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| {{SI}}
| | #Redirect: [[No reflow phenomenon]] |
| {{WikiDoc Cardiology Network Infobox}}
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| {{CMG}}<br/>
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| '''Associate Editors-In-Chief:''' Jennifer Giuseffi, M.D.; David M. Leder, M.D.
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| ==Background==
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| The [[no reflow]], or slow flow, phenomenon refers to inadequate myocardial perfusion with evidence of persistent myocardial [[ischemia]] of a target vessel following [[thrombolysis]] or [[PCI|percutaneous coronary intervention (PCI)]] without angiographic evidence of mechanical obstruction.
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| ==Prevalence==
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| The prevalance of no flow and slow flow varies according to definition. It has been reported in anywhere from 11-30% of patients following [[thrombolysis]] or intervention in [[acute myocardial infarction]]. However, in routine, elective coronary intervention, the prevalence has been reported to be as low as 0.6-2%. This phenomenon appears to be more frequent during interventions on [[SVG|saphenous vein grafts (SVG)]] or thrombus containing lesions as well as during the use of rotational [[atherectomy]].
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| ==Associations==
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| Gender does not appear to play a role in this phenomenon, but it seems to occur more frequently in older patients and in those who did not experience pre-infarct [[angina]]. Admission [[hyperglycemia]] has also been associated with higher incidence of [[no reflow]] as well as worse outcomes. Lesions at high-risk for [[no reflow]] and slow flow include: [[diffuse]] [[atherosclerotic]] involvement, angiographic demonstrable [[thrombus]], irregular or ulcerative lesions, and long lesions with large plaque volume.
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| ==Mechanism==
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| The primary mechanism is [[micro-embolization]] of either plaque debris or thrombotic material to the distal micro-vasculature following balloon inflation or stent deployment. Another possible additional mechanism is [[arteriole]] [[vasospasm]] secondary to vasoactive agents, i.e. [[serotonin]], [[adenosine diphosphate]], [[thromboxane A2]], released by the embolized [[platelet]]-rich [[atheromatous]] material. Other factors that may contribute as well include microvascular plugging with [[platelets]] or [[leukocytes]], endothelial swelling, tissue edema compressing [[vasculature]], oxidative stress and inflammation.
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| ==Clinical Implications==
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| No reflow often appears suddenly, is associated with severe chest pain, ischemic ECG changes, and/or hemodynamic deterioration. This needs to be distinguished from slow flow, which can be caused by coronary dissection, macrothrombus formation, coronary vasospasm, or distal macroembolization.
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| The presence of no reflow is clinically important as its presence has been associated with a five to ten fold increase in mortality, as well as a high incidence of myocardial infarction (MI), left ventricular dysfunction, ventricular arrhythmias, early congestive heart failure and cardiogenic shock.
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| ==Goals of Treatment==
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| Restore normal blood flow through epicardial coronary arteries & microvasculature to prevent persistence of myocardial ischemia. No reflow needs to be distinguished from slow flow resulting from coronary artery dissection, thrombus, coronary vasospasm, or residual stenosis. These etiologies must be excluded as part of the treatment of no reflow. Ultimately, the goals are to improve outcomes, relieve chest pain and alleviate myocardial ischemia.
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| {{SIB}}
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| [[Category:Cardiology]]
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