New York/New Jersey VA Health Care Network

Aggression and violence represent a significant public health concern and a clinical challenge for the mental healthcare provider. A great deal has been revealed regarding the neurobiology of violence and aggression, and an integration of this body of knowledge will ultimately serve to advance clinical diagnostics and therapeutic interventions. We will review here the latest findings regarding the neurobiology of aggression and violence. First, we will introduce the construct of aggression, with a focus on issues related to its heterogeneity, as well as the importance of refining the aggression phenotype in order to reduce pathophysiologic variability. Next we will examine the neuroanatomy of aggression and violence, focusing on regional volumes, functional studies, and interregional connectivity. Significant emphasis will be on the amygdala, as well as amygdala-frontal circuitry. Then we will turn our attention to the neurochemistry and molecular genetics of aggression and violence, examining the extensive findings on the serotonergic system, as well as the growing literature on the dopaminergic and vasopressinergic systems. We will also address the contribution of steroid hormones, namely, cortisol and testosterone. Finally, we will summarize these findings with a focus on reconciling inconsistencies and potential clinical implications; and, then we will suggest areas of focus for future directions in the field.

BACKGROUND: Percutaneous coronary intervention (PCI) relieves angina in patients with stable ischemic heart disease, but clinical trials have not shown that it improves survival. Between June 1999 and January 2004, we randomly assigned 2287 patients with stable ischemic heart disease to an initial management strategy of optimal medical therapy alone (medical-therapy group) or optimal medical therapy plus PCI (PCI group) and did not find a significant difference in the rate of survival during a median follow-up of 4.6 years. We now report the rate of survival among the patients who were followed for up to 15 years. METHODS: We obtained permission from the patients at the Department of Veterans Affairs (VA) sites and some non-VA sites in the United States to use their Social Security numbers to track their survival after the original trial period ended. We searched the VA national Corporate Data Warehouse and the National Death Index for survival information and the dates of death from any cause. We calculated survival according to the Kaplan-Meier method and used a Cox proportional-hazards model to adjust for significant between-group differences in baseline characteristics. RESULTS: Extended survival information was available for 1211 patients (53% of the original population). The median duration of follow-up for all patients was 6.2 years (range, 0 to 15); the median duration of follow-up for patients at the sites that permitted survival tracking was 11.9 years (range, 0 to 15). A total of 561 deaths (180 during the follow-up period in the original trial and 381 during the extended follow-up period) occurred: 284 deaths (25%) in the PCI group and 277 (24%) in the medical-therapy group (adjusted hazard ratio, 1.03; 95% confidence interval, 0.83 to 1.21; P=0.76). CONCLUSIONS: During an extended-follow-up of up to 15 years, we did not find a difference in survival between an initial strategy of PCI plus medical therapy and medical therapy alone in patients with stable ischemic heart disease. (Funded by the VA Cooperative Studies Program and others; COURAGE ClinicalTrials.gov number, NCT00007657.).

This article examines the evolution of and need for "end-of-life conversations." Barriers to end-of-life discussions that have been identified in patients and families, health care professionals, and health care systems can seriously interfere with the quality of remaining life for terminally ill patients. Strategies for enhancing end-of-life discussions are most productively linked to (1) physicians' interpersonal communication skills, (2) a patient-centered model of care, (3) a focus on quality of remaining life, and (4) innovative clinical models for implementing these discussions earlier in the care process. We conclude that end-of-life conversations must become a routine, structured intervention in health care and that advance care planning is best viewed as one component in a series of ongoing end-of-life discussions. Randomized trials are needed to examine new approaches and models for enhancing end-of-life conversations. JAMA. 2000;284:1573-1578.

Thyroid hormone [L-thyroxine (T4)] rapidly induced phosphorylation and nuclear translocation (activation) of mitogen-activated protein kinase (MAPK) in HeLa and CV-1 cells in the absence of cytokine or growth factor. A pertussis toxin-sensitive and guanosine 5'-O-(3-thiotriphosphate)-sensitive cell surface mechanism responsive to T4 and agarose-T4, suggesting a G protein-coupled receptor, was implicated. Cells depleted of MAPK or treated with MAPK pathway inhibitors showed reduced activation of MAPK and of the signal transducer and activator of transcription STAT1alpha by T4; they also showed reduced T4 potentiation of the antiviral action of interferon-gamma (IFN-gamma). T4 treatment caused tyrosine-phosphorylated MAPK-STAT1alpha nuclear complex formation and enhanced Ser-727 phosphorylation of STAT1alpha, in the presence or absence of IFN-gamma. STAT1alpha-deficient cells transfected with STAT1alpha containing an alanine-for-serine substitution at residue 727 (STAT1alphaA727) showed minimal T4-stimulated STAT1alpha activation. IFN-gamma induced the antiviral state in cells containing wild-type STAT1alpha (STAT1alphawt) or STAT1alphaA727; T4 potentiated IFN-gamma action in STAT1alphawt cells but not in STAT1alphaA727 cells. T4-directed STAT1alpha Ser-727 phosphorylation is MAPK mediated and results in potentiated STAT1alpha activation and enhanced IFN-gamma activity.

The effectiveness of thyroid hormone suppressive therapy in reducing the volume of benign thyroid nodules is controversial. It is important to clarify this therapeutic effect of thyroid hormone, because its prolonged use needs to be carefully weighed against its potential deleterious effects in the skeletal and cardiovascular systems. To evaluate the best available evidence, we conducted a systematic review and meta-analysis of the randomized controlled trials that fulfill the following inclusion criteria: single thyroid nodules proven benign by fine needle aspiration, treatment, and follow-up of at least 6 months; documented suppression of TSH; measurement of thyroid nodule volume by ultrasound; and response to therapy defined as more than 50% volume reduction from baseline. Six randomized clinical trials published between 1987 and 1999, with 346 patients, were included in the meta-analysis. Ninety percent of the participants were female. Using a random effects model, the overall effect size showed a relative risk of 1.9 (95% confidence interval, 0.95-3.81) favoring a treatment effect. A sensitivity analysis showed significant changes in the results. Suppressive thyroid hormone therapy for longer than 6 months is associated with a trend toward a reduction of more than 50% in volume of benign thyroid nodules, without achieving statistical significance. The results are highly sensitive to changes in the statistical analysis, especially if the method used ignores heterogeneity among the effect sizes. More studies are needed before this therapy can be widely recommended.

3-hydroxy-3-methylglutaryl coenzyme A reductase (HMG CoA-reductase) inhibitors, otherwise known as statins, are currently the medical treatment of choice for hypercholesterolemia. Hypercholesterolemia is a known risk factor for cardiovascular disease, and statin therapy has led to a significant reduction in morbidity and mortality from adverse cardiac events, stroke, and peripheral arterial disease. In addition to achieving a therapeutic decrease in serum cholesterol levels, statin therapy appears to promote other effects that are independent of changes in serum cholesterol. These ''pleiotropic'' effects include attenuation of vascular inflammation, improved endothelial cell function, stabilization of atherosclerotic plaque, decreased vascular smooth muscle cell migration and proliferation, and inhibition of platelet aggregation. This article is part I of a 2-part review, and it focuses on the pleiotropic effects of statins at the cellular level.

Serum concentration of hepatic enzymes are linked to liver dysfunction, metabolic and cardiovascular diseases. We perform genetic analysis on serum levels of alanine transaminase (ALT), alkaline phosphatase (ALP) and gamma-glutamyl transferase (GGT) using data on 437,438 UK Biobank participants. Replication in 315,572 individuals from European descent from the Million Veteran Program, Rotterdam Study and Lifeline study confirms 517 liver enzyme SNPs. Genetic risk score analysis using the identified SNPs is strongly associated with serum activity of liver enzymes in two independent European descent studies (The Airwave Health Monitoring study and the Northern Finland Birth Cohort 1966). Gene-set enrichment analysis using the identified SNPs highlights involvement in liver development and function, lipid metabolism, insulin resistance, and vascular formation. Mendelian randomization analysis shows association of liver enzyme variants with coronary heart disease and ischemic stroke. Genetic risk score for elevated serum activity of liver enzymes is associated with higher fat percentage of body, trunk, and liver and body mass index. Our study highlights the role of molecular pathways regulated by the liver in metabolic disorders and cardiovascular disease.

L-T3 and L-T4 activated the Na+/H+ exchanger of L-6 myoblasts, with a fast nongenomic mechanism, both in the steady state and when cells undergo acid loading with ammonium chloride. Monitored with the intracellular pH-sensitive fluorescent probe 2',7'-bis(carboxyethyl)-5(6)-carboxyfluorescein, activation of the exchanger appeared to be initiated at the plasma membrane, because T3-agarose reproduced the effect of L-T3, and triiodothyroacetic acid, a hormone analog previously shown to inhibit membrane actions of thyroid hormone, blocked the action of L-T3 on the exchanger. We show here for the first time that transduction of the hormone signal in this nongenomic response requires tyrosine kinase-dependent phospholipase C activation and two different signaling pathways: 1) mobilization of intracellular calcium, assessed by the fluorescent probe fura-2, through activation of inositol trisphosphate receptors and without contributions from extracellular calcium or ryanodine receptors; and 2) protein phosphorylation involving protein kinase C and MAPK (ERK1/2), as shown by the use of kinase inhibitors and by immunoblotting for activated kinases.

Cognitive impairments in schizophrenia are well documented and correlated with functional disability. Although some patients demonstrate normal neuropsychological (NP) functioning, little is known about their functional disability. We examined the cross-sectional functional implications of NP normality and symptomatic remission in older outpatients diagnosed with schizophrenia or schizoaffective disorder, who were administered a NP battery and performance-based measures of functional and social competence, with their real-world functioning rated by case managers. NP status was classified by the General Deficit Score (GDS) and remission status was based on the Positive and Negative Syndrome Scale (PANSS), yielding four subsamples of patients: NP normal-remitted (n = 21), NP normal-symptomatic (n = 22), NP impaired-remitted (n = 90), and NP impaired-symptomatic (n = 97). NP normal patients demonstrated better functional and social competence and better ratings of real world functioning, after controlling for premorbid abilities. However, compared to normative date, NP normal patients manifested disability in several real-world domains, including residential status. These results suggest that NP status is a better predictor of functional outcome then symptom status or the interaction of the two factors. The disability seen in NP normal cases indicates that factors other than cognitive impairments may determine aspects of everyday outcomes in schizophrenia.

OBJECTIVE: To evaluate the Advanced Illness Coordinated Care Program (AICCP), delivered by allied health personnel to improve care for patients coping with advanced illness and in need of preparation for end-of-life (EOL) care. STUDY DESIGN: Clinical trial involving 275 patients and 143 surrogates in 6 settings who were randomly assigned to the AICCP or usual care (UC). METHODS: The AICCP participants met with a care coordinator for assistance with provider communication, care coordination, and support. The AICCP was evaluated for effects on satisfaction with care, advance planning, consistency of care with patient preferences, and healthcare costs. RESULTS: The AICCP increased patient satisfaction with care and communication (P = .03), and AICCP surrogates reported fewer problems with provider support (P = .03). More AICCP than UC participants completed an advance directive (AD) (69.4% vs 48.4%; P = .006), and the AICCP group completed more ADs per participant (P = .01). Median time to AD documentation was 46 days for AICCP and 238 days for UC (P = .02). There was no difference in survival (AICCP 43% vs UC 42%). Six-month costs were lower with AICCP than with UC (12,123 US dollars vs 16,295 US dollars); however, the difference did not reach statistical significance. CONCLUSIONS: The AICCP improved satisfaction with care and helped patients develop and revise more ADs, sooner, without affecting mortality. This program may be delivered in a range of managed care, fee-for-service, and group-model settings.

We have examined the effects of l-thyroxine (T4) on the activation of signal transducer and activator of transcription 3 (STAT3) and on the STAT3-dependent induction of c-Fos expression by epidermal growth factor (EGF). T4, at a physiological concentration of 100 nM, caused tyrosine phosphorylation and nuclear translocation (i.e. activation) of STAT3 in HeLa cells in as little as 10–20 min. Activation by T4 of STAT3 was maximal at 30 min (15±4-fold enhancement; mean±S.E.M.) in 18 experiments. This effect was reproduced by T4–agarose (100 nM) and blocked by CGP 41251, genistein, PD 98059 and geldanamycin, inhibitors of protein kinase C (PKC), protein tyrosine kinase (PTK), mitogen-activated protein kinase (MAPK) kinase and Raf-1 respectively. Tyrosine-phosphorylated MAPK also appeared in nuclear fractions within 10 min of treatment with T4. In the nuclear fraction of T4-treated cells, MAPK immunoprecipitate also contained STAT3. The actions of T4 were similar in HeLa and CV-1 cells, which lack thyroid hormone receptor (TR), and in TR-replete skin fibroblasts (BG-9). T4 also potentiated the EGF-induced nuclear translocation of activated STAT1α and STAT3 and enhanced the EGF-stimulated expression of c-Fos. Hormone potentiation of EGF-induced signal transduction and c-Fos expression was inhibited by CGP 41251, geldanamycin and PD 98059. Therefore the non-genomically induced activation by T4 of STAT3, and the potentiation of EGF by T4, require activities of PKC, PTK and an intact MAPK pathway.

