Occlusion of saphenous vein grafts is a major problem after coronary artery bypass grafting. Segments of occluded and suboccluded implanted aortocoronary grafts were obtained during re-intervention bypass grafting in 47 patients yielding a total of 80 vein grafts. The grafts were studied by immunohistochemistry for smooth muscle cells (alpha-SMC actin), macrophages (HAM56), cell replication (PCNA, Ki-67) and transmission and scanning electronmicroscopy (TEM, SEM). In 81% of the examined grafts the (sub)occlusion was due to a myo-intimal thickening and an associated luminal accumulation of foam cells and mural thrombi. The foam cells were constantly found at the luminal site of the myo-intimal thickening and within the luminal part of adherent thrombi. Transmission electronmicroscopy demonstrated phagocytosis of platelets and platelet fragments by the foam cells. A significant fraction of the foam cells demonstrated nuclear immunoreactivity for Ki-67 and PCNA. The myo-intimal thickening of the vein grafts was composed of smooth muscle cells lying in a fibrous tissue matrix. The smooth muscle cells were surrounded by prominent basal lamina and showed ultrastructural features of apoptosis. Our results support the hypothesis that phagocytosis of lipid rich platelets by monocytes set up a mechanism for foam cell formation and replication in human saphenous vein grafts. The transformation of a smooth muscle cell rich myointimal thickening towards a fibrous, cell poor intimal thickening could be induced by progressive smooth muscle cell loss through apoptosis.
The morphological changes in human vein grafts occurring in the first days after a coronary bypass operation (CBP) are rarely reported in the literature. Sections of aorto-coronary vein grafts from 11 patients who died during the first 10 days after a CBP were obtained at autopsy. The number of vein grafts per patient ranged from 1 to 4, yielding a total of 28 vein grafts. The early changes in the vein grafts have been studied by light microscopy, immunohistochemistry, transmission and scanning electron microscopy. The study demonstrates that soon after grafting, the vein wall is infiltrated by polymorphonuclear leucocytes (PMN). At 24 h the endothelium shows extensive desquamation. The massive migration of PMN through the venous wall occurs simultaneously with the endothelial damage. The circular layer of the media is severely damaged, resulting in a loss of smooth muscle cells (SMC). The remaining SMC in this layer show a change toward the synthetic phenotype and a reduced expression of alpha-smooth muscle actin. These early changes in the SMC function may initiate the process of fibrosis in the intima and the media of the vein grafts.
The haemodynamic basis for paradoxical embolization in patients with stroke and decompression sickness has not yet been fully elucidated. Therefore right and left atrial pressures were measured simultaneously with peroperatively placed catheters after coronary artery bypass grafting in 17 patients with sinus rhythm and normal left ventricular function. Recordings were made both during spontaneous breathing and positive pressure ventilation. A cyclic pressure reversal in which right atrial pressure exceeded left atrial pressure was reproducibly recorded. It started on average 215 +/- 5 ms (mean +/- SEM) after the onset of the electrocardiographic P-wave, lasted on average 179 +/- 14 ms and had a maximal amplitude of on average 4.1 +/- 0.3 mmHg. During the expiration phase of spontaneous breathing and inspiration phase of positive pressure ventilation, the onset of the pressure reversal occurred later, its duration was shorter and its amplitude smaller. These observations demonstrate the presence of a cyclic inter-atrial pressure reversal and illustrate the importance of the breathing mode for the time course and amplitude of this reversal.
This article describes a case of infective aortic valve endocarditis due to Fusarium oxysporum occurring 4 years after coronary artery bypass grafting. It is the first reported case of endocarditis caused by Fusarium.
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