Background: Pleural effusion is not pathognomic and distinguishing between transudates and exudates often presents a diagnostic dilemma. The purpose of our study was to examine whether the inclusion of pleural fluid brain natriuretic peptide (BNP) measurement into the analysis improves the diagnostic accuracy of pleural effusion. Methods: The pleural effusion of 14 patients with CHF (group A) and 14 subjects with different pleural pathology (group B) were analyzed. Samples of pleural fluid and serum were obtained from all patients on admission and biochemical analysis, bacterial and fungal culture, acid-fast bacilli smear and culture and cytology were performed on the pleural fluid. In vitro quantitative determination of N-terminal pro-Brain natriuretic peptide (NTproBNP) in serum and pleural fluid were performed by electrochemiluminescence immunoassay proBNP method on an Elecsys 2010 (Roche) analyzer. Results: The median NT-proBNP levels in groups A and B were 6295 pg/ml and 276 pg/ml, respectively: ( P=0.0001). There was no overlap between the two groups. While the Light's criteria had a sensitivity of 93% and specificity of 43% for transudates, the pleural fluid NT-proBNP level accurately differentiated between the two groups. Conclusions: The pleural NT-proBNP levels were elevated in all patients who had transudate. Therefore if the NT-proBNP levels of pleural effusion are within the normal range, transudate resulting from congestive heart failure can be ruled out. Our results suggest that the inclusion of pleural fluid NT-proBNP measurement in the routine diagnostic panel would enhance discrimination among the different causes of pleural effusions.
Case ReportWe report the case of a 24-year-old man patient, who was admitted with exercise-induced tachycardia. His medical history and physical examination were negative. The resting electrocardiogram (ECG) showed a sinus rhythm and sporadic ventricular premature beats with left bundle branch block morphology and right-axis deviation (Fig. 1). The tachycardia shown in Figure 2 (which was accompanied by palpitation) is an alternating wide and narrow QRS complex tachycardia with identical heart rates. What is the mechanism of the tachycardia? Address for reprints: János Tomcsányi, M.D., Figure 1. An ECG showing a sinus rhythm and sporadic ventricular premature beats with left bundle branch block morphology and right-axis deviation. Paper speed 25 mm/s.
DiscussionThe most common explanation for alternating narrow and wide QRS tachycardia with identical heart rates is supraventricular tachycardia with alternating bundle branch block. If so, the tachycardia can be atrial, atrioventricular (AV) nodal, or an orthodromic reciprocating tachycardia involving a right accessory pathway. There are three problems, however. First, the morphology of the left bundle branch block is very unusual. Second, the patient has ventricular premature beats with the same morphology. Third, there are three beats during the tachycardia, which suggest gradual widening of the QRS complex (see the aVR and aVF leads in Fig. 2), although the wandering baseline makes the interpretation a little difficult. These problems would suggest that this tachycardia cannot be explained by a single mechanism. The most plausible origin of the wide QRS complexes is the right ventricular outflow tract. The intermediary QRS complexes are fusion beats, rather than beats with incomplete 568June 2005 PACE, Vol. 28
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