Background: Health care workers (HCWs) play a critical role in prevention of health care-associated infections such as methicillin-resistant Staphylococcus aureus (MRSA), but glove and gown contact precautions and hand hygiene may not be consistently used with vulnerable patients.Methods: A cross-sectional survey of MRSA knowledge, attitudes/perceptions, and practices among 276 medical, nursing, allied health, and support services staff at an acute-care hospital in the eastern United States was completed in 2012. Additionally, blinded observations of hand hygiene behaviors of 104 HCWs were conducted.Results: HCWs strongly agreed that preventive behaviors reduce the spread of MRSA. The vast majority reported that they almost always engage in preventive practices, but observations of hand hygiene found lower rates of adherence among nearly all HCW groups. HCWs who reported greater comfort with telling others to take action to prevent MRSA transmission were significantly more likely to self-report adherence to recommended practices.Conclusions: It is important to reduce barriers to adherence with preventive behaviors and to help all HCWs, including support staff who do not have direct patient care responsibilities, to translate knowledge about MRSA transmission prevention methods into consistent adherence of themselves and their coworkers to prevention guidelines. Copyright (C) 2014 by the Association for Professionals in Infection Control and Epidemiology, Inc. Published by Elsevier Inc. All rights reserved.

Background: Health care workers' (HCWs) perceptions and attitudes affect implementation of precautions to prevent transmission of drug-resistant pathogens such as methicillin-resistant Staphylococcus aureus (MRSA). Identification of challenges and barriers to recommended practices is a critical component of promoting a safe clinical environment of care.Methods: Semistructured interviews addressed how MRSA affects HCWs, prevention of transmission, and challenges and barriers HCWs experience when entering a MRSA isolation room and performing appropriate hand hygiene.Results: The purposive sample of 26 acute care HCWs (16 registered nurses; 1 physician; 6 allied health professionals; and 3 support staff) self-selected from 276 responding to a questionnaire on MRSA. Analysis identified 18 themes across seven categories. Most participants reported feeling responsible for preventing transmission, and having the knowledge and desire to do so. However, many also reported challenges to following consistent hand hygiene and use of contact precautions. Barriers included patient care demands, equipment and environmental issues such as availability of sinks, time pressures, the practices of other HCWs, and the need for additional signs indicating which patients require contact precautions.Conclusions: The HCWs reported a need for improved clarity of isolation protocols throughout patients' hospital journey, additional rooms and staff for isolation patients, improved education and communication (including timely and appropriate signage), and an emphasis on involving all HCWs in reducing contamination. Copyright (C) 2014 by the Association for Professionals in Infection Control and Epidemiology, Inc. Published by Elsevier Inc. All rights reserved.

BACKGROUND Coronary artery disease (CAD) patients experience chest pain (CP) from cardiac and non-cardiac etiologies. OBJECTIVE Proton pump inhibitor (PPI) treatment of CAD patients with atypical CP would result in less CP, as well as fewer emergency room (ER) visits for CP, medical evaluations, and hospitalizations. METHODS A randomized, prospective, placebo-controlled trial in patients with a history of severe CAD, without current ischemia, and not receiving acid reducing therapy. Patients received esomeprazole 40 mg or placebo daily added to standard cardiac medications for 6 months. The primary endpoint was percentage of patients experiencing CP. RESULTS In 162 patients randomized, 78 received esomeprazole and 84 received placebo. Esomeprazole significantly reduced the primary endpoint of patients experiencing CP (24.4% versus 54.8%; p < 0.001). The absolute number of CP episodes and CP days was also significantly reduced. Fewer patients experienced the combined endpoint of doctor office/ER visits for CP (19.2% versus 48.8%; p < 0.001), mainly due to significantly fewer office visits for CP (14.1% versus 39.3%; p < 0.001). ER visits for CP trended less with esomeprazole (12.8% versus 22.6%; p = 0.10), as did hospitalizations for CP (14.1% versus 20.2%; p = 0.30). However, the study lacked statistical power to reach these secondary endpoints. CONCLUSIONS Concomitant esomeprazole therapy in CAD patients without active ischemia but with a history of atypical CP reduces number of patients with further CP symptoms and medical office visits for CP. Larger studies are needed to further evaluate PPI treatment on ER CP visits and hospitalizations in this patient population.

