propensity score matching was performed.CUAR was calculated by using the following formula: log10 (CRP x UA /Albumin). CUAR levels were significantly higher in patients with no-reflow than in those with reflow (P < 0.001). CUAR levels above 1.28 predicted no-reflow with higher sensitivity of 74% and specificity of 71% than all including CRP, UA and albumin (AUC = 0.80 [95%CI: 0.76–0.83], P < 0.001). In multivariate logistic regression analysis, CUAR levels above 1.28 (OR: 4.43 [3.04–6.46], 95% CI; P < 0.001) wereindependently associated with no-reflow phenomenon. Our results showed that CUAR could be a basic and available marker to predict no-reflow in patients with STEMI who underwent primary percutaneous coronary intervention. • The no-reflow phenomenon is still a challenge, which is associated with long-term mortality and morbidity in STEMI patients. • The mechanism of no-reflow includes interactions among inflammation, reactive oxygen damage, and endothelial dysfunction. • CUAR could indicate the composite effect of inflammation, endothelial damage and oxidative stress. • CUAR is independently associated with no-reflow phenomenon in STEMI patients. • It can be used as a simple and available new marker to predict high-risk patients with the no-reflow phenomenon. [ABSTRACT FROM AUTHOR]

Background The no-reflow phenomenon is a serious complication after primary percutaneous coronary intervention (PCI) for ST-elevation Myocardial Infarction (STEMI). Coronary artery ectasia (CAE) may increase the risk of no-reflow, however, only limited data is available on the potential impact of CAE. The aim of this study was to determine the potential association between CAE and no-reflow after primary PCI. Methods A case control study was performed based on a prospective cohort of STEMI patients from January 2000 to December 2011. All patients with TIMI 0–1 flow post primary PCI, in the absence of dissection, thrombus, spasm or high-grade residual stenosis, were considered as no-reflow case. Control subjects were two consecutive STEMI patients after each case, with TIMI flow ≥2 after primary PCI. CAE was defined as dilatation of an arterial segment to a diameter at least 1.5 times that of the adjacent normal coronary artery. Results In the no-reflow group, frequency of CAE was significantly higher (33.8% vs 3.9%, p < 0.001) compared to the control group. Baseline variables were comparable between patients with and without CAE. Patients with CAE had more often TIMI 0–1 flow pre-PCI (91% vs 71% p = 0.03), less often anterior STEMI (3% vs 37%, p < 0.001) and underwent significantly less often a PCI with stenting (47% vs 74%, p = 0.003). After multivariate analysis, CAE remained a strong and independent predictor of no-reflow (OR 13.9, CI 4.7–41.2, p < 0.001). Conclusion CAE is a strong and independent predictor of no-reflow after primary PCI for STEMI. Future studies should assess optimal treatment. [ABSTRACT FROM AUTHOR]

Background Adjunctive therapies, given in addition to reperfusion to reduce myocardial infarct size, have been disappointing based on clinical trials. New therapeutic targets independent of infarct size modification are needed. The no-reflow phenomenon occurs commonly after the infarct-related coronary artery is opened and predicts poor clinical outcome. We investigated the effects of a single application of delayed (post-reperfusion) therapeutic hypothermia (TH) in a rat model of coronary artery occlusion/reperfusion. Methods Rats were subjected to 60 min of coronary artery occlusion followed by 3 h of reperfusion. Rats were divided into normothermic ( n = 5) and TH ( n = 5) groups. In the TH, hypothermia was initiated at 1 min after coronary artery reperfusion by pumping room-temperature (22 °C) saline into and out of the thoracic cavity for 1 h. This decreased intrathoracic temperature to around 26 °C within 12 min. At 3 h after reperfusion, hearts were excised for infarct size and no-reflow zone measurement. Results Ischemic risk area and infarct size were similar between the 2 groups. No-reflow area (expressed as % of risk area) was significantly reduced in TH group (18.0 ± 4.4%) compared with normothermic group (39.5 ± 2.9%, P = 0.005). When expressed as % of necrotic area, no-reflow area was reduced by more than half in TH group (25.5 ± 6.4%) versus in normothermic group (54.4 ± 5.3%, P = 0.01). Conclusions In this preliminary study, hypothermia initiated after reperfusion following 60 min of coronary artery occlusion had no effect on infarct size yet substantially reduced the extent of no-reflow. [ABSTRACT FROM AUTHOR]

