Are ejection fraction measurements by echocardiography and left ventriculography equivalent?

BACKGROUND: Left ventricular ejection fraction (EF) is an important parameter in the diagnosis and treatment of patients with coronary heart disease. Previous studies comparing echocardiography and contrast left ventriculography (CVG) for the measurement of EF have shown considerable variation in results, yet, in clinical practice, EF measurements are used interchangeably. The purpose of this study was to assess the concordance between echocardiography and CVG for the determination of EF in routine clinical practice and to identify factors associated with variation in test results. METHODS: We reviewed the medical records of 5,385 patients hospitalized for acute myocardial infarction between 1997 and 2005 as part of a community-based surveillance project. Of these, 741 patients had EF measurements recorded by both echocardiography and CVG during hospitalization. RESULTS: While good correlation (r = 0.73) and no systematic bias were noted between the measurement of EF by echocardiogram compared to CVG, there was wide variation between the 2 methods for any given patient. In approximately one third of patients with acute myocardial infarction, the measurement of EF by echocardiography and CVG differed by >10 points, while in approximately 1 in 20 patients, EF measurements by echocardiography and CVG differed by >20 points. The number of days between tests to measure EF, level of EF, temporal order of EF testing, and patient-related factors made only a minor contribution to the variation in test results. CONCLUSIONS: Our results demonstrate that, in routine clinical practice, EF determinations obtained by echocardiography and CVG may vary widely, with potentially important clinical implications.

Adenosine A2A receptor antagonists exert motor and neuroprotective effects by distinct cellular mechanisms.

OBJECTIVE: To investigate whether the motor and neuroprotective effects of adenosine A(2A) receptor (A(2A)R) antagonists are mediated by distinct cell types in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) model of Parkinson's disease. METHODS: We used the forebrain A(2A)R knock-out mice coupled with flow cytometric analyses and intracerebroventricular injection to determine the contribution of A(2A)Rs in forebrain neurons and glial cells to A(2A)R antagonist-mediated motor and neuroprotective effects. RESULTS: The selective deletion of A(2A)Rs in forebrain neurons abolished the motor stimulant effects of the A(2A)R antagonist KW-6002 but did not affect acute MPTP neurotoxicity. Intracerebroventricular administration of KW-6002 into forebrain A(2A)R knock-out mice reinstated protection against acute MPTP-induced dopaminergic neurotoxicity and attenuated MPTP-induced striatal microglial and astroglial activation. INTERPRETATION: A(2A)R activity in forebrain neurons is critical to the control of motor activity, whereas brain cells other than forebrain neurons (likely glial cells) are important components for protection against acute MPTP toxicity.