ABSTRACT: Chest pain units have been used to monitor and investigate emergency department (ED) patients with potential ischemic chest pain to reduce the possibility of missed acute coronary syndrome. We seek to optimize the use of hospital resources by implementing a chest pain diagnostic algorithm.
This was a prospective cohort study of ED patients with potential ischemic chest pain. High-risk patients were referred to cardiology, and patients without ECG or biomarker evidence of ischemia were discharged home after 2 to 6 hours of observation. Emergency physicians scheduled discharged patients for outpatient stress ECGs or radionuclide scans at the hospital within 48 hours. Patients with positive provocative test results were immediately referred back to the ED. The primary outcome was the rate of missed diagnosis of acute coronary syndrome at 30 days.
We prospectively followed 1,116 consecutive patients who went through the chest pain diagnostic algorithm, of whom 197 (17.7%) were admitted at the index visit and 254 (22.8%) received outpatient testing on discharge. The 30-day acute coronary syndrome event rate was 10.8%, and the 30-day missed acute coronary syndrome rate was 0% (95% confidence interval 0% to 2.4%). Of the 120 acute coronary syndrome cases, 99 (82.5%) were diagnosed at the index ED visit, and 21 patients (17.5%) received the diagnosis during outpatient stress testing.
In ED patients with chest pain, a structured diagnostic approach with time-focused ED decision points, brief observation, and selective application of early outpatient provocative testing appears both safe and diagnostically efficient, even though some patients with acute coronary syndrome may be discharged for outpatient stress testing on the index ED visit.
Annals of emergency medicine 01/2012; 59(4):256-264.e3. · 4.23 Impact Factor
ABSTRACT: Emergency department (ED) crowding has been associated with a variety of adverse outcomes. Current guidelines suggest that patients with potentially ischemic chest pain should undergo rapid assessment and treatment in a monitored setting to optimize the diagnosis of acute coronary syndrome. These patients may be at high risk of incorrect diagnosis and adverse events when their evaluation is delayed because of crowding. To mitigate crowding-related delays, we developed processes that enabled emergency physicians to evaluate potentially sick patients in the waiting room when all nurse-staffed stretchers are occupied. The objective of this study was to investigate the safety of waiting room chest pain evaluation.
This prospective comparative cohort study was conducted in a busy urban, tertiary care ED. Explicit triage and waiting room evaluation processes were introduced. One thousand one hundred seven patients with chest pain of potential cardiac origin were triaged either to a monitored bed or a waiting room chair, depending on bed availability and triage judgment. After diagnostic evaluation, patients were followed for 30 days to identify the proportion of missed cases of acute coronary syndrome (primary outcome) and other prespecified adverse events. Analysis was based on intention to treat.
Eight hundred four patients were triaged to monitored bed and 303 to waiting room evaluation. Initial vital signs were similar, but the waiting room group was younger and had lower rates of some cardiovascular risk factors. The rate of acute coronary syndrome, defined as acute myocardial infarction or objective unstable angina, was 11.7% in the monitored bed group and 7.6% in waiting room patients. There were no missed acute coronary syndrome cases in either the monitored bed group (0%; 95% confidence interval [CI] 0% to 0.4%) or the waiting room group (0%; 95% CI 0% to 1.0%). There were 32 adverse events in the monitored bed group (4.0%; 95% CI 2.6% to 5.3%) and 2 in the waiting room group (0.7%; 95% CI 0% to 1.6%).
Our organized approach to triage and waiting room evaluation for stable chest pain patients was safe and efficient. Although waiting room evaluation is not ideal, it may be a feasible contingency strategy for periods when ED crowding compromises access to monitored, nurse-staffed ED beds.
Annals of emergency medicine 11/2010; 56(5):455-62. · 4.23 Impact Factor
ABSTRACT: We sought to determine N-terminal pro-Brain Natriuretic Peptide (NTproBNP) levels among a population of individuals with type 2 diabetes, and to correlate these levels with diabetes medications and patient demographics.
We analyzed data from 506 patients with type 2 diabetes. We compared NT-proBNP levels of these patients with those from the general population. We also sought to determine whether patients' NT-proBNP levels were correlated with diabetes medications, age, gender, creatinine, hemoglobin A1C levels, BMI, blood pressure, and lipid levels.
Increasing doses of sulfonylureas were associated with increasing levels of NT-proBNP. However, patients on combined sulfonylurea and metformin therapy had lower NT-proBNP levels than those on sulfonylureas alone. Neither thiazolidinediones nor insulin were associated with NT-proBNP levels. The majority of patients with type 2 diabetes had similar NT-proBNP levels compared to a reference group from the general population. In no age category did NT-proBNP levels differ significantly between men and women. Levels of NT-proBNP were positively associated with age (p<0.0001), systolic blood pressure (p<0.01) and creatinine levels (p<0.0001), and negatively associated with diastolic blood pressure (p<0.001). Levels of NT-proBNP were not associated with A1C, BMI, triglycerides, and high density lipoprotein (p=NS).
