Okada E, Solti F, Jellinek H, Shozawa T
2nd Dept. of Pathology, Semmelweis Medical University Budapest, Hungary.
Acta Morphol Hung. 1986;34(4):249-60.
The mechanism of sinus node dysfunction caused by cardiac lymphostasis was studied in dogs with histological and electrophysiological methods. A total of seventeen mongrel dogs were used in this study. Out of them 12 animals were operated to induce cardiac lymphostasis and sacrificed 3, 6, and 10 days after operation. In 3 of the dogs, in addition to cardiac lymphostasis, local cardiac hypertension was induced by constricting the descending aorta (artificial coarctation of the aorta). The other five dogs were sacrificed as normal controls. The signs of deteriorated pacemaker function of the sinus nodes; sinus arrest escape rhythm, and bradycardia were observed in electrocardiographic (ECG) tracings in dogs with cardiac lymphostasis. The sinus node cells of the animals revealed cytoplasmic oedema, and swelling of the cells developed progressively parallel to the time elapsed after the operation. The pathological changes in the animals with combined lymphostasis and local hypertension were more severe than those seen in the animals with lymphostasis only. In one out of the three dogs with combined operation, scattered foci of necrobiotic sinus node cells and necrobiosis of the medial smooth muscle cells in sinus node arteries were also observed. It was concluded in the present study that cardiac lymphostasis induced water and electrolyte imbalance in sinus nodes. The disturbed water and electrolyte homeostasis resulted in alterations in the electrophysiological activity of the sinus nodes. In order to elucidate the exact relationship between cardiac lymphostasis and human sick sinus syndrome, further experimental and clinical studies will be necessary.
