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.

suggestive of ST-segment elevation myocardial infarction in patients who were found not to have ST-segment elevation myocardial infarction. 1 Typical of those cases were a critical illness, a unique dome-and-spike pattern always in the inferior leads, and high in-hospital mortality.We recently reported a case in which the "spiked helmet" sign appeared in the anteroapical leads ( Figure). 2 Coronary angiography excluded coronary artery disease as a cause of ST-segment elevation. The cause of death, as established by autopsy, was traumatic aortic dissection due to a car accident. The morphology of the ST-segment elevation resembled the second case in the series of Littmann and Monroe. The exact mechanism of this pseudo-STsegment elevation is not known, but in the case of inferior ST-segment elevation, the proposed mechanism was diaphragmatic movement or an acute rise in intra-abdominal pressure. In our case, an acute rise in intrathoracic pressure due to aortic dissection may have been the cause of the pseudo-ST-segment elevation. In reply: We thank Tomcsányi et al for their interest in our work. The presented case extends our observations by demonstrating that with a sudden rise in intrathoracic pressure, the spiked helmet pattern can also show up in the chest leads. As was typical of our series, their patient did not have myocardial infarction (according to standard diagnostic criteria) and did not survive to hospital discharge. Our purpose in describing the spiked helmet sign was to raise physician awareness of this potential electrocardiographic marker of a high risk of death. 1 We hope that if physicians can recognize the spiked helmet sign in real time, it will assist in the rapid evaluation and management of critically ill patients. The case presented by Tomcsányi et al is a further step in this direction. FIGURE.The "spiked helmet" sign. Atrial fibrillation and ST-segment elevation in leads V 2 through V 4 . The dome-and-spike sign is most pronounced in leads V 3 and V 4 . Reprinted from J Electrocardiol, 2 with permission from Elsevier.

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Objective: To test the hypothesis that gene-gene interaction of the renin-angiotensin system is associated with an effect on the extent of coronary atherosclerosis. Setting and results: A cohort of 1162 patients with coronary artery disease were genotyped for genetic polymorphisms in the renin-angiotensin system. Patients carrying the D allele of the angiotensin I converting enzyme (ACE) gene had greater coronary extent scores (defined as the number of coronary segments with 5% to 75% stenosis) than those not carrying this allele (p = 0.006 in non-parametric analysis and p = 0.019 in parametric analysis). This association remained significant after adjusting for age, body mass index, hypertension, and diabetes, which were also significantly associated with coronary extent scores. There was a significant interaction (p = 0.033) between genotypes of ACE and angiotensin II type 1 receptor (AGTR1). The association between the ACE gene D allele and increased coronary extent scores was significant (p = 0.008 in non-parametric and p = 0.027 in parametric analysis) in those carrying the +1166 C allele of the AGTR1 gene, but was absent in those not carrying the AGTR1 gene +1166 C allele. Conclusion: These findings suggest that variation in the ACE and AGTR1 genes and their interaction may not only contribute to susceptibility of coronary artery disease as previously found but also modify the disease process, thus contributing to interindividual differences in severity of the disease.