Histological and morphometric changes in cardiac conduction fibers after spontaneous myocardial infarction in horses and dogs.

BACKGROUND AND AIM

Arrhythmic sudden cardiac death in dogs and horses often results from ventricular arrhythmia secondary to myocardial damage. Despite this, limited data exist on the histomorphometric changes in cardiac conduction fibers (CCFs) and cardiac conduction cells (CCCs) following spontaneous myocardial infarction (MI). This study aimed to characterize morphometric and histological alterations in conduction fibers and their junctions with cardiomyocytes in infarcted hearts of horses and dogs.

MATERIALS AND METHODS

Ten hearts from horses and 10 from dogs that had died suddenly were examined. Histological and immunohistochemical analyses were performed using hematoxylin and eosin, Masson's trichrome, and periodic acid-Schiff staining to identify conduction fibers and assess glycogen accumulation. The thickness and density of conduction fibers, as well as the diameter of conduction cells, were measured using image analysis software. Statistical comparisons were conducted using t-tests, analysis of variance, and Cohen's d-test.

RESULTS

In horses, the diameter of CCCs was significantly smaller in infarcted cases (55.74 μm) compared to normal hearts (79.08 μm) (p < 0.001). In dogs, slight hypertrophy of CCCs (31.21 μm) was observed in normal hearts, whereas infarcted hearts exhibited reduced diameters (26.83 μm) (p = 0.114). The density of CCFs was 9.06% in horses and 7.99% in dogs (p = 0.846), while fiber thickness was 30.06 μm in horses and 29.86 μm in dogs (p = 0.263). Horses exhibited extensive myocardial fibrosis, particularly in the middle third and posterior left ventricle, while dogs displayed milder lesions distributed across the ventricle.

CONCLUSION

This study demonstrates a reduction in CCC size in horses and minor hypertrophy in dogs, coupled with fibrotic myocardial lesions of varying severity. The observed histomorphometric changes provide insight into the structural impact of MI on conduction cells, which may contribute to ventricular arrhythmias in these species. These findings have implications for veterinary cardiology and the management of MI-related arrhythmic conditions.