Definite stent thrombosis among Malaysian population: predictors and insights of mechanisms from intracoronary imaging.

INTRODUCTION: Stent thrombosis (ST) is an uncommon, but significant complication following angioplasty. We aimed to examine the predictors, clinical outcomes and mechanism of definite ST cases among patients who underwent percutaneous coronary intervention (PCI). METHODS: This was a retrospective observational registry of 14,935 patients from the year 2011 till 2015. Clinical characteristics, clinical outcome and intracoronary imaging data were recorded in all the patients. The SPSS Statistic version 24 was used for statistical analysis. The Cox regression hazard model was used to report calculate the hazard ratio (HR) with a 95% confidence interval (95%CI). Independent predictors of ST were identified by univariate logistic regression analysis. Variables that showed a statistically significant effect in univariate analyses were entered in a multivariate Cox proportional hazards model. A p-value<0.05 was regarded as significant. RESULTS: The incidence of definite ST was 0.25% (37 out of 14935 patients). 75% of ST group patients presented with ST elevation myocardial infarction (75% vs. 19.8%, p<0.01). There was higher mortality among patients with ST when compared to the group without ST (Hazard Ratio, HR=10.69, 95%CI: 1.13, 100). Two independent predictors of ST were 1) previous history of acute myocardial infarction (HR=2.36, 95%CI: 1.19, 4.70) and 2) PCI in the context of acute coronary syndrome when compared to elective PCI (HR=37, 95%CI: 15.7, 91.5). Examination of 19 ST cases with intracoronary imaging identified nine cases (47%) of underexpanded stents and five cases (26%) of malopposition of stents. CONCLUSIONS: ST is associated with high mortality. PCI in acute coronary syndrome setting and a previous history of acute myocardial infarction were significant predictors for ST. Intracoronary imaging identified stent underexpansion and malopposition as common reasons for ST. In cases where the risk of ST is high, the use of intracoronary imaging guided PCI is recommended.

Clinical and economic outcomes with appropriate or partial prophylaxis.

INTRODUCTION: Despite the existence of evidence-based guidelines for venous thromboembolism (VTE) prevention, prophylaxis is often inappropriately prescribed. This study compared the efficacy, safety, and cost of appropriate (ACCP-recommended) prophylaxis with partial prophylaxis (not completely conforming to ACCP guidelines) in patients at-risk of VTE receiving enoxaparin or unfractionated heparin. METHODS: The MarketScan((R)) Hospital Drug Database from Thomson Reuters (January 2004-March 2007), was queried for medical and surgical patients at high risk of VTE, aged > or =40years, and with a hospital stay > or =6days. Univariate and multivariate analyses compared hospital-acquired VTE events, adverse events, and hospital costs between appropriate or partial prophylaxis discharges. RESULTS: Of the 21,001 discharge records included, appropriate prophylaxis was received by 5136 (24.5%) patients. Compared with partial prophylaxis, appropriate prophylaxis was associated with significantly lower incidences of hospital-acquired pulmonary embolism (0.9% vs 0.5%; adjusted odds ratio [OR] 0.55, 95% confidence intervals [CI] 0.35-0.87, P=0.010), and bleeding events (10.7% vs 5.1%; adjusted OR 0.57, 95% CI 0.50-0.66, P<0.001). Total costs per discharge were lower for appropriate prophylaxis ($17,386+/-12,004) than partial prophylaxis ($23,823+/-19,783) with an adjusted mean difference of $6370 in favor of appropriate prophylaxis (P<0.001). CONCLUSION: This retrospective study suggests that ACCP-guideline recommended appropriate prophylaxis reduces hospital-acquired pulmonary embolism and bleeding events in patients at-risk of VTE and is cost-saving when total direct medical costs are considered. The substantial US clinical and economic VTE burden may, therefore, be reduced by improving prophylaxis adherence with guideline recommendations.

Islet perturbations in rats fed a high-fat diet.

The islet response to a high-fat diet, which induces insulin resistance, was investigated in Sprague-Dawley rats. It was found that the insulin response to glucose (15 or 25 mg/min, i.v.) was not different between rats given a high-fat diet and control rats after 2 weeks but was significantly reduced in rats fed high-fat diets after 4 (by 46+/-9%; p<0.001) and 8 weeks (by 68+/-12%; p<0.001). However, after 2 weeks of a high-fat diet, stimulated insulin secretion from isolated islets incubated for 60 min in 5.6, 8.3, and 11.1 mM glucose was impaired. When islets isolated from rats given a high-fat diet for 2 weeks were perifused, it was evident that the first-phase insulin secretion was impaired (seen during the first 6 min after increase of glucose from 3.3 to 8.3 mM). Insulin gene expression, examined by quantitative in situ hybridization, was impaired after 2 weeks of high-fat diet (52% decrease in mRNA-labeling; p<0.001). Islet hypertrophy was not evident in rats given high-fat diet, as determined by areas of either islet profiles in dark-field images or isolated islets. Islet innervation, as revealed by immunostaining for vasoactive intestinal peptide (VIP) and neuropeptide Y (NPY), was increased after 2, 4, and 8 weeks of high-fat diet. Thus induction of insulin resistance by high-fat diet in Sprague-Dawley rats results after 2 weeks in impaired glucose-stimulated insulin secretion in vitro, impaired insulin gene expression, and hyperinnervation of the islets without any sign of islet hypertrophy, whereas the in vivo insulin response to glucose, although normal after 2 weeks, is impaired after 4 weeks.