CORRESPONDENCE: LETTER TO THE EDITOR
Reply
Clyde W. Yancy, MD, FACC*
* Baylor University Medical Center, Baylor Heart and Vascular Institute, 3500 Gaston Avenue, Suite H-030, Dallas, Texas 75246 (Email: clydey{at}baylorhealth.edu).
The letter by Drs. O'Rourke and Nichols appropriately addresses alternative modalities for assessing aortic impedance (a component of left ventricular afterload), and importantly expands on our earlier discussion regarding the measurement of peripheral resistance and incorporating the use of those measurements in the treatment of advanced decompensated heart failure. The paper by Mullens et al. (1) and accompanying editorial comment (2) do not exclude other monitoring modalities, but rather address what is practically available and importantly highlight the potential benefit of vasodilator therapy and emphasize the need to consider decompensated heart failure as a disease entity driven not only by congestion but also by altered ventricular loading conditions. There is reasonable hesitancy to the full embrace of the use of nitroprusside if indeed that use requires invasive hemodynamic monitoring. Not only does invasive hemodynamic monitoring seem to be necessary, but also skill in caring for such catheters in an intensive care unit setting and skill in interpreting the data are required. Titrating the vasodilator dose to hemodynamics is yet another unique skill set required to use nitroprusside successfully in this clinical scenario.
A noninvasive strategy that addresses one of several components of left ventricular afterload, be it aortic impedance, brachial/radial arterial resistance, or transthoracic bioimpedance, would be preferable. The dilemma is that use of those noninvasive strategies in an intensive care unit setting for patients with advanced decompensated heart failure cannot be assumed to be accurate and reproducible without undergoing prospective testing. The test should be proven to be reliable, reproducible, and accurate when compared with a known conventional hemodynamic parameter. Utility of certain modalities in the realm of hypertension is not sufficient to verify utility in the setting of heart failure, especially when aortic flow characteristics and tissue factors related to impedance may be strikingly different. As well, if the noninvasive strategy introduces a new metric, the ability to titrate therapy according to that metric should be proven.
It is agreed that any evidence-based beneficial measurement of peripheral resistance that obviates the need for right heart catheterization would be preferable as greater use of vasodilator therapy seems warranted in the setting of advanced decompensated heart failure.
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1. Mullens W, Abrahams Z, Francis GS, et al. Sodium nitroprusside for advanced low-output heart failure J Am Coll Cardiol 2008;52:200-207.[Abstract/Free Full Text]2. Yancy CW. Vasodilator therapy for decompensated heart failure J Am Coll Cardiol 2008;52:208-210.[Free Full Text]
Related Article
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Vasodilator Therapy in Cardiac Failure: What Was New Is Old
- Michael F. O'Rourke and Wilmer W. Nichols
J. Am. Coll. Cardiol. 2009 53: 898.
[Full Text]
[PDF]
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