Sharing experiences to improve bereavement support and clinical care after stillbirth: report of the 7th annual meeting of the International Stillbirth Alliance.

Stillbirth remains a global health challenge which is greatly affected by social and economic inequality, particularly the availability and quality of maternity care. The International Stillbirth Alliance (ISA) exists to raise awareness of stillbirth and to promote global collaboration in the prevention of stillbirth and provision of appropriate care for parents whose baby is stillborn. The focus of this ISA conference was to share experiences to improve bereavement support and clinical care. These issues, relevant throughout the globe, are not discrete but closely interrelated, with both similarities and differences depending on the specific country and cultural context. Counting stillbirths and understanding the causes of stillbirth are essential not only for providing optimal care and support to parents whose babies die, but also for reducing the future burden of stillbirth. This summary highlights novel work from obstetricians, midwives, psychologists, parents and peer support organizations that was presented at the ISA meeting. It covers topics including the bereavement process, peer support for parents, support and training for staff, evidence for clinical care, and the need for accurate data on stillbirths and perinatal audits. Representatives from the maternity services of the region presented their outcome data and shared their experiences of clinical and bereavement care. Data and developments in practice within stillbirth and bereavement care must be widely disseminated and acted upon by those responsible for maternity care provision, both to prevent stillbirths and to provide high-quality care when they do occur.

The neuropeptide substance P mediates adventitial mast cell activation and induces intraplaque hemorrhage in advanced atherosclerosis.

RATIONALE: Although we and others have recently shown that mast cells play an important role in plaque progression and destabilization, the nature of the actual trigger for (peri)vascular mast cell activation during atherosclerosis is still unresolved. OBJECTIVE: In this study, we confirm that perivascular mast cell content correlates with the number of nerve fibers in the adventitia of human coronary atherosclerotic plaque specimen. Because peripheral C-type nerve fibers secrete, among others, substance P, a potent mast cell activator, we set out to study effects of adventitial administration of this neuropeptide on mast cell dependent destabilization of carotid artery plaques in apolipoprotein E-deficient (apoE(-/-)) mice. METHODS AND RESULTS: Substance P treatment significantly enhanced the number and activation status of adventitial mast cells compared to controls and promoted intraplaque hemorrhages. These phenomena could be prevented by coadministration of the neurokinin-1 receptor antagonist spantide I and did not occur in mast cell deficient apoE(-/-) mice, establishing the critical involvement of mast cells in substance P-elicited plaque destabilization. CONCLUSIONS: Our data suggest that neurotransmitters such as substance P are capable of promoting mast cell dependent plaque destabilization and provide a new, direct link between neural factors and vascular inflammation.

Human coronary artery remodeling, beginning and end of the atherosclerotic process.

UNLABELLED: BACKGROUND, AIMS OF THE STUDY: The objective of the study was to relate the progress of coronary artery remodeling to the earliest stages of the atherosclerotic process. For this purpose, a mathematical model for description of dimensional change of the coronary artery wall and its constituent components was developed and applied. MATERIALS AND METHODS: The study used coronary artery samples randomly taken from each of 83 consecutive, unselected postmortems. All samples were routinely fixed and processed to paraffin for the preparation of right-angled, 5-micron sections, routinely stained and mounted for subsequent analysis. Computer assisted image analysis, using 32 systematic random, radial sampling lines, was used for interactive measurements of distance from centre of lumen to points defining intima, media and adventitia thickness along the radial intercept, which were subsequently tabled for analysis of variance, calculations of (group-vessel) means, and related to stage of pathology. RESULTS: Pre-atherosclerotic changes, before any localised changes in especially intima dimensions, are found, consisting of a process of gradual vascular widening, associated with temporally at least partly dissociated increases in width, which as a fraction of total vessel radius show a phased process. In these, the intima first increases, subsequently remains stable, and finally reduces in width proportionally to the increasing diameter. The media shows a similar initial increase, on average stabilising in the third phase after reaching a plateau value in the second. The adventitia, already increasing in phase 1, continues to increase in phase 2, accelerating in phase 3. The complex process, as found, occurs systematically in all vessels, is distributed circumferentially, and precedes the development of localised lesions of the intima. CONCLUSIONS: The findings suggest the existence of a diffuse complex of changes, consisting of a gradual vascular widening followed by narrowing, with associated mural changes reflecting the atherosclerotic process.