Background-Increased plasma levels of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) have been identified as predictors of cardiac dysfunction and prognosis in congestive heart failure and ischemic heart disease. In severe sepsis patients, however, no information is available yet about the prognostic value of natriuretic peptides. Therefore, the aim of the present study was to determine the role of the N-terminal prohormone forms of ANP (NT-proANP) and BNP (NT-proBNP) in the context of outcome of septic patients. Furthermore, the effect of treatment with recombinant human activated protein C [drotrecogin alfa (activated)] on plasma levels of natriuretic peptides in severe sepsis was evaluated. Methods and Results-Fifty-seven patients with severe sepsis were included. Levels of NT-proANP and NT-proBNP were measured on the second day of sepsis by ELISA. Septic patients with NT-proBNP levels Ͼ1400 pmol/L were 3.9 times more likely (relative risk [RR], 3.9; 95% CI, 1.6 to 9.7) to die from sepsis than patients with lower NT-proBNP values (PϽ0.01). NT-proANP levels, however, were not predictive of survival in our patient population. A highly significant correlation was found between troponin I levels and plasma concentrations of NT-proBNP in septic patients (rϭ0.68, PϽ0.0001). In addition, troponin I significantly accounted for the variation in NT-proBNP levels (PϽ0.0001), suggesting an important role for NT-proBNP in the context of cardiac injury and dysfunction in septic patients. Twenty-three septic patients who received treatment with drotrecogin alfa (activated) presented with significantly lower concentrations of NT-proANP, NT-proBNP, and troponin I compared with patients not receiving drotrecogin alfa (activated). Conclusions-NT-proBNP

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OBJECTIVES-The purpose of this study was to compare the effect of intravenous flecainide and ajmaline with respect to their ability to induce or accentuate the typical ECG pattern of Brugada syndrome.BACKGROUND-Brugada syndrome is associated with a high incidence of sudden cardiac death. The typical ECG pattern of ST-segment elevation in the right precordial leads often is concealed, but it can be unmasked with sodium channel blockers such as flecainide and ajmaline. Little is known about the relative effectiveness of these provocative agents in unmasking Brugada syndrome.

In this prospective study, asymptomatic cerebral infarction following cardiac catheterization occurred in 15% of patients in whom duration of the procedure was significantly longer than in those without infarction (P = .017).

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MRI Findings in Brugada Patients. Introduction: Cardiac magnetic resonance imaging (CMR) is a powerful diagnostic tool for evaluating cardiac structure and function. Recently, right ventricular wallmotion abnormalities were described using electron beam tomography in patients with Brugada syndrome. In the present study, we prospectively evaluated CMR findings in patients with Brugada syndrome compared to matched controls.Methods and Results: CMR was performed on 20 consecutive patients with proven Brugada syndrome. The imaging protocol included breath-hold dark blood prepared T1-weighted multislice turbo spin-echo and gradient-echo images. Ventricular volumes and dimensions were compared to age-and sex-matched normal volunteers. The right ventricular outflow tract area was significantly enlarged in patients with Brugada syndrome compared to controls (11 vs 9 cm 2 , P = 0.018). There was a trend to larger right ventricular end-diastolic and end-systolic volumes and lower right ventricular ejection fraction in patients with Brugada syndrome compared to controls. However, none of the differences reached significance (P = 0.3, P = 0.08, and P = 0.06, respectively). There was no statistically significant difference in the left ventricular parameters between patients and controls. High intramyocardial T1 signal similar to fat signal was observed in 4 (20%) of the 20 patients compared to none of the controls.Conclusion: The findings support the view that subtle structural changes, such as right ventricular outflow tract dilation may point to a localized arrhythmogenic substrate in patients with Brugada syndrome.

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