Cellular mechanisms of myocardial infarct expansion.

Infarct expansion is acute regional dilatation and thinning of the infarct zone. There are several possibilities for the mechanism of this alteration in cardiac shape: thinning could be caused by 1) cell rupture, 2) a reduction in the intercellular space, or 3) stretching of myocytes or 4) slippage of groups of myocytes so that less cells are distributed across the wall. To determine the relative contributions of these cellular mechanisms of wall thinning and dilatation, detailed study of transverse histological sections of rat hearts with infarct expansion was performed 1, 2, and 3 days after coronary ligation. The number of cells across the wall was determined in six regions within, adjacent to, and remote from the infarct. Cell counting was performed so that the total number of cells across the wall and the number of cells per unit length (cell density) across the wall were determined. The transmural cell count and the cell density were correlated with the wall thickness in each region. Myocyte cross-sectional areas and sarcomere lengths were also measured. The results from the infarct expansion hearts were compared with those of sham-operated control hearts that had been similarly analyzed. To ensure that mechanisms identified in the rat were applicable to human infarct expansion, five hearts from patients who died within 3 days of infarction and two hearts from patients without coronary disease were studied histologically in a similar fashion. Wall thinning occurred in all regions of the rat infarct expansion hearts compared with controls (p less than 0.0001) but, as expected, was most pronounced in the infarct zone. A decrease in the number of cells across the wall accompanied the wall thinning at each site (p less than 0.0001), and this change in cell number was highly correlated with the changes in wall thickness (r = 0.915, p less than 0.001). Cell density increased from controls only within the infarct zone (p less than 0.001) and accounted for at most 20% of the thinning in that region. The change in cell density was attributable to both cell stretch (measured by increased sarcomere length and decreased myocyte cross-sectional area) and a decrease in the intercellular space. A similar strong correlation between wall thinning and decreased number of cells across the wall was identified in the human hearts (r = 0.94, p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

[1]  E. Sonnenblick,et al.  Profound structural alterations of the extracellular collagen matrix in postischemic dysfunctional ("stunned") but viable myocardium. , 1987, Journal of the American College of Cardiology.

[2]  H. Weisman,et al.  Steroid administration after myocardial infarction promotes early infarct expansion. A study in the rat. , 1987, The Journal of clinical investigation.

[3]  G. Hutchins,et al.  Infarct expansion: pathologic analysis of 204 patients with a single myocardial infarct. , 1986, Journal of the American College of Cardiology.

[4]  M. Pfeffer,et al.  Survival after an experimental myocardial infarction: beneficial effects of long-term therapy with captopril. , 1985, Circulation.

[5]  P. Anversa,et al.  Left ventricular failure induced by myocardial infarction. I. Myocyte hypertrophy. , 1985, The American journal of physiology.

[6]  B. Bulkley,et al.  Global cardiac remodeling after acute myocardial infarction: a study in the rat model. , 1985, Journal of the American College of Cardiology.

[7]  H J Berger,et al.  Functional left ventricular aneurysm formation after acute anterior transmural myocardial infarction. Incidence, natural history, and prognostic implications. , 1984, The New England journal of medicine.

[8]  J. Weiss,et al.  Early dilation of the infarcted segment in acute transmural myocardial infarction: role of infarct expansion in acute left ventricular enlargement. , 1984, Journal of the American College of Cardiology.

[9]  W. Gaasch,et al.  Acute Alterations in Left Ventricular Diastolic Chamber Stiffness: Role of the “Erectile” Effect of Coronary Arterial Pressure and Flow in Normal and Damaged Hearts , 1982, Circulation research.

[10]  J. Perloff,et al.  Development and regression of increased ventricular mass. , 1982, The American journal of cardiology.

[11]  B. Bulkley,et al.  Pathogenesis of left ventricular aneurysms: an experimental study in the rat model. , 1982, The American journal of cardiology.

[12]  J S Hochman,et al.  Expansion of acute myocardial infarction: an experimental study. , 1982, Circulation.

[13]  L. W. Eaton,et al.  Expansion of Acute Myocardial Infarction: Its Relationship to Infarct Morphology in a Canine Model , 1981, Circulation research.

[14]  A E Becker,et al.  Left ventricular fibre architecture in man. , 1981, British heart journal.

[15]  W Grossman,et al.  Cardiac hypertrophy: useful adaptation or pathologic process? , 1980, The American journal of medicine.

[16]  B. Bulkley,et al.  Expansion of Transmural Myocardial Infarction A Pathophysiologic Factor in Cardiac Rupture , 1979, Circulation.

[17]  T K Borg,et al.  The collagen network of the heart. , 1979, Laboratory investigation; a journal of technical methods and pathology.

[18]  P. Anversa,et al.  Morphometric study of myocardial hypertrophy induced by abdominal aortic stenosis. , 1979, Laboratory investigation; a journal of technical methods and pathology.

[19]  J. B. Garrison,et al.  Regional cardiac dilatation after acute myocardial infarction: recognition by two-dimensional echocardiography. , 1979, The New England journal of medicine.

[20]  Dd. Streeter,et al.  Gross morphology and fiber geometry of the heart , 1979 .

[21]  G. Hutchins,et al.  Infarct expansion versus extension: two different complications of acute myocardial infarction. , 1978, The American journal of cardiology.

[22]  M. Fishbein,et al.  Experimental myocardial infarction in the rat: qualitative and quantitative changes during pathologic evolution. , 1978, The American journal of pathology.

[23]  J. Ross,et al.  Sarcomere length in experimental myocardial infarction: evidence for sarcomere overstretch in dyskinetic ventricular regions. , 1977, Journal of molecular and cellular cardiology.

[24]  A. Linzbach Hypertrophy, hyperplasia and structural dilatation of the human heart. , 1976, Advances in cardiology.

[25]  W D Spotnitz,et al.  Cellular basis for volume related wall thickness changes in the rat left ventricle. , 1974, Journal of molecular and cellular cardiology.

[26]  E. Sonnenblick,et al.  Structural conditions in the hypertrophied and failing heart. , 1973, The American journal of cardiology.

[27]  J W Covell,et al.  Diastolic Geometry and Sarcomere Lengths in the Chronically Dilated Canine Left Ventricle , 1971, Circulation research.

[28]  J W Covell,et al.  The Ultrastructure of the Heart in Systole and Diastole: >Changes In Sarcomere Length , 1967, Circulation research.

[29]  E. Sonnenblick,et al.  Relation of Ultrastructure to Function in the Intact Heart: Sarcomere Structure Relative to Pressure Volume Curves of Intact Left Ventricles of Dog and Cat , 1966, Circulation research.

[30]  W. J. Langford Statistical Methods , 1959, Nature.

[31]  F. P. Mall,et al.  On the muscular architecture of the ventricles of the human heart , 1911 .

[32]  James Bell Pettigrew On the Arrangement of the Muscular Fibres in the Ventricles of the Vertebrate Heart: With Physiological Remarks , 1866, The British and Foreign Medico-Chirurgical Review.