ABSTRACT
AIMS: The aortic dissection detection (ADD) risk score has been proposed by guidelines to standardise the approach to patients with suspected acute aortic dissection (AD). However, the ADD risk score has not been validated so far. METHODS AND RESULTS: Patients with suspected AD from two clinical centres were prospectively enrolled in a registry from 2008 to 2012. The ADD risk score was calculated retrospectively by review of medical charts, according to the number of risk categories where patients met criteria. Of 1328 patients, 291 (21.9%) were diagnosed with AD. The ADD risk score was=0 in 439 (33.1%) patients, =1 in 646 (48.6%) patients and >1 in 243 (18.3%) patients. The incidence of AD was 5.9%, 27.3% and 39.1% respectively in patient groups identified by ADD risk score=0, =1 and >1. ADD risk score>0 had a sensitivity of 91.1% (95% confidence interval (CI) 87.2-94.1%) and a specificity of 39.8% (95% CI 36.8-42.9%) for the diagnosis of AD, while ADD risk score>1 had a sensitivity of 32.7% (95% CI 27.3-38.4%) and a specificity of 85.7% (95% CI 83.5-87.8%). Among patients with ADD risk score=0, mediastinum widening on chest X-ray had a sensitivity of 16.7% (95% CI 3.6-41.4%) and a specificity of 86.3% (95% CI 81.9-90.0%). CONCLUSION: The ADD risk score stratifies patients for the risk of AD. ADD risk score>0 is highly sensitive and poorly specific for the diagnosis in AD. The presence of ADD risk score=0 per se does not accurately exclude AD. In patients with ADD risk score=0, chest X-ray provides limited diagnostic information.
Subject(s)
Aortic Aneurysm, Thoracic/diagnosis , Aortic Dissection/diagnosis , Aged , Diagnosis, Differential , Female , Humans , Male , Prospective Studies , Retrospective Studies , Risk Assessment/methodsABSTRACT
OBJECTIVE: The aim of the present study was to investigate whether the improvement of pulmonary capillary wedge pressure (PCWP) non-invasively assessed with tissue Doppler imaging is able to predict prognosis and cardiac-related mortality in patients with heart failure (HF), as previously demonstrated for NT-proBNP. METHODS: We prospectively studied 23 patients (74 +/- 10 y; 17 M, 6 F) with acute HF. NT-proBNP and PCWP were measured at admission and discharge. NT-proBNP concentrations were determined by a chemiluminescent immunoassay kit. PCWP was assessed using the ratio of transmitral E velocity to the early diastolic mitral annulus velocity (E'), with the formula PCWP = 1.9 + 1.24 (E/E'). Patients were divided in two groups according to the clinical end-point based on cardiac death and hospital readmission for HF. RESULTS: After a mean follow-up of 230 days, 10 patients reached the end-point (group A), while 13 patients resulted event-free (group B). In group B, NT-proBNP values significantly decreased (3816 +/- 7424 vs. 6799 +/- 10537 pg/mL, P < 0.01) and PCWP improved (17 +/- 7 vs. 23 +/- 12 mmHg, P < 0.01). The decrease in both NT-proBNP and PCWP values was able to identify the majority of patients (77%) with an event-free survival at follow-up, whereas 70% of patients who reached the end-point had discordant changes in NT-proBNP and PCWP (chi2 = 5.06, P < 0.05). CONCLUSIONS: The combination of a biochemical marker such as NT-proBNP and a new indicator of LV filling pressure (E/E') allows to estimate the prognostic impact of standard medical therapy even in a small group of HF patients.