As advances in neuroscience have furthered our understanding of the role of brain circuitry, genetics, stress, and neuromodulators in the regulation of normal behavior and in the pathogenesis of psychopathology, an increasing appreciation of the role of neurobiology in individual differences in personality and their pathology in personality disorders has emerged. Individual differences in the regulation and organization of cognitive processes, affective reactivity, impulse/action patterns, and anxiety may in the extreme provide susceptibilities to personality disorders such as borderline and schizotypal personality disorder. A low threshold for impulsive aggression, as observed in borderline and antisocial personality disorders, may be related to excessive amygdala reactivity, reduced prefrontal inhibition, and diminished serotonergic facilitation of prefrontal controls. Affective instability may be mediated by excessive limbic reactivity in gabaminergic/glutamatergic/cholinergic circuits, resulting in an increased sensitivity or reactivity to environmental emotional stimuli as in borderline personality disorder and other cluster B personality disorders. Disturbances in cognitive organization and information processing may contribute to the detachment, desynchrony with the environment, and cognitive/perceptional distortions of cluster A or schizophrenia spectrum personality disorders. A low threshold for anxiety may contribute to the avoidant, dependent, and compulsive behaviors observed in cluster C personality disorders. These alterations in critical regulatory domains will influence how representations of self and others are internalized. Aspects of neurobiological functioning themselves become cognized through the medium of figurative language into an ongoing narrative of the self, one that can be transformed through the analytic process, allowing for the modulation of genetic/biological thresholds.

OBJECTIVE: The study examined the effect of adding a full-time family support coordinator to the surgical intensive care unit team on family satisfaction, length-of-stay, and cost in the surgical intensive care unit. DESIGN, SETTING, AND PATIENTS: A quasi-experimental design was conducted in two phases: baseline (8 mos) and intervention (10 mos) phases. Data on family satisfaction, length-of-stay, and costs from both phases were collected. INTERVENTIONS: The intervention added a new role, the family support coordinator, to the surgical intensive care unit team. The family support coordinator functioned as a liaison between the patient's family and the health care team. MEASUREMENTS AND MAIN RESULTS: The results revealed that generally the intervention was associated with increases in family satisfaction with communication for all surgical intensive care unit team members, with physicians, social workers, and respiratory care therapists showing increases in significance. The largest increase was for physician communication (p = .0034). Families also rated their perceptions of the quality of care provided to their family members by various members of the surgical intensive care unit team. Mean ratings increased for all areas of care, with respiratory and nursing care showing the largest increases. Families' perceptions of the care and treatment they received during the stay of their family member showed increases in all areas of satisfaction between baseline and intervention, particularly those areas most related to the intervention. CONCLUSIONS: The implementation of the family support coordinator intervention increased family satisfaction across a range of parameters. Although there were decreases in length-of-stay and costs, they were not statistically significant. Further research is needed to determine whether intervention refinement could produce lower length-of-stay and costs.

Although posttraumatic stress disorder (PTSD) is common in primary care patients, many do not seek mental health treatment. Existing research on barriers and facilitators to receiving PTSD treatment are not specific to primary care patients. In this study, we sought to understand the psychosocial concerns, treatment barriers, and treatment facilitators among non-treatment-seeking primary care veterans with PTSD who reside in both rural and urban settings. Using a concurrent triangulation design, we collected qualitative focus group and quantitative self-report data concurrently, analyzed them separately, and merged the results for interpretation. In total, 27 veteran primary care patients with PTSD participated in 1 of 4 focus groups. A modified conventional content analysis approach was used. Team-based coding began with three broad primary codes (psychosocial concerns, barriers, and facilitators) and subcodes were allowed to emerge from the data. Self-report measures were used to collect clinical characteristics and barriers to care. The results expanded upon existing models of PTSD treatment initiation by (a) specifying treatment preferences, such as patient-centered care, peer support services, and open access scheduling, and (b) presenting concerns, such as anger and core symptoms of PTSD. Results also indicated that a commonly used quantitative barriers measure may offer an incomplete picture of why veterans do not seek treatment as it does not assess how past negative treatment experiences may affect utilization. Strategies to help veterans overcome barriers to care may benefit from a focus on negative treatment-seeking beliefs and tailoring based on a veteran's rural or urban status.

