Korean Circ J.  2007 Jun;37(6):235-243. 10.4070/kcj.2007.37.6.235.

The Open Artery Hypothesis

Affiliations
  • 1Cardiology Division, Department of Internal Medicine, St. Vincent's Hospital, College of Medicine, The Catholic University of Korea, Suwon, Korea. cmkim@vincent.cuk.ac.kr

Abstract

There is considerable clinical and experimental evidence of the benefit of late reperfusion of infarct-related arteries, referred to as the open artery hypothesis, in patients with acute myocardial infarction who presented too late to salvage at-risk ischemic myocardium. In addition to myocardial salvage, reperfusion of the infarct-related artery prevents infarct expansion, reduces development of ventricular remodeling, and decreases ventricular arrhythmia. The Occluded Artery Trial recently answered a major question related to the open artery hypothesis in a high-risk, asymptomatic patient with an occluded infarct artery. In this review, clinical and experimental evidence of the benefit of the open artery hypothesis will be discussed.

Keyword

Myocardial infarction; Reperfusion; Ventricular remodeling

MeSH Terms

Arrhythmias, Cardiac
Arteries*
Humans
Myocardial Infarction
Myocardium
Reperfusion
Ventricular Remodeling

Figure

  • Fig. 1. Temporary circumflex coronary artery ligation and infarct size in a dog. Reperfusion after 18 and 25 minutes represents a period of reversible ischemia in which infarct transmurality is negligible. After 40 minutes, 3 hours, and 6 hours, however, reperfusion results showed a graded and time-dependent limitation of infarct size. The infarct size limitation following reperfusion after 40 minutes and 3 hours is significant compared with prolonged coronary artery occlusion (24 hours).4)

  • Fig. 2. Bar graph of left ventricular volume as determined by biplane angiography in survivors of first anterior Q wave infarction with paired studies performed at 3 weeks and 1 year after this initial infarction. Patients with a patent left anterior descending coronary artery at the initial catheterization did not demonstrate progressive enlargement over time. In contrast, patients with an occluded vessel supplying their infarcted region showed time-dependent ventricular enlargement; by 1 year (solid bar), these enlargements had increased above their baseline size († p<0.05) and had greater volumes (*p<0.05) than patients with patent vessels.10) LV: left ventricle.

  • Fig. 3. Univariate survival curves for total mortality by infarct artery patency.9)

  • Fig. 4. Photographs of transverse sections of rat left ventricle (LV) subjected to coronary occlusion for 21 days. A: noninfarcted (normal) sham-control rat with normal thickness of the LV wall. B: myocardial infarction without treatment (control), large transmural infarction of the anterior wall showing considerable thinning of the infarct compared with the septal wall and sham-control. The LV cavity was dilated. C: myocardial infarction with 2-(3-benzoyl-phenyl)-propionic acid(ketoprofen) injection. The LV cavity was more dilated than in the control, and the infarct scar is thinner than that of the control (A: hematoxylin-eosin stain, B&C: Masson's trichrome stain).32)

  • Fig. 5. Baseline left ventricular size and subsequent cardiovascular mortality. Baseline end-diastolic and end-systolic areas measured 11 days post-infarction are represented in quartiles. The figure shows that the 3-year cardiovascular mortality rate was greatest in the patients whose left ventricular size was in the upper quartile early post-infarction.34)

  • Fig. 6. Mechanisms of benefit. Early versus late open artery after acute myocardial infarction.3) AMI: acute myocardial infarction, CHF: congestive heart failure, LV: left ventricle.


Reference

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