Trial reportPloS one2015
Intravascular ultrasound observation of the mechanism of no-reflow phenomenon in acute myocardial infarction.
Trial report in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
4 citing papers in PubMed, 8 citations in OpenAlex.
- The role and mechanisms of microvascular damage in the ischemic myocardium.Cellular and molecular life sciences : CMLS · 2023Review
- Targeting the dominant mechanism of coronary microvascular dysfunction with intracoronary physiology tests.The international journal of cardiovascular imaging · 2017Review
- Prognostic Association of Circulating Neutrophil Count with No-Reflow in Patients with ST-Segment Elevation Myocardial Infarction following Successful Primary Percutaneous Intervention.Disease markers · 2017Article
- Clinic Predictive Factors for Insufficient Myocardial Reperfusion in ST-Segment Elevation Myocardial Infarction Patients Treated with Selective Aspiration Thrombectomy during Primary Percutaneous Coronary Intervention.BioMed research international · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo study the mechanism of the no-reflow phenomenon using coronary angiography (CAG) and intravascular ultrasound (IVUS).
methodsA total of 120 patients with acute myocardial infarction (AMI) who successfully underwent indwelling intracoronary stent placement by percutaneous coronary intervention (PCI). All patients underwent pre- and post-PCI CAG and pre-IVUS. No-reflow was defined as post-PCI thrombolysis in myocardial infarction (TIMI) grade 0, 1, or 2 flow in the absence of mechanical obstruction. Normal reflow was defined as TIMI grade 3 flow. The pre-operation reference vascular area, minimal luminal cross-sectional area, plaque cross-sectional area, lesion length, plaque volume and plaque traits were measured by IVUS.
resultsThe no-reflow group was observed in 14 cases (11.6%) and normal blood-flow group in 106 cases (89.4%) based on CAG results. There was no statistically significant difference in the patients' medical history, reference vascular area (no-flow vs. normal-flow; 15.5 ± 3.2 vs. 16.2 ± 3.3, p > 0.05) and lesion length (21.9 ± 5.1 vs. 19.5 ± 4.8, p > 0.05) between the two groups. No-reflow patients had a longer symptom onset to reperfusion time compared to normal blood-flow group [(6.6 ± 3.1) h vs (4.3 ± 2.7) h; p < 0.05] and higher incidence of TIMI flow grade < 3 (71.4% vs 49.0%, p < 0.05). By IVUS examination, the no-reflow group had a significantly increased coronary plaque area and plaque volume compared to normal blood-flow group [(13.7 ± 3.0) mm2 vs (10.2 ± 2.9) mm2; (285.4 ± 99.8) mm3 vs (189.7 ± 86.4) mm3; p < 0.01]. The presence of IVUS-detected soft plaque (57.1% vs. 24.0%, p < 0.01), eccentric plaque (64.2% vs. 33.7%, p < 0.05), plaque rupture (50.0% vs. 21.2%, p < 0.01), and thrombosis (42.8% vs. 15.3%) were significantly more common in no-reflow group.
conclusionThere was no obvious relationship between the coronary risk factors and no-reflow phenomenon. The symptom onset to reperfusion time, TIMI flow grade before stent deployment, plaque area, soft plaques, eccentric plaques, plaque rupture and thrombosis may be risk factors for the no-reflow phenomenon after PCI.
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