BACKGROUND:The present study was undertaken to investigate the effect of statins plus omega-3 polyunsaturated fatty acids (PUFAs) on endothelial function and lipid profile in South Asians with dyslipidemia and endothelial dysfunction, a population at high risk for premature coronary artery disease.METHODS:Thirty subjects were randomized to rosuvastatin 10 mg and omega-3-PUFAs 4 g or rosuvastatin 10 mg. After 4 weeks, omega-3-PUFAs were removed from the first group and added to subjects in the second group. All subjects underwent baseline, 4-, and 8-week assessment of endothelial function and lipid profile.RESULTS:Compared to baseline, omega-3-PUFAs plus rosuvastatin improved endothelial-dependent vasodilation (EDV: -1.42% to 11.36%, p = 0.001), and endothelial-independent vasodilation (EIV: 3.4% to 17.37%, p = 0.002). These effects were lost when omega-3-PUFAs were removed (EDV: 11.36% to 0.59%, p = 0.003). In the second group, rosuvastatin alone failed to improve both EDV and EIV compared to baseline. However, adding omega-3-PUFAs to rosuvastatin, significantly improved EDV (-0.66% to 14.73%, p = 0.001) and EIV (11.02% to 24.5%, p = 0.001). Addition of omega-3-PUFAs further improved the lipid profile (triglycerides 139 to 91 mg/dl, p = 0.006, low-density lipoprotein cholesterol 116 to 88 mg/dl, p = 0.014).CONCLUSIONS:Combined therapy with omega-3-PUFAs and rosuvastatin improves endothelial function in South Asian subjects with dyslipidemia and endothelial dysfunction.

Increased creatine kinase-MB isoenzymes after coronary stenting are common, and many studies have suggested an association of this increase with an adverse long-term prognosis. How such postprocedural creatine kinase-MB release affects long-term prognosis remains unclear. Whether any actual causal relation exists remains unanswered.

The predictors of troponin release after percutaneous coronary intervention were prospectively assessed in 405 consecutive patients. Troponin release occurred frequently (27%) and was associated with complications during the procedure, including sapheneous vein graft interventions, multistent use, glycoprotein IIb/IIIa use, and a history of hypercholesterolemia.

In conclusion, high plasma CRP levels are associated with more myocardial ischemia early in primary UAP. Although the underlying mechanisms are not well understood, these data could have important pathophysiologic and clinical implications. Whether the increased CRP represents a marker either for the extent of atherosclerosis or an inflammatory process in the coronary arteries or directly exerts a pro-inflammatory or prothrombotic effect on the vessel wall leading to the increased ischemia is currently unknown.

Several studies have correlated conduction abnormalities on the 12-lead electrocardiogram (ECG) with echocardiographic findings.(1-3) Echocardiographic studies on left bundle branch block (LBBB) produce variable findings that are related to the underlying cardiac pathophysiology. However, paradoxical septal motion on echocardiography is seen in most and is presumed secondary to abnormal septal activation related to a proximal conduction abnormality. We have previously reported that nonspecific widening of the QRS complex in the absence of typical electrocardiographic criteria for right bundle branch block (RBBB) or LBBB is associated with evidence of left ventricular (LV) dysfunction.(4) Although the mechanism of QRS widening was unknown, it was hypothesized that increased LV fibrosis in the presence of LV dysfunction led to an intraventricular conduction delay (IVCD), suggesting the presence of peripheral conduction disease. The present report has 3 purposes: (1) to support the existence of peripheral conduction disease by evaluating upper septal motion on echocardiography in patients with typical electrocardiographic criteria for either an IVCD or LBBB-peripheral conduction block was presumed in the presence of normal upper septal motion (no paradoxical septal motion) using echocardiography; (2) to compare LBBB versus IVCD in relation to echocardiographic findings of LV dysfunction; and (3) to compare the LV echocardiographic systolic function in patients with LBBB and paradoxical septal motion in comparison with normal septal motion.

