Fig 1.
Macroscopic section of the pig heart after acute myocardial infarction, stained with 2,3,5-triphenyltetrazolium chloride.
A. Sample from the subacute reperfused infarction group. B. Sample from the chronic reperfused infarction group. Arrows indicate the area of infarction (not stained with 2,3,5-triphenyltetrazolium chloride). Note the transmural nature of the infarction zone, which appears well defined and paler. LV, left ventricle; RV, right ventricle.
Fig 2.
Tissue changes in the different spatial distributions of Purkinje cardiomyocytes after myocardial infarction.
A. Healthy intramyocardial Purkinje cells. Control group. 200x magnification. Hematoxylin-eosin. B. Subendocardial layer of Purkinje fibers in the subacute reperfused infarction group. 100x magnification. Hematoxylin-eosin. Practically all the myocardial tissue has been replaced by mixed granulation and inflammatory tissue. Purkinje cells appear only slightly vacuolated, before a layer of disrupted surviving cardiomyocytes. Inflammatory infiltrate can also be seen in the endocardium. C. Detail of an unaltered intramyocardial Purkinje bundle delimitating an area of necrotic tissue and inflammatory infiltrate in preserved myocardium in the subacute reperfused infarction group. 200x magnification. Hematoxylin-eosin. D. Preserved subendocardial Purkinje cells within an extensive fibrous tissue scar. Chronic infarction group. 100x magnification. Hematoxylin-eosin. Note the presence of several cardiomyocytes as well as the appearance of capillaries. C, capillary; CM, cardiomyocyte; E, endocardium; FT, fibrous tissue; GT, granulation tissue; PC, Purkinje cell.
Fig 3.
Cellular changes in Purkinje cardiomyocytes after myocardial infarction.
A. Detail of a vacuolated subendocardial Purkinje cell. Subacute reperfused infarction group. 400x magnification. Hematoxylin-eosin. Microvacuoles predominate in this micrograph. B. Cluster of perivascular Purkinje cells with large vacuoles. Subacute reperfused infarction group. 200x magnification. Hematoxylin-eosin. An active fibroblastic response and hemorrhage can be seen. C. Intramyocardial Purkinje and transitional cells in the acute phase. Acute reperfused infarction group. 200x magnification. Hematoxylin-eosin. Note microvascular obstruction of the capillaries. D. Necrotic subendocardial Purkinje cells and cardiomyocytes in the acute non-reperfused infarction group. 200x magnification. Hematoxylin-eosin. C, capillary; CM, cardiomyocyte; E, endocardium; e, eosinophil; m, mononuclear cell; TC, transitional cell; PC, Purkinje cell; V, vein; v, vacuoles.
Fig 4.
Perivascular Purkinje cardiomyocytes.
A. Intramyocardial perivascular Purkinje cells. Acute reperfused infarction group. 200x magnification. Hematoxylin-eosin. Note acute hypereosinophilia of inferior cardiomyocytes. B. Small epicardial cluster of pericoronary Purkinje cells. Subacute reperfused infarction group. 200x magnification. Hematoxylin-eosin. C. Perivascular penetrating Purkinje cells. Chronic infarction group. 200x magnification. Hematoxylin-eosin. D. Cluster of perivascular vacuolated Purkinje cells. Subacute reperfused infarction. 100x magnification. Hematoxylin-eosin. Tissue necrosis and inflammatory infiltrate are evident. A, artery; CM, cardiomyocyte; PC, Purkinje cell; V, vein.
Fig 5.
Density of Purkinje fibers in the control and infarction groups.
Density is expressed as a percentage of the total area of the tissue (***p<0.001, Fisher exact test).
Fig 6.
Density of Purkinje fibers in the acute reperfused infarction, subacute reperfused infarction, chronic reperfused infarction, control and acute non-reperfused infarction groups (***p<0.001, Fisher exact test).
Table 1.
Summary of the main morphometric parameters of the Purkinje cardiomyocytes in all the experimental groups.
Fig 7.
Purkinje bundle thickness (μm) in the control and infarction groups (***p<0.001, Kruskal-Wallis test).
Fig 8.
Purkinje bundle thickness in the acute reperfused infarction, subacute reperfused infarction, chronic reperfused infarction, control and acute non-reperfused groups (***p<0.001, Kruskal-Wallis test).
Table 2.
Frequency of the different patterns of Purkinje-cardiomyocyte junctions in the control and infarction groups.
Fig 9.
Frequency of the different types of PMJs in the acute reperfused infarction, subacute reperfused infarction, chronic reperfused infarction, control and acute non-reperfused groups (p = 0.23, Pearson's chi-squared test with simulated p-value (based on 2000 replicates)).
CCB, contact through the cell body; CCP, contact through cell prolongations; CTC, contact through transitional cells; PMJ, Purkinje-cardiomyocyte junction.
Table 3.
Frequency of the different patterns of Purkinje-cardiomyocyte junctions in all the experimental groups.
Table 4.
Frequency of different localization patterns of Purkinje cardiomyocytes in all the experimental groups.