ABSTRACT
The objectives of the present study were to determine predictors for target lesion revascularization (TLR) and to examine the clinical usefulness of the Driver(®) stent (a cobalt alloy, modular-type) in Japanese patients with coronary artery disease. Data on 631 Japanese patients including 241 with stable angina and 361 with acute coronary syndrome-who had been implanted with the Driver(®) stent (805 lesions) between August 2004 and February 2005-were collected retrospectively; 95.0 and 81.7% of these lesions were de novo and ACC/AHA classification B2/C type, respectively. Early angiography of 622 patients revealed 1) the preprocedural minimal lumen diameter (MLD) of 0.80 ± 0.51 mm, with lesion lengths of 17.1 ± 7.3 mm, and 2) the postprocedural MLD of 2.95 ± 0.55 mm, with MLD gains of 2.14 ± 0.68 mm. At 270 days of clinical follow-up, the incidences of major adverse cardiac events (MACE), TLR, and early stent thrombosis (ST) were 18.8, 14.7, and 0.2%, respectively; the TLR rate decreased statistically significantly to 5.3 and 5.9% when implanting the Driver(®) stent (3.5 and 4.0 mm) and by IVUS, respectively. Absence rate of diabetes mellitus, presence rate of AMI, presence rate of stent diameters of ≥3.5 mm, and presence rate of IVUS-guided PCI showed lower TLR rates, with statistically significant differences. Uni- and multivariate analyses revealed that AMI and stent diameter (≥3.5 mm) are significant predictors for TLR (0.048 and 0.047, respectively), indicating that physicians are recommended to consider these variables when selecting candidate real-world patients for IVUS-guided PCI.
ABSTRACT
To examine the physiological role of the histamine H(2) receptor, histamine H(2) receptor-null mice were generated by homologous recombination. Histamine H(2) receptor-null mice, which developed normally and were fertile and healthy into adulthood, exhibited markedly enlarged stomachs and marked hypergastrinemia. The former was due to hyperplasia of gastric gland cells (small-sized parietal cells, enterochromaffin-like cells and mucous neck cells which were rich in mucin), but not of gastric surface mucous cells, which were not increased in number as compared with those in wild-type mice despite the marked hypergastrinemia. Basal gastric pH was slightly but significantly higher in histamine H(2) receptor-null mice. Although carbachol but not gastrin induced in vivo gastric acid production in histamine H(2) receptor-null mice, gastric pH was elevated by both muscarinic M(3) and gastrin antagonists. Thus, both gastrin and muscarinic receptors appear to be directly involved in maintaining gastric pH in histamine H(2) receptor-null mice. Interestingly, gastric glands from wild-type mice treated with an extremely high dose of subcutaneous lansoprazole (10 mg/kg body weight) for 3 months were very similar to those from histamine H(2) receptor-null mice. Except for hyperplasia of gastric surface mucous cells, the findings for gastric glands from lansoprazole-treated wild-type mice were almost identical to those from gastric glands from histamine H(2) receptor-null mice. Therefore, it is possible that the abnormal gastric glands in histamine H(2) receptor-null mice are secondary to the severe impairment of gastric acid production, induced by the histamine H(2) receptor disruption causing marked hypergastrinemia. Analyses of the central nervous system (CNS) of histamine H(2) receptor-null mice revealed these mice to be different from wild-type mice in terms of spontaneous locomotor activity and higher thresholds for electrically induced convulsions. Taken together, these results suggest that (1) gastrin receptors are functional in parietal cells in histamine H(2) receptor-null mice, (2) abnormal gastric glands in histamine H(2) receptor-null mice may be secondary to severe impairment of gastric acid production and secretion and (3) histamine H(2) receptors are functional in the central nervous system.