Background— Our group has previously shown that human umbilical vein endothelial cells exposed to smokers’ serum decreased nitric oxide (NO) production and endothelial nitric oxide synthase (eNOS) activity in the presence of increased eNOS expression. In the present study, we examined whether these observations extended to human coronary artery endothelial cells (HCAECs). In addition, the role of reactive oxygen species in the observed alterations was examined. Methods and Results— HCAECs were incubated with serum from 10 nonsmokers and 15 smokers for 12 hours with or without the addition of either polyethylene glycol-superoxide dismutase (PEG-SOD, 300 U/mL), PEG-SOD+PEG-catalase (1000 U/mL), chelerythrine (3 μmol/L), or tetrahydrobiopterin (20 μmol/L). At the end of incubation, NO, eNOS protein, and eNOS activity were measured from the same culture. HCAECs incubated with smokers’ serum alone showed significantly lower NO production ( P <0.05) and eNOS activity ( P <0.005) but higher eNOS expression ( P <0.005) compared with nonsmokers. In smokers, addition of PEG-SOD, PEG-SOD+PEG-catalase, or tetrahydrobiopterin significantly ( P <0.05) improved NO levels and eNOS activity. Interestingly, in the same smokers, a significant decrease in eNOS expression was only seen with the addition of PEG-SOD+PEG-catalase ( P <0.05) and treatment with PEG-SOD alone insignificantly increased eNOS expression. Conclusions— The present study indicates that in vitro, HCAECs show similar changes in NO biosynthesis as human umbilical vein endothelial cells when exposed to smokers’ serum and also confirms that oxidative stress plays a central role in smoking-mediated dysfunction of NO biosynthesis in endothelial cells. Furthermore, these data support other studies suggesting a role for hydrogen peroxide in the upregulation of eNOS.

Fifty-one patients with human immunodeficiency virus infection and acute coronary syndromes were identified. Nearly all patients (98%) had traditional coronary risk factors. Revascularization procedures were performed safely with low in-hospital mortality.

OBJECTIVES The objective of this study was to evaluate the association of high plasma levels of either C-reactive protein (CRP), lipoprotein (a) (Lp[a]) or total homocysteine (tHCY) with the long-term prognosis after successful coronary stenting (CS).BACKGROUND High plasma levels of either CRP, Lp(a) or tHCY may have an impact in coronary artery disease. However, long-term prospective data after coronary stenting (CS) are limited.METHODS Four-hundred and eighty-three consecutive patients with either stable or unstable coronary syndromes were followed for up to three years after successful CS. The composite of cardiac death, myocardial infarction or rehospitalization for rest unstable angina, whichever occurred first, was the prespecified primary end point. Moreover, the one-year incidence of clinical recurrence of symptoms, in-stent restenosis (ISR) and progression of atherosclerosis to a significant lesion (PTSL) were additionally evaluated. PTSL was defined as an increase by at least 25% in the luminal diameter stenosis of a known nonsignificant lesion (less than or equal to50% luminal diameter stenosis) that was located in a nonintervened vessel at restudy, resulting in an angiographically significant lesion (greater than or equal to70% luminal diameter stenosis).RESULTS By the end of the follow-up, high plasma levels of either CRP or Lp(a) but not tHCY were independently associated with the primary end point. In particular, CRP greater than or equal to 0.68 mg/dl (p < 0.001) or Lp(a) greater than or equal to 25 mg/dl (p = 0.003) conferred a significantly increased risk. By 1 year, a CRP greater than or equal to0.68 mg/dl conferred a significantly increased risk for clinical recurrence of symptoms (p < 0.001) or PTSL (p < 0.001). None of the studied biochemical markers was related to ISR.CONCLUSIONS High plasma levels of either CRP or Lp(a) but not tHCY may be associated with a higher incidence of late adverse events after successful CS. PTSL in vessels not previously intervened upon may play a significant role in the underlying pathophysiology as opposed to ISR. (J Am Coll Cardiol 2002;40:1375-82) (C) 2002 by the American College of Cardiology Foundation.