Background The objectives of this study were to evaluate the incidence of no-reflow as independent predictor of adverse events and to assess whether baseline pre-procedural treatment options may affect clinical outcomes. Methods Data were derived from the ISACS-TC registry ( NCT01218776 ) from October 2010 to January 2015. No-reflow was defined as post-PCI TIMI flow grades 0–1, in the absence of post-procedural significant (≥ 25%) residual stenosis, abrupt vessel closure, dissection, perforation, thrombus of the original target lesion, or epicardial spasm. The outcome measure was in-hospital mortality. Results No-reflow was identified in 128 of 5997 patients who have undergone PCI (2.1%). On multivariate analysis, patients with no-reflow were more likely to be older (OR: 1.20, 95% CI: 1.01–1.44), to have a history of hypercholesterolemia (OR: 1.95, 95% CI: 1.31–2.91) and to be admitted with a diagnosis of STEMI (OR: 2.96, 95% CI: 1.85–4.72). Angiographic characteristics associated with no-reflow phenomenon were: stenosis ≥ 50% of the right coronary artery, presence of multivessel disease and pre-procedural TIMI blood flow grades 0–1. No-reflow was highly predictive of in-hospital mortality (17.2% vs. 4.2%; adjusted OR: 4.60, 95% CI: 2.61–8.09). Administration of pre-procedural unfractioned heparin or 600 mg clopidogrel loading dose was associated with less incidence of no-reflow (OR: 0.65, 95% CI: 0.43–0.99 and 0.61, 95% CI: 0.37–1.00, respectively). Aspirin, enoxaparin, and 300 mg clopidogrel loading dose, did not significantly impact the occurrence of the no-reflow. Conclusions We found that pre-procedural administration of 600 mg loading dose of clopidogrel and/or unfractioned heparin is associated with reduced incidence of no-reflow. [ABSTRACT FROM AUTHOR]

Background The ‘no-reflow’ phenomenon after a percutaneous coronary intervention (PCI) in patients with acute ST-segment elevation myocardial infarction (STEMI) is a strong predictor of both short- and long-term mortality. Glucagon-like peptide-1 (GLP-1) exerts a cardioprotective effect during ischemia reperfusion injury. We planned to evaluate the effects of liraglutide on myocardial no-reflow after PCI for STEMI. Methods A total of 284 patients with STEMI undergoing PCI were enrolled in this study between September 2013 and March 2015. Of these, 210 patients were randomized 1:1 to receive either liraglutide or placebo 30 min before PCI (1.8 mg). Results The primary end point, the prevalence of no-reflow, was significantly lower in the liraglutide group than in the control group (5% vs. 15%, P = 0.01). Administration of liraglutide was consistently identified as a significant determinant for no-reflow ratio. There was a significant decrease in serum high-sensitivity C-reactive protein levels at 6-hour reperfusion in the liraglutide group compared to the control group (0.87 ± 0.09 mg/dL vs. 0.96 ± 0.10 mg/dL, P < 0.001). During a 3-month follow-up period, no difference was observed in the incidence of major adverse cardiovascular event. Conclusions Liraglutide may be associated with less no-reflow in STEMI, which should be confirmed by larger-scale trials. [ABSTRACT FROM AUTHOR]

Background Aim of the present study was to evaluate all randomized trials, comparing intracoronary adenosine versus placebo in STEMI patients undergoing primary PCI. Methods and results PubMed, the Cochrane Library and ISI Web of Knowledge electronic databases were scanned for eligible studies up to February 23rd 2015. The summary measure used was risk ratio (RR) with 95% confidence intervals. A total of 13 studies were eligible, including 1487 patients. Incidence of ST resolution was significantly higher in the IC adenosine group than in the placebo group (RR = 1.20 [1.05–1.38]; p = 0.008). At metaregression, a significant correlation was found between the magnitude of the adenosine-related effect on ST resolution and the mean ischemic time (p = 0.011) or the percentage of patients with the LAD as the infarct-related artery (p = 0.03). Furthermore, we found a larger increase in LVEF (p = 0.02) with a parallel reduction in the incidence of heart failure (HF) (RR = 0.50 [0.28–0.89]; p = 0.02) in the IC adenosine group. Finally, IC adenosine administration was associated with a significantly lower incidence of major adverse cardiac events (MACE) both at short- (RR = 0.62 [0.39–0.98] p = 0.04) and long-term (RR = 0.61 [0.39–0.95] p = 0.03). Conclusions This is the first meta-analysis demonstrating a clinical benefit for IC adenosine in hard endpoints, such as adverse cardiovascular events, in patients undergoing primary PCI. [ABSTRACT FROM AUTHOR]

Background No-reflow in ST-segment elevation acute myocardial infarction (STEMI) is associated with a poor clinical prognosis. Its pathophysiological mechanisms are not fully elucidated yet but enhanced vascular permeability plays a key role in this phenomenon. Angiopoietin-like 4 (ANGPTL4) has been implicated in vascular permeability in experimental models of acute myocardial infarction (AMI). We therefore sought to investigate whether baseline ANGPTL4 serum levels are associated with no-reflow after primary percutaneous coronary intervention (PPCI). Methods We studied a group of 41 patients presenting with a first STEMI within 12 h of onset of symptoms and who underwent successful PPCI. Blood samples were obtained from all patients on admission before the start of the procedure, for ANGPTL4 level measurement. No-reflow was assessed by cardiac magnetic resonance imaging (MRI), the reference method. Results MRI-detected no-reflow was observed in 20 patients (48.8%). Variables independently associated with no-reflow on multivariate logistic regression analysis were: lower ANGPTL4 serum levels (odds ratio 0.82, 95% CI 0.70-0.98, P = 0.02), higher troponin T peak (odds ratio 1.03, 95% CI 1.00-1.05, P = 0.03), higher incidence of left anterior descending coronary artery (LAD) as culprit artery (odds ratio 14.61, 95% CI 1.24-172.49, P = 0.03), and higher C-reactive protein levels (odds ratio 1.18, 95% CI 1.00-1.39, P = 0.05). Conclusion ANGPTL4 serum levels predict MRI-detected no-reflow after successful PPCI in STEMI patients. Given the recently demonstrated therapeutic role of ANGPTL4 in diminishing no-reflow and limiting infarct size in pre-clinical animal models, these findings in humans may open up new possibilities in the field of research. [ABSTRACT FROM AUTHOR]

Abstract: Background and objective: Myocardial edema plays a role in myocardial no-reflow and infarction during ischemia and reperfusion. The effects of statins against no-reflow and infarction may relate to the inhibition of myocardial edema. The current study investigated the role of protein kinase A (PKA) in statin-reduced myocardial edema in reperfused swine hearts. Methods and results: Minipigs were treated with simvastatin (SIM, 2mg/kg), SIM+H-89 (a PKA inhibitor, 1.0μg/kg/min), or H-89 alone 1h before 90-min ischemia and 3-h reperfusion or sham operation. Ischemia or ischemia–reperfusion induced severe myocardial edema, PKA activation, and up-regulation of aquaporin-1, -4, -8, and ‐9 in the reflow and no-reflow myocardium. SIM pretreatment reduced the sizes of no-reflow and infarct areas by 18.5% and 11.1% (P <0.01), decreased water content in the left ventricle, reflow and no-reflow myocardium by 1.4%, 5.3%, and 4.3% (P <0.05), inhibited cardiomyocytes swelling in the reflow and no-reflow areas by 19.8% and 13.1% (P <0.01), suppressed mitochondrial water accumulation in the reflow and no-reflow areas by 49.0% and 35.9% (P <0.01), increased PKA activity (P <0.01), and blocked the up-regulation of aquaporin-1, -4, -8, and ‐9 in the reflow and no-reflow myocardium. However, these beneficial effects of SIM were partially abolished by inhibiting PKA with H-89. Conclusions: The cardioprotective effects of acute SIM therapy against myocardial no-reflow and infarction relate to the reduction of myocardial edema by suppressing the expression of aquaporin-1, -4, -8, and ‐9 in a partially PKA-dependent manner. [Copyright &y& Elsevier]

