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. 1982 Sep;48(3):265–271. doi: 10.1136/hrt.48.3.265

Coronary artery narrowing without irreversible myocardial damage or development of collaterals. Assessment of "critical" stenosis in a human model.

E Falk
PMCID: PMC481240  PMID: 7104120

Abstract

Postinfarction cardiac rupture is the result of thrombotic occlusion of a functional end artery with no previous myocardial damage in the perfusion area of the occluded artery. The pre-existing atherosclerotic stenosis at the site of thrombosis is thus"non-critical" in relation to development of collateral vessels and/or irreversible myocardial damage. Eleven cases of postinfarction cardiac rupture were studied by microscopy of cross-sections of the thrombosed segments. At the site of the thrombosis, pre-existing atherosclerosis had narrowed the lumen to 11% or less of its normal cross-sectional area. Maximal pre-existing narrowing of the proximal left anterior descending artery was found in a case with 97% stenosis (histologically measured cross-sectional area reduction) and an estimated residual lumen of 0.71 mm2. The prestenotic luminal area which is usually considered angiographically as "normal" was in all cases shown histologically to be severely narrowed by a diffuse intimal thickening. It is concluded that organic coronary stenosis must be far greater than 75% to be responsible for the development of collateral vessels and/or irreversible myocardial damage.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

  1. Arnett E. N., Isner J. M., Redwood D. R., Kent K. M., Baker W. P., Ackerstein H., Roberts W. C. Coronary artery narrowing in coronary heart disease: comparison of cineangiographic and necropsy findings. Ann Intern Med. 1979 Sep;91(3):350–356. doi: 10.7326/0003-4819-91-3-350. [DOI] [PubMed] [Google Scholar]
  2. BAHR G. F., BLOOM G., FRIBERG U. Volume changes of tissues in physiological fluids during fixation in osmium tetroxide or formaldehyde and during subsequent treatment. Exp Cell Res. 1957 Apr;12(2):342–355. doi: 10.1016/0014-4827(57)90148-9. [DOI] [PubMed] [Google Scholar]
  3. Baroldi G. Functional morphology of the anastomotic circulation in human cardiac pathology. Methods Achiev Exp Pathol. 1971;5:438–473. [PubMed] [Google Scholar]
  4. Cohen M. V. The functional value of coronary collaterals in myocardial ischemia and therapeutic approach to enhance collateral flow. Am Heart J. 1978 Mar;95(3):396–404. doi: 10.1016/0002-8703(78)90372-1. [DOI] [PubMed] [Google Scholar]
  5. Davies M. J., Woolf N., Robertson W. B. Pathology of acute myocardial infarction with particular reference to occlusive coronary thrombi. Br Heart J. 1976 Jul;38(7):659–664. doi: 10.1136/hrt.38.7.659. [DOI] [PMC free article] [PubMed] [Google Scholar]
  6. Gould K. L., Lipscomb K., Hamilton G. W. Physiologic basis for assessing critical coronary stenosis. Instantaneous flow response and regional distribution during coronary hyperemia as measures of coronary flow reserve. Am J Cardiol. 1974 Jan;33(1):87–94. doi: 10.1016/0002-9149(74)90743-7. [DOI] [PubMed] [Google Scholar]
  7. Hori M., Inoue M., Ohgitani N., Tsujioka K., Abe H., Fukui S., Minamino T. Site and severity of coronary narrowing and infarct size in man. Br Heart J. 1980 Sep;44(3):271–279. doi: 10.1136/hrt.44.3.271. [DOI] [PMC free article] [PubMed] [Google Scholar]
  8. Jones A. M. The functional role of intercoronary anastomoses. Acta Cardiol. 1965;(Suppl):130+–130+. [PubMed] [Google Scholar]
  9. Kalbfleisch H., Hort W. Quantitative study on the size of coronary artery supplying areas postmortem. Am Heart J. 1977 Aug;94(2):183–188. doi: 10.1016/s0002-8703(77)80278-0. [DOI] [PubMed] [Google Scholar]
  10. Lee J. T., Ideker R. E., Reimer K. A. Myocardial infarct size and location in relation to the coronary vascular bed at risk in man. Circulation. 1981 Sep;64(3):526–534. doi: 10.1161/01.cir.64.3.526. [DOI] [PubMed] [Google Scholar]
  11. Levin D. C., Kauff M., Baltaxe H. A. Coronary collateral circulation. Am J Roentgenol Radium Ther Nucl Med. 1973 Nov;119(3):463–473. doi: 10.2214/ajr.119.3.463. [DOI] [PubMed] [Google Scholar]
  12. MacAlpin R. N. Relation of coronary arterial spasm to sites of organic stenosis. Am J Cardiol. 1980 Jul;46(1):143–153. doi: 10.1016/0002-9149(80)90616-5. [DOI] [PubMed] [Google Scholar]
  13. Maseri A. Pathogenetic mechanisms of angina pectoris: expanding views. Br Heart J. 1980 Jun;43(6):648–660. doi: 10.1136/hrt.43.6.648. [DOI] [PMC free article] [PubMed] [Google Scholar]
  14. McMahon M. M., Brown B. G., Cukingnan R., Rolett E. L., Bolson E., Frimer M., Dodge H. T. Quantitative coronary angiography: measurement of the "critical" stenosis in patients with unstable angina and single-vessel disease without collaterals. Circulation. 1979 Jul;60(1):106–113. doi: 10.1161/01.cir.60.1.106. [DOI] [PubMed] [Google Scholar]
  15. Proudfit W. L., Shirey E. K., Sones F. M., Jr Distribution of arterial lesions demonstrated by selective cinecoronary arteriography. Circulation. 1967 Jul;36(1):54–62. doi: 10.1161/01.cir.36.1.54. [DOI] [PubMed] [Google Scholar]
  16. Rafflenbeul W., Urthaler F., Lichtlen P., James T. N. Quantitative difference in "critical" stenosis between right and left coronary artery in man. Circulation. 1980 Dec;62(6):1188–1196. doi: 10.1161/01.cir.62.6.1188. [DOI] [PubMed] [Google Scholar]
  17. WESSLER S., ZOLL P. M., SCHLESINGER M. J. The pathogeneis of spontaneous cardiac rupture. Circulation. 1952 Sep;6(3):334–351. doi: 10.1161/01.cir.6.3.334. [DOI] [PubMed] [Google Scholar]

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