The present study explored longitudinal evidence for prodromal symptoms of depression episodes. A model based on previous findings of the relations between prodromal and residual symptoms was described and used to generate hypotheses tested in this study. Data were analyzed from 160 participants from the Cognitive Vulnerability to Depression (CVD) project (L. Alloy & L. Abramson, 1999) who experienced an episode of depression during the prospective follow-up period and 60 CVD participants who did not. Congruent with the hypothesis, individuals who subsequently developed an episode of depression experienced significantly greater numbers of depression symptoms in the period of time leading up to the acute episode compared with those who did not develop a depressive episode. Seven depression symptoms were particularly likely to appear before the onset of an acute episode. Furthermore, all 3 predictions from the model were supported: the durations of prodromal and residual phases were correlated, the prodromal and residual symptom profiles were quite similar, and the order of symptom onset was significantly and highly negatively correlated with the order of symptom remission. Additionally, residual symptom profiles were similar to subsequent prodromal symptom profiles in individuals who experienced more than 1 depressive episode. These findings are discussed in terms of the importance of understanding the earliest prodromal symptoms to appear and their relation to the symptomatic course of depression episodes. Implications for early intervention are also discussed.

Working memory abnormalities, which are particularly pronounced on context processing tasks, appear relatively specific to schizophrenia spectrum illnesses compared with other psychotic disorders. However, the specificity of context processing deficits to schizotypal personality disorder (SPD), a prototype of schizophrenia, has not been studied. The authors administered 3 versions of the modified AX Continuous Performance Test and an N-back working memory test to 63 individuals with SPD and 25 with other personality disorders, as well as 42 healthy controls. For the AX Continuous Performance Test standard and degraded versions, there was a significant Trial Type x Delay x Group interaction, as SPDs made significantly more errors reflecting poor maintenance of context and fewer errors reflecting good maintenance of context. SPDs also demonstrated poor performance on the N-back, especially at the 2-back condition. Context processing errors and N-back accuracy scores were related to disorganization symptoms. These findings, which are quite similar to those previously reported in patients with schizophrenia, suggest that context processing deficits are specific to the schizophrenia spectrum and are not a reflection of overall psychopathology.

PTSD symptoms and substance use commonly co-occur, but information is limited regarding their interplay. We used ecological momentary assessment (EMA) to capture fluctuations in PTSD symptoms and drinking within and across days. Fifty Iraq and Afghanistan War veterans completed four daily Interactive Voice Response (IVR) assessments of PTSD and substance use with cell phones for 28 days. The aims of this study were to (1) describe participant compliance and reactions to the protocol and (2) identify participant characteristics and protocol reactions that predict compliance. Protocol compliance was high, with participants completing an average of 96 out of a total of 112 IVR assessments (86%). While some participants perceived that the IVR assessments increased their drinking (21%) and PTSD symptoms (60%), self-report measures showed significant decreases in PTSD symptoms and nonsignificant decreases in drinking over the assessment period. Analyses revealed demographic (e.g., older than 24, full-time employment, more education), clinical (e.g., less binge drinking, less avoidance symptoms), and perceived benefit from participation predicted better protocol compliance. Results can guide future research on participant predictors of compliance with intensive EMA methods.

INTRODUCTION: Although the safety of celecoxib has been investigated, limited data are available on complications affecting the entire (upper and lower) gastrointestinal (GI) tract, with no patient-level pooled analyses of upper and lower GI outcomes available. We therefore evaluated the upper and lower GI safety of celecoxib by using patient-level data from randomized controlled trials (RCTs). METHODS: This patient-level pooled analysis included 52 prospective, randomized, double-blind parallel-group studies from the Celecoxib Clinical Database. Each study had a planned duration of continuous treatment with celecoxib or a nonselective nonsteroidal antiinflammatory drug (nsNSAID), rofecoxib, or the placebo comparator arm for at least 4 weeks. All studies with final reports completed by 1 October 2007 were included. The primary end point was the combined incidence of clinically significant upper and lower GI events (CSULGIEs). An independent blinded committee reviewed and adjudicated all end points by using predefined criteria and all available reported adverse events, laboratory data, and case narratives. All doses of celecoxib and all doses of all nsNSAIDs were pooled for analysis. RESULTS: The pooled analysis involved 51,048 patients; 28,614 were randomized to celecoxib; 15,278 to nsNSAIDs (including 3,248 patients taking naproxen, 2,640 taking ibuprofen, 8,066 taking diclofenac, 1,234 taking loxoprofen, and 90 taking ketoprofen); 5,827 to placebo and 1,329 to rofecoxib. The mean age was 60 years, and 65% were women. Data on 1,042 patients with potential GI events were reviewed for end-points adjudication; the adjudication committee confirmed 89 patients with CSULGIEs. The majority were in the celecoxib and nsNSAID groups (with raw incidence proportions of 37 (0.1%) and 40 (0.3%), respectively). The incidence rates were 0.3, 0.9 and 0.3 per 100 patient-years in the celecoxib, nsNSAID, and placebo groups, respectively. The time to incidence of CSULGIEs was significantly longer with celecoxib than with nsNSAIDs (P=0.0004). CONCLUSIONS: When compared with nsNSAIDs, celecoxib is associated with a significantly lower risk of all clinically significant GI events throughout the entire GI tract. This pooled analysis of 52 RCTs significantly advances the understanding of the upper and lower GI safety profile of celecoxib and its potential benefits to patients.

