Coronary artery bypass grafting: Part 1--the evolution over the first 50 years.

Surgical treatment for angina pectoris was first proposed in 1899. Decades of experimental surgery for coronary artery disease finally led to the introduction of coronary artery bypass grafting (CABG) in 1964. Now that we are approaching 50 years of CABG experience, it is appropriate to summarize the advancement of CABG into a procedure that is safe and efficient. This review provides a historical recapitulation of experimental surgery, the evolution of the surgical techniques and the utilization of CABG. Furthermore, data on contemporary clinical outcomes are discussed.

Increasing the antioxidative capacity of neonatal cardiopulmonary bypass prime solution: an in vitro study.

Inflammation and oxidative damage are believed to play an important role in the postoperative complications after cardiopulmonary bypass (CPB) in neonates. During the preparation of the prime, red blood cells (RBCs) release non-protein-bound iron (NPBI) and free haemoglobin/haem (Hb/haem). The presence of these prooxidants in the prime solution may increase oxidative stress in neonates undergoing CPB. The solution used as the basis of the prime solution may influence the degree of this oxidative stress. We investigated the NPBI and the Hb/haem binding capacities of two different prime solutions: a prime based on pasteurized human albumin and a prime based on fresh frozen plasma. The presence of NPBI and free Hb/haem were measured during and after the preparation of the prime solution. Only in the albumin prime was NPBI detectable. However, in both primes, the concentrations of free Hb/haem increased. Thus, to reduce the prooxidative effects of NPBI and free Hb/haem, RBCs should be added to the prime at the last possible moment. Adding fresh frozen plasma should be considered, as this would result in no detectable NPBI in the prime solution.

Structural degeneration of pulmonary homografts used as aortic valve substitute underlines early graft failure.

OBJECTIVES: The limited availability of donor valves and experimental evidence that pulmonary valves can withstand systemic pressure made us use cryopreserved pulmonary homografts as aortic valve substitutes. We observed a high incidence of early reoperation because of severe graft insufficiency due to cuspal tears. The mid-term results are evaluated in this study and histological analysis of explanted homografts is performed to investigate the cause of graft failure. METHODS: From December 1991 to April 1994, 16 patients (13 male; mean age 37.3 years, range 21-59 years) underwent aortic valve replacement with a cryopreserved pulmonary homograft. The indication was endocarditis (n = 4), bioprosthesis degeneration (n = 3) or congenital aortic valve disease (n = 9). All homografts were implanted freehand in the subcoronary position. All patients were contacted for follow-up and recent echo-Doppler studies were reviewed. Six explanted homografts were examined microscopically using routine histological techniques to analyze changes in cell population, collagen and elastic fiber structure. RESULTS: Follow-up was complete in all patients. Reoperation was required in ten patients because of severe graft incompetence (mean implantation time 5.9 years, range 2.8-8.0 years). In two patients, recurrent endocarditis was the cause of graft failure. In the other eight patients the leaflets looked pliable and thin with gross tearing in one or more cusps. The histopathologic changes observed were remarkably similar in all examined grafts: the cusp tissue was almost non-cellular and the collagen fiber structure had mostly disappeared. At the site of rupture, the tissue had become thin with strongly degenerated collagen and elastic fiber structure. In the six patients with a homograft remaining in situ, echo-Doppler showed trivial to mild insufficiency in five cases and moderate to severe in one case, whereas no significant gradients were observed. CONCLUSIONS: We concluded that structural reduction of cell number and degenerative alterations in the molecular composition of the extracellular matrix in valve tissue is the main cause of early graft failure in this series. The use of cryopreserved pulmonary homografts in the systemic circulation is therefore not advised.

The pathology of fresh and cryopreserved homograft heart valves: an analysis of forty explanted homograft valves.

OBJECTIVE: Tissue degeneration reduces the durability of aortic and pulmonary homograft heart valves. Homograft valves can evoke cellular and humoral immune responses that might be detrimental to the valve tissue. Analyzing explanted homograft valves helps in understanding the different factors that eventually lead to tissue degeneration. METHODS: A total of 40 homografts was acquired from patients whose grafts had been explanted because of stenosis (n = 22), insufficiency (n = 8), paravalvular leakage (n = 4), other technical problems (n = 4), noncardiac death (n = 1), and stenosis with endocarditis (n = 1). The period of implantation varied from 14 days to 16 years (median, 4 years). Cryopreserved valves (n = 31) were, in the majority, derived from beating-heart donors, whereas the fresh valves were sterilized with antibiotics and stored at 4 degrees C for an average of 32 days. Four unimplanted cryopreserved valves, 1 native aortic valve, and 1 native pulmonary valve were used as references. Analysis included macroscopy, light microscopy with routine hematoxylin and eosin staining (cellularity and tissue structure), and immunohistochemical studies to allow identification of macrophages (CD68) and T lymphocytes (CD3), endothelial cells, leukocyte adhesion molecules (CD54, CD106, and CD62E), and immunoglobulin (IgG) and complement factor (C3) depositions. In situ hybridization for the Y chromosome was performed in 10 cases, with host-donor sex mismatch, to distinguish between host and donor cells. The outcomes of histology and immunohistochemistry were related to clinical factors, such as implantation time and reason for explantation. RESULTS: In the first year after implantation, a strong reduction in cellularity of the valve tissue was observed, with almost acellular tissues after 1 year. Trilaminar tissue architecture disappeared with the same speed, whereas endothelial cells were almost absent in all explants. Macrophages and T lymphocytes were encountered in 85% and 78% of the leaflets, respectively. Expression of leukocyte adhesion molecules was low in almost all grafts, and IgG and C3 depositions were not increased. Valve tissue cellularity consisted mainly of ingrown host cells when the implantation time exceeded 1 year. CONCLUSIONS: During the first year of implantation, homograft valves rapidly lose their cellular components and normal tissue architecture. A low-grade inflammatory response was observed, but no convincing evidence of immune-mediated injury was found.