Levels of NT-proBNP are associated with increasing sulfonylurea dosage, age, blood pressure, and creatinine levels. There is unlikely to be clinically significant differences in NT-proBNP levels between patients with type 2 diabetes and a normal population.
International journal of cardiology 03/2007; 115(3):312-7. · 7.08 Impact Factor
ABSTRACT: Current risk stratification tools do not identify very-low-risk patients who can be safely discharged without prolonged emergency department (ED) observation, expensive rule-out protocols, or provocative testing. We seek to develop a clinical prediction rule applicable within 2 hours of ED arrival that would miss fewer than 2% of acute coronary syndrome patients and allow discharge within 2 to 3 hours for at least 30% of patients without acute coronary syndrome.
This prospective, cohort study enrolled consenting eligible subjects at least 25 years old at a single site. At 30 days, investigators assigned a diagnosis of acute coronary syndrome or no acute coronary syndrome according to predefined explicit definitions. A recursive partitioning model included risk factors, pain characteristics, physical and ECG findings, and cardiac marker results.
Of 769 patients studied, 77 (10.0%) had acute myocardial infarction and 88 (11.4%) definite unstable angina. We derived a clinical prediction rule that was 98.8% sensitive and 32.5% specific. Patients have very low risk of acute coronary syndrome if they have a normal initial ECG, no previous ischemic chest pain, and age younger than 40 years. In addition, patients at least 40 years old and with a normal ECG result, no previous ischemic chest pain, and low-risk pain characteristics have very low risk if they have an initial creatine kinase-MB (CK-MB) less than 3.0 microg/L or an initial CK-MB greater than or equal to 3.0 microg/L but no ECG or serum-marker increase at 2 hours.
The Vancouver Chest Pain Rule for early discharge defines a group of patients who can be safely discharged after a brief evaluation in the ED. Prospective validation is needed.
Annals of emergency medicine 02/2006; 47(1):1-10. · 4.23 Impact Factor
ABSTRACT: Tenofovir (TDF) exposure has been associated with renal dysfunction. Mitochondrial nephrotoxicity was investigated as an underlying mechanism. Given the interaction between TDF and didanosine (ddl), their concurrent use was also investigated.
Relative kidney biopsy mitochondrial DNA (mtDNA) to nuclear DNA ratios were measured retrospectively. HIV+ individuals on TDF within 6 months preceeding the biopsy (HIV+/TDF+, n=21) were compared to HIV+ individuals who never received TDF (HIV+/TDF-, n=10) and to HIV uninfected controls (HIV-,n=22). Twelve of the HIV+/TDF+ individuals received concurrent ddl, 10 of those once at unadjusted ddl dosage. Tubular mitochondria morphology was also examined by electron microscopy. Statistical analyses were done on log-transformed mtDNA/nDNA, using non-parametric tests.
Kidney mtDNA levels were different among the three groups (P=0.046). mtDNA ratios were lower in HIV+/TDF+ subjects (7.5 [2.0-12.1]) than in HIV- ones (14.3 [6.0-16.5], P=0.014), but not lower than HIV+/TDF- controls (6.4 [2.8-11.9], P=0.82). Among HIV+ subjects, there was a difference between TDF-, TDF+/ddl- and TDF+/ddl+ (P=0.005), with concurrent TDF/ddl use associated with lower mtDNA (2.1 [1.9-5.5], n=12) than TDF+/ddl- (13.8 [7.5-16.4], n=9, P=0.003). No TDF-/ddl+ biopsies were available. In regression analyses, only HIV infection (P=0.03), and TDF/ddl use (P=0.003) were associated with lower mtDNA. At the ultrastructural level, abnormal tubular mitochondria was more prevalent in HIV+/TDF+ biopsies than HIV+/TDF- and HIV- ones together (P<0.001) but not more so in TDF+/ddl+ biopsies than TDF+/ddl- ones (P=0.67).
Renal dysfunction in this population may be mediated through mitochondrial nephrotoxicity that involves more than one drug and/or pathogenesis. Kidney mtDNA depletion was associated with HIV infection and concurrent TDF/ddl therapy but not TDF use alone, while kidney ultrastructural mitochondrial abnormalities were seen with TDF use. The interaction between TDF and ddl may be relevant in the kidney where both drugs are cleared. The clinical relevance of our findings needs to be evaluated given the current recommendation for reduced doses of ddl when used in conjunction with TDF.
Antiviral therapy 01/2006; 11(1):79-86. · 3.16 Impact Factor