Biomedical subjects

Robert-Jan van Suylen

Publications and source records attributed to Robert-Jan van Suylen.

4 recordsLinked to original sources

PubMed2006

Degeneration of the pulmonary autograft: an explant study.

OBJECTIVE: We sought to determine the histologic features of pulmonary autografts explanted after the Ross operation. METHODS: Histologic sections of 30 explanted autografts and 8 normal heart valves were compared and semiquantitatively scored by a blinded cardiovascular pathologist. RESULTS: Pulmonary autografts (n = 30) were explanted on average 6.1 +/- 0.6 years (median, 6.6 years; range, 0.1-11.7 years) after the Ross operation (n = 28) or removed at autopsy (n = 2). Twelve (43%) of the patients undergoing reoperation had no or negligible autograft insufficiency on early transthoracic echocardiography, 12 (43%) had grade 1 autograft insufficiency, and 4 (14%) had grade 1-2 autograft insufficiency. Valve regurgitation with root dilatation was the most common indication for reoperation after root replacement (n = 26 [93%]) and regurgitation after subcoronary implanted autografts (n = 2 [7%]). Microscopy of the autograft explants revealed normal laminar architecture and cellularity. Wall specimens were characterized by reduced and fragmented elastin and increased collagen levels (fibrosis). Medial elastin changes were associated with the presence of hypertrophic smooth muscle cells. Fibrosis was most severe in the adventitia. Intimal thickening was a common finding. Valve explants showed significant thickening caused by fibrocellular tissue on the ventricular surface and marked thickening of the free margin. An autopsy explant with normal function before death showed similar features. CONCLUSIONS: Pulmonary autograft explants showed severe aneurysmal degeneration of the wall, which was characterized by intimal thickening, medial elastin fragmentation, and adventitial fibrosis. Valve leaflets were thickened. The presence of these features in a nonfailing explant suggests these changes represent a common mode of remodeling.

Adolescent↗

PubMed2005

Post-mortem histologic evaluation of microwave lesions after epicardial pulmonary vein isolation for atrial fibrillation.

BACKGROUND: Surgical pulmonary vein isolation has gained widespread use as a treatment modality for patients with concomitant atrial fibrillation. However, several uncertainties persist concerning the appropriate energy source, approach, and the need for lesion transmurality. In this study, we present an in-depth histologic investigation of epicardial ablation lesions in 3 patients. METHODS: Within a large clinical series of adjuvant epicardial beating-heart microwave isolation of the pulmonary veins, with intraoperative measurement of electrical block, 3 nonablation-related deaths allowed detailed histologic investigation of the lesions. All three patients were in sinus rhythm prior to death. Transmural histologic sections from the box lesion encircling the pulmonary veins were microscopically examined for tissue damage, lesion depth, width, and transmurality, as well as for signs of ongoing repair. RESULTS: Three out of 13 tissue samples showed transmural lesions. In three sections no histologic damage was observed and in the remaining samples transmural extent of myocardial damage ranged from 48% to 82% (mean, 64 +/- 13%). Lesion depths varied between 1.2 mm and 5.7 mm (mean 2.6 +/- 1.3 mm). The lesion depth did not differ significantly among patients and was not related to the thickness of the epicardial or myocardial layers. Interestingly, several sections showed clear necrosis of nerve bundles located in the epicardial tissue. CONCLUSIONS: This post-mortem histologic study showed that in the majority of samples the lesions were not transmural and that the extent of myocardial damage was highly variable. Even in this validated approach of epicardial beating heart ablation with satisfactory clinical results, transmurality of lesions cannot be assumed.

Aged↗

PubMed2003

Atherosclerotic plaque rupture: local or systemic process?

It is generally established that the unstable plaque is the major cause of acute clinical sequelae of atherosclerosis. Unfortunately, terms indicating lesions prone to plaque instability, such as "vulnerable plaque," and the different phenotypes of unstable plaques, such as plaque rupture, plaque fissuring, intraplaque hemorrhage, and erosion, are often used interchangeably. Moreover, the different phenotypes of the unstable plaque are mostly referred to as plaque rupture. In the first part of this review, we will focus on the definition of true plaque rupture and the definitions of other phenotypes of plaque instability, especially on intraplaque hemorrhage, and discuss the phenotypes of available animal models of plaque instability. The second part of this review will address the pathogenesis of plaque rupture from a local and a systemic perspective. Plaque rupture is thought to occur because of changes in the plaque itself or systemic changes in the patient. Interestingly, contributing factors seem to overlap to a great extent and might even be interrelated. Finally, we will propose an integrative view on the pathogenesis of plaque rupture.

Animals↗

PubMed2003

The dynamic extracellular matrix: intervention strategies during heart failure and atherosclerosis.

The extracellular matrix is no longer seen as the static embedding in which cells reside; it has been shown to be involved in cell proliferation, migration and cell-cell interactions. Turnover of the different extracellular matrix components is an active process with multiple levels of regulation. Collagen, a major extracellular matrix constituent of the myocardium and the arterial vascular wall, is synthesized by (myo)fibroblasts in the myocardium and smooth muscle cells in the medial arterial vascular wall. Its degradation is controlled by proteinases, which include matrix metalloproteinases. This review will focus on the impact of fibrosis and especially collagen turnover on the progression of heart failure and atherosclerosis, two of the main cardiovascular pathologies. We will discuss data from human studies and animal models, with an emphasis on the effects of interventions on collagen synthesis and degradation. We conclude that there is a dynamic (dis)balance in the rate of collagen synthesis and degradation during heart failure and atherosclerosis, which makes the outcome of interventions not always predictable. Alternative approaches for intervening in collagen metabolism will be discussed as possible therapeutic intervention strategies.

Animals↗