Tags

Type your tag names separated by a space and hit enter

Heterogeneity of ventricular remodeling after acute myocardial infarction in rats.
Am J Physiol. 1992 Feb; 262(2 Pt 2):H486-95.AJ

Abstract

To determine the effects of acute myocardial infarction on the extent and distribution of systolic and diastolic wall stress on the surviving myocardium, coronary artery occlusion was produced in rats, and the animals were killed 1 wk later. After hemodynamic measurements in vivo, the characteristics of cardiac anatomy at end diastole and peak systole were mimicked in vitro by fixing hearts under diastolic conditions or barium-induced contracture. In the presence of infarcts inducing a 48% loss of myocytes, left ventricular failure was documented by increases in left ventricular minimal and end-diastolic pressures and decreases in peak systolic pressure and positive and negative rates of pressure change with time. End-diastolic and end-systolic volumes increased, whereas stroke volume and cardiac output diminished. Ventricular remodeling in diastole consisted of an increase in the longitudinal axis while both longitudinal and transverse mid-chamber diameters were augmented after systolic contraction. Left ventricular chamber volume enlarged by 44% through a 20% augmentation in the longitudinal diameter and increases in the transverse luminal diameter of 13, 21, 32, and 37% in four consecutive sites from the equatorial region to the apex. As a consequence of infarction, systolic thickening of the spared myocardium of the free wall was reduced progressively from the base to the apex. In the interventricular septum of the infarcted heart, systole thickening occurred mostly in the equatorial region and was reduced at the basal and apical portions. The interaction of hemodynamic impairment with the architectural rearrangements of the wall and chamber provoked a 1.9-fold increase in overall stress on the spared myocardium. However, diastolic stress was augmented by 6.8-fold, markedly exceeding the 1.1-fold increase in systolic stress. Thus large infarcts of the rat left ventricle due to left main coronary occlusion lead to a change in shape of the heart from ellipsoidal to cylindrical. The elevation in overall stress may condition the unfavorable long-term outcome of the infarcted heart.

Authors+Show Affiliations

Department of Medicine, New York Medical College, Valhalla 10595.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

1539707

Citation

Capasso, J M., et al. "Heterogeneity of Ventricular Remodeling After Acute Myocardial Infarction in Rats." The American Journal of Physiology, vol. 262, no. 2 Pt 2, 1992, pp. H486-95.
Capasso JM, Li P, Zhang X, et al. Heterogeneity of ventricular remodeling after acute myocardial infarction in rats. Am J Physiol. 1992;262(2 Pt 2):H486-95.
Capasso, J. M., Li, P., Zhang, X., & Anversa, P. (1992). Heterogeneity of ventricular remodeling after acute myocardial infarction in rats. The American Journal of Physiology, 262(2 Pt 2), H486-95.
Capasso JM, et al. Heterogeneity of Ventricular Remodeling After Acute Myocardial Infarction in Rats. Am J Physiol. 1992;262(2 Pt 2):H486-95. PubMed PMID: 1539707.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Heterogeneity of ventricular remodeling after acute myocardial infarction in rats. AU - Capasso,J M, AU - Li,P, AU - Zhang,X, AU - Anversa,P, PY - 1992/2/1/pubmed PY - 1992/2/1/medline PY - 1992/2/1/entrez SP - H486 EP - 95 JF - The American journal of physiology JO - Am J Physiol VL - 262 IS - 2 Pt 2 N2 - To determine the effects of acute myocardial infarction on the extent and distribution of systolic and diastolic wall stress on the surviving myocardium, coronary artery occlusion was produced in rats, and the animals were killed 1 wk later. After hemodynamic measurements in vivo, the characteristics of cardiac anatomy at end diastole and peak systole were mimicked in vitro by fixing hearts under diastolic conditions or barium-induced contracture. In the presence of infarcts inducing a 48% loss of myocytes, left ventricular failure was documented by increases in left ventricular minimal and end-diastolic pressures and decreases in peak systolic pressure and positive and negative rates of pressure change with time. End-diastolic and end-systolic volumes increased, whereas stroke volume and cardiac output diminished. Ventricular remodeling in diastole consisted of an increase in the longitudinal axis while both longitudinal and transverse mid-chamber diameters were augmented after systolic contraction. Left ventricular chamber volume enlarged by 44% through a 20% augmentation in the longitudinal diameter and increases in the transverse luminal diameter of 13, 21, 32, and 37% in four consecutive sites from the equatorial region to the apex. As a consequence of infarction, systolic thickening of the spared myocardium of the free wall was reduced progressively from the base to the apex. In the interventricular septum of the infarcted heart, systole thickening occurred mostly in the equatorial region and was reduced at the basal and apical portions. The interaction of hemodynamic impairment with the architectural rearrangements of the wall and chamber provoked a 1.9-fold increase in overall stress on the spared myocardium. However, diastolic stress was augmented by 6.8-fold, markedly exceeding the 1.1-fold increase in systolic stress. Thus large infarcts of the rat left ventricle due to left main coronary occlusion lead to a change in shape of the heart from ellipsoidal to cylindrical. The elevation in overall stress may condition the unfavorable long-term outcome of the infarcted heart. SN - 0002-9513 UR - https://www.unboundmedicine.com/medline/citation/1539707/Heterogeneity_of_ventricular_remodeling_after_acute_myocardial_infarction_in_rats_ L2 - https://journals.physiology.org/doi/10.1152/ajpheart.1992.262.2.H486?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -