Angiographic Assessment of Reperfusion in Acute Myocardial Infarction by Myocardial Blush Grade

Henriques, José P.S.; Zijlstra, Felix; Hof, Arnoud W J van ‘t; Boer, Menko‐Jan de; Dambrink, Jan‐Henk E.; Gosselink, Marcel; Hoorntje, Jan C.A.; Suryapranata, Harry

doi:10.1161/01.cir.0000065221.06430.ed

Cited by 346 publications

(134 citation statements)

References 48 publications

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“…The frequency of MO of just over 30% observed in our population study with NSTEMI is close to that observed in patients with STEMI determined by CMR, myocardial contrast echography and angiographic methods (TIMI frame count score, myocardial blush grade) [1,2,3,4,5,6,7, 17, 18,20,21,22]. …”

Section: Discussionsupporting

confidence: 84%

“…Experimentally induced MO was initially described only after transient but complete obstruction (TIMI = 0) of a coronary artery [26]. In clinical studies, the infarct-related artery status at baseline correlated well (p < 0.05) with the microvascular status, and patients with MO had a significantly lower TIMI score at baseline than patients without [1, 20, 27]. One of the reasons for this difference is the low number of patients in our study, and therefore, the low statistical power.…”

Section: Discussionmentioning

confidence: 99%

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Presence and Extent of Cardiac Magnetic Resonance Microvascular Obstruction in Reperfused Non-ST-Elevated Myocardial Infarction and Correlation with Infarct Size and Myocardial Enzyme Release

Mewton¹,

Bonnefoy²,

Revel³

et al. 2008

Cardiology

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Objective: Microvascular obstruction (MO) is a factor of adverse outcome in patients with ST-elevated myocardial infarction (STEMI). We assessed the presence and extent of MO and its relationship with infarct size and left ventricular (LV) functional parameters after acute non-ST-elevated myocardial infarction (NSTEMI). Methods: Twenty-five patients with first acute NSTEMI underwent a cine and first-pass perfusion cardiac magnetic resonance (CMR) study, with late gadolinium enhancement imaging 72 h after myocardial infarction. Results: MO was detected in 32% of patients, and its extent comprised 0.5–3.1% of the total LV mass (mean 1.9 ± 1.2%). Patients with MO had a significantly larger infarct size than patients without (14.1 ± 5.9 vs. 5.3 ± 4.1% LV mass; p < 0.001). There was no significant difference between both groups for the LV functional parameters and LV ejection fraction (58.5 ± 6.8 vs. 62.6 ± 9.6%; p = 0.29). Patients with MO showed a higher troponin I release (570 ± 364 vs. 148 ± 103 IU; p = 0.003) and a higher creatine kinase release (29,887 ± 18,263 vs. 10,287 ± 5,283 IU; p = 0.007). Conclusions: In patients with acute NSTEMI, MO has a frequency similar to that observed in patients with STEMI and also correlates with the infarct extent. The prognostic significance on clinical outcome remains to be shown in this specific population.

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Section: Discussionsupporting

confidence: 84%

Section: Discussionmentioning

confidence: 99%

Presence and Extent of Cardiac Magnetic Resonance Microvascular Obstruction in Reperfused Non-ST-Elevated Myocardial Infarction and Correlation with Infarct Size and Myocardial Enzyme Release

Mewton¹,

Bonnefoy²,

Revel³

et al. 2008

Cardiology

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“…Nonetheless, effective epicardial and microcirculatory reperfusion, which was more frequently observed in patients treated with the MGuard than with a standard metallic stent, may improve long-term survival. 3,4,14 These observations require confirmation in larger randomized trials.…”

Section: Discussionmentioning

confidence: 96%

Mesh-Covered Embolic Protection Stent Implantation in ST-Segment–Elevation Myocardial Infarction

