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Aim Elevated brain natriuretic peptide (BNP) and tumour marker antigen carbohydrate 125 (CA125) levels have shown to be associated with higher risk for adverse outcomes in patients with acute heart failure (AHF). Nevertheless, no attempt has been made to explore the utility of combining these two biomarkers. We sought to assess whether CA125 adds prognostic value to BNP in predicting 6-month all-cause mortality in patients with AHF. Methods and results We analysed 1111 consecutive patients admitted for AHF. Antigen carbohydrate 125 (U/mL) and BNP (pg/mL) were measured at a median of 72 ± 12 h after instauration of treatment. Antigen carbohydrate 125 and BNP were dichotomized based on proposed prognostic cutpoints, and a variable with four categories was formed (BNP–CA125): C1 = BNP < 350 and CA125 < 60 ( n = 394); C2 = BNP ≥ 350 and CA125 < 60 ( n = 165); C3 = BNP < 350 and CA125 ≥ 60 ( n = 331); and C4 = BNP ≥ 350 and CA125 ≥ 60 ( n = 221). The independent association between BNP–CA125 and mortality was assessed with the Cox regression analysis, and their added predictive ability tested by the integrated discrimination improvement (IDI) index. At 6 months, 181 deaths (16.3%) were identified. The cumulative rate of mortality was lower for patients in C1 (7.8%), intermediate for C2 and C3 (17.8% and 16.9%, respectively), and higher for C4 (37.2%), and P -value for trend

A study was made of nodal conduction times of atrial stimuli with fixed coupling intervals, in 23 patients divided into two groups according to their atrial stimulus test response: Group I (continuous AV node function curve; 17 cases) and Group II (dual AV node pathway; six cases). The stimulation protocol involved the delivery of 75 stimuli with a fixed coupling interval 20 ms greater than the effective refractory period (ERP) of the AV node (Group I) or fast pathway (Group II). The atrial coupling intervals (A1A2) and node conduction times (A2H2) were measured. An evaluation was made of the dispersion of intervals with range (R) and of the distribution of A2H2 times (X2 test). In both Groups, R (A2H2) was greater than R(A1A2) (P less than 0.05); R(A2H2) in Group II was greater than R(A2H2) in Group I (P less than 0.001). In Group I the distribution of A2H2 was non-normal in four cases and bimodal in five; in Group II the distribution was non-normal and bimodal in all cases. It is concluded that: (1) the AV node generates a dispersion in its conduction times in the vicinity of its ERP, although the nodal conduction curve is continuous; and (2) the so-called dual pathway may constitute an exaggeration of AV node response inhomogeneity.