Affiliations: University of Colorado Health Sciences Center,Denver, CO,
Brown Medical School, Pawtucket, RI
Correspondence to: Thomas L. Petty, MD, Health ONE Center, 1850 High St, Denver, CO 80218; e-mail: email@example.com
To the Editor:
The recent article “Ratio Between Forced Expiratory Flow Between 25% and 75% of Vital Capacity [FEF25–75%] and FVC Is a Determinant of Airway Reactivity and Sensitivity to Methacholine” by Parker et al (July 2003)1
is confusing and perhaps misleading. Whereas the term vital capacity is in the title and suggests slow vital capacity, FVC is used in the ratio with FEF25–75%. Thus, ambiguity is suggested.
Of greater importance is the fact that the ratio between FEF25–75% and FVC involves two numbers, a numerator and a denominator. Thus, the reduction of the ratio could be a reduction in FEF25–75% or an increase in FVC (although unlikely). The authors do not mention whether they measured the FEF25–75% under isovolume conditions (ie, from the same part of the FVC as the prebronchodilator FEF25–75%). Of greater concern is the omission of the FEV1/FVC ratio. This ratio is not given for comparison with the FEF25–75%/FVC ratio. The absolute response of FVC to methacholine is also not given in the article. Thus, the article presents many unanswered questions that require elaboration.
For some time, I have been trying to get rid of the FEF25–75% as being unnecessary and misleading.2–
The most common complaint I receive even from board-certified internists at medical meetings is that spirometric values are difficult to interpret. Previous studies3
have shown that the FEF25–75% and other “sensitive tests” for small airways dysfunction were not predictors of decline in FEV1 or the emergence of clinical illness.
The National Lung Health Education Program recommends using only two parameters (FEV1 and FVC) or a surrogate (forced expiratory volume in 6 s) for the spirometric assessment of lung function.4
Testing for early stages of disease, of course, is somewhat different than methacholine challenge, but comparing the FEV1 number with a ratio that has two determinants seems inappropriate.
We thank Dr. Petty for his interest in our article (July 2003).1
In regard to the ambiguity of the title, the original title of the article was “FEF25–75 [forced expiratory flow between 25% and 75% of vital capacity]/FVC Ratio Is a Determinant of Airway Reactivity and Sensitivity to Methacholine.” The change to its present title was an editorial decision.
The FEF25–75/FVC ratio as an indicator of disproportionately small airways for a given lung size, was derived from the description by Mead and colleagues2–3
of airway-lung size dysanapsis. This was manifested as an inverse relationship between vital capacity (VC) and the product of the ratio of maximal flow at 50% of VC divided by VC and the static recoil pressure of the lung at 50% of VC (Vmax50/VC × Pst[L]50).2–5
The FEF25–75/FVC ratio may be reduced either by reducing the FEF25–75 or by increasing the FVC. Since this ratio is used to gain insight into the presence of dysanapsis, it does not matter whether the ratio is low because the person has small airways with a normal-sized lung (a reduction in FEF25–75) or normal-sized airways with a large-sized lung (an increase in forced VC).
Dr. Petty’s preference to use the FEV1/FVC ratio is well-understood. It has been well-described that subjects with airway obstruction, that is, a low FEV1/FVC ratio, are more likely to have airway hyperresponsiveness (AHR). We evaluated the association between the “new” ratio (ie, FEF25–75/FVC) and AHR because we believed that it describes a potentially different mechanism that leads to AHR. A low FEF25–75/FVC ratio may identify subjects who have relatively small airways for their lung size but do not have airway obstruction, whereas the FEV1/FVC ratio would identify subjects with airway obstruction.
The purpose of our article was not to advocate the use of FEF25–75 or the FEF25–75/FVC ratio in the clinical interpretation of pulmonary function test results. We agree that these parameters have not been shown to be good predictors of the development of obstructive airway disease. Rather, the focus of our article was to demonstrate that small airway size relative to lung size was a more important determinant than the absolute airway size alone for AHR. This relationship between dysanapsis and AHR may provide another potential mechanism for the pathogenesis of asthma.
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