LETTERS TO THE EDITOR Note: This copy is for your personal non-commercial use only. To order presentation-ready copies for distribution to your colleagues or clients, contact us at www.rsna.org/rsnarights.
Editor: It is uncommon to follow up a clinical trial for 3 decades and, for this reason and others, the article by Tabár and col leagues about the Swedish Two-County Trial of mammographic screening in the September 2011 issue of Radiology (1) merits careful reading. What I miss is information about to tal mortality. This is important because the screening cohorts in the Swedish trial appeared to exhibit a higher total mor tality than did control subjects in the follow-up until 1989. Later on, in 1996, it was demonstrated that there was no more mortality but a misunderstanding about the age-adjustment process. When such an adjustment was made, there was no significant difference be tween the in tervention and control groups. In fact, the age-adjusted risk for total mortality was 0.98 (range, 0.96–1.00) (2). The net effect of screening on allcause mortality was minimal at that time, perhaps because overdiagnosis and overtreatment increases mortality. That means an association in between mam mographic screening and death to balance the impact of screening in decreasing breast cancer mortality. So I ask authors to present data about total mortality after 3 decades of follow-up of the Swedish Two-County Trial. Disclosures of Potential Conflicts of Interest: No potential conflicts of interest to disclose.
References 1. Tabár L, Vitak B, Chen TH, et al. Swedish two-county trial: impact of mammographic screening on breast cancer mortality during 3 decades. Radiology 2011;260(3):658–663. 2. Nyström L, Andersson I, Bjurstam N, Frisell J, Nordenskjöld B, Rutqvist LE. Long-term ef fects of mammography screening: updated overview of the Swedish randomised trials. Lancet 2002;359(9310):909–919.
Response From László Tabár, MD,* Robert A. Smith, PhD,† Tony H. H. Chen, PhD,‡ and Stephen W. Duffy, Msc§
308
Department of Mammography, Falun Central Hospital, Sweden* American Cancer Society, Atlanta, Ga† Graduate Institute of Epidemiology and Preventive Medicine, National Taiwan University, Taipei, Taiwan‡ Centre for Cancer Prevention, Wolfson Institute of Preventive Medicine, Barts & the London School of Medicine & Dentistry, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, England§ e-mail:
[email protected] The interest in deaths from other causes in a breast screening trial arises from the possibility of misclassification of cause of death in breast cancer cases and from the concern that treatments for breast cancers detected with screening might result in deaths from other causes (eg, cardiovascular deaths as a result of radiation therapy). Because these circum stances pertain only to women with breast cancer (1), interest should be focused on monitoring deaths from all causes in breast cancer cases. In 2002, we pub lished follow-up results to 1998 showing a significant 31% decrease in breast cancer death (relative risk: 0.69; 95% confidence interval: 0.58, 0.80; P , .001), no significant increase in deaths from other causes, and a significant 19% reduction in deaths from all causes among breast cancer cases in the invited group (relative risk: 0.81; 95% confidence interval: 0.72, 0.90; P , .001) (2). An up date of our most recent follow-up (3) is under preparation. In 1989, we published the results with respect to all-cause mortality among all women in the Two-County Trial (4). We found that there was no evidence of bias in cause of death assessment and that all-cause mortality was indeed lower in women offered screening compared with all women in the control group, commensurate with the proportion of deaths that were due to breast cancer. In view of these results, follow-up for all-cause mortality in the entire popula tion was discontinued. This is supported by the view of independent reviewers that all-cause mortality, unless restricted to
women with a breast cancer diagnosis, is an inappropriate end point in a breast screening trial (1). Disclosures of Potential Conflicts of Interest: L.T. No potential conflicts of interest to disclose. R.A.S. No potential conflicts of interest to dis close. T.H.H.C. No potential conflicts of interest to disclose. S.W.D. No potential conflicts of in terest to disclose.
