Coronary stenting and abciximab in primary angioplasty for ST-segment-elevation myocardial infarction

Advances in anti-platelet therapy and improvement of stent deployment techniques have improved the safety and efficacy of stenting in the setting of ST-segment-elevation myocardial infarction (STEMI). However, in randomized trials, routine coronary stenting does not reduce mortality and re-infarction, compared to balloon angioplasty. Further, the benefits in target vessel revascularization seem to be reduced when applied to unselected patients with STEMI. Direct stenting represents an attractive strategy with potential benefits in terms of myocardial perfusion. Future large randomized trials are needed to evaluate whether this strategy has a significant impact on outcome, and to provide a cost-benefit analysis of the unrestricted use of drug-eluting stents in this high-risk subset of patients. The additional use of abciximab reduces mortality in primary angioplasty. Since the feasibility of long-distance transportation has been shown in several randomized trials, early pharmacological pre-treatment may confer further advantages by early recanalization and shorter ischaemic time, particularly in high-risk patients. Further randomized trials are needed to clarify the potential benefits from early abciximab administration and the potential role of small molecules in primary angioplasty for STEMI.     

The Role of Circulating Bone Cell Precursors in Fracture Healing

Fracture healing is a complex process that involves several cell types; as a previous report suggested an increase in osteoblast (OB) precursors in peripheral blood during this process, this paper examines the role of circulating bone cell precursors in this process in the light of a prior suggestion that OB precursors are increased. Nine healthy men less than 60 years old with traumatic fractures were enrolled. The parameters circulating OB precursors (osteocalcin+/alkaline phosphatase+/CD15− cells) and osteoclast precursors (CD14+/CD11b+/vitronectin receptor + cells) were measured by flow cytometry; bone formation markers and TGFβ1, by ELISA; and PTH, by RIA in serum on arrival at the emergency department (baseline) and 15 days after fracture. Bone cell precursors behaved differently during healing. TGFβ1 was inversely correlated with OB number, but increased their degree of maturation at baseline. Bone formation markers and TGFβ1 were increased after fracture, whereas PTH was decreased. The TGFβ1 increase was directly correlated with age, whereas age was not correlated with the precursors. In conclusion, we confirm the role of TGFβ1 in fracture healing; and its possible role in the control of pre-OB homeostasis. There was no variation in circulating precursor cells during healing, though the increase in TGFβ1 may suggest increased pre-OB maturation and homing to the injured site.     

Repeated immune and non immune insults to the graft after heart transplantation

The clinical transplantation outcome is related to both effects of immunological and non immunological factors degenerating into hyperacute, acute and chronic rejection. Modern immunosuppressive treatments have resolved most events linked to acute rejection while long-term survival still remains the major problem after heart transplantation. The goal of personalized immunosuppressive therapy is to prevent rejection without inducing toxic effects. The aim of future studies could be to clarify the pathogenesis of chronic rejection and develop new and less toxic therapeutic approaches to induce “tolerance” to the graft without major side effects.