Citations

Left ventricular assist devices (LVADs) and total artificial hearts (TAHs) are surgically implanted as permanent treatment of unrecoverable heart failure. Both LVADs and TAHs are durable mechanical circulatory support (MCS) devices that can prolong patient survival but also alter end-of-life trajectory. The permissibility of discontinuing assisted circulation is controversial because device deactivation is a life-ending intervention. Durable MCS is intended to successfully replace native physiological functions in heart disease. We posit that the presence of new lethal pathophysiology (ie, a self-perpetuating cascade of abnormal physiological processes causing death) is a central element in evaluating the permissibility of deactivating an LVAD or a TAH. Consensual discontinuation of durable MCS is equivalent with allowing natural death when there is an onset of new lethal pathophysiology that is unrelated to the physiological functions replaced by an LVAD or a TAH. Examples of such lethal conditions include irreversible coma, circulatory shock, overwhelming infections, multiple organ failure, refractory hypoxia, or catastrophic device failure. In all other situations, deactivating the LVAD/TAH is itself the lethal pathophysiology and the proximate cause of death. We postulate that the onset of new lethal pathophysiology is the determinant factor in judging the permissibility of the life-ending discontinuation of a durable MCS.

Published literature have not discerned end-of-life palliative versus life-shortening effects of pharmacologically maintaining continuous deep sedation until death (ie, dying in deep sleep) compared with common sedation practices relieving distress in the final conscious phase of dying. Continuous deep sedation predictably suppresses brainstem vital centers and shortens life. Continuous deep sedation remains controversial as palliation for existential suffering and in elective death requests by discontinuation of chronic ventilation or circulatory support with mechanical devices. Continuous deep sedation contravenes the double-effect principle because: (1) it induces permanent coma (intent of action) for the contingency relief of suffering and for social isolation (desired outcomes) and (2) because of its predictable and proportional life-shortening effect. Continuous deep sedation should be distinguished from common sedation practices for palliation and characterized instead as physician-assisted death.

OBJECTIVE The negative results of two randomized controlled trials (RCTs) have challenged current guideline recommendations for using aspirin for primary prevention of cardiovascular events among patients with diabetes. We therefore sought to determine if the effect of aspirin for primary prevention of cardiovascular events and mortality differs between patients with and without diabetes. RESEARCH DESIGN AND METHODS We conducted a systematic search of MEDLINE, EMBASE, Cochrane Library, Web of Science, and Scopus since their inceptions until November 2008 for RCTs of aspirin for primary prevention of cardiovascular events. Blinded pairs of reviewers evaluated studies and extracted data. Random-effects meta-analysis and Bayesian logistic regression were used to estimate the ratios of relative risks (RRs) of outcomes of interest among patients with and without diabetes. A 95% CI that crosses 1.00 indicates that the effect of aspirin does not differ between patients with and without diabetes. RESULTS Nine RCTs with moderate to high methodological quality contributed data to the analyses. The ratios of RRs comparing the benefit of aspirin among patients with diabetes compared with patients without diabetes for mortality, myocardial infarction, and ischemic stroke were 1.12 (95% CI 0.92–1.35), 1.19 (0.82–1.17), and 0.70 (0.25–1.97), respectively. CONCLUSIONS Whereas estimates of benefit among patients with diabetes remain imprecise, our analysis suggests that the relative benefit of aspirin is similar in patients with and without diabetes.

An analysis is presented of the deformation of a homogeneous, isotropic, elastic half space subjected to a constant radial strain in a circular area on the boundary. Explicit analytic expressions for the normal and radial displacements and the shear stress on the boundary are used to interpret experiments performed on inflated pig lungs. The boundary strain was induced by inflating or deflating the lung after bonding a flexible disk to the lung surface. The prediction that the surface bulges outward for positive boundary strain and inward for negative strain was observed in the experiments. Poisson’s ratio at two transpulmonary pressures was measured, by use of the normal displacement equation evaluated at the surface. A direct estimate of Poisson’s ratio was possible because the normal displacement of the surface depended uniquely on the compressibility of the material. Qualitative comparisons between theory and experiment support the use of continuum analyses in evaluating the behavior of the lung parenchyma when subjected to small local distortions.