Resurgence of interest in the hemodynamic alterations of advanced heart failure

Historically, cardiac insufficiency has always being allocated to be the culprit lesion of the heart failure syndrome. However, contemporary heart failure pharmacotherapy solely focuses on preservation of neurohormonal homeostasis. The research described in this manuscript is the result of thorough investigation of the hemodynamic alterations of hundreds of patients admitted for advanced decompensated heart failure (ADHF). Firstly, our data suggest that progressive cardiac insufficiency and hemodynamic derangements assessed through invasive hemodynamic monitoring, are still contributing to short- and long-term compromise, and this independent of race or gender. In addition, we demonstrated that restoring an optimal hemodynamic balance with add-on afterload reduction provides incremental intermediate- and long-term benefits over evidence based neurohormonal blockade alone. Indeed parental vasodilator therapy with sodium nitroprusside can be safely administered to achieve more hemodynamic improvement in patients presenting with ADHF. In addition, the institution of a more aggressive oral vasodilator regimen with isosorbide diniatrate / hydralazine over standard neurohormonal antagonists at the time of discharge after an episode of ADHF can safely maintain these hemodynamic improvements leading to improved outcomes. Another novel insight comes from the notice that venous congestion and raised intra-abdominal pressure, more than impaired cardiac output, seem to be related to the development of worsening renal function in patients admitted with ADHF. Treatment strategies with the aim of better renal preservation should therefore focus how to safely reduce this renal venous congestion with diuretic therapy, ultrafiltration or paracentesis whenever indicated. Finally, we demonstrated that cardiac resynchronization therapy (CRT) really acts as a novel "hemodynamic therapy" for advanced heart failure patients even in the patient population previously categorized as "non-responders". Moreover, we have proven that the phenotypic improvement in heart failure status after prolonged CRT is paralleled by a reversed left ventricualr remodeling and recovery of left ventricular contractility. Thus, prolonged (hemodynamic) unloading of the heart will lead to physiological changes on the myocyte level in hearts once destined to only further deteriorate