The challenge of the volume status assessment in heart failure

We read with great interest the recently published report by Nguyen et al1 validating, in nonspecialized community settings, the handheld echocardiography in the assessment of clinical volume status in heart failure (HF) patients with severe left ventricular systolic dysfunction. We agree that most hospitalizations because of HF are associated with volume overload and that the assessment of fluid accumulation is an essential evaluative and therapeutic target in HF management requiring an accurate estimation. However, we have some issues of potential interest to discuss.

Firstly, the authors, by using as standard of reference the clinical assessment of volume status, conclude that pseudonormal or restrictive filling patterns, which identify the high filling pressure profile, predict hypervolemia with high accuracy; instead, normal or abnormal relaxation patterns, which identify the low filling pressure profile, predict euvolemia. This finding is clinically very interesting and noteworthy. However, in clinical practice, the clinical assessment as a marker of hemodynamic status (recognized as the first step in the evaluation of congestion), has a degree of uncertainly and lack of accuracy, which limits its use in therapeutic decision making: Framingham score for congestive HF was reported to be only 85% sensitive and 58% specific. Moreover, the hemodynamic profiling of patients with HF based on clinical signs/symptoms is not highly reliable2 and may lead to inaccurate estimation of hemodynamic status in chronic HF.3 In few words, a mismatch between clinical and central hemodynamics is not rare in coronary patients with severe left ventricular (LV) systolic dysfunction. Conversely, the reliability of central hemodynamics, particularly by using echocardiography, to predict physical signs may be fairly limited. The gold standard as study reference in this setting is, in fact, the heart catheterization to estimate hemodynamic indices of left ventricular filling pressure or pulmonary capillary wedge pressure; as second option, B-type natriuretic peptide assay has been largely validated as an important parameter of severity in congestive HF.

Secondly, handheld echocardiography is certainly a charming and also useful way to evaluate the fluid overload; however, we are not sure to exclude that the filling pattern of abnormal relaxation could be also associated with fluid accumulation despite normal or near-normal LV filling pressure (LVFP) in eupnoeic subjects. In fact, fluid retention may precede the signs/symptoms of congestion and, sometimes, the increase of E/Ea ratio (ratio of Early to late-Atrial-ventricular filling) over cutoff of 15 mm Hg too. In the current clinical practice, it is not infrequent, in fact, to find fluid overloaded patients with an abnormal relaxation pattern (eg, HF patients with preserved systolic function) requiring diuretic treatment. In other words, the questions are these: Are filling patterns always discriminating between subjects with and without fluid retention, considering that Doppler echocardiography may permit only an estimation of LVFP and not a direct measurement of the central hemodynamic indexes? or Are the filling patterns able to identify a preclinical condition of fluid retention which is a potential cause of subsequent central fluid overload and, finally, of cardiac decompensation?

Thirdly, we agree with the authors that there is a pressing need to find a practical, safe, and reliable point-of-care tool that would complement clinical assessment in monitoring volume status and optimize HF management. To this proposal, other methods are available to evaluate the fluid accumulation in clinical practice today, such as bioelectrical impedance analysis.4, 5 This method, which assesses body hydration status rapidly, accurately and noninvasively, is correlated with New York Functional Class6 and has preliminarily demonstrated high diagnostic accuracy in differentiating dyspnea from decompensated HF.7 It could play an important and promising new role (other studies are needed) in managing the care of patients with HF and in monitoring fluid balance. We believe, in fact, that the chief aim in management of volume overload is the objective estimation of fluid accumulation in a reproducible and easy manner useful to monitor it routinely.

The best way to treat HF is to prevent acute HF and progression of disease. It is possible to identify such early warnings (pulmonary or systemic fluid accumulation), which indicate a timely and appropriate therapy. In HF practice, it is not unusual the coexistence of a still normal clinical profile (eupnoeic patients) with fluid retention (weight gain and/or edema) and/or radiographic finding of pulmonary congestion. For this reason, it is more important in this situation to determine rapidly and easily a subclinical profile of fluid overload rather than high filling pressure profile and subsequently to treat it accordingly. Indeed, in our opinion, the achievement and maintenance of dry-wet is the key approach leading to euvolemic status and realizing lower LVFP.

In conclusion, the study results should be carefully considered; however, further investigations are needed (particularly in HF with a normal left ventricular ejection fraction or with atrial fibrillation or mitral valve disease and in right ventricular overload) before translating these findings in the current clinical practice to assess volume status. Novel methods may open up new horizons in monitoring the clinical volume status and body hydration in HF, focusing on the preclinical condition of fluid overload.