OBJECTIVES The goal of this study was to investigate the dose-dependent effects of active cigarette smoking on endothelial nitric oxide (NO) and endothelin-1 (ET-1) biosynthesis.BACKGROUND Limited studies have suggested that active cigarette smoking may be associated with a dose-dependent reduction of endothelium-dependent vasodilation (EDV). The underlying biochemical changes that cause this dose-specific effect, such as changes in the endothelial NO biosynthetic pathway and ET-1 production, have not been examined.METHODS Flow- and nitroglycerin-mediated reactivity of the brachial artery were measured in eight nonsmokers, seven light smokers (less than or equal to1 pack/week) and eight heavy smokers (greater than or equal to1 pack/day), and their sera were added to confluent (similar to85%) monolayers of human umbilical endothelial cells (HUVECs) for 12 h. Basal and substance P-stimulated NO and basal ET-1 production were measured. The HUVECs used for measuring basal NO production were lysed, and both endothelial NO synthase (eNOS) protein expression and eNOS activity were determined.RESULTS Serum cotinine level and pack-years of smoking were significantly lower in light smokers compared with heavy smokers (p < 0.006 and p < 0.004, respectively). There were no significant differences between heavy smokers and light smokers in EDV (p = 0.52), basal (p = 0.70) and stimulated-NO production (p = 0.95), eNOS protein (p = 0.40) and eNOS activity (p = 0.63). Compared with nonsmokers, all the parameters were significantly altered in both of the smokers' groups. No differences were found in nitroglycerin-mediated vasodilation and in vitro ET-1 production among the three groups.CONCLUSIONS These results indicate light smoking may have similar detrimental effects on EDV and NO biosynthetic pathway as does heavy smoking. These data may have important implications concerning the amount of active cigarette exposure that imparts cardiovascular risk. (C) 2002 by the American College of Cardiology Foundation.

The correlates of troponin positivity were assessed in 423 consecutive patients with an acute coronary syndrome and an identifiable culprit lesion. Complex lesions (disrupted plaques and/or intracoronary thrombus) were found in 72% of troponin-positive patients versus 41% of troponin-negative patients, strengthening the association between intracoronary thrombus and microvascular infarction.

Background—The mechanisms involved in the dysfunction of both endothelium-dependent vasodilatation (EDV) and NO biosynthesis related to smoking are unclear. In this study, EDV was assessed in healthy smokers and nonsmokers in vivo and, using serum from the same individuals, was related to the NO biosynthetic pathway in vitro. Methods and Results—Flow-mediated EDV of the brachial artery was measured in 23 male patients (8 nonsmokers and 15 smokers). Serum was collected, added to confluent (≈85%) monolayers of human umbilical vein endothelial cells (HUVECs), and incubated for 12 hours. Basal and substance P–stimulated NO production was measured. The HUVECs used for measuring basal NO production were lysed, and both endothelial NO synthase (eNOS) protein expression and eNOS activity were determined. EDV was lower in smokers compared with nonsmokers (P <0.001). HUVECs treated with serum from smokers compared with nonsmokers showed significantly lower basal (P <0.0001) and stimulated (P <0.02) NO production, higher eNOS expression (P <0.0001), but lower eNOS activity (P <0.004). There was a significant positive correlation between in vivo EDV and in vitro substance P–stimulated NO production (rho=0.57, P <0.01) and between basal NO production and eNOS activity (r =0.54, P <0.008) and a negative correlation between basal NO production and eNOS protein expression (r =−0.60, P <0.003). Conclusions—This is the first study to combine an in vivo model with a near-physiological in vitro model to demonstrate an association between decreased NO production and reduced EDV. Cigarette smoking was associated with reduced EDV, NO generation, and eNOS activity in the presence of increased eNOS protein expression.