2862 days after ACF induction, the extent of heart failure was determined morphologically, and hemodynamically by means of an intraventricular pressure-volume conductance catheter. Specific adaptations in BNP plasma concentrations and the expression of the b1-, b2- and b3-adrenoreceptor mRNA expression were examined in this modified ACF model. Finally, electron microscopy should reveal subcellular changes according to CHF. In previous publications heart failure was inconsistent and started to develop earliest $8 weeks after fistula induction using a 18G-needle. Therefore, our goal was to modify the needletechnique to achieve a predictable CHF within a short time period to facilitate interventional studies with an improved assay sensitivity. In vivo hemodynamic assessment of rats by means of a pressurevolume catheter has become the gold standard – besides echocardiography – in experimental models investigating adaptive changes due to myocardial infarction or volume overload. In using this modified approach, a complete hemodynamic characterization derived from a conductance catheter in vivo in this modified approach is shown for the first time. Intraventricular pressures and volumes in the control group were comparable to values previously published for healthy rats. A nearly two-fold increase in the lung weight index accompanied by elevated central venous and left end-diastolic pressures denotes backward failure. Finally, we demonstrated a clear separation between an increased heart and lung weight indices and a reduced LVEF in every ACF animal compared to every animal in the control group. This clearly depicts the transition from eccentric hypertrophy with preserved cardiac function to severe biventricular dilatation with decompensated heart failure due to pronounced volume overload in our modified approach. Today, progressive heart failure has been recognized to develop from a combination of genetic, neurohumoral, inflammatory, and biochemical factors. Therefore, biomarkers have become important for clinical risk stratification. Beside Troponin in the case of acute coronary syndrome, BNP is one of the most interesting biomarkers to grade the extent of heart failure to support medical decisions making and to monitor responses to therapy. An increase in BNP plasma concentration reliably reflects the neurohumoral activation due to persistent hemodynamic overload of the heart. 2862 days after fistula induction BNP plasma concentrations were significantly increased in our modified experimental model. This is consistent with previous results by Langenickel et al. demonstrating the superiority of cardiac BNP mRNA expression as a marker of the transition from compensated to overt heart failure in volume overloaded rats. Also, subcellular fragmentation consistent with apoptotic changes of the Dasatinib myocardium has been recognized as an important pathophysiological mechanism promoting progression of heart failure. This holds true for several causes of heart failure, including myocardial infarction, and pressure and volume overload.