CORRESPONDENCE: LETTER TO THE EDITOR
Reply
Wilfried Mullens, MD,
Gary S. Francis, MD,
Randall C. Starling, MD, MPH,
David O. Taylor, MD and
W.H. Wilson Tang, MD*
* Cleveland Clinic, Cardiovascular Medicine, 9500 Euclid Avenue, Desk J3-4, Cleveland, Ohio 44195 (Email: tangw{at}ccf.org).
We appreciate the enthusiastic interests and insightful comments regarding our report on the potential role of venous congestion as a driver for worsening renal function (WRF) in patients admitted with advanced decompensated heart failure (ADHF) (1). We have acknowledged in the report that many factors can contribute in the pathophysiology of WRF in the setting of ADHF. While our existing data cannot demonstrate direct causation between elevated central venous pressure and WRF, our current treatment goals are to reduce filling pressures and to improve cardiac output using a wide range of drug and device therapies according to protocols established in our heart failure intensive care unit. It is important to clarify that the mean dosages of furosemide during intensive medical therapy were similar among patients who did and did not develop WRF, with similar percentages of patients in both groups receiving furosemide through continuous parental infusion. While the biggest hemodynamic determinant of the subsequent development of WRF in this patient population with initially depressed cardiac index appeared to be elevated central venous pressure rather than low cardiac output, we believe our data supported the presence of venous congestion as the driver of the process, either due to underlying restrictive physiology, overzealous diuretic use, neurohormonal up-regulation, or more likely the severity of congestion. Dissecting these factors may be challenging in the clinical setting, and may vary widely among individual patients. Regardless, this is a clear departure from the traditional "cardio-centric" concept of impaired cardiac output as the primary determinant of cardio-renal compromise in some patients with ADHF.
Contrary to animal experiments, we did not observe a direct correlation between baseline renal function and severity of venous congestion; several reasons might account for this discrepancy. First, the duration and onset of venous congestion in the quoted animal experiments always was acute and short-lived while in patients admitted with ADHF venous congestion most often arises slowly and gradually over the preceding weeks. Second, some of our patients have been treated with long-term neurohormonal antagonists and may have pre-existing/intrinsic renal dysfunction contrary to animal models, which had normal renal function at the moment venous pressure was artificially raised. Furthermore, other extrinsic factors as a result of long-term venous congestion (such as raised intra-abdominal pressure caused by visceral edema or ascites) may contribute to this cardio-renal pathophysiology (2). However, the first step is to recognize that venous congestion is a major feature of the syndrome, which is the primary message of this and several other recent papers in different patient populations (3,4). We fully agree that more rigorous studies are needed, and we believe that the search for future ADHF therapies should focus on strategies that allow safe and optimal reduction and prevention of venous congestion to prevent such a devastating complication.
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References
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1. Mullens W, Abrahams Z, Francis GS, et al. Importance of venous congestion for worsening of renal function in advanced decompensated heart failure J Am Coll Cardiol 2009;53:589-596.[Abstract/Free Full Text]2. Mullens W, Abrahams Z, Skouri H, et al. Elevated intra-abdominal pressure in acute decompensated heart failure: a potential contributor to worsening renal function? J Am Coll Cardiol 2008;51:300-306.[Abstract/Free Full Text] 3. Damman K, van Deursen VM, Navis G, et al. Increased central venous pressure is associated with impaired renal function and mortality in a broad spectrum of patients with cardiovascular disease J Am Coll Cardiol 2009;53:582-588.[Abstract/Free Full Text] 4. Damman K, Navis G, Smilde TD, et al. Decreased cardiac output, venous congestion and the association with renal impairment in patients with cardiac dysfunction Eur J Heart Fail 2007;9:872-878.[Abstract/Free Full Text]
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