renal artery stenosis and peripheral vascular disease

1
879 prepared by the PEG/SDS method and cDNA synthesised as described,3 but with random primers in place of D95. Serum samples from 20 haemophiliacs treated repeatedly with unheated commercial factor V I I I concentrate were tested with both the original set of primers (D94, D95, N 1, N2) and the new set. The original set detected HCV RNA in 7 serum samples (35%), whereas the new set detected HCV RNA in 17 (85%). Serum from 30 healthy blood donors gave no signals with either set of primers. We conclude that the NCR series primers will, to a significant degree, circumvent the problem of false-negative PCR results arising from sequence variation. We thank Dr P. Jones, Dr G. Savidge, and Dr J. Barbara for kindly providing clinical materials. Virology Division, Department of Medical Microbiology, University College and Middlesex School of Medicine, London W1P 7PN, UK J. A. GARSON C. RING P. TUKE R. S. TEDDER 1 Okamoto H, Okada S, Sugiyama Y, et al. The 5’-terminal sequence of the hepatitis C virus genome. Jpn J Exp Med 1990; 60: 167-77. 2 Okamoto H, Okada S, Sugiyama Y, et al. Detection of hepatitis C virus RNA by a two-stage polymerase chain reaction with two pairs of primers deduced from the 5’-noncoding region. Jpn J Exp Med 1990; 60: 215-22. 3 Garson JA, Tuke PW, Makris M, et al. Demonstration of multiple viraemia patterns in haemophiliacs treated with hepatitis C virus contaminated factor VIII concentrates Lancet (in press). Renal artery stenosis and peripheral vascular disease S)R,&mdash;Dr Salmon and Dr Brown (Aug 4, p 321) report that in a group of 374 patients referred for angiographic assessment of lower-limb peripheral vascular disease (PVD), but not selected for the presence of hypertension, 31% had a renal artery stenosis, which was bilateral in 12%. This high prevalence is interesting but not really surprising since atherosclerosis is a diffuse disease that can affect renal arteries. A very important point for the management of hypertensive patients is the true prevalence of renal artery stenosis when peripheral vascular disease coexists with hypertension.1 From Sept 1, 1987, to Aug 31, 1988, 565 consecutive hypertensive adults were referred to our clinic for evaluation of hypertension either on an ambulatory basis or during admission. 99 patients (mean age 66) had PVD and 466 (mean age 51) did not. For each patient a standardised collection of information was checked and registered with a computerised system (’A-rtemis’).’ The evaluation included the search for a curable cause of hypertension, the investigation of cardiovascular risk factors, and a complete clinical review. Peripheral arterial disease was confirmed at least by clinical observation, including a pedo/brachial systolic blood pressure ratio of less than 0 90 at rest. If suggested by the clinical history, initial diagnostic work-up, or duplex doppler examination 3 renal artery stenosis was confirmed by angiography. Renovascular hypertension was finally diagnosed in 14 (14-1%) hypertensive patients with PVD and in only 23 (4-9%) hypertensive patients without PVD (p < 0-05). The reported prevalence of renovascular hypertension varies widely but frequently ranges from 3% to 5 %. Our findings suggest that lower-limb PVD can be used to identify a subpopulation of hypertensive adults with a higher prevalence of renovascular hypertension. Departments of Hypertension, Vascular Medicine, and Internal Medicine, Saint-Joseph Hospital, 75014 Paris, France P. PRIOLLET I. LAZARETH D. MANI&Egrave;RE-CONSTANTIN Medical Information Department, Broussais Hospital, Paris F. AIM&Eacute; 1 Mani&egrave;re-Constantin D, Aim&eacute; F, Priollet P. L’art&eacute;rite des membres inf&eacute;rieurs chez l’hypertendu est-elle un indice d’hypertension r&eacute;no-vasculair? Presse Med 1990; 19: 176 2 Degeulet P, Menard J, Berger C, Plouin PF, Devnes C, Hirel JC. Hypertension management: the computer as a participant Am J Med 1980; 68: 559-67 3 Taylor DC, Kettler MD, Moneta GL, et al. Duplex ultrasound scanning in the diagnosis of renal artery stenosis, a prospective evaluation J Vasc Surg 1988; 7: 364-69. Interatrial shunts and decompression sickness SIR,--Our criticisms of Dr Wilmshurst and colleagues’ paper1 have not been directed at discrediting the value of this work. We wish simply to note deficiencies in the design of the study. In our letter of April 14, we asked if those performing the echocardiograms were blinded to the history of the subjects and if those interpreting the echocardiograms were independent of subject selection and examination. Wilmshurst replied, "Our paper makes it clear that those who did the echocardiograms also interpreted them, and did so blind to the history of the divers". Our specific question is did the investigators interview and examine the subjects, irrespective of subsequent blind reading of the results? The quality and extent of the examination is investigator dependent. If those who performed the echocardiograms knew the history, they may have biased the outcome inadvertently. Our second point is that those entered into the investigation were all cases referred to Wilmshurst; the study group was not randomly selected and may have been subject to a referral bias-eg, including primarily those who wanted to return to diving. Furthermore, we have referred cases to Wilmshurst because we felt that their CNS dysbarism was unusual or unexpected from the dive profile. Such unintentional selection bias could be overcome if the study was designed to comprise all cases of dysbarism treated at one centre or from a given catchment area. Institute of Naval Medicine, Alverstoke, Gosport PO12 2DL, UK D. J. SMITH 1. Wilmshurst PT, Byme JC, Webb-Peploe MM. Relation between interatrial shunts and decompression sickness in divers. Lancet 1989; ii: 1302-05 *** This letter has been shown to Dr Wilmshurst, whose reply follows.-ED. L. SiR,&mdash;The divers we examined did a series of manoeuvres to accentuate intracardiac shunting. If shunting was seen, the test was judged positive and no more manoeuvres were done, to minimise the amount of systemic gas embolism. Scans were recorded on videotape and individual injections were reviewed before proceeding to the next manoeuvre, but a decision was always reached before the subject left the couch. Those doing the scans were blind to the history and examination and since they simultaneously interpreted the scans, interpretation was also blinded. I have reviewed all the medical records. Some divers had been treated for decompression sickness at the Institute of Naval Medicine (INM) but they were referred to me by others and none of the referrals came from the INM. The cases treated by INM were, however, typical of the whole series in respect of proportion of individuals in clinical subgroupings used, proportion of subjects who had done provocative dives, and proportion in each subgroup who had shunts. Smith’s misunderstanding about the INM patients may have arisen because he was not seconded from the US Navy until our study had been completed. He suggests studying cases from just one centre or catchment area. However, there are regional differences in diving practices. In our study selection bias was countered by asking the regional medical referees of the British SubAqua Club and sympathetic recompression chamber operators to refer as many individuals who had had decompression sickness as possible. We did not ask for any specific clinical subgroup and many of those we saw did not intend to return to diving. Our aim was to avoid selection bias by recruiting a large sample. In two years, we studied 61 individuals who had dysbaric illness-ie, about one- third of the total UK cases of dysbaric illness during that period. The relative frequency of different clinical manifestations, the distribution of speed of onset of symptoms, and the proportion of divers affected without provocative dives is similar to that described in British SubAqua Club accident statistics.’ We have confirmed our observations in an extended study of over 200 divers.2 Smith and colleagues are aware of previous supervised replication studies at another centre (April 14, p 915). I have told Smith that if

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Page 1: Renal artery stenosis and peripheral vascular disease

879

prepared by the PEG/SDS method and cDNA synthesised asdescribed,3 but with random primers in place of D95.Serum samples from 20 haemophiliacs treated repeatedly with

unheated commercial factor V I I I concentrate were tested with both

the original set of primers (D94, D95, N 1, N2) and the new set. Theoriginal set detected HCV RNA in 7 serum samples (35%), whereasthe new set detected HCV RNA in 17 (85%). Serum from 30healthy blood donors gave no signals with either set of primers. Weconclude that the NCR series primers will, to a significant degree,circumvent the problem of false-negative PCR results arising fromsequence variation.

We thank Dr P. Jones, Dr G. Savidge, and Dr J. Barbara for kindly providingclinical materials.

Virology Division,Department of Medical Microbiology,University College and Middlesex School of Medicine,London W1P 7PN, UK

J. A. GARSONC. RINGP. TUKER. S. TEDDER

1 Okamoto H, Okada S, Sugiyama Y, et al. The 5’-terminal sequence of the hepatitis Cvirus genome. Jpn J Exp Med 1990; 60: 167-77.

2 Okamoto H, Okada S, Sugiyama Y, et al. Detection of hepatitis C virus RNA by atwo-stage polymerase chain reaction with two pairs of primers deduced from the5’-noncoding region. Jpn J Exp Med 1990; 60: 215-22.

3 Garson JA, Tuke PW, Makris M, et al. Demonstration of multiple viraemia patterns inhaemophiliacs treated with hepatitis C virus contaminated factor VIIIconcentrates Lancet (in press).

Renal artery stenosis and peripheralvascular disease

S)R,&mdash;Dr Salmon and Dr Brown (Aug 4, p 321) report that in agroup of 374 patients referred for angiographic assessment oflower-limb peripheral vascular disease (PVD), but not selected forthe presence of hypertension, 31% had a renal artery stenosis,which was bilateral in 12%. This high prevalence is interesting butnot really surprising since atherosclerosis is a diffuse disease that canaffect renal arteries. A very important point for the management ofhypertensive patients is the true prevalence of renal artery stenosiswhen peripheral vascular disease coexists with hypertension.1From Sept 1, 1987, to Aug 31, 1988, 565 consecutive

hypertensive adults were referred to our clinic for evaluation ofhypertension either on an ambulatory basis or during admission. 99patients (mean age 66) had PVD and 466 (mean age 51) did not. Foreach patient a standardised collection of information was checkedand registered with a computerised system (’A-rtemis’).’ Theevaluation included the search for a curable cause of hypertension,the investigation of cardiovascular risk factors, and a completeclinical review. Peripheral arterial disease was confirmed at least byclinical observation, including a pedo/brachial systolic blood

pressure ratio of less than 0 90 at rest. If suggested by the clinicalhistory, initial diagnostic work-up, or duplex doppler examination 3renal artery stenosis was confirmed by angiography. Renovascularhypertension was finally diagnosed in 14 (14-1%) hypertensivepatients with PVD and in only 23 (4-9%) hypertensive patientswithout PVD (p < 0-05).The reported prevalence of renovascular hypertension varies

widely but frequently ranges from 3% to 5 %. Our findings suggestthat lower-limb PVD can be used to identify a subpopulation ofhypertensive adults with a higher prevalence of renovascularhypertension.

Departments of Hypertension,Vascular Medicine, and Internal Medicine,

Saint-Joseph Hospital,75014 Paris, France

P. PRIOLLETI. LAZARETHD. MANI&Egrave;RE-CONSTANTIN

Medical Information Department,Broussais Hospital, Paris F. AIM&Eacute;

1 Mani&egrave;re-Constantin D, Aim&eacute; F, Priollet P. L’art&eacute;rite des membres inf&eacute;rieurs chezl’hypertendu est-elle un indice d’hypertension r&eacute;no-vasculair? Presse Med 1990; 19:176

2 Degeulet P, Menard J, Berger C, Plouin PF, Devnes C, Hirel JC. Hypertensionmanagement: the computer as a participant Am J Med 1980; 68: 559-67

3 Taylor DC, Kettler MD, Moneta GL, et al. Duplex ultrasound scanning in thediagnosis of renal artery stenosis, a prospective evaluation J Vasc Surg 1988; 7:364-69.

Interatrial shunts and decompressionsickness

SIR,--Our criticisms of Dr Wilmshurst and colleagues’ paper1 havenot been directed at discrediting the value of this work. We wishsimply to note deficiencies in the design of the study.

In our letter of April 14, we asked if those performing theechocardiograms were blinded to the history of the subjects and ifthose interpreting the echocardiograms were independent of

subject selection and examination. Wilmshurst replied, "Our papermakes it clear that those who did the echocardiograms also

interpreted them, and did so blind to the history of the divers". Ourspecific question is did the investigators interview and examine thesubjects, irrespective of subsequent blind reading of the results?The quality and extent of the examination is investigatordependent. If those who performed the echocardiograms knew thehistory, they may have biased the outcome inadvertently.Our second point is that those entered into the investigation were

all cases referred to Wilmshurst; the study group was not randomlyselected and may have been subject to a referral bias-eg, includingprimarily those who wanted to return to diving. Furthermore, wehave referred cases to Wilmshurst because we felt that their CNS

dysbarism was unusual or unexpected from the dive profile. Suchunintentional selection bias could be overcome if the study wasdesigned to comprise all cases of dysbarism treated at one centre orfrom a given catchment area.

Institute of Naval Medicine,Alverstoke, Gosport PO12 2DL, UK D. J. SMITH

1. Wilmshurst PT, Byme JC, Webb-Peploe MM. Relation between interatrial shuntsand decompression sickness in divers. Lancet 1989; ii: 1302-05

*** This letter has been shown to Dr Wilmshurst, whose replyfollows.-ED. L.

SiR,&mdash;The divers we examined did a series of manoeuvres toaccentuate intracardiac shunting. If shunting was seen, the test wasjudged positive and no more manoeuvres were done, to minimisethe amount of systemic gas embolism. Scans were recorded onvideotape and individual injections were reviewed before

proceeding to the next manoeuvre, but a decision was alwaysreached before the subject left the couch. Those doing the scanswere blind to the history and examination and since theysimultaneously interpreted the scans, interpretation was also

blinded.I have reviewed all the medical records. Some divers had been

treated for decompression sickness at the Institute of NavalMedicine (INM) but they were referred to me by others and none ofthe referrals came from the INM. The cases treated by INM were,however, typical of the whole series in respect of proportion ofindividuals in clinical subgroupings used, proportion of subjectswho had done provocative dives, and proportion in each subgroupwho had shunts. Smith’s misunderstanding about the INMpatients may have arisen because he was not seconded from the USNavy until our study had been completed. He suggests studyingcases from just one centre or catchment area. However, there areregional differences in diving practices. In our study selection biaswas countered by asking the regional medical referees of the BritishSubAqua Club and sympathetic recompression chamber operatorsto refer as many individuals who had had decompression sickness aspossible. We did not ask for any specific clinical subgroup and manyof those we saw did not intend to return to diving. Our aim was toavoid selection bias by recruiting a large sample. In two years, westudied 61 individuals who had dysbaric illness-ie, about one-third of the total UK cases of dysbaric illness during that period.The relative frequency of different clinical manifestations, thedistribution of speed of onset of symptoms, and the proportion ofdivers affected without provocative dives is similar to that describedin British SubAqua Club accident statistics.’ We have confirmedour observations in an extended study of over 200 divers.2

Smith and colleagues are aware of previous supervised replicationstudies at another centre (April 14, p 915). I have told Smith that if