Requirements for improving social capital among faculty members of medical universities: A multicenter qualitative study.

Introduction: Social capital is critical to organizational dynamics, particularly in developing countries. This study explored strategies for enhancing social capital among faculty members at seven medical universities in the south of Iran. Methods: This qualitative study was conducted in 2021. We used a purposeful sampling technique to recruit faculty members and conducted individual semi-structured interviews with them. Thematic analysis was used to analyze and describe the collected data. Results: A total of 49 faculty members (34 males; 15 females) participated in this study. The participants expressed satisfaction with their affiliations with medical universities. Social capital was related to the feeling of belonging to the organization, as well as to interpersonal and intra-organizational relations. Social capital was associated with three components: empowerment, organizational policy change, and organizational identification. Additionally, a dynamic relationship between the individual, interpersonal, and macro-organizational levels reinforced the organization's social capital. This means that, just as the macro-organizational level affects the members' identities, the members' activism affects the macro-organizational level. Conclusion: To strengthen the organization's social capital, managers should work on the mentioned components at the individual, interpersonal, and macro-organizational levels.

Extraluminal atherosclerosis: an under-recognised finding in human aortocoronary venous bypass grafts.

BACKGROUND: Coronary artery bypass grafting (CABG) is commonly compromised by graft atherosclerosis. Histopathologic studies confirm various forms of atherosclerosis, including positively remodelled lesions in native coronary arteries but there are no histopathologic reports of extraluminal atherosclerosis in vein grafts. METHODS: We prospectively investigated the histopathologic presence and pattern of extraluminal atherosclerosis in human old vein grafts in a two-year interval among patients undergoing redo-CABG at three university hospitals in Tehran. We separately documented clinical and angiographic findings. RESULTS: We evaluated 100 segments from 20 human old vein grafts obtained during the redo CABG. All but four segments demonstrated some degrees of luminal narrowing. Luminal atherosclerotic plaques were detectable in 61 segments. We detected extraluminal atheroscleoris in seven segments. Mean vessel wall thickness was greater in segments containing extraluminal plaques (1.41±0.26 mm versus 0.91±0.04 mm, P=0.008). Angiographic findings had a modest correlation with presence or absence of luminal atheromatous lesions (Spearman's rho: 0.331, P=0.007). Angiographic degree of stenosis could not predict the presence of positively remodelled atherosclerotic plaques (Spearman's rho: -2.21, P=0.073). CONCLUSION: Previous studies suggested positive remodelling in vein grafts. Out study provides histopathologic evidence on extraluminal atherosclerosis in human aortocoronary vein grafts.

Histopathologic insight into saphenous vein bypass graft disease.

OBJECTIVES: Vein graft disease is a major drawback of coronary artery bypass grafting. However, histopathologic studies of old human aortocoronary grafts are scarce. METHODS: We screened patients undergoing redo coronary artery bypass grafting at three university hospitals and selected those with at least one excisable old vein graft. Native non-grafted saphenous veins were also obtained as controls. Clinical and angiographic data were separately documented. RESULTS: We evaluated 117 segments from 29 veins. All but 4 old graft segments showed degrees of luminal narrowing and fibrointimal proliferation. Moreover, 61 segments demonstrated atherosclerotic plaques. Such plaques were typically concentric and, compared with other segments, more frequently represented necrosis, calcification and giant cells (p < 0.001 for all comparisons) and had a higher inflammatory cell count, predominantly of lymphocytic origin. Native saphenous veins frequently showed fibrosis, but no calcification or active inflammation. Angiographic findings showed moderate correlation with the histological degree of luminal stenosis (Spearman's ρ = 0.564, p < 0.001). CONCLUSIONS: Human vein graft atherosclerosis and arterial atherosclerosis share many features; however, we found lymphocytes to be the dominant inflammatory cells within plaques. Conventional angiography underestimated the atherosclerosis burden in vein grafts. Improved understanding of disease pathophysiology could lead to the development of novel interventions that reduce costly and suboptimal repeat revascularizations.

Pathophysiology of aortocoronary saphenous vein bypass graft disease.

Aortocoronary saphenous vein bypass grafting relieves anginal pain in patients with coronary artery disease. However, its effectiveness is limited due to graft failure; the 10-year patency rate is 50%-60%. Early, 1-year and late graft failure may be due to thrombosis, fibrointimal hyperplasia and atherosclerosis, respectively. There is general agreement that vein graft atherosclerosis differs from arterial lesions in terms of temporal and histological changes. Vein graft atherosclerosis is more rapid, with diffuse concentric changes and a less noticeable fibrous cap, making venous plaques more vulnerable to rupture and subsequent thrombus formation. Despite progress in understanding the pathophysiology, some aspects of vein graft atherosclerosis need to be clarified. This review focuses on the pathophysiologic aspects of this widespread, costly and disabling disease, with emphasis on late graft occlusion and distinctions between arterial and venous atherosclerosis in terms of histology, pathophysiology and risk factors.