Abstract: In acute ST-segment elevation myocardial infarction (STEMI), improvement in reperfusion strategies has contributed to improvement in mortality. Nonetheless up to 40–50% of patients who achieve satisfactory epicardial patency do not necessarily achieve patency at the coronary microvascular level, a condition referred to as the ‘no-reflow’ phenomenon. The ‘no-reflow’ phenomenon is associated with a worse prognosis at follow up. The pathogenic mechanisms underlying the ‘no-reflow’ phenomenon is complex and dynamic. This includes a variable combination of mechanisms including distal atherothrombotic embolisation, ischaemic injury, reperfusion injury and heightened susceptibility of coronary microcirculation to injury. Accurate detection of ‘no-reflow’ is crucial because it is independently associated with adverse ventricular remodelling and patient prognosis. The diagnosis of ‘no-reflow’ can be made using angiography, electrocardiography, nuclear scintigraphy, myocardial contrast echocardiography or cardiovascular magnetic resonance (CMR). Despite our improved understanding on the pathogenesis and diagnosis of ‘no-reflow’, the treatment of ‘no-reflow’ remains the ‘Achilles heel’ in the treatment of patients with acute myocardial infarction. Several therapeutic strategies have been tested for the prevention and treatment of ‘no-reflow’, however none have been associated with improvement in clinical outcomes. Therefore there exists a need for ‘in-lab’ tools that will be able to aid early identification of patients at increased risk of ‘no-reflow’. This may enable patients at heightened risk of ‘no-reflow’ to be treated with the most appropriate individualised treatment early. We review the pathogenic mechanisms and diagnostic techniques of the ‘no-reflow’ phenomenon as well as the prevention and treatment strategies of the candidate mechanisms. [Copyright &y& Elsevier]

Abstract: Aims: Primary percutaneous coronary intervention (PPCI) has become the treatment of choice in patients with ST-elevation myocardial infarction (STEMI) over the recent years. A number of studies have demonstrated a morbidity and mortality benefit over thrombolysis, which has been attributed to better coronary perfusion in patients undergoing PPCI. However although PPCI usually achieves normal flow in the affected epicardial vessel, myocardial reperfusion is not fully restored in a significant percentage of patients. This is commonly the result of distal thrombus embolization with subsequent impairment of myocardial microcirculation. Recognition of this has led to the development of a number of devices with different mechanisms of action that aim to reduce such distal embolization and therefore improve end myocardial perfusion. Recent studies indeed demonstrate that the use of such devices offer additional clinical advantage in patients undergoing PPCI compared to the current practice. This report focuses on thrombectomy devices and reviews the evidence that advocates their routine use in PPCI patients. Methods and results: We have performed a systematic review of currently available thrombectomy devices. We also performed a literature search, using the terms “thrombectomy” and “thrombus aspiration” in PubMed and EMBASE. Thrombectomy devices were divided in “manual” and “non-manual” groups. We performed a meta-analysis of the available randomized control trials that compared adjunctive thrombectomy in PPCI to standard PPCI. The use of manual thrombectomy devices is associated with significant improvements in ST-segment resolution (STR) (p<0.00001), Myocardial Blush Grade (MBG) 3 (p<0.00001), Thrombolysis in Myocardial Infarction (TIMI) grade 3 flow (p=0.01) as well as clinical parameters (43% reduction in mortality, p=0.04) in patients undergoing PPCI. Conclusion: Current evidence advocates the routine use of manual thrombectomy devices in PPCI. Non-manual (mechanical) thrombectomy may have a role in selected PPCI patients with large caliber vessels and heavy thrombus burden although their routine use is not presently supported. [Copyright &y& Elsevier]

