CORRESPONDENCE: LETTER TO THE EDITOR
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Giampaolo Niccoli, MD, PhD*,
Francesco Burzotta, MD, PhD,
Leonarda Galiuto, MD, PhD and
Filippo Crea, MD, PhD
* Istituto di Cardiologia, Università Cattolica del Sacro Cuore, L.go A. Gemelli, 8, Rome 00168, Italy (Email: gniccoli73{at}hotmail.it).
We thank Drs. John R. and Roger Kapoor for their interest in our article (1) and for their comments on the role of coronary stent overexpansion in no-reflow. Iatrogenic coronary microvascular dysfunction (type D in the Camici-Crea classification) (2) has emerged as an important cause of microvascular dysfunction, especially in the setting of primary percutaneous coronary interventions (PCIs) (2). Thrombus and plaque material can mechanically plug microcirculation and further increase vasoconstriction due to the release of potent vasoconstrictors by platelets. Accurate planning of a primary PCI is of paramount importance including pharmacological prevention of distal embolization and vasoconstriction by administration of glycoprotein IIb-IIIa inhibitors and vasodilators, as well as mechanical prevention of thrombus dislodgment by thrombus aspiration, which has been shown to substantially improve microvascular function and survival in patients treated by a primary PCI (3). Another technical point to consider, whenever possible, is direct stenting, which seems to improve the microvascular function compared with stenting preceded by balloon pre-dilation (4). Furthermore, stent overexpansion as well as aggressive post-dilation should be avoided in this setting because of the higher risk of no-reflow, as shown by Maekawa et al. (5), probably due to the higher risk of distal embolization from unstable plaques compared with stable plaques (6). Finally, recent reports on the safety of the drug-eluting stent in the setting of a primary PCI (7) suggest its possible use in the attempt to reduce target lesion revascularization, as is the case in stable patients.
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1. Niccoli G, Burzotta F, Galiuto L, Crea F. Myocardial no-reflow in humans J Am Coll Cardiol 2009;54:281-292.[Abstract/Free Full Text]2. Camici PG, Crea F. Coronary microvascular dysfunction N Engl J Med 2007;356:830-840.[CrossRef][Web of Science][Medline] 3. Burzotta F, Crea F. Thrombus-aspiration: a victory in the war against no reflow Lancet 2008;371:1889-1890.[CrossRef][Web of Science][Medline] 4. Loubeyre C, Morice MC, Lefèvre T, Piéchaud JF, Louvard Y, Dumas P. A randomized comparison of direct stenting with conventional stent implantation in selected patients with acute myocardial infarction J Am Coll Cardiol 2002;39:15-21.[Abstract/Free Full Text] 5. Maekawa Y, Asakura Y, Anzai T, et al. Relation of stent overexpansion to the angiographic no-reflow phenomenon in intravascular ultrasound-guided stent implantation for acute myocardial infarction Heart Vessels 2005;20:13-18.[CrossRef][Web of Science][Medline] 6. Prati F, Pawlowski T, Gil R, et al. Stenting of culprit lesions in unstable angina leads to a marked reduction in plaque burden: a major role of plaque embolization?. A serial intravascular ultrasound study. Circulation 2003;107:2320-2325.[Abstract/Free Full Text] 7. Stone GW, Lansky AJ, Pocock SJ, et al. Paclitaxel-eluting stents versus bare-metal stents in acute myocardial infarction N Engl J Med 2009;360:1946-1959.[CrossRef][Web of Science][Medline]
Related Article
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Stent Overexpansion and Myocardial No-Reflow
- John R. Kapoor and Roger Kapoor
J. Am. Coll. Cardiol. 2009 54: 2340-2341.
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