Fibrillar collagen and remodeling of dilated canine left ventricle

Karl Weber, Ruth Pick, Marc A. Silver, Gordon W. Moe, Joseph S. Janicki, Irving H. Zucker, Paul W. Armstrong

Research output: Contribution to journalArticle

218 Citations (Scopus)

Abstract

To test the hypothesis that in the failing volume-overloaded ventricle, the extracellular matrix and fibrillar collagen in particular are major determinants of the architectural remodeling of the myocardium, this histopathological study of the dilated, postmortem canine left ventricle secondary to rapid ventricular pacing or aortocaval fistula was undertaken. Using the picrosirius-polarization technique to enhance collagen birefringence, we sought to examine the structural integrity of the collagen matrix and interstitium. In the dilated failing ventricle secondary to rapid pacing, we found 1) interstitial edema and a disruption or disappearance of collagen fibers that were apparent within 6 hours of pacing, persisted for weeks, and subsequently were associated with muscle fiber disorganization within the endomyocardium, 2) interstitial fibrosis that was present in the midwall and epimyocardium with chronic pacing, and 3) an early remodeling of intramyocardial coronary arteries that included medial swelling with smooth muscle degeneration followed by proliferative lesions involving fibroblasts and a subsequent perivascular and medial fibrosis. Many of these findings were still evident 48 hours after pacing had been discontinued. In contrast, the collagen matrix and interstitium seen with ventricular dilatation secondary to the circulatory overload that accompanies an aortocaval fistula were indistinguishable from that in sham-operated controls. Thus, we conclude that unlike the chamber enlargement and preserved ventricular function that accompany an aortocaval fistula, ventricular dilatation and failure caused by rapid pacing are based on an architectural remodeling of the myocardium. This structural dilatation involves the extracellular matrix and interstitium and appears to be related to altered permeability of intramyocardial coronary arteries. The mechanism or mechanisms involved in the pathogenesis of. myocardial remodeling with rapid ventricular pacing require further investigation.

Original languageEnglish (US)
Pages (from-to)1387-1401
Number of pages15
JournalCirculation
Volume82
Issue number4
DOIs
StatePublished - Jan 1 1990

Fingerprint

Fibrillar Collagens
Heart Ventricles
Canidae
Collagen
Fistula
Dilatation
Extracellular Matrix
Coronary Vessels
Myocardium
Fibrosis
Birefringence
Ventricular Function
Smooth Muscle
Permeability
Edema
Fibroblasts
Muscles

All Science Journal Classification (ASJC) codes

  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

Cite this

Weber, K., Pick, R., Silver, M. A., Moe, G. W., Janicki, J. S., Zucker, I. H., & Armstrong, P. W. (1990). Fibrillar collagen and remodeling of dilated canine left ventricle. Circulation, 82(4), 1387-1401. https://doi.org/10.1161/01.CIR.82.4.1387

Fibrillar collagen and remodeling of dilated canine left ventricle. / Weber, Karl; Pick, Ruth; Silver, Marc A.; Moe, Gordon W.; Janicki, Joseph S.; Zucker, Irving H.; Armstrong, Paul W.

In: Circulation, Vol. 82, No. 4, 01.01.1990, p. 1387-1401.

Research output: Contribution to journalArticle

Weber, K, Pick, R, Silver, MA, Moe, GW, Janicki, JS, Zucker, IH & Armstrong, PW 1990, 'Fibrillar collagen and remodeling of dilated canine left ventricle', Circulation, vol. 82, no. 4, pp. 1387-1401. https://doi.org/10.1161/01.CIR.82.4.1387
Weber K, Pick R, Silver MA, Moe GW, Janicki JS, Zucker IH et al. Fibrillar collagen and remodeling of dilated canine left ventricle. Circulation. 1990 Jan 1;82(4):1387-1401. https://doi.org/10.1161/01.CIR.82.4.1387
Weber, Karl ; Pick, Ruth ; Silver, Marc A. ; Moe, Gordon W. ; Janicki, Joseph S. ; Zucker, Irving H. ; Armstrong, Paul W. / Fibrillar collagen and remodeling of dilated canine left ventricle. In: Circulation. 1990 ; Vol. 82, No. 4. pp. 1387-1401.
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