BACKGROUND: The existence of a gap between research evidence and clinical practice has been described recently. Several drugs are effective in preventing secondary events after acute myocardial infarction (AMI), but it is not certain whether this evidence is employed in daily practice. We investigated the drugs currently employed for patients with a history of AMI in Japan.
METHODS: Medical records of patients who developed AMI during the calendar year of 1999 were retrospectively identified at three teaching hospitals in Japan. We collected data on drugs prescribed at three time points (upon admission for AMI, at the time of discharge, and one year after discharge) for each patient.
RESULTS: Data were available for 149 patients with AM!. Drugs prescribed at the time of discharge were aspirin (77.5%), nitrates (68.3%), and angiotensin converting enzyme inhibitors (52.8%) . β-blockers were prescribed for only 12.0% of patients. The drugs used one year after discharge were to a large extent similar to those at the time of discharge. There were no significant correlations between the use of these drugs and comorbidity.
CONCLUSION: Despite established evidence that β-blockers offer benefits to patients with a history of AMI, they have not been prescribed frequently, for reasons that remain unclear. To improve the quality of clinical care, further systematic effort is needed to bridge this evidence to practice gap.

OBJECTIVESThe toxicity of microglass fibers (MG), one of the man-made mineral fibers, has not been sufficiently evaluated. The aim of the current study was to evaluate the cytotoxicity of MGin vitro.

METHODSAlveolar macrophages were obtained from the bronchoalveolar lavage of male F344/N rats. The macrophages were exposed to MG at concentrations of 0, 40, 80, 160 and 320 μg/ml. The effects of MG on the macrophages were examined by cell magnetometry, LDH assay and morphological observation.

RESULTSIn the cell magnetometry experiment, a significant delay of relaxation (the reduction of remanent magnetic field strength) was observed in the cells treated with 160 and 320 μg/ml of MG in a dose-dependent manner. A significant increase in LDH release was also observed in the cells with 160 and 320 μg/ml in a dose-dependent manner. Changes in the cytoskeleton were observed after exposure to MG by immunofluorescent microscopy using an α-tubulin antibody.

CONCLUSIONSThe cytotoxicity of MG on alveolar macrophages was demonstrated with cell magnetometry. The mechanism of the toxic effects of MG was related to cytoskeleton damage.