Previous studies have shown that transient no-reflow during coronary intervention but with Thrombosis in Myocardial Infarction (TIMI) grade 3 flow at the completion of the procedure is associated with increased in-hospital and 6-month mortality. We hypothesized that the use of intravascular ultrasound before intervention could identify morphologic features that were predictive of transient no-reflow in patients who had acute coronary syndrome (ACS). We analyzed 220 patients with ACS who had suitable intravascular ultrasound images that were acquired before intervention. We defined "transient no-reflow" as TIMI grade 0, 1, or 2 flow during the procedure and TIMI grade 3 flow at the completion of the procedure. We defined "reflow" as good coronary flow (TIMI grade 3 flow) during and after the procedure. Patients were categorized to a transient no-reflow group (n = 20) or a reflow group (n = 200). In the transient no-reflow group, vessel area and amount of plaque burden in the culprit lesion were significantly greater than in the reflow group (vessel 20.8 +/- 5.4 vs 16.4 +/- 6.2 mm(2), p < 0.01; plaque burden 0.90 +/- 0.03 vs 0.83 +/- 0.08, p < 0.001). The presence of ruptured plaque, lipid pool-like images, and thrombus formation were significantly higher in the transient no-reflow group than in the reflow group. Multivariate analysis identified the presence of thrombus formation (odds ratio 4.53, 95% confidence interval 1.03 to 20.0, p = 0.04) and larger plaque burden (odds ratio 1.79, 95% confidence interval 1.01 to 3.23, p = 0.05) as independent predictors of transient no-reflow. In conclusion, lesion morphologies are different for transient no-reflow and reflow. These findings suggest that the presence of thrombus formation and large plaque burden increase the risk for developing transient no-reflow during coronary intervention for ACS.
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http://dx.doi.org/10.1016/j.amjcard.2005.07.104 | DOI Listing |
Curr Issues Mol Biol
January 2025
Institute of Experimental Medicine, Almazov National Medical Research Centre, 15B Parkhomenko Street, 194021 Saint Petersburg, Russia.
Myocardial ischemia-reperfusion injury increases myocardial microvascular permeability, leading to enhanced microvascular filtration and interstitial fluid accumulation that is associated with greater microvascular obstruction and inadequate myocardial perfusion. A burst of reactive oxygen species and inflammatory mediators during reperfusion causes myosin light chain kinase (MLCK)-dependent endothelial hyperpermeability, which is considered a preventable cause of reperfusion injury. In the present study, a single intravenous injection of MLCK peptide inhibitor PIK7 (2.
View Article and Find Full Text PDFLasers Med Sci
December 2024
Department of Cardiovascular Medicine, Hiroshima University Graduate School of Biomedical and Health Sciences, 1-2-3, Kasumi, Minami-ku, Hiroshima, 734-8551, Japan.
Excimer laser coronary angioplasty (ELCA) in percutaneous coronary intervention (PCI) is safe and effective. However, thrombotic complications after ELCA occasionally occur. This study aimed to evaluate the impact of lipid-rich plaque in both in-stent restenosis (ISR) and de novo lesions on thrombus formation and transient no-reflow after ELCA.
View Article and Find Full Text PDFNeurol Res Pract
November 2024
Department of Neurology, University Hospital Wurzburg, Josef-Schneider-Str. 11, 97080, Wurzburg, Germany.
Background: Despite high recanalization rates of > 90% after endovascular thrombectomy (EVT) clinical outcome in around 50% of treated acute ischemic stroke (AIS) patients is still poor. Novel treatments augmenting the beneficial effects of recanalization are eagerly awaited, but this requires mechanistic insights to explain and overcome futile recanalization.
Main Body: At least two mechanisms contribute to futile recanalization after cerebral large vessel occlusions (LVO): (i) the no reflow phenomenon as evidenced by randomly distributed areas without return of blood flow despite reperfusion of large cerebral arteries, and (ii) ischemia/reperfusion (I/R) injury, the paradoxically harmful aspect of blood flow return in transiently ischemic organs.
Commun Biol
March 2024
Key Laboratory of Growth Regulation and Translational Research of Zhejiang Province, School of Life Sciences, Westlake University, Hangzhou, China.
Ischemic stroke produces the highest adult disability. Despite successful recanalization, no-reflow, or the futile restoration of the cerebral perfusion after ischemia, is a major cause of brain lesion expansion. However, the vascular mechanism underlying this hypoperfusion is largely unknown, and no approach is available to actively promote optimal reperfusion to treat no-reflow.
View Article and Find Full Text PDFIran J Basic Med Sci
January 2024
Pharmaceutical Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran.
Ischemic disorders, including myocardial infarction, cerebral ischemia, and peripheral vascular impairment, are the main common reasons for debilitating diseases and death in Western cultures. Ischemia occurs when blood circulation is reduced in tissues. Reperfusion, although commanded to return oxygen to ischemic tissues, generates paradoxical tissue responses.
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