Skip to main content
Log in

Contraction band necrosis at the lateral borders of the area at risk in reperfused infarcts

Observations in a pig model of in situ coronary occlusion

  • Original Article
  • Published:
Virchows Archiv Aims and scope Submit manuscript

Abstract

The aim of this study was to test the hypothesis that increased mechanical stress at the lateral borders of the area at risk may render this area more susceptible to ischaemia/reperfusion injury in the absence of collateral flow. The spatial distribution of myocardial necrosis within the territory of a transiently occluded left anterior descending coronary artery was investigated in 31 porcine hearts submitted to 48 min of coronary occlusion and 6 h of reperfusion. Immediately before excising the heart, the left anterior descending coronary artery was re-occluded and 10% fluorescein was injected in the left atrium. The area at risk was imaged by ultraviolet illumination of the myocardial slices, and the area of necrosis by incubation in triphenyltetrazolium chloride. The area at risk was divided in four sectors and an index of eccentricity was calculated as the percent of the area of necrosis located in the two lateral sectors of the area at risk. The area of contraction band necrosis was measured in whole heart histological sections. Infarcts were generally small, and were composed almost exclusively of contraction band necrosis. There was a good correlation between the extent of the area of contraction band necrosis and infarct size (r=0.831, P<0.0005). The area of necrosis had a patchy appearance and was predominantly distributed along the lateral borders of the area at risk. This eccentric distribution was more prominent in smaller infarcts, and the eccentricity index was inversely correlated with infarct size (r=−0.471, P=0.007), suggesting that contraction band necrosis occurres first at the interface between control and reperfused myocardium in this model. These results are in agreement with a prominet role of mechanical factors in the genesis of myocardial necrosis during transient coronary occlusion.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

Similar content being viewed by others

References

  1. Batts K, Ackerman D, Edwards W (1990) Postinfarction rupture of the left ventricular free wall: clinicopathologic correlates in 100 consecutive autopy cases. Hum Pathol 21:530–535

    Google Scholar 

  2. Cinca J, Worner F, Carreño A, Coronel R, Soldevilla A, Pérez-Villa F, Janse MJ, Soler-Soler J (1992) T-Q, S-T segment mapping and hyperemia in reperfused pig heart with ischemic preconditioning. Am J Physiol 263:H1732-H1738

    Google Scholar 

  3. Coronel R, Fiolet JWT, Wilms-Shopman FJG, Opthof T, Schaapherder AFM, Janse MJ (1989) Distribution of extracellular potassium and electrophysiologic changes during two-stage coronary ligation in the isolated, perfused canine heart. Circulation 80:165–177

    Google Scholar 

  4. Fishbein MC, Maclean D, Maroko PR (1978) The histopathologic evolution of myocardial infarction. Chest 73:843–849

    Google Scholar 

  5. Frank JS, Brady AJ, Fransworth S, Mottino G (1986) Ultrastructure and function of isolated myocytes after calcium depletion and repletion. Am J Physiol 250:H265-H275

    Google Scholar 

  6. Fujiwara H, Ashraf M, Sato S, Millard RW (1982) Transmural cellular damage and blood flow distribution in early ischemia in pig hearts. Circ Res 51:683–693

    Google Scholar 

  7. Ganote C, Armstrong S (1993) Ischaemia and the myocyte cytoskeleton: review and speculation. Cardiovasc Res 27:1387–1403

    Google Scholar 

  8. Hearse J, Humphrey SM, Chain EB (1973) Abrupt reoxygenation of the anoxic potassium-arrested perfused rat heart: a study of myocardial enzyme release. J Mol Cell Cardiol 5:395–407

    Google Scholar 

  9. García-Dorado D, Théroux P, Desco M, Solares J, Elizaga J, Fernandez-Avilés F, Alonso J, Soriano J: Cell-to-cell interaction (1989) A mechanism to explain wave-front progression of myocardial necrosis. Am J Physiol 256:H1266-H1273

    Google Scholar 

  10. Garcia-Dorado D, Théroux P, Solares J, Alonso J, Fernandez-Avilés F, Elizaga J, Soriano J, Botas J, Muñoz R (1990) Determinants of hemorrhagic infarcts. Histologic observations from experiments involving coronary occlusion, coronary reperfusion and reocclusion. Am J Pathol 173:301–311

    Google Scholar 

  11. Garcia-Dorado D, Théroux P, Duran JM, Solares J, Alonso J, Sanz E, Muñoz R, Elizaga J, Botas J, Fernandez-Avilés F, Soriano J, Esteban E (1992) Selective inhibition of the contractile apparatus. A new approach to modification of infarct size, infarct composition, and infarct geometry during coronary artery occlusion and reperfusion. Circulation 85:1160–1174

