Coronary no-reflow phenomenon: from the experimental laboratory to the cardiac catheterization laboratory.

Abstract

Coronary no-reflow occurs commonly during acute percutaneous coronary intervention, particularly in patients with acute myocardial infarction and those with degenerated vein grafts. It is associated with a guarded prognosis, and thus needs to be recognized and treated promptly. The pathophysiology originates during the ischemic phase and is characterized by localized and diffuse capillary swelling and arteriolar endothelial dysfunction. In addition, leukocytes become activated and are attracted to the lumen of the capillaries, exhibit diapedesis and may contribute to cellular and intracellular edema and clogging of vessels. At the moment of perfusion, the sudden rush of leukocytes and distal atheroemboli further contributes to impaired tissue perfusion. Shortening the door-to-balloon time, use of glycoprotein IIb/IIIa platelet receptor inhibitors and distal protection devices are predicted to limit the development of no-reflow during percutaneous interventions. Distal intracoronary injection of verapamil, nicardipine, adenosine, and nitroprusside may improve coronary flow in the majority of patients. Hemodynamic support of the patient may be needed in some cases until coronary flow improves.

• Authors: Shereif H Rezkalla, Robert A Kloner
• Journal: Catheterization and cardiovascular interventions : official journal of the Society for Cardiac Angiography & Interventions (Catheter Cardiovasc Interv) Vol. 72 Issue 7 Pg. 950-7 (Dec 01 2008) ISSN: 1522-726X [Electronic] United States
• PMID: 19021281 (Publication Type: Journal Article, Review)
• Copyright: Copyright 2008 Wiley-Liss, Inc.

Chemical References

• Platelet Aggregation Inhibitors
• Platelet Glycoprotein GPIIb-IIIa Complex
• Vasodilator Agents

Topics

• Angioplasty, Balloon, Coronary (adverse effects, instrumentation)
• Animals
• Coronary Circulation
• Diagnostic Techniques, Cardiovascular
• Embolism, Cholesterol (etiology, physiopathology)
• Humans
• Myocardial Ischemia (pathology, physiopathology, therapy)
• Myocardial Reperfusion Injury (etiology, physiopathology)
• Myocardium (pathology)
• No-Reflow Phenomenon (etiology, pathology, physiopathology, prevention & control)
• Platelet Aggregation Inhibitors (therapeutic use)
• Platelet Glycoprotein GPIIb-IIIa Complex (antagonists & inhibitors)
• Stents
• Vasodilator Agents (therapeutic use)