References 1. Freedman DA, Petitti DB, Robins JM. On the efficacy of screening for breast cancer. Int J Epidemiol 2004;33(1):43–55. 2. Tabár L, Duffy SW, Yen MF, et al. All-cause mortality among breast cancer patients in a screening trial: support for breast cancer mortality as an end point. J Med Screen 2002;9(4):159–162. 3. Tabár L, Vitak B, Chen TH, et al. Swedish two-county trial: impact of mammographic screening on breast cancer mortality during 3 decades. Radiology 2011;260(3):658–663. 4. Tabár L, Fagerberg G, Duffy SW, Day NE. The Swedish two county trial of mammo graphic screening for breast cancer: recent results and calculation of benefit. J Epidemiol Community Health 1989;43(2):107–114.
Hepatic Artery Stenosis after Liver Transplantation From Edward I. Bluth, MD, Richard Tupler, MD, and Neil Lall, MD Department of Radiology, Ochsner Clinic Foundation, 1514 Jefferson Hwy, New Orleans, LA 70121 e-mail:
[email protected] Editor: We read with interest the article by Park and colleagues in the September 2011 issue of Radiology (1). We found this article contrary to our experience with the diagnosis of hepatic arterial stenosis (HAS) in patients after liver transplan tation. Park and colleagues described a high false-positive rate for HAS on the basis of the tardus parvus waveform (TPW) but found that, in combination with a peak systolic velocity (PSV) of 48 cm/sec or less, the specificity for ste
radiology.rsna.org n Radiology: Volume 263: Number 2—April 2012
LETTERS TO THE EDITOR
noses of more than 50% was improved. The presence of the TPW should trigger further evaluation to determine whether there is HAS. The finding of low velocities at a sig nificant stenosis (.90%) is a well-known phenomenon in carotid ultrasonography (US). This relates to decreased velocities from decreased flow as the vessel nears occlusion. We suspect that Park and col leagues have confused stenoses of more than 90% with stenoses of 50%–90% (where, as in the carotids, PSVs increase in direct proportion to the severity of the stenosis). Our experience is similar to that of Dodd et al (2) and Muradali and Chawla (3), with HAS usually associated with PSV of more than 200 cm/sec in the main hepatic artery as well as TPW. We believe it is important for readers of Radiology to recognize that the defin itive diagnosis of HAS is still made with direct interrogation of the extrahepatic anastomosis site. In 50%–90% stenosis, PSV at this level is elevated more than 200 cm/sec, a direct sign of stenosis; the presence of TPW and a resistive in dex of less than 0.5 distally are indirect indications of HAS. It would be a dis service to patients to adopt the criteria described by Park and colleagues. This would result in lowering the sensitivity of what the authors recognize to be a screening examination. Given the bene fit of early detection of HAS, sensitivity should be favored over specificity. Many patients with early treatable HAS could be overlooked with the limited criteria of TPW with PSV of 48 cm/sec or less. Disclosures of Potential Conflicts of Interest: E.I.B. No potential conflicts of interest to dis close. R.T. No potential conflicts of interest to disclose. N.L. No potential conflicts of interest to disclose.
References 1. Park YS, Kim KW, Lee SJ, et al. Hepatic arte rial stenosis assessed with Doppler US after liver transplantation: frequent false-positive diagnoses with tardus parvus waveform and value of adding optimal peak systolic velocity cutoff. Radiology 2011;260(3):884–891. 2. Dodd GD 3rd, Memel DS, Zajko AB, Baron RL, Santaguida LA. Hepatic artery stenosis and thrombosis in transplant recipients: Doppler
diagnosis with resistive index and systolic acceleration time. Radiology 1994;192(3): 657–661. 3. Muradali D, Chawla T. Organ transplantation. In: Rumack CM, Wilson SR, Charboneau JW, Levine D, eds. Diagnostic ultrasound. 4th ed. Philadelphia, Pa: Elsevier, 2010; 639–706.