Abstract: Background: It is unknown whether adenosine triphosphate disodium (ATP) administration during primary percutaneous coronary intervention (PCI) is useful in anterior acute myocardial infarction (AMI). Methods: The study was a prospective, non-randomized, open-label trial. Primary PCI was successfully performed in 204 consecutive patients with first anterior AMI. ATP at a mean dose of 117 μg/kg/min for 45 min on an average was infused intravenously during PCI in 100 patients (Group 1). In the other 104 patients, normal saline was administered (Group 2). ST-segment resolution (STR) was estimated 90 min after recanalization. The no-reflow ratio was measured 2 weeks later, using intravenous myocardial contrast echocardiography. Left ventricular ejection fraction (LVEF), LV regional wall motion (LVRWM), and LV end-diastolic volume index (LVEDVI) were measured 6 months later. Results: Baseline patient characteristics of the two groups were similar, including TIMI risk scores. Significant STR (≧50% resolution compared to baseline) (66% versus 50%; Group 1 versus Group 2, p =0.02), no-reflow ratio (24% versus 34%, indicated by mean values, p =0.02), LVEF (61% versus 55%, p =0.0007), LVRWM (−1.56 versus −2.05, using the SD/chord, p =0.0001), and LVEDVI (60 ml/m2 versus 71 ml/m2, p =0.0007) were significantly better in Group 1, and the no-reflow ratio, LVEF, LVRWM and LVEDVI were significantly better in ATP-administered patients, regardless of antecedent angina or advanced age. ATP Administration was consistently identified as a significant determinant for STR, no-reflow ratio, LVEF, LVRWM, and LVEDVI. Conclusions: Intravenous ATP administration during reperfusion is an independent determinant of STR and the no-reflow ratio, and LVEF, LVRWM, and LVEDVI at 6 months after primary PCI. [Copyright &y& Elsevier]

Abstract: Remote periconditioning is induced by brief cycles of ischemia and reperfusion of a remote organ applied during sustained myocardial ischemia. It remains unknown whether the remote periconditioning reduces myocardial no-reflow. The adenosine triphosphate-sensitive potassium (KATP) channel opening and inhibition of Rho-kinase may be the important mechanism of protection against myocardial no-reflow. Therefore, this study was sought to assess the effect of remote periconditioning on myocardial no-reflow and explore the possible mechanism. Methods: Coronary ligation area and area of no-reflow were determined with pathological means in 58 mini-swines randomized into 7 study groups: 9 controls, 8 in remote periconditioning, 8 in hydroxyfasudil (a specific inhibitor of Rho-kinase)-treated, 9 in glibenclamide (KATP channel blocker)-treated, 8 in remote periconditioning and glibenclamide, 8 in hydroxyfasudil and glibenclamide and 8 sham-operated. The ischemia and reperfusion model was created with 3 h of left anterior descending artery occlusion followed by 2 h of reperfusion. Results: Compared with the control group, remote periconditioning decreased Rho-kinase activity (P <0.01), increased coronary blood volume (P <0.05), decreased area of no-reflow (from 82.3±3.9% to 45.5±5.7% of ligation area, P <0.01) and reduced necrosis size (from 98.5±1.3% to 74.7±6.3% of ligation area, P <0.05). Hydroxyfasudil had the same effect on the above parameters as remote periconditioning. Glibenclamide abrogated the effect of remote periconditioning or hydroxyfasudil on area of no-reflow and necrosis area, but not Rho-kinase activity. Conclusion: Remote periconditioning can reduce myocardial no-reflow after ischemia and reperfusion. This beneficial effect could be due to its activation of KATP channel via inhibition of Rho-kinase. [Copyright &y& Elsevier]