    Google Scholar 

  12. Garcia-Dorado D, Oliveras J, Gili J, Sanz E, Pérez-Villa F, Barrabés J, Carreras MJ, Solares J, Soler Soler J (1993) Analysis of myocardial oedema by magnetic resonance imaging early after coronary artery occlusion with or without reperfusion. Cardiovasc Res 27:1462–1469

    Google Scholar 

  13. Griffith GCG, Hegde B, Oblath RW (1961) Factors in myocardial rupture. An analysis of two hundred and four cases at Los Angeles County Hospital between 1924 and 1955. Am J Cardiol 8:792–798

    Google Scholar 

  14. Litt MR, Jerremy RW, Wisman HS, Winkestein JA, Becker LC (1989) Neutrophil depletion limited to reperfusion reduces myocardial infarct size after 90 minutes of ischemia. Evidence for neutrophil mediated reperfusion injury. Circulation 80:1816–1827

    Google Scholar 

  15. Miyazaki S, Fujiwara H, Onodera T, Kihara Y, Matsuda M, Wu D-J, Nakamura Y, Kumada T, Sasayama S, Kawai C, Hamashima Y (1987) Quantitative analysis of contraction band and coagulation necrosis after ischemia and reperfusion in the porcine heart. Circulation 75:1074–1082

    Google Scholar 

  16. O'Brien P, Bosnjak Z, Warltier DC (1993) Recovery of contractile function of postischemic, reperfused myocardium. Influence of 2,3-Butanedione-2-monoxime. J Cardiovasc Pharmacol 21:693–700

    Google Scholar 

  17. Oliva PB, Hammill SC, Edwards WD (1993) Cardiac rupture: a clinically predictable complication of acute myocardial infarction. Report of 70 cases with clinicopathologic correlations. J Am Coll Cardiol 22:720–726

    CAS  PubMed  Google Scholar 

  18. Reimer KA, Jennings RB (1979) The “wavefront phenomenon” of myocardial ischemic cell death. II. Transmural progression of necrosis within the framework of ischemic bed size (myocardium at risk) and collateral flow. Lab Invest 40:633–644

    Google Scholar 

  19. Reimer KA, Jennings RB (1992) Myocardial ischemia, hypoxia, and infarction. In: Fozzard HA, Haber E, Jennings RB, Katz A, Morgan HE (eds) The heart and cardiovascular scientific fundations. Raven Press, New York, p 1886

    Google Scholar 

  20. Rousseau G, Hebert D, Libersan D, Khadil A, G SJ, Latour JG (1993) Importance of platelets in myocardial injury after reperfusion in the pressence of residual coronary stenosis in dogs. Am Heart J 125:1553–1563

    Google Scholar 

  21. Sabbah HN, Stein PD (1982) Effect of acute regional ischemia on pressure in the subepicardium and subendocardium. Am J Physiol 242:H240-H244

    Google Scholar 

  22. Savage RM, Wagner GS, Ideker RE, Podolsky SA, Hackel DB (1977) Correlation of postmortem anatomic findings with electrocardiographic changes in patients with myocardial infarction. Retrospective study of patients with typical anterior and posterior infarcts. Circulation 55:279–285

    Google Scholar 

  23. Siegmund B, Klietz T, Schwartz P, Piper HM (1991) Temporary contractile blockade prevents hypercontracture in anoxic-reoxygenated cardiomyocytes. Am J Physiol 260:H426-H435

    Google Scholar 

  24. Siegmund B, Koop A, Klietz T, Schwartz P, Piper HM (1990) Sarcolemmal integrity and metabolic competence of cardiomyocytes under anoxia-reoxygenation. Am J Physiol 258: H285-H291

    Google Scholar 

  25. Steenbergen C, Hill ML, Jennings RB (1985) Volume regulation and plasma membrane injury in aerobic, anaerobic, and ischemic myocardium in vitro. Effects of osmotic cell swelling on plasma membrane integrity. Circ Res 57:864–875

    Google Scholar 

  26. Steenbergen C, Hill ML, Jennings RB (1987) Cytoskeletal damage during myocardial ischemia: changes in vinculin immunofluorescence staining during total in vitro ischemia in canine heart. Circ Res 60:478–486

    Google Scholar 

Download references

Author information

Authors and Affiliations

Authors

Additional information

Partially supported by Grants 92/0443 from the Fondo de Investigaciones Sanitarias de la Seguridad Social, CRHG 07-92/79 from the Institut Català de la Salut, and Concerted Action BMH1-CT92/1501, BIOMED I Program from the European Union.

Rights and permissions

Reprints and permissions

About this article

Cite this article

Solares, J., Garcia-Dorado, D., Oliveras, J. et al. Contraction band necrosis at the lateral borders of the area at risk in reperfused infarcts. Vichows Archiv A Pathol Anat 426, 393–399 (1995). https://doi.org/10.1007/BF00191349

Download citation

  • Received:

  • Accepted:

  • Issue Date:

  • DOI: https://doi.org/10.1007/BF00191349

Key words

Navigation