ABSTRACT
BACKGROUND: The routine use of natiuretic peptides in severely dyspneic patients has recently been called into question. We hypothesized that the diagnostic utility of Amino Terminal pro Brain Natiuretic Peptide (NT-proBNP) is diminished in a complex elderly population. METHODS: We studied 502 consecutive patients in whom NT-proBNP values were obtained to evaluate severe dyspnea in the emergency department. The diagnostic utility of NT-proBNP for the diagnosis of congestive heart failure (CHF) was assessed utilizing several published guidelines, as well as the manufacturers suggested age dependent cut-off points. RESULTS: The area under the receiver operator curve (AUC) for NT-proBNP was 0.70. Using age-related cut points, the diagnostic accuracy of NT-proBNP for the diagnosis of CHF was below prior reports (70% vs. 83%). Age and estimated creatinine clearance correlated directly with NT-proBNP levels, while hematocrit correlated inversely. Both age > 50 years and to a lesser extent hematocrit < 30% affected the diagnostic accuracy of NT-proBNP, while renal function had no effect. In multivariate analysis, a prior history of CHF was the best predictor of current CHF, odds ratio (OR) = 45; CI: 23-88. CONCLUSIONS: The diagnostic accuracy of NT-proBNP for the evaluation of CHF appears less robust in an elderly population with a high prevalence of prior CHF. Age and hematocrit levels, may adversely affect the diagnostic accuracy off NT-proBNP. KEYWORDS: Congestive Heart Failure; Natriuretic peptides; Diagnosis; Elderly Patients.
Subject(s)
Blood Pressure/physiology , Echocardiography, Doppler , Heart Failure, Systolic/diagnostic imaging , Heart Failure, Systolic/physiopathology , Mitral Valve/diagnostic imaging , Mitral Valve/physiopathology , Diastole/physiology , Humans , Pulmonary Wedge Pressure/physiology , Ventricular Dysfunction, Left/physiopathologyABSTRACT
Aspirin resistance (AR) still lacks a universally accepted definition, but it may be discussed as either a laboratory phenomenon or a clinical presentation. Laboratory resistance is mainly defined as abnormal platelet response to aspirin, whereas the clinical manifestation is the failure of aspirin to prevent cardiovascular events. Although there is evidence of an association, it appears that a laboratory abnormality in platelet function is not the only risk factor for the clinical manifestation of AR. Therapies for primary and secondary prevention of AR still need to be elucidated, but there are some data to suggest that in an acute episode of aspirin failure because of AR, different therapeutic interventions need to be considered.