OBJECTIVE: Suicide is a significant public health problem. Suicidal ideation (SI) increases the risk for completed suicide. However, the brain basis of SI is unknown. The objective of this study was to examine the neural correlates of self-monitoring in individuals at risk for suicide. We hypothesized that combat veterans with a history of SI relative to those without such a history would show altered activation in the anterior cingulate cortex and related circuitry during self-monitoring. METHODS: Two groups of combat-exposed war veterans (13 men with and 13 men without history of SI) were studied. Both the SI and non-SI participants had two or more of the following: a) current major depressive disorder, b) current posttraumatic stress disorder, and c) history of mild traumatic brain injury, and each subject performed a validated stop task during functional magnetic resonance imaging. Error-related activation was compared between the SI and non-SI groups. RESULTS: The SI group demonstrated more error-related activation of the anterior cingulate (8256 mm(3), t = 2.51) and prefrontal cortex (i.e., clusters >2048 mm(3), voxelwise p < .05). The SI and non-SI participants showed similar behavioral task performance (i.e., mean error rate, F values < 0.63, p values > .43; and mean reaction times, F = 0.27, p = .61). CONCLUSIONS: These findings suggest neural correlates of altered self-monitoring in individuals with a history of SI and may further suggest that functional magnetic resonance imaging could be used to identify individuals at risk for suicide before they engage in suicidal behavior.

OBJECTIVE: To describe provider practice patterns in the diagnosis and treatment of Nursing Home-Acquired Pneumonia (NHAP) and to document associations with cure, mortality, and transfer. DESIGN: A retrospective cohort. SETTING: Six nursing homes in Seattle, Washington. PARTICIPANTS: A total of 94 patients, 65 years of age or older (mean 83 +/- SD 9), in whom the diagnosis of pneumonia was documented in the nursing home medical record between July 1, 1994, and June 6, 1995. MEASUREMENTS: Multivariate logistic regression was used to assess the relationship between descriptive, diagnostic, or therapeutic measures and three outcomes, cure, 30-day mortality, and hospital transfer. RESULTS: Ninety-four episodes of pneumonia were identified. Allowing for more than one outcome per patient, there were 71 (75.5%) cures, 16 (17%) deaths, and nine (9.6%) transfers. Eighty-five percent of patients identified as having NHAP by their providers had chest X-rays (CXRs), and 69% had physical examinations. Sputum examination was ordered in 5%, blood cultures in 6%, and white blood cell counts in 33% of patients. In multivariate analysis, patients with functional decline were more likely to die (Odds Ratio (OR) 36.5 (95% CI 6.1, 220)). Cognitive decline was a risk factor for mortality (OR 6.8 l (CI 1.8, 26)) and transfer (OR 7.5 (CI 1.2, 46)). Those patients receiving only oral antibiotics (OR 3.2 (CI 1.1, 9.7)) were more likely to be cured. Length of therapy >1 week was also associated with cure (OR 2.9 (CI 1.0, 8.6)). Providers with Certificate of Added Qualifications (CAQ) in Geriatric Medicine were more likely to achieve cure (OR 3.1 (CI 1.0, 9.0)). CONCLUSIONS: Most patients with NHAP had diagnostic CXRs and physical examinations. In multivariate analysis, death was more likely to occur in patients with cognitive or functional decline. Cure was associated with the use of oral antibiotics alone and with care by providers with CAQ in Geriatric Medicine.