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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]

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]

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]

Copyright of Herz is the property of Springer Nature 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.)

Background: Endothelial dysfunction and no-reflow share microcirculatory obstruction as a common pathophysiological mechanism. This study evaluated the relationship between systemic peripheral endothelial dysfunction assessed by flow-mediated dilatation (FMD) of the brachial artery and no-reflow in patients with ST-segment elevation myocardial infarction (STEMI) who received successful fibrinolysis. Results: This study included 150 patients managed by the percutaneous coronary intervention (PCI) after successful fibrinolysis. Patients were divided according to coronary angiographic success into normal flow versus no-reflow groups. According to FMD measured through brachial artery ultrasound, patients were divided based on their endothelial function into endothelial dysfunction versus normal endothelial function. No-reflow occurred in 44 patients (29.3%). No-reflow patients had longer pain to door time (6.52 ± 1.82 vs 5.19 ± 1.85 h), more Killip class II (36.4% vs 16%, p = 0.006), and lower FMD (7.26 ± 1.92 vs 8.23 ± 2.76%, p = 0.036). Also, they showed more endothelial dysfunction; however, this difference was statistically nonsignificant (97.7% vs 87.7%, p = 0.055). One hundred and thirty-six patients (90.7%) had endothelial dysfunction. They were older (57.51 ± 5.92 vs 50.86 ± 4.55 years, p value ≤ 0.001), more smokers (41.2% vs 14.3%, p = 0.04). Patients with normal endothelial function had a more myocardial blush grade (MBG) 3 (78.6% vs 26.5%, p value = 0.001) in comparison with more MBG 2 in those with endothelial dysfunction (41.9% vs 14.3%, p value = 0.001). Endothelial dysfunction patients had nonsignificant more no-reflow (31.6% vs 7.1%, p-value: 0.06). There was a significant weak positive correlation between thrombolysis in myocardial infarction (TIMI) flow and FMD (r = 0.174, p = 0.033) and a significant moderate positive correlation between MBG and FMD (r = 0.366, p < 0.001). Patients with TIMI I flow had significantly lower FMD compared with patients with TIMI II and TIMI III flow post-PCI. FMD ≤ 6% could predict post-procedural TIMI I flow. Conclusions: In STEMI patients who underwent PCI within 24 h after successful fibrinolysis, those who had no-reflow showed worse peripheral systemic endothelial function as they had lower brachial artery FMD. Also, FMD showed a significant positive correlation with the post-procedural angiographic flow (TIMI flow and MBG). FMD ≤ 6% could predict TIMI I flow. [ABSTRACT FROM AUTHOR]

Copyright of Herz is the property of Springer Nature 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.)

Background: Following primary percutaneous coronary intervention (PCI), no-reflow is associated with a high rate of long-term unfavorable clinical outcomes. Despite the importance of early no-reflow prediction in cardiovascular medicine, noninvasive assessment is lacking. This study aimed to evaluate the preprocedural CHA2DS2 VASc score and the brachial artery flow-mediated dilation percentage (FMD%) as predictors of the no-reflow phenomenon in patients with acute ST-segment elevation myocardial infarction (STEMI) undergoing primary PCI. Results: This study included 150 patients who presented with acute STEMI, underwent primary PCI, and were divided into two groups according to the flow result, reflow group and a no-reflow group. The CHA2DS2 VASc score was calculated and evaluation of endothelial function by measuring the brachial artery FDM% was done for each patient before the procedure. There were 39 (26%) patients in the no-reflow group and 111 (74%) in the reflow group. The no-reflow patients were older and had significantly higher body mass index (BMI), higher frequency of diabetes mellitus, hypertension, history of heart failure, dyslipidemia, Killip class IV on admission, thrombus grade V, multiple affected vessels, conventional stenting, and multiple stents placement, longer ischemic times, higher CHA2DS VASc score, and lower brachial artery FMD% (p-values of < 0.05 for all). Moreover, there was a significant negative correlation between CHA2DS VAS score and preprocedural FMD%, with the higher the score indicating lower FMD among cases (p-value = 0.000). Conclusions: Preprocedural CHA2DS2 VASc score and the brachial artery FMD can be used as predictors for the no-reflow phenomenon in patients with STEMI, undergoing primary PCI. [ABSTRACT FROM AUTHOR]

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 < 0.001 respectively, with no significant difference between groups A and B, only the thrombus resolution in group B was significantly higher than group A; p < 0.001. Finally, 6-months, over-all MACE was significantly higher in group C (34.7% vs. 14.6% and 16.3%, 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. [ABSTRACT FROM AUTHOR]

It remains uncertain whether plasma D-dimer level can predict no-reflow in patients with STEMI who had pPCI after 48 h of symptom onset. This study retrospectively enrolled 229 consecutive patients who had pPCI for acute STEMI within 2–7 days of symptom onset between January 2008 and December 2018. Patients were divided into no-reflow group (TIMI flow grade 0–2) and reflow group (TIMI flow grade 3). Predictors of no-reflow were assessed by univariate and multivariate binary logistic regression analyses. Plasma D-dimer level can independently predict no-reflow in patients with STEMI who had pPCI within 2–7 days of symptom onset (OR 2.52 per 1 mg/L increase, 95% CI 1.16–5.47, p = 0.019). This finding indicated that pPCI may be safe and feasible for STEMI patients within 2–7 days of symptom onset with low D-dimer level. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Because the phenomenon of no reflow has a poor prognosis in ST-segment elevation myocardial infarction (STEMI) patients and the atherogenic index of plasma (AIP) has been shown to be a strong predictor of coronary heart disease, we aimed to investigate the relationship between AIP and no-reflow in patients with acute STEMI who underwent primary percutaneous coronary intervention (PCI). A total of 763 consecutive STEMI patients (648 men; mean age 58 ± 12 years) who underwent primary PCI were recruited for this study. The patients were classified into a reflow group (n = 537) and a no-reflow group (n = 226) according to the postprocedural angiographic features of thrombolysis in the myocardial infarction flow of the infarct-related artery. The AIP value was significantly higher in the no-reflow group than in the reflow group [0.50 (0.38-0.65) vs. 0.39 (0.25-0.49) p < .001], and AIP was found to be an independent predictor of no-reflow development. The best cut-off value of AIP for predicting no-reflow was 0.54, with sensitivity of 46.02 and specificity of 84,73. In addition, the predictive power of AIP was greater than that of triglycerides and high-density lipoprotein cholesterol based on a receiver operator curve comparison. The AIP was independently associated with no-reflow in patients with STEMI after primary PCI. This might be a superior indicator compared to traditional lipid profiles. [ABSTRACT FROM AUTHOR]

Cardioprotection aims at infarct size reduction and improvement of clinical outcome from myocardial infarction. The translation of cardioprotection from preclinical and promising proof-of-concept studies to clinical benefit for patients has been largely disappointing. Almost all of these studies which did not translate into clinical benefit had infarct size reduction as the primary endpoint and used protocols selected to achieve infarct size reduction. The present review puts forward the hypothesis that the coronary circulation is a so far neglected target of cardioprotection. Mechanisms of ischemia–reperfusion injury to the coronary circulation are detailed. Clinical methods and measures to assess coronary microvascular impairment in reperfused acute myocardial infarction are presented. A comparison of magnetic resonance imaging data on infarct size vs. coronary microvascular obstruction is made. Finally, the design of studies which are optimized not only for infarct size reduction but also for salvage of the coronary microcirculation is advocated. [ABSTRACT FROM AUTHOR]

No-reflow (NR) is one of the major complications of primary percutaneous coronary intervention (PCI) in patients with non-ST-segment elevation myocardial infarction (NSTEMI). We aim to assess the value of multilayer longitudinal strain parameter to predict NR in patients with NSTEMI and preserved ejection fraction. 230 consecutive patients who were admitted to the emergency department and diagnosed with NSTEMI were prospectively included in this study. Echocardiography was performed 1 h before angiography. Specific analysis for endocardial, mid-myocardial and epicardial layers were performed by two-dimensional (2D) speckle tracking echocardiography (STE) for multilayer longitudinal strain. NR was described as flow grade of ≤ TIMI 2 when mechanical occlusions like dissection, intimal tear, arterial spasm and thromboembolism during angiography were excluded. 49 of 168 patients admitted to the study had NR. No significant differences were observed between the groups regarding age and gender. Multilayer longitudinal strain imaging (endocard, midmyocard and epicard) revealed lower strain values particularly in endocardial layer in patients with NR (GLS-endocard: - 14.14 ± 1.39/- 17.41 ± 2.34, p < 0.001; GLS-midmyocard: - 14.81 ± 1.40/17.81 ± 2.22, p < 0.001; GLS-epicard: - 16.14 ± 1.38/18.22 ± 2.00, p < 0.001). GLS-endocard, GLS-midmyocard, GLS-epicard and ST depression were found to be statistically significant independents parameters respectively to predict NR phenomenon (GLS-endocard: OR: 2.193, p < 0.001; GLS-midmyocard: OR: 1.510, p: 0.016; GLS-epicard: OR: 1.372, p: 0.035; ST depression: OR: 3.694, p: 0.014). We revealed that left ventricular strain study with speckle tracking echocardiography predicts NR formation. This noninvasive method may be useful for detecting NR formation in patients with NSTEMI. [ABSTRACT FROM AUTHOR]

Abstract 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 < 0.001). In adjusted multivariate analysis, preprocedural RWPT was found to be among independent predictors for NR (OR: 26.2, 95% CI: 6.5–105.1, P < 0.001). The predictive power of preprocedural RWPT was statistically non-inferior to ST-resolution (STR)% (difference between area under curves = 0.029, P = 0.595). Conclusion RWPT is strongly associated with and significantly predicts the development of NR. This association was statistically non-inferior to the well-known association between STR% and NR. [ABSTRACT FROM AUTHOR]

Attenuated plaque on intravascular ultrasound (IVUS) and low attenuation plaque on computed tomography angiography (CTA) are associated with no-reflow phenomenon during percutaneous coronary intervention (PCI). However, evaluation by a single modality has been unable to satisfactorily predict this phenomenon. We investigated whether the combination of IVUS and CTA findings can ameliorate the predictive potential for no-reflow phenomenon after stent implantation during PCI in stable coronary artery disease (CAD). A total of 988 lesions of 707 stable CAD patients who underwent coronary CTA before PCI were enrolled. PCI was performed with preprocedural IVUS and stent implantation. As for plaque characters, very low attenuation plaque (CTA v-LAP) whose minimum density was < 0 Hounsfield units on CTA and attenuated plaque (IVUS AP) on IVUS were evaluated. No-reflow phenomenon was observed in 22 lesions (2.2%) of 19 patients (2.7%). Both CTA v-LAP and IVUS AP were much more frequently observed in patients with no-reflow phenomenon. Positive (PPV) and negative predictive values (NPV) and accuracy for prediction of no-reflow were almost equivalent between CTA v-LAP (13.2, 99.6, and 87.0%) and IVUS AP (15.7, 99.8, and 89.0%). The combination of CTA v-LAP and IVUS AP markedly ameliorated PPV (31.7%) without deterioration of NPV (99.7%) and increased the diagnostic accuracy (95.5%). These findings showed that the combination of CTA v-LAP and IVUS AP improved the predictive power for no-reflow phenomenon after coronary stenting in stable CAD patients, suggesting the usefulness of combined estimation by using CTA and IVUS for predicting no-reflow phenomenon during PCI in clinical practice. [ABSTRACT FROM AUTHOR]

