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the near future. To be accepted, however, the nitrate respiratory rate and a greater increase in oxygen saturation formulation may need further refinement.
with isosorbide dinitrate than with furosemide. The fall in heart rate is of interest, because it suggests reduced Department of Cardiovascular Medicine, University of Birmingham and sympathetic drive; in other studies heart rate did not University Hospital Birmingham NHS Trust, Edgbaston, change significantly with infusion of isosorbide dinitrate or nitroprusside,1,2 but it did fall with isosorbide mononitrategiven as bolus9 (table). However, the mean initial heart Chatterjee K, Parmley WW, Ganz W, et al. Haemodynamic andmetabolic responses to vasodilator therapy in acute myocardial rate was only 91 (SD 5) beats per minute in the study by infarction. Circulation 1973; 48: 1183–93.
Nelson and colleagues and 94 (14) in that by Chatterjee Nelson GIC, Silke B, Ahuja RC, Hussain M, Taylor SH.
and colleagues; these heart rates suggest that the Haemodynamic advantages of isosorbide dinitrate over frusemide in pulmonary oedema in these two studies was not too acute heart failure following myocardial infarction. Lancet 1983; i:730–32.
severe, although nine out of 36 patients had clinical Biddle TL,Yu PN. Effect of furosemide on haemodynamics and lung features of cardiogenic shock at presentation and there water in acute pulmonary edema secondary to myocardial infarction.
was significant mortality among Chatterjee’s patients.1,2 Am J Cardiol 1979; 43: 86–90.
Another interpretation of the lack of effect on heart rate of Mukherjee SK, Katz MA, Michael UF