(Circulation. 2000;101:e87.)
© 2000 American Heart Association, Inc.
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-Adrenergic Blockade in Myocardial Infarction
Department of Pathology Health Science Center at Syracuse, State University of New York, Syracuse, NY
| Introduction |
|---|
I read with interest the article by Gregorini et al1 that
showed that
-adrenergic blockade improves recovery of myocardial
perfusion and function after stenting in acute myocardial infarction
(AMI), and I suggest that this finding can be explained by a basic
principle of the spasm of resistance vessel (S-RV) concept of
ischemic heart disease (IHD), a theory that asserts that S-RV
induces symptoms in IHD.2
A basic premise of the concept is that severe ischemic injury is a major cause of S-RV, and it is known that injury incites S-RV.3 It seems reasonable that stenotic coronary artery disease (CAD) can cause sufficient ischemic injury to induce ischemic injuryinduced (II-I) S-RV, and the concept attributes effort angina to II-I S-RV; however, other vasoconstrictive forces, such as emotional stress, can also be operative. The severe necrotic injury of AMI is considered to cause continuing II-I S-RV and no-reflow (reduced myocardial perfusion),2 and the reduced perfusion studied by Gregorini et al1 is regarded as no-reflow. In keeping with these positions, there is evidence for both ischemic- and injury-induced coronary S-RV,2 and no-reflow has recently been attributed to S-RV by others.4
II-I S-RV is regarded as an expression of the hemostatic
response, which is a basic defensive or homeostatic mechanism designed
to prevent exsanguination after injury.3 Hemostasis
includes initial vasoconstriction and subsequent thrombosis, but local
thromboses would not be expected with ischemic injury because,
unlike the usual injury, vascular disruption does not occur; however,
no-reflow secondary to S-RV is assumed to
Milano, Italy
Pisa, Italy
Essen, Germany
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