Response From Yang Shin Park, MD,*† Kyoung Won Kim, MD,* and So Jung Lee, MD* Department of Radiology, Asan Medical Center, University of Ulsan College of Medicine, 388-1, Pungnap 2-dong, Songpa-ku, Seoul, 138-736, Korea* Department of Radiology, Korea University Guro Hospital, Seoul, Korea† e-mail:
[email protected] We thank Dr Bluth and colleagues for their interesting comments concerning our work (1). As they mentioned, we consider a PSV of more than 200 cm/sec at an anastomosis to be a sign of HAS, in addition to TPW of the distal hepatic artery. If surgical anastomosis can be interrogated directly and the PSV ex ceeds 200 cm/sec at the anastomosis, a possibility of stenosis can be suggested and it is often the case in whole-liver transplant recipients in whom the hepatic artery can be continuously traced from recipient to graft side. However, in pa tients who undergo living donor liver transplantation, a continuous trace of the hepatic artery and direct Doppler evalua tion of the hepatic artery anastomosis are not possible. Therefore, although it may be an indirect sign, TPW is a useful indicator of anastomotic stenosis in pa tients after living donor liver transplanta tion. However, TPW can also be seen in various conditions other than HAS (2–5). Thus, it is important to recognize the di agnostic power and pitfalls of this sign. In our study, we observed that false-positive diagnoses of HAS with TPW tend to oc cur in patients with a higher PSV. The model by Spencer and Reid (6) has shown the relationship between the degree of stenosis and blood velocity. However, the relationship between the
Radiology: Volume 263: Number 2—April 2012 n radiology.rsna.org
degree of stenosis and appearance of TPW at the distal artery has not been shown. It may be possible that low-grade stenosis may accompany TPW of the dis tal artery together with a PSV of more than 200 cm/sec, but we think that it should be proved by further studies. We agree that sensitivity should be favored over specificity with Doppler US because it is a screening examination. However, with an awareness of the fre quent false-positive diagnoses with TPW with high PSV, we can search for other possible reasons for TPW (if any). If not explained by other possible causes or if there is a clinical suspicion (surgical finding or enzyme abnormality) as well, we think that computed tomographic ar teriography should be performed with out hesitation. Disclosures of Potential Conflicts of Interest: Y.S.P. No potential conflicts of interest to dis close. K.W.K. No potential conflicts of interest to disclose. S.J.L. No potential conflicts of inter est to disclose.
References 1. Park YS, Kim KW, Lee SJ, et al. Hepatic arte rial stenosis assessed with Doppler US after liver transplantation: frequent false-posi tive diagnoses with tardus parvus waveform and value of adding optimal peak systolic ve locity cutoff. Radiology 2011;260(3):884–891. 2. Dodd GD 3rd, Memel DS, Zajko AB, Baron RL, Santaguida LA. Hepatic artery stenosis and thrombosis in transplant recipients: Doppler diagnosis with resistive index and systolic acceleration time. Radiology 1994;192(3): 657–661. 3. Sidhu PS, Ellis SM, Karani JB, Ryan SM. Hepatic artery stenosis following liver trans plantation: significance of the tardus parvus waveform and the role of microbubble con trast media in the detection of a focal stenosis. Clin Radiol 2002;57(9):789–799. 4. García-Criado A, Gilabert R, Berzigotti A, Brú C. Doppler ultrasound findings in the hepatic artery shortly after liver transplan tation. AJR Am J Roentgenol 2009;193(1): 128–135. 5. Urbani L, Morelli L, Campatelli A, et al. False positive tardus-parvus waveforms after liver transplantation: a case of wide discrepancy between donor and recipient hepatic arteries mimicking anastomotic stenosis. Transplant Proc 2008;40(10):3816–3818. 6. Spencer MP, Reid JM. Quantitation of carotid stenosis with continuous-wave (C-W) Dop pler ultrasound. Stroke 1979;10(3):326–330.
309