Abstract: Objectives: To overview and summarize the results emerging from the studies on adjunctive devices (AD) with theoretical anti-embolic properties in patients with ST-elevation acute myocardial infarction (STEMI) undergoing percutaneous coronary interventions (PCI). Background: A series of small-to-medium size randomized studies have compared different AD with standard PCI (SP) in the setting of STEMI. The reported results are conflicting. Methods: Eighteen prospective randomized studies on 3180 STEMI patients comparing AD with SP were identified and entered the meta-analysis. Pre-specified angiographic, electrocardiographic (absence of ST-segment resolution, STR) and early (up to 30 days) clinical end-points were assessed. Results: AD were associated with lower rates of angiographically evident distal embolization: OR (95% CI): 0.54 (0.37–0.81). Analyses of angiographic and electrocardiographic reperfusion showed striking heterogeneity among studies and an overall trend toward better results with AD: OR (95% CI) 0.76 (95% CI 0.51–1.12) for TIMI<3, 0.53 (0.37–0.76) for myocardial blush grade (MBG)<3, 0.60 (0.45–0.78) for absence of STR. Subgroup analysis according to the type of AD for the end-point of no STR showed concordant absence of benefit in studies testing distal protection devices, positive results being confined to the studies using thrombectomy devices (OR 0.46, 95% CI 0.32–0.66). However, the possibility of a “small study” bias within thrombectomy studies cannot be discharged (significant heterogeneity and positive Egger''s test). Early major adverse cardiac events were not different between AD and SP. Conclusions: AD use may be associated with reduced rate of angiographic distal embolization, and improved MBG 3 and STR rates. However, efficacy might vary with the type of device employed. Moreover, early clinical outcome is not modified suggesting that further, larger, studies are needed to assess the clinical impact of AD. Condensed abstract: We conducted a meta-analysis of 18 prospective randomized trials comparing adjunctive devices (AD) with standard PCI in the setting of STEMI. The use of AD was associated with lower rates of (angiographically evident) distal embolization. Analyses of angiographic and electrocardiographic reperfusion showed striking heterogeneity and an overall trend toward better results with AD. Subgroup analysis suggested that different types of device may have different effects. Early major adverse cardiac events were similar between AD and SP. [Copyright &y& Elsevier]

Abstract: Background: Systemic inflammation is involved in several pathological cardiovascular processes. However, whether it plays a role in the no-reflow phenomenon occurring in patients with acute myocardial infarction (AMI) after percutaneous coronary intervention (PCI) is unknown. Methods: We studies 60 consecutive patients (59.5±12 years, 82% males) with a first ST-segment elevation AMI, treated by primary or rescue PCI within 6 h of symptom onset. Angiographic indexes of no-reflow, evaluated at the end of the procedure, included coronary TIMI flow grading, corrected TIMI frame count (c-TFC) and myocardial blush grade (MBG). ECG indexes of no-reflow included the lack of ST segment resolution (defined as a reduction <50% of the measured ST-segment elevation at 90 min, compared to the admission ECG), as analyzed both in the single lead with the maximal ST elevation and in all leads showing ST elevation on admission. Patients were divided into two groups according to baseline high-sensitivity C-reactive protein (CRP) serum levels measured on admission: high CRP group (CRP>5 mg/L) and low CRP group (CRP<5 mg/L). Results: A similar prevalence of final TIMI flow<3 and MBG<3 was observed in patients with high and low CRP serum levels (30% vs. 12%, p =0.1, and 50% vs. 53%, p =1.0, respectively), and c-TFC was also similar in the two groups (26±4.5 vs. 24±6, p =0.5). Accordingly, the prevalence of lack of ST-segment resolution in the two groups was similar, both by the single-lead method (25% vs. 25%, p =1.0) and the multiple-lead method (29% vs. 19%, p =0.4). Conclusion: In this study we failed to demonstrate any significant association between CRP serum levels on admission and coronary no-reflow, as assessed by both angiographic and ECG parameters in AMI patients treated by successful primary or rescue PCI within 6 h of chest pain onset. [Copyright &y& Elsevier]

Abstract: Introduction: Myocardial no-reflow, has been associated with alterations in endothelial junctions, which is regulated in part by endothelial dysfunction. Carvedilol is an alpha1 and nonselective beta-adrenergic receptor antagonist with antioxidative properties known to protect endothelial function. Therefore, we hypothesized that carvedilol might also have protective effects on myocardial no-reflow and endothelial junctions. Methods: Thirty-two mini-swines were randomized into 4 study groups: 8 in control, 8 pretreated with carvedilol (1 mg/kg/d) for 3 days, 8 in propranolol (nonselective beta-adrenergic receptor antagonist)-pretreated for 3 days and 8 in sham-operated. Acute myocardial infarction and reperfusion model was created with 3 h occlusion of the left anterior descending coronary artery followed by 1 h reperfusion. Coronary ligation area (LA) and area of no-reflow were determined with both myocardial contrast echocardiography (MCE) in vivo and pathological means (Path). Myocardial vascular endothelial (VE)-cadherin, beta-catenin and gamma-catenin were assessed by immunoblot. Results: Compared with the control group, carvedilol significantly improved ventricular function, increased coronary blood flow from 50.6±3.1% to 72.1±3.8% of the baseline at 1 h of reperfusion (P <0.01), decreased area of no-reflow (MCE: from 78.5±4.5% to 24.9±4.1%, Path: from 82.3±1.9% to 25.8±4.3% of LA respectively, all P <0.01), reduced necrosis area from 98.5±1.3% to 74.4±4.7% of LA (P <0.05). The levels of VE-cadherin, β-catenin, and γ-catenin in the reflow myocardium were significantly greater in the carvedilol group (all P <0.05). However, propranolol failed to significantly modify area of no-reflow, VE-cadherin, β-catenin and γ-catenin levels (all P >0.05). Conclusion: Pretreatment with carvedilol preserves endothelial junctions and reduces myocardial no-reflow after acute myocardial infarction and reperfusion. The beneficial effect of carvedilol was not due to its β-blocking action. [Copyright &y& Elsevier]

Abstract: The no-reflow phenomenon is frequently associated with adverse outcomes in patients undergoing percutaneous coronary intervention (PCI). We describe two cases in which the no-reflow phenomenon developed during PCI and was successfully resolved by direct intracoronary aspiration using the Export aspiration catheter. [Copyright &y& Elsevier]

Abstract: Background: Distal protection devices are increasingly used to prevent embolization during percutaneous coronary interventions (PCI) in saphenous vein grafts (SVG) and native coronary arteries (NV). During interventions with the Filterwire device we have observed reduced flow that is reversible following removal of the filter (filter no reflow, FNR), which might be erroneously interpreted as true no reflow and might be associated with reduced capture efficiency of the basket. Methods: We analyzed the incidence of FNR in 58 patients (60 lesions) at high risk of embolization undergoing PCI of either a SVG or a NV using the Filterwire (Boston Scientific, Natick, MA). Qualitative and quantitative angiographic analysis was performed, and the volume of collected debris was estimated using a photographic technique. Results: In our population, about 1/3 of the cases showed FNR, which was associated with angiographically visible filling defects within the basket, indicating macroembolism. However some patients (especially those undergoing vein graft interventions) showed filling defects without FNR, and some others FNR without filling defects. Thus we tried to understand the predictors of FNR: FNR was associated with higher amount of collected debris (36.97±42.98 mm3 vs. 11.31±18.47 mm3, p =0.005), was neither prevented by abciximab, nor predicted by high thrombotic burden, increasing stent volume or need for predilatation. When patient with and without angiographically evident macroembolisation were separately analyzed, a linear correlation of FNR with the quantity of debris was only apparent in the macroembolization group. Conclusions: Interventionalists should be aware of the “Filter No Reflow”, a common but reversible angiographic complication when the Filterwire device is used. Reduced flow seen during these procedures should be treated conservatively. Mechanical obstruction of the filter, but also other mechanisms (pharmacologically active debris? platelet aggregates?) play a role in this phenomenon. [Copyright &y& Elsevier]

Abstract: Background: Large thrombus burden remains challenging in the setting of acute myocardial infarct. Initial thrombosuction (IT) followed by actual angioplasty may be advantageous over conventional strategy in primary percutaneous coronary intervention (PCI). Methods: With a case-control design, 22 consecutive patients receiving primary PCI with IT were designated as group 1. Another 22 well-matched patients undergoing primary PCI with conventional strategy in the same period were enrolled as group 2. Clinical and angiographic outcomes, procedural parameters and resource usage were compared. Results: Baseline characteristics were comparable, including the symptom onset-to-needle time (250±101 vs. 261±149 min, p=NS). Total procedure time (33±14 vs. 47±20 min, p=0.011), fluoroscopy time (10±6 vs. 16±10 min, p=0.014) and contrast medium consumption (140±40 vs. 170±50 ml, p=0.024) were all significantly reduced with group 1. No-reflow occurred less frequently with group 1 (5% vs. 32%, p=0.046) during intervention, and TIMI 3 flow was established more quickly (19±10 vs. 30±20 min, p=0.024). Final TIMI 3 flow rates and stent rates were similar. The time to myocardial enzyme peak was shorter with group 1 (9.7±3.1 vs. 12.8±6.3 h, p=0.048), but no difference was found in 3 months cumulative major cardiac adverse event rates. Conclusions: Primary PCI with IT achieves earlier reperfusion and is more efficient in terms of time and resource, comparing to conventional strategy. [Copyright &y& Elsevier]

Abstract: No-reflow phenomenon is associated with a poor prognosis and its underlying mechanisms are still poorly understood. von Willebrand Factor (vWF) is a central molecule in haemostasis which plays an important role in acute coronary syndromes. However its possible role in no-reflow has not been assessed prior to this study. Quantitative baseline vWF plasma antigen was measured by immunoturbidometric assay in 54 consecutive patients with a first ST segment elevation acute myocardial infarction, treated by primary percutaneous coronary intervention within 12h of symptom onset. Definitions of no-reflow were (1) angiographic: final TIMI flow ≤2 or final TIMI flow 3 with a myocardial blush grade <2; (2) electrocardiographic: lack of ST segment resolution (≤50% reduction of ST segment elevation at 90min). Angiographic and electrocardiographic no-reflow was observed in 32 (59%) and 30 (56%) patients, respectively (only 9 patients had both type of no-reflow). Plasma levels of vWF were significantly higher in patients with angiographic no-reflow but not in those with electrocardiographic no-reflow. Also, vWF was the most powerful independent predictors of angiographic no-reflow (OR 3.8, 95% CI 1.1–12.9, p =0.033). Our results provide new insights into no-reflow pathophysiology with appealing therapeutic implications. [ABSTRACT FROM AUTHOR]

Abstract: The role of admission CRP levels on the prediction of poor myocardial perfusion grades after percutaneous coronary interventiın (PCI) in patients with acute myocardial infarction (AMI) has not been clearly elucidated. Dynamic nature of acute coronary syndromes is usually associated with spontaneous ischemia-reperfusion injury in infarct related artery. So we considered that poor myocardial perfusion after primary PCI is not only related to procedural factors and clinical characteristics of the patients but may also be related to microvascular damage starting before coronary intervention. We suggested that CRP mediated complement activation and neutrophil plugging may be the factors contributing to the development of microvascular damage in patients with AMI. [Copyright &y& Elsevier]

Abstract: When considering the clinical significance of admission high CRP levels in patients with acute myocardial infarction (AMI), it can be concluded that the development of poor myocardial perfusion may partially explain the relation between high CRP levels and poor clinical outcomes. We considered that poor myocardial perfusion after primary percutaneous coronary intervention (PCI) is not only related to procedural factors and clinical characteristics of the patients but may also be related with microvascular damage starting before PCI. We suggested that CRP mediated complement activation and neutrophil plugging may be the factors contributing to the development of microvascular damage in patients with AMI. Further large-scale randomized studies are needed to clarify the clinical utility of admission CRP levels in the prediction of poor myocardial perfusion after PCI in patients with ST segment elevation myocardial infarction. [Copyright &y& Elsevier]