Dudek

Dziewierz

Brener

et al. 2015

Circ: Cardiovascular Interventions

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P rimary percutaneous coronary intervention (PCI), with stent implantation when feasible, is the recommended method of reperfusion in patients with ST-segment-elevation myocardial infarction (STEMI).1,2 Although stent implantation frequently restores normal epicardial coronary flow in patients with STEMI, myocardial reperfusion is often suboptimal and results in increased infarct size and mortality.3-5 Numerous strategies have been proposed to improve microvascular perfusion, including pharmacological agents (eg, glycoprotein IIb/IIIa inhibitors, adenosine) and mechanical approaches (eg, thrombus aspiration, distal protection devices).6-10 Meta-analyses of underpowered randomized trials suggested that manual aspiration thrombectomy might be associated with reduced 30-day mortality, with underlying improvements in epicardial and myocardial perfusion.11,12 However, in the large-scale, randomized Thrombus Aspiration in ST-Elevation Myocardial Infarction in Scandinavia (TASTE) trial, a survival benefit of routine manual aspiration thrombectomy during primary PCI was not observed. Background-The MGuard, a bare metal stent covered with a polymer mesh, was designed to reduce distal embolization during percutaneous coronary intervention in ST-segment-elevation myocardial infarction. In the MGUARD for Acute ST Elevation Reperfusion trial, the primary end point of complete ST-segment resolution was significantly improved with the MGuard compared with control. We evaluated 1-year clinical and angiographic results. Methods and Results-Patients with ST-segment-elevation myocardial infarction ≤12 hours undergoing primary percutaneous coronary intervention of a single de novo native lesion were randomized to the MGuard versus any commercially available metallic stent (39.8% drug-eluting). Clinical follow-up was performed through 1 year, and angiography at 13 months was planned in 50 MGuard patients. There was no difference in major adverse cardiac events (1.8% versus 2.3%; P=0.75) at 30 days between the groups. Major adverse cardiac events at 1 year were higher with the MGuard, driven by greater ischemia-driven target lesion revascularization (8.6% versus 0.9%; P=0.0003). Conversely, mortality tended to be lower with the MGuard at 30 days (0% versus 1.9%; P=0.04) and at 1 year (1.0% versus 3.3%; P=0.09). Late lumen loss at 13 months in the MGuard was 0.99±0.80 mm, and binary restenosis was 31.6%. Conclusions-In patients with ST-segment-elevation myocardial infarction undergoing primary percutaneous coronary intervention, a trend toward reduced 1-year mortality was present in patients treated with the MGuard stent. Target lesion revascularization and major adverse cardiac events rates during follow-up were higher in the MGuard group than in the control stent group, and angiographic late loss of the MGuard was consistent with that expected from bare metal stents. Clinical Trial Registration-URL: http://www.clinicaltrials.gov. Unique identifier: NCT01368471.(Circ Cardiovasc Interv. 2015;8:e001484.

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“…The mechanism of NR in primary angioplasty is thought to include peripheral embolism caused by debris (that originates in and is flushed from the atherosclerotic plaque), ischemia/reperfusion injury, coronary anatomy variability and individual predisposition [2]. NR predictors include male gender, advanced age [3], multivessel coronary disease [4], impaired kidney function [5], an elevated thromboxane A 2 (TXA 2 ) level [6], increased platelet reactivity [7], high levels of C-reactive protein (CRP) [8] and endothelin-1 [9], neutrophilia [10], elevated baseline glucose [3], anterior wall myocardial infarction [3] and a visible free-floating thrombus in a target coronary vessel [11]. …”

Section: Introductionmentioning

confidence: 99%

Aspirin ‘Resistance': Impact on No-Reflow, Platelet and Inflammatory Biomarkers in Diabetics after ST-Segment Elevation Myocardial Infarction

et al. 2015

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Background: The no-reflow (NR) phenomenon exists despite percutaneous coronary intervention (PCI), and is especially prevalent in diabetics. The causes(s) of NR are not fully elucidated, but may be associated with impaired residual platelet and inflammatory reactivity during dual-antiplatelet therapy. Objective: To assess the relationship between dual-antiplatelet therapy, NR and conventional biomarkers suggestive of platelet and inflammatory response in diabetics following ST-segment elevation myocardial infarction (STEMI) treated with PCI. Methods: Sixty diabetics with (n = 27) and without NR (n = 33) were prospectively enrolled. All patients were treated with clopidogrel and aspirin. Platelet and inflammatory biomarkers were assessed serially in the peripheral blood and right atrium before and after PCI and then at 24 h, 7 days and 30 days. Results: Arachidonic acid (AA)-induced platelet aggregation and the serum thromboxane B₂ level before and after PCI (in the peripheral and right atrium blood) were significantly higher in the NR patients than in those with no NR. AA-induced aggregation >100 (AUC*min) before PCI predicted NR in diabetic patients with 96.2% sensitivity and 38.5% specificity (AUC 0.66; 95% CI 0.52-0.71; p = 0.029). There were no other correlations between NR and platelet reactivity (collagen, adenosine diphosphate, thrombin receptor agonist peptide-induced aggregation, vasodilator-stimulated phosphoprotein platelet reactivity index, soluble P-selectin, soluble CD40 ligand, platelet-derived growth factor AB and the level of platelet-monocyte aggregates) or between NR and inflammatory indices (i.e. high-sensitivity C-reactive protein, interleukin 6 and interleukin 10). Conclusion: An inadequate response to aspirin, but not to clopidogrel, may be associated with the occurrence of the NR phenomenon in diabetics with STEMI who have been treated with primary PCI.

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Angiographic Assessment of Reperfusion in Acute Myocardial Infarction by Myocardial Blush Grade

Cited by 346 publications

References 48 publications

Presence and Extent of Cardiac Magnetic Resonance Microvascular Obstruction in Reperfused Non-ST-Elevated Myocardial Infarction and Correlation with Infarct Size and Myocardial Enzyme Release

Presence and Extent of Cardiac Magnetic Resonance Microvascular Obstruction in Reperfused Non-ST-Elevated Myocardial Infarction and Correlation with Infarct Size and Myocardial Enzyme Release

Mesh-Covered Embolic Protection Stent Implantation in ST-Segment–Elevation Myocardial Infarction

Aspirin ‘Resistance': Impact on No-Reflow, Platelet and Inflammatory Biomarkers in Diabetics after ST-Segment Elevation Myocardial Infarction

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