Changes in tissue-Doppler echocardiographic assessment of left ventricular filling during NT-proBNP guided heart failure treatment titration: a pilot study.

BACKGROUND: Although brain natriuretic peptide (BNP) and E/Ea are closely related in heart failure (HF) patients and may be helpful to guide HF therapy, the response of E/Ea to changes in BNP over several weeks of intensive HF treatment optimisation is unknown. This study was designed to investigate this relationship. METHODS AND RESULTS: In 17 patients with decompensated HF, treatment was titrated to reduce the NT-proBNP level to <200pg/mL over 10 weeks. Paired NT-proBNP measurements and echocardiograms were performed at two weekly intervals during the study. Treatment titration was associated with a reduction in E/Ea (17.6+/-6.8S.D. to 13.7+/-5.0S.D., p=0.018) in keeping with the reduction in NT-proBNP (median 603 [S.E. 561] to 311 [S.E. 235], p=0.045). This relationship remained in those who responded to titration (reduction in NT-proBNP of >or=50%), and those who did not. The overall change in E/Ea was similar to the changes observed in NT-proBNP in each group however there appeared to be temporal differences in the changes in E/Ea and NT-proBNP. CONCLUSION: This pilot study demonstrates that the E/Ea decreases after NT-proBNP guided HF therapy. E/Ea may be a complementary target for HF therapy optimisation; this hypothesis should be further evaluated in larger scale randomised trials.

The relationship between BNP and E/Ea in patients hospitalized with acute heart failure.

BNP and echocardiographic E/Ea are variables helpful in the management of patients with heart failure (HF). The response of E/Ea to treatment for acute decompensated HF remains uncertain. This pilot study aimed to explore this relationship. 24 patients (17 male, mean age 69 years, median ejection fraction 26%) hospitalized with HF were enrolled in this study. Paired clinical examination, BNP-32 level, and echocardiogram were performed at admission and discharge. By discharge patient symptoms and BNP-32 had significantly improved, however E/Ea did not change. Our data suggests that BNP-32 and E/Ea may not be interchangeable indices and may respond differently during treatment of acute decompensated HF.

The effect of type 2 diabetes on diastolic function.

PURPOSE: This study aimed to determine whether sedentary overweight subjects with type 2 diabetes have impaired diastolic function compared with equally sedentary and overweight nondiabetic subjects. METHODS: Mitral valve pulsed Doppler echocardiography and tissue Doppler imaging (TDI) were used to assess left ventricular structure and diastolic function in 40- to 60-yr-old sedentary overweight subjects with type 2 diabetes (N = 13) and age- and body mass-matched sedentary nondiabetic subjects (N = 15). Pseudonormal filling was identified using preload reduction and TDI. RESULTS: Traditional Doppler mitral inflow parameters were not different between groups; however, early diastolic relaxation, as measured by peak early mitral annular velocity (E') and the ratio of E' and peak late mitral annular velocity (E'/A'), was reduced in type 2 diabetic subjects (P < 0.05). The ratio of peak early mitral inflow (E) to E' (E/E'), an estimate of left ventricular filling pressure, was also higher in the type 2 diabetes group (P < 0.05). The proportions of diastolic impairment (69 vs 40%) and pseudonormal filling (39 vs 20%) were not different between groups (P = 0.18). CONCLUSION: These findings suggest that type 2 diabetes has an effect on diastolic function that is independent of age and body composition.

Effects of carvedilol on left ventricular remodeling after acute myocardial infarction: the CAPRICORN Echo Substudy.

BACKGROUND: The CAPRICORN trial has shown that carvedilol improved outcome in patients with left ventricular dysfunction after acute myocardial infarction treated with ACE inhibitors. The aim of this substudy was to determine the effects of carvedilol on left ventricular remodeling in this patient group. METHODS AND RESULTS: Patients entering the CAPRICORN trial from 13 centers in New Zealand, Australia, and Spain were recruited for this echocardiographic substudy. In 127 patients, quantitative 2D echocardiography was performed according to a standard protocol before randomization and repeated after 1, 3, and 6 months of treatment with carvedilol or placebo. Left ventricular volumes, ejection fraction (Simpson's method), and wall motion score index were determined in a blinded analysis at the Core Echo Laboratory. At 6 months, left ventricular end systolic volume was 9.2 mL less in the carvedilol group than in the placebo group (P=0.023), and left ventricular ejection fraction was 3.9% higher (P=0.015). Left ventricular end diastolic volume and wall motion score index were not statistically different between the 2 groups at 6 months. CONCLUSIONS: In patients with left ventricular dysfunction after acute myocardial infarction treated with ACE inhibitors, carvedilol had a beneficial effect on ventricular remodeling, which may, in part, mediate the substantial clinical beneficial effects of carvedilol in this patient population.