The Role of Metallic Nanoparticles in Inhibition of Mycobacterium Tuberculosis and Enhances Phagosome Maturation into the Infected Macrophage.

This review focuses on the role of gallium (Ga) nanoparticles (NPs) to enhance phagosome maturation into the Mycobacterium tuberculosis-infected macrophage and the role of magnetic iron NPs as nanocarriers of antituberculosis drugs. The literature shows that silver (Ag) and zinc oxide (ZnO) NPs with dimensions less than 10 nm can penetrate directly through the macrophage bilayer membrane. Ag NPs increase the permeability membrane by motiving the aggregation of proteins in the periplasmic space and forming nano-sized pores. ZnO NPs can interact with the membrane of M. tuberculosis, which leads to the formation of surface pores and the release of intracellular nucleotides. The colloidal Ag:ZnO mixture NPs with 1:1 ratio can eliminate M. tuberculosis and shows the lowest cytotoxicity effects on MCF-7 and THP-1 cell lines. Ag/ZnO nanocrystals are not able to kill M. tuberculosis alone ex-vivo. Hence, bimetallic gold (Au)/Ag NPs possessed high efficiency to inhibit M. tuberculosis in an ex-vivo THP-1 infection model. Co-delivery of mixed MeNPs into a polymeric carrier collaborated to selective uptake by macrophages through passive targeting, initial burst release of ions from the encapsulated metallic (Me) NPs, and eventually, reduction of MeNPs toxicity, and plays a pivotal role in increasing the antitubercular activity compared to use alone. In addition, Ga NPs can import drugs to the macrophage, inhibit M. tuberculosis growth, and reduce the inhibition of phagosome maturation. Magnetic encapsulated NPs exhibited good drug release properties and might be suitable as carriers of antituberculosis drugs.

Impact of congestive heart failure in patients with non-ST-segment elevation acute coronary syndromes.

The presence of congestive heart failure (CHF) has been associated with treatment disparities and worse outcomes in patients with ST-segment elevation myocardial infarction, but the incidence and effect of CHF in patients with non-ST-segment elevation acute coronary syndromes (NSTE ACSs) has not been well characterized. We evaluated 45,744 patients with NSTE ACS (positive cardiac markers and/or ischemic ST-segment changes) who were treated at 424 hospitals in the CRUSADE Quality Improvement Initiative between March 2000 and March 2003. Treatment patterns and in-hospital outcomes in patients with signs of CHF on presentation and those who developed in-hospital CHF were compared with those in patients without CHF. In total, 10,398 patients (22.7%) had signs of CHF on presentation, and 1,664 patients (3.6%) later developed in-hospital CHF. Compared with patients without CHF, early (<24 hours from presentation) medications and invasive cardiac procedures were used less often in patients with signs of CHF on presentation. Likewise, patients with in-hospital CHF were less likely than those without CHF to receive acute antiplatelet agents and undergo cardiac catheterization but more likely to receive acute beta blockers, angiotensin-converting enzyme inhibitors, and heparin and to undergo coronary artery bypass grafting. Adjusted mortality was higher in patients with signs of CHF on presentation (odds ratio 2.64, 95% confidence interval 2.31 to 3.01) and those with in-hospital CHF (odds ratio 4.93, 95% confidence interval 4.05 to 5.99) than in patients without CHF. In conclusion, CHF occurs frequently in patients with NSTE ACS but is associated with less aggressive treatment and a higher risk of mortality. Further study is needed to determine the causes of these treatment differences and the optimal therapeutic approach for patients with NSTE ACS and concomitant CHF.

Incidence, risk factors, and prognosis of inhospital heart failure after percutaneous coronary intervention: insight from the Blue Cross Blue Shield of Michigan Cardiovascular Consortium (BMC2).

BACKGROUND: Prior history of heart failure (HF) has been shown to be a predictor of poor outcomes after percutaneous coronary intervention (PCI). Clinical predictors of the development of inhospital HF and its prognostic significance after PCI have yet to be defined. In this study, we sought to identify the incidence, risk factors, and prognosis of inhospital HF after PCI. METHODS: Using a contemporary registry of consecutive PCIs, the incidence of HF after PCI was identified. Multivariate logistic regression analysis was used to determine predictors of the development of HF after PCI as well as the impact of HF on inhospital mortality. RESULTS: The incidence of HF after PCI in the overall patient population was 1.4%. Independent predictors of HF were female sex, age > or = 60 years, exceeding a maximum weight- and creatinine-adjusted contrast dose, diabetes, prior HF, prior gastrointestinal bleeding, prior chronic obstructive pulmonary disease, history of atrial fibrillation, American College of Cardiology type B2 or C vessel, emergency PCI, ejection fraction < 50%, myocardial infarction with or without cardiogenic shock, and repeat angiography. After adjustment for comorbidities, the development of HF was independently associated with an increased risk of inhospital death (adjusted OR 2.48, 95% CI 1.77-3.48). CONCLUSIONS: The development of HF is a relatively uncommon occurrence after PCI and is associated with a poor prognosis. The identification of risk factors for HF could foster the development of interventions aimed toward its prevention in high-risk patients.