No Reflow and Slow Flow
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Associate Editors-In-Chief: Jennifer Giuseffi, M.D.; David M. Leder, M.D.
Background
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 percutaneous coronary intervention (PCI) without angiographic evidence of mechanical obstruction.
Prevalence
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 saphenous vein grafts (SVG) or thrombus containing lesions as well as during the use of rotational atherectomy.
Associations
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.
Mechanism
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.
Clinical Implications
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.
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.
Goals of Treatment
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.
Treatment Choices
Prophylaxis
When intervening on high-risk lesions (see above for description) limit the amount of instrumentation within the target vessel, which includes minimizing overaggressive balloon or stent expansion. In patients undergoing rotational atherectomy, shorter runs, slower speeds and smaller initial burr size with small stepwise increases in burr size should be employed to help prevent no reflow. In addition, a cocktail of heparin, nitroglycerin and calcium channel blockers (CCB) should be infused simultaneously. Adding two arteriolar vasodilators, i.e. nicardipine and adenosine, to the flush "cocktail" may be helpful in further reducing incidence of no reflow, however traditionally the CCB used is verapamil.