This study sought to investigate the association of baseline serum cystatin C levels with myocardial perfusion and cardiac functional recovery in patients with ST-segment elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PPCI). 108 patients with a first anterior STEMI who underwent PPCI were enrolled. Serum cystatin C was measured by immunoturbidimetric method. Patients were divided into two groups according to the median cystatin C levels on admission: group 1 (≥median, n = 54) and group 2 (

Early reperfusion represents the key strategy in ST elevation myocardial infarction. However, reperfusion may induce myocardial damage due to the reperfusion myocardial injury, compromising the full potential of reperfusion therapy and accounting for unfavourable results in high risk patients. Adenosine seems to attenuate ischemia reperfusion injury, and thus represents a promising therapeutic option for treating such patients. However, previous randomized clinical trials have collectively failed to demonstrate whether adenosine can effectively reduce measures of myocardial injury and improve clinical outcome, despite its good basic evidence. The failure of such trials to show a real beneficial action may be in part related to specific factors other than adenosine's clinical efficacy. The purpose of this review is to explain the rationale for the use of adenosine as an adjunctive pharmacological cardio-protective agent following reperfusion of the ischemic myocardium, to address the weakness of previous trials and to summarize the current state of knowledge regarding the effect of adenosine administration on reperfusion myocardial injury in patients with myocardial infarction. Although some preclinical and clinical studies point towards the beneficial role of adenosine in the prevention and treatment of no-reflow phenomenon in myocardial infarction, many unanswered questions still remain, including the optimal clinical indication, mode, dosage, duration and timing of application, and the exact mechanisms leading to potential benefits. Clarifying these issues will depend on further properly designed, adequately powered and well conducted clinical trials, which will probably provide us with the definite answers. [ABSTRACT FROM AUTHOR]

A high proportion of primary percutaneous coronary interventions performed in the setting of acute myocardial infarction, concur with inadequate myocardial perfusion at the microvascular level. This phenomenon, known as 'no-reflow' contributes to reperfusion injury, poor prognosis and to unfavorable clinical outcome. In this study, we evaluated the hypothesis that the synthetic 17β-aminoestrogen Prolame, may confer cardioprotection and prevent against no-reflow. In an open-chest model of 30-min ischemia and 90-min reperfusion, male Wistar rats were randomly assigned to different groups: Control, Prolame, Prolame followed by the nitric oxide synthase inhibitor ( l-NAME), and 17β-estradiol. Areas of risk, infarct size and no-reflow were determined by planimetry with triphenyltetrazolium chloride and thioflavin- S stains. Structural damage of the vasculature was measured as capillary compression in clarified tissue after intra-atrial injection of Microfil. Hemodynamic function was obtained at the end of stabilization, ischemia and reperfusion; nitric oxide (NO·) content was determined indirectly using the Griess reaction. Activation of the eNOS signaling cascade was determined by western blot. Prolame reduced the infarcted area, decreased the zones of no-reflow and capillary compression by activating the PI3K/Akt/eNOS signaling pathway in correlation with NO· increase. Prolame also activated endothelial cells augmenting NO· production, which was inhibited by ICI182780 (a selective estrogen receptor down-regulator), supporting the notion that the cardioprotective effect of Prolame involves the preservation of endothelium through the activation of estrogen receptor downstream signaling. Our results provide evidence that Prolame has potential therapeutic application in patients with AMI, as it prevents from both vascular and cardiac tissue damage. [ABSTRACT FROM AUTHOR]

D-dimer is a final product of fibrin degradation and gives an indirect estimation of the thrombotic burden. We aimed to investigate the value of plasma D-dimer levels on admission in predicting no-reflow after primary percutaneous coronary intervention (p-PCI) and long-term prognosis in patients with ST segment elevation myocardial infarction (STEMI). We retrospectively involved 569 patients treated with p-PCI for acute STEMIs. We prospectively followed up the patients for a median duration of 38 months. Angiographic no-reflow was defined as postprocedural thrombolysis in myocardial infarction (TIMI) flow grade <3 or TIMI 3 with a myocardial blush grade <2. Electrocardiographic no-reflow was defined as ST-segment resolution <70 %. The primary clinical end points were mortality and major adverse cardiovascular events (MACE). The incidences of angiographic and electrocardiographic no-reflow were 31 and 39 % respectively. At multivariable analysis, D-dimer was found to be an independent predictor of both angiographic ( p < 0.001), and electrocardiographic ( p < 0.001) no-reflow. Both mortality (from Q1 to Q4, 5.7, 6.4, 11.3 and 34.1 %, respectively, p < 0.001) and MACE (from Q1 to Q4, 17.9, 29.3, 36.9 and 52.2 %, respectively, p < 0.001) rates at long-term follow-up were highest in patients with admission D-dimer levels in the highest quartile (Q4), compared to the rates in other quartiles. However, Cox proportional hazard model revealed that high D-dimer on admission (Q4) was not an independent predictor of mortality or MACE. In contrast, electrocardiographic no-reflow was independently predictive of both mortality [Hazard ratio (HR) 2.88, 95 % confidence interval (CI) 1.04-8.58, p = 0.041] and MACE [HR 1.90, 95 % CI 1.32-4.71, p = 0.042]. In conclusion, plasma D-dimer level on admission independently predicts no-reflow after p-PCI. However, D-dimer has no independent prognostic value in patients with STEMI. [ABSTRACT FROM AUTHOR]

The aim of the study was to assess the frequency and predictive factors of microvascular obstruction (MVO) in patients with non-ST-segment elevation myocardial infarction (NSTEMI). This study included 190 consecutive patients with NSTEMI who underwent percutaneous coronary intervention (PCI) within 24 h after admission and cardiac magnetic resonance (CMR) imaging, 4.1 days after angiography. MVO was defined using the CMR criteria. MVO was detected 26 of 190 patients (13.8 %). Patients with MVO had higher peak high-sensitivity troponin T, creatine-kinase and creatine kinase-myocardial band levels and higher proportions of those with baseline thrombolysis in myocardial infarction (TIMI) flow grade 0-1, absence of collateral circulation, post-PCI TIMI flow grade <3, myocardial blush grade <3 and angiographic no-reflow than patients without MVO. Patients with MVO had larger initial area at risk [median (25th-75th percentiles), 23.9 % (17.4-33.9 %) vs. 16.1 % (7.8-27.7 %), P = 0.018] and infarct size [11.4 % (6.6-19.2 %) vs. 1.4 % (0-4.7 %) of the left ventricle, P < 0.001] than patients without MVO. In multivariable analysis, the culprit lesion localization in the circumflex coronary artery [adjusted odds ratio (OR) 13.71, 95 % confidence interval 2.91-64.58, P < 0.001] and the infarct size [adjusted OR 3.37 (1.80-6.29), P < 0.001, for each 5 % of the left ventricle] were independently associated with the increased risk for MVO. In patients with NSTEMI undergoing early PCI, the MVO defined by CMR imaging was present in 13.8 % of the patients. The localization of culprit lesion in the circumflex coronary artery and larger infarct size were independently associated with the increased risk for MVO. [ABSTRACT FROM AUTHOR]

Objective: To evaluate whether garlicin can prevent reperfusion no-reflow in a catheter-based porcine model of acute myocardial infarction (AMI). Methods: Twenty-two male Chinese mini swines were randomized into 3 groups: sham-operation group ( n=6), control group ( n=8), and garlicin group ( n=8). The distal part of left anterior descending coronary artery (LAD) in swines of the latter two groups was completely occluded by dilated balloon for 2 h and a successful AMI model was confirmed by coronary angiography (CAG) and electrocardiograph (ECG), which was then reperfused for 3 h. In the sham-operation group, balloon was placed in LAD without dilatation. Garlicin at a dosage of 1.88 mg/kg was injected 10 min before LAD occlusion until reperfusion for 1 h in the garlicin group. To assess serial cardiac function, hemodynamic data were examined by catheter method before AMI, 2 h after occlusion and 1, 2, and 3 h after reperfusion. Myocardial contrast echocardiography (MCE) and double staining with Evans blue and thioflavin-S were performed to evaluate myocardial no-reflow area (NRA) and risk area (RA). Results: Left ventricular systolic pressure and left ventricular end-diastolic pressure significantly improved in the garlicin group after reperfusion compared with the control group P<0.05) and 2 h after AMI ( P<0.05). MCE showed garlicin decreased reperfusion NRA after AMI compared with the control group ( P <0.05). In double staining, NRA/RA in the garlicin group was 18.78%, significantly lower than that of the control group (49.84%, P<0.01). Conclusions: Garlicin has a preventive effect on the porcine model of myocardial infarction reperfusion no-reflow by improving hemodynamics and decreasing NRA. [ABSTRACT FROM AUTHOR]

The objective of this study was to evaluate the clinical efficacy and safety of nitroprusside injection for preventing the slow-flow/no-reflow phenomenon after percutaneous coronary intervention (PCI). We searched the Cochrane Central Register of Controlled Trials (Issue 2, 2011), PubMed, EMbase, and Google Scholar for data. Two reviewers independently evaluated the quality of the included studies and extracted the data. A meta-analysis was performed using RevMan 5.0 software. Four randomized controlled trials (RCTs) involving 319 patients were included. The results of the meta-analyses showed that intracoronary nitroprusside is beneficial in preventing no-reflow/slow-flow, in reducing corrected TIMI frame count, and in improving left ventricular ejection fraction. It also likely reduces adverse reactions in patients after PCI and rehospitalization due to cardiovascular events. However, we must caution that in this review, there is a moderate possibility of bias with regard to patient selection, performance, and publication because of the small number of included studies. A larger sample size and high-quality RCTs are needed for a more reassuring analysis. [ABSTRACT FROM AUTHOR]

The present study evaluated the efficacy of intracoronary administration of verapamil to attenuate the no-reflow phenomenon following the primary percutaneous coronary intervention (PCI) in patients with the ST-segment elevation acute myocardial infarction (STEMI). A total of 201 patients with STEMI who underwent primary PCI within 12 h from the beginning of the heart attack were included. The no-reflow phenomenon was defined as substantial coronary anterograde flow of TIMI ≤2. Verapamil (100–200 μg) was injected into coronary artery immediately after no-reflow; the coronary arteriography was repeated later. Hundred and ninety-eight patients with STEMI successfully underwent primary PCI, and 246 stents were implanted with the average of 1.2 stents per patient. No-reflow occurred in 25 out of 198 patients (12.6 %). Twenty-one (84 %) patients developed the flow of TIMI ≥3 after intracoronary administration of verapamil, as revealed by repeated coronary angiography. Two patients developed transient hypotension which normalized without treatment within 3–5 min. Three patients showed sinus bradycardia, in one patient there was transient II sinoatrial block, and one patient developed type 1 atrioventricular block. All adverse effects were alleviated after intravenous injection of atropine (0.5–1 mg). In conclusion, the no-reflow phenomenon following primary PCI in patients with STEMI is significantly improved by intracoronary administration of verapamil which is useful to reduce cardiovascular events during operation. [ABSTRACT FROM AUTHOR]

No-reflow after primary percutaneous coronary intervention (pPCI) may be reversible. 40 patients undergoing pPCI were evaluated by assessing either improvement or lack of changes regarding angiographic and electrocardiographic indexes of no-reflow between admission and pre-discharge. Myeloperoxidase (MPO; in nanograms per milliliter), C-reactive protein (CRP; in milligrams per liter), endothelin-1 (ET-1; in nanograms per milliliter), angiopoietin-2 (Ang-2, in picograms per milliliter), and their pre-discharge/basal values variations (Δ) were related to no-reflow evolution. ΔMPO and ΔCRP were greater in patients with sustained no-reflow or lack of ST-segment resolution (STR) as compared with those with reversible no-reflow or lack of STR ( p = 0.033, p = 0.04, p < 0.001, and p = 0.001, respectively), whereas ΔET-1 was similar in the two groups. ΔAng-2 was greater in patients with sustained no-reflow or lack of STR as compared with those with reversible no-reflow or lack of STR ( p = 0.01 and 0.044, respectively). Bigger ΔMPO, ΔCRP (increasing levels), and ΔAng-2 (decreasing levels) are associated with sustained no-reflow, thus they might have a role in no-reflow evolution. [ABSTRACT FROM AUTHOR]

The myocardial microcirculation provides the vital pressure control and metabolic homeostasis for normal muscle function. Microvascular dysfunction is implicated in chronic cardiac disease and can signify higher risk, but its effect in acute myocardial infarction (AMI) can be profound. Modern management of AMI is focussed entirely on timely epicardial coronary patency, but as a result can leave microcirculatory devastation in its wake. The 'no-reflow' phenomenon occurs in up to 40 % of those successfully reperfused following an ST-elevation AMI (STEMI), and reflects significant microvessel injury that at its most severe involves both microvascular obstruction (MVO) and intramyocardial haemorrhage. Myocardial contrast echocardiography and cardiac magnetic resonance imaging have both led the field in establishing MVO as the prime determinant of adverse left ventricular (LV) remodeling, LV dysfunction, heart failure and increased mortality. These imaging techniques will be essential to support future research endeavours and shift focus to the maintenance of microvascular flow in AMI. [ABSTRACT FROM AUTHOR]

Although epicardial blood flow can be restored by an early intervention in most cases, a lack of adequate reperfusion at the microvascular level is often a limiting prognostic factor of acute myocardial infarction (AMI). Our group has recently found that paracrine factors secreted from apoptotic peripheral blood mononuclear cells (APOSEC) attenuate the extent of myocardial injury. The aim of this study was to determine the influence of APOSEC on microvascular obstruction (MVO) in a porcine AMI model. A single dose of APOSEC was intravenously injected in a closed chest reperfused infarction model. MVO was determined by magnetic resonance imaging and cardiac catheterization. Role of platelet function and vasodilation were monitored by means of ELISA, flow cytometry, aggregometry, western blot and myographic experiments in vitro and in vivo. Treatment of AMI with APOSEC resulted in a significant reduction of MVO. Platelet activation markers were reduced in plasma samples obtained during AMI, suggesting an anti-aggregatory capacity of APOSEC. This finding was confirmed by in vitro tests showing that activation and aggregation of both porcine and human platelets were significantly impaired by co-incubation with APOSEC, paralleled by vasodilator-stimulated phosphoprotein (VASP)-mediated inhibition of platelets. In addition, APOSEC evidenced a significant vasodilatory capacity on coronary arteries via p-eNOS and iNOS activation. Our data give first evidence that APOSEC reduces the extent of MVO during AMI, and suggest that modulation of platelet activation and vasodilation in the initial phase after myocardial infarction contributes to the improved long-term outcome in APOSEC treated animals. [ABSTRACT FROM AUTHOR]

Independent no-reflow predictors should be evaluated in female patients with ST-segment elevation acute myocardial infarction (STEMI) and successfully treated with primary percutaneous coronary intervention (PPCI) in the current interventional equipment and techniques, thus to be constructed a no-reflow predicting model. In this study, 320 female patients with STEMI were successfully treated with PPCI within 12 h after the onset of AMI from 2007 to 2010. All clinical, angiographic, and procedural data were collected. Multiple logistic regression analysis was used to identify independent no-reflow predictors. The no-reflow was found in 81 (25.3%) of 320 female patients. Univariate and multivariate stepwise logistic regression analysis identified that low SBP on admission <100 mmHg (OR 1.991, 95% CI 1.018-3.896; p = 0.004), target lesion length >20 mm (OR 1.948, 95% CI 1.908-1.990; p = 0.016), collateral circulation 0-1 (OR 1.952, 95% CI 1.914-1.992; p = 0.019), pre-PCI thrombus score ≥4 (OR 4.184, 95% CI 1.482-11.813; p = 0.007), and IABP use before PCI (OR 1.949, 95% CI 1.168-3.253; p = 0.011) were independent no-reflow predictors. The no-reflow incidence significantly increased as the numbers of independent predictors increased [0% (0/2), 10.8% (9/84), 14.5% (17/117), 37.7% (29/77), 56.7% (17/30), and 81.8% (9/11) in female patients with 0, 1, 2, 3, 4, and 5 independent predictors, respectively; p < 0.0001]. The five no-reflow predicting variables were admission SBP <100 mmHg, target lesion length >20 mm, collateral circulation 0-1, pre-PCI thrombus score ≥4, and IABP use before PCI in female patients with STEMI treated with PPCI. [ABSTRACT FROM AUTHOR]

lthough slow/no-reflow is a serious problem complicating primary percutaneous coronary interventions (PCI) for acute myocardial infarction (AMI) and is associated with a poor prognosis, its efficacious treatment remains problematic. We compared the acute, in-hospital and long-term (1 year) effects of nitroprusside (NTP) with those of nicorandil (NC) on the slow/no-reflow phenomenon. Forty-nine of 442 consecutive patients with AMI who underwent primary PCI complicated by slow/no-reflow and who received intracoronary NTP ( n = 25) or NC ( n = 24) administration were studied. Both NTP and NC induced significant improvements in coronary flow, with increases in TIMI flow grade from 1.64 ± 0.62 to 2.74 ± 0.36 ( p < 0.001) and 1.60 ± 0.86 to 2.23 ± 0.91 ( p < 0.001), and in corrected TIMI frame count from 37.8 ± 15.1 to 13.7 ± 7.1 ( p < 0.001) and 30.8 ± 20.7 to 19.3 ± 17.9 ( p < 0.001), respectively. The degree of improvement in TIMI flow grade (post-pre/pre) and TIMI frame count (pre-post/pre) showed that NTP was more effective than NC (NTP vs. NC: 0.88 ± 0.79, 0.37 ± 0.37, p = 0.008; 0.59 ± 0.23, 0.36 ± 0.27, p = 0.003, respectively). Congestive heart failure did not tend to last beyond 3 days after onset in the NTP group, which was more than in the NC group, during hospitalization (1/25, 4/24, p = 0.143, respectively). At the 1-year follow-up, the NTP group tended to show more improvement than the NC group in MACE (5/25, 9/24, p = 0.175, respectively). NTP is a more effective treatment for slow/no-reflow associated with PCI in patients with AMI and may improve long-term clinical outcomes compared with NC. [ABSTRACT FROM AUTHOR]

We developed a new filter-type distal protection guide wire, Filtrap, that uses a polyurethane filter with 1834 100-μm micropores covering the distal half of a spindle-shaped spiral Ni-Ti basket. The basket is 5 mm in diameter, self-expandable, and is mounted at the distal end of the system. This study aimed to assess the usefulness and safety of Filtrap during percutaneous coronary intervention (PCI). Early angiographic and in-hospital outcomes were reviewed in 14 patients, including 9 acute coronary syndrome patients, treated with Filtrap during PCI. All lesions were located in native coronary arteries but one was located in a saphenous vein graft. The Filtrap was successfully delivered and deployed distal to the lesion in 13 of 14 patients (93%). All PCI procedures including stent implantation were successfully completed except for 2 AMI patients, who ended up with Thrombolysis in Myocardial Infarction (TIMI) 2 coronary flow. One of these 2 patients had a distal embolization which occurred after thrombectomy before Filtrap insertion. The mean time of device insertion was 9.4 ± 3.2 min. Five patients showed transient no-reflow that was completely restored immediately with removal of the device. Embolic debris was entrapped in 8 (62%) of these cases. All patients were free from in-hospital events except for one patient with a large anterior acute myocardial infarction who received an emergency surgery due to a free wall cardiac rupture. These results suggest that the Filtrap is a practical and safe device for embolic protection during PCI. [ABSTRACT FROM AUTHOR]

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We have read with a great pleasure the letter of Dr. Cure et al. to the editor about our recent study which showed an association between atherogenic index of plasma (AIP) and no-reflow in patients with ST segment elevation myocardial infarction who underwent primary percutaneous coronary intervention. Dr Cure raises concerns about the miscalculation of AIP value that suggested choosing 'mmol/l' in equation instead of 'mg/dl'. As the AIP is the logarithmic transformation of triglyceride/high density lipoprotein; 'mmol/l' and an alternatively 'mg/dl' units can be used in the equation to calculate AIP values. Cure et al. also argue that our patients' lipoprotein levels were lower than expected. However, in a population based study and in several studies which were held in Turkey, the mean values of lipoprotein levels in Turkish population were nearly similar with our study population findings. We thank the authors' letter for pointing out these issues which we hope to have addressed. [ABSTRACT FROM AUTHOR]

No-reflow developed after coronary revascularization is an independent predictor of in-hospital mortality and poor clinical outcome. In this study, we investigated the difference between direct stenting and stenting with predilation, regarding to development of no-reflow in patients with acute coronary syndromes (ACS) and the role of fibrinolytic system in that phenomenon. Fifty eight patients with the diagnosis of ACS in whom percutaneous coronary intervention (PCI) was applied were included in study. Patients were divided into two groups according to stent application with and without predilation. Pre- and post-intervention corrected TIMI frame counts (cTFC) were calculated. Post-PCI plasminogen activator inhibitor-1 (PAI-1), tissue plasminogen activator (tPA), plasminogen and D-Dimer levels were measured. Pre-intervention cTFC values were similar between stenting with and without predilation groups ( P > 0.05). There was a significant decrease in post-intervention cTFC values in both groups ( P < 0.002 and P < 0.05, respectively). But, there was no significant difference between post-intervention cTFC values of the groups, regardless to stent implantation techniques. ( P > 0.05). In patients having high cTFC values compared with having low cTFC values; PAI-1 ( P = 0.002), tPA ( P = 0.015), plasminogen ( P = 0.040) and D-dimer ( P = 0.049) levels were significantly higher. Also, significant relationship was determined between cTFC and PAI-1, tPA, plasminogen, D-dimer levels ( P values 0.003, <0.05, <0.05, and <0.002, respectively). Results of this study indicated an important role of increased fibrinolytic activity in development of no-reflow phenomenon after PCI. We didn’t observe any differences between direct stenting and stenting with predilation according to the occurrence of no-reflow. [ABSTRACT FROM AUTHOR]

Obstruction of the coronary microvasculature contributes to the pathophysiology of MI and adversely affects post-MI recovery. This "no-reflow" phenomenon resulting from microvascular obstruction is an indicator of lack of adequate tissue perfusion within the infarcted myocardium, even after restoration of epicardial blood flow. Regions of microvascular obstruction can be detected and quantifed because of rapid advances in and refinement of imaging technologies over the past decade. This article focuses on the non-invasive imaging modalities used to assess MO, discusses the prognostic implications of MO, and briefly addresses strategies for reducing MO. [ABSTRACT FROM AUTHOR]

Both animal models of experimental myocardial infarction and clinical studies on reperfusion therapy for acute myocardial infarction have provided evidence of impaired tissue perfusion at the microvascular level after initiation of reperfusion despite adequate restoration of epicardial vessel patency. Characteristics of this “no-reflow” phenomenon found in basic science investigations, such as distinct perfusion defects, progressive decrease of resting myocardial flow with ongoing reperfusion and functional vascular alterations are paralleled by clinical observations demonstrating similar features during the course of reperfusion. In experimental animal investigations of coronary occlusion and reperfusion, this no-reflow phenomenon could be characterized as a fundamental mechanism of myocardial ischemia and reperfusion. Major determinants of the amount of no-reflow are the duration of occlusion, infarct size, but also the length of reperfusion, as rapid expansion of perfusion defects occurs during reperfusion. Moreover, no-reflow appears to persist over a period of at least four weeks, a period when major steps of infarct healing take place. The significant association of the degree of compromised tissue perfusion at four weeks and indices of infarct expansion, found in chronic animal models of reperfused myocardial infarction, might be the pathoanatomic correlate for the prognostic significance observed in the clinical setting. [ABSTRACT FROM AUTHOR]

Ischemic myocardial injury can be broadly characterized as either reversible or irreversible. Within irreversibly injured (infarcted) regions microvascular perfusion can vary from nearly normal to nearly zero, even in the presence of an open infarct-related artery (‘no-reflow’). Historically, non-invasive assessment of heterogeneous microvascular perfusion within myocardial infarcts has been problematic. More recently, however, contrast-enhanced MRI has emerged as a promising approach to the examination of these regions in patients with myocardial infarction. In this review we highlight a number of important animal and human studies of no-reflow regions examined using contrastenhanced MRI. These studies provide evidence that contrast- enhanced MRI can accurately characterize the presence and spatial extent of no-reflow regions, discriminate between areas of necrosis with and without no-reflow, and provide clinically meaningful predictive information regarding left ventricular remodeling and patient outcome [ABSTRACT FROM AUTHOR]

Background. During the past decade, experimental studies have provided convincing evidence that microcirculatory dysfunction plays a pivotal role in the manifestation of tissue injury in ischemia–reperfusion and osteomyocutaneous flap transfer. The study of the mechanisms of injury, however, requires sophisticated experimental in vivo models. With the use of microsurgical techniques, osteomyocutaneous flap transfer can successfully be performed in rat hind limbs, allowing in vivo fluorescent microscopic analysis of post-ischemic microcirculatory dysfunction in all tissues involved, including periosteum, striated muscle, subcutis and skin. The drawback of this “acute” model is that the period of analysis is restricted to a few hours only. Method. To overcome this limitation, the “chronic” dorsal skinfold chamber preparation, containing striated muscle and subcutis, can be used. This model allows one to study microcirculatory dysfunction after both tourniquet-induced and pressure-induced ischemia–reperfusion-induced tissue injury over a period of up to 3 weeks. Results. With the use of these models, recent investigations have demonstrated that ischemia–reperfusion and osteomyocutaneous flap transfer are associated with capillary perfusion failure (no-reflow), mediated by intravascular hemoconcentration, endothelial swelling and endothelin (ET)-1-mediated microvascular constriction. In addition, post-ischemic reperfusion provokes an inflammatory response (reflow paradox) in post-capillary venules, which is characterized by β2-integrin-mediated and intercellular adhesion molecule (ICAM)-1-mediated leukocyte adhesion and vascular hyperpermeability, which results in interstitial edema formation. Treatment studies have produced evidence that isovolemic hemodilution and heat shock protein induction are successful in ameliorating capillary no-reflow, while blockade of adhesion molecules, inactivation of oxygen radicals and, also, induction of heat shock proteins, are capable of reducing the post-ischemic inflammatory response. Conclusion. These experimental results not only demonstrate the importance of the use of advanced in vivo methods to delineate pathophysiological mechanisms in complex disease models, but may also provide a basis for potential prospective randomized trials to test the benefit for the patient in the daily clinical routine. [ABSTRACT FROM AUTHOR]

The effects of oral pretreatment with mioflazine (2.5 mg·kg) on regional myocardial reflow, infarct size reduction and hemodynamic recovery were studied in 24 anesthetized open-chest dogs undergoing 90 minutes of acute left anterior descending coronary artery (LAD) occlusion followed by 150 minutes of reperfusion. Regional myocardial blood flow was measured with tracer microspheres, and infarct size was determined by triphenyl tetrazolium chloride staining. Pretreatment with mioflazine resulted in a reduced diastolic aortic pressure (p<0.05) and an elevated cardiac output and LV dpdt max (p<0.05). These effects persisted throughout the experiment. In control animals (n=12) a hyperemic reflow response was found in the perfusion area of the LAD during the first minutes of reperfusion. After 150 min of reperfusion, however, the viable myocardium of the LAD area became underperfused, and almost no reflow was found in the infarcted zones. In the animals pretreated with mioflazine (n=12) the hyperemic response persisted throughout the reperfusion phase and the no-reflow phenomenon was prevented. Infarct size (expressed as percentage of perfusion area) tended to be smaller in this group: 23.7±12.4% versus 33.7±19.2% (p>0.05). Left atrial pressure increased during LAD occlusion in both groups but normalized completely in the drug-pretreated animals (p<0.05). It is concluded that pretreatment with mioflazine prevents the no-reflow phenomenon after reperfusion of an evolving infarction, tends to reduce infarct size and improves hemodynamic recovery. [ABSTRACT FROM AUTHOR]

The relationships among coronary perfusion pressure (0-150 cm HO), ventricular contracture, vascular resistance, and loss of perfusion of subendocardial myocardium were studied in anoxic isolated rat hearts. Coronary flow and myocardial pH and lactate concentrations were measured during 60 minutes, and the perfusable proportion of the ventricular wall determined after 15 and 60 minutes of global, substrate-free anoxic perfusion. Myocardial contracture in similarly treated hearts was indicated by the pressure exerted on left intraventricular balloons. Decreased perfusion pressure proportionately decreased both coronary flow and the extent of perfusion, and delayed the onset of contracture. The slower development of contracture was associated with a measured increase in lactate content and fall in pH within the ventricular wall. During anoxia the subendocardial myocardium progressively lost its capacity to be perfused, commencing at the onset of ventricular contracture, and continuing to extend even after maximum contracture pressures had been developed. Increased coronary perfusion pressures accelerated the rate of development of contracture but significantly reduced the extent of the perfusion defect, probably by opposing vascular compression. [ABSTRACT FROM AUTHOR]

Post-ischemic reperfusion impairment, ('no-reflow phenomenon'), was studied in rats subjected to 8-30 minutes of global brain ischemia. During ischemia, rapid and complete loss of cerebral blood flow, EEG andP-high energy phosphates (ATP/PCr) was observed. Brain intravascular perfusion defects were examined by injecting carbon black intravenously in a group of rats with stable cardiopulmonary function and in another group subjected to rapid thoracotomy and intraarterial infusion of the carbon marker. Results indicate that global brain ischemic or non-ischemic control rats given intraarterial carbon black after thoracotomy had varying degrees of vessel filling defects in brain resulting in 'pale tissue areas' suggestive of impaired perfusion (no-reflow). All rats given carbon black intravenously whether global brain ischemic or not, showed normal cerebrovascular filling of the carbon black and absence of 'pale tissue areas'. In addition, post-ischemic cerebral reperfusion following 8-30 minutes global brain ischemia can reverse neuroelectric, energy metabolite and cerebral blood flow loss in rats whose cardiopulmonary function is not compromised. These findings indicate that the 'no-reflow phenomenon' is an agonal or post-mortem artifact observed in the presence of cardiopulmonary failure. [ABSTRACT FROM AUTHOR]

Reperfusion after transient tissue ischemia constitutes an irrevocable need to preserve tissue viability. However, release of prolonged ischemia will either result in failure of the microcirculation to reperfusion ( no-reflow) and thus the prolongation of hypoxia, or in restoration of blood flow resulting in reoxygenation of the inflicted tissue. While ischemia damages the tissue primarily through hypoxia-induced depletion of energy stores, reoxygenation paradoxically contributes to tissue damage through the formation of oxygen radicals, the release of chemoattractant mediators (TNF, IL-1, LTB), and the activation of circulating polymorphonuclear leukocytes (PMNs). Through the action of chemoattractant mediators and the upregulation of leukocytic (CD11/CD18) and endothelial adhesion receptors (ICAM, GMP-140), activated PMNs adhere to the endothelium, release further chemoattractants and oxygen radicals and undertain a vicious circle, which will ultimately result in further tissue damage. Both the no-reflow phenomenon and the events initiated by reflow - termed herein as the reflow-paradox - contribute to the failure of the nutritive microvascular perfusion and loss of tissue viability following ischemia and reperfusion. [ABSTRACT FROM AUTHOR]

Objective: Successful resuscitation of the brain requires unimpaired blood recirculation. The study addresses the question of the severity and reversibility of no-reflow after cardiac arrest.Design: Adult normothermic cats were submitted to 5, 15 and 30 min cardiac arrest by ventricular fibrillation. The extent of no-reflow was assessed in each cardiac arrest group after 5 min closed chest cardiac massage in combination with 0.2 mg/kg epinephrine or after successful resuscitation followed by 30 min recirculation.Measurements and Results: Reperfusion of the brain was visualized by labelling the circulating blood with FITC-Albumin. Areas of no-reflow, defined as absence of microvascular filling, were identified by fluorescence microscopy at 8 standard coronal levels of forebrain, and expressed as percent of total sectional area. During cardiac massage, no-reflow affected 21 +/- 5%, 42 +/- 38% and 70 +/- 27% of forebrain after 5, 15 and 30 min cardiac arrest, respectively. After 30 min spontaneous recirculation following successful resuscitation of the heart, no-reflow significantly declined to 7 +/- 11% after 5 min cardiac arrest (p < 0.05) but persisted in 30 +/- 11% and 65 +/- 21% of forebrain after 15 and 30 min cardiac arrest, respectively (n.s.).Conclusion: Our observations demonstrate that resuscitation of the heart by closed chest massage causes severe (and after prolonged cardiac arrest irreversible) no-reflow of the brain. This suggests that no-reflow is an important cause of post-resuscitation brain pathology. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Purpose of Review: Coronary artery no-reflow phenomenon is an incidental outcome of percutaneous coronary intervention in patients presenting with acute myocardial infarction. Despite advances in pharmacologic and non-pharmacologic therapies, coronary no-reflow phenomenon occurs more commonly than desired. It often results in poor clinical outcomes and remains as a relevant consideration in the cardiac catheterization laboratory. In this systematic review, we have sought to discuss the topic in detail, and to relay the most recent discoveries and data on management of this condition.Recent Findings: We discuss several pharmacologic and non-pharmacologic treatments used in the prevention and management of coronary no-reflow and microvascular obstruction. Covered topics include the understanding of pharmacologic mechanisms of current and future agents, and recent discoveries that may result in the development of future treatment options.Summary: We conclude that the pathophysiology of coronary no-reflow phenomenon and microvascular obstruction still remains incompletely understood, although several plausible theories have led to the current standard of care for its management. We also conclude that coronary no-reflow phenomenon and microvascular obstruction must be recognized as a multifactorial condition that has certain predispositions and characteristics, therefore its prevention and treatment must begin pre-procedurally and be multi-faceted including certain medications and operator techniques in the cardiac catheterization laboratory. [ABSTRACT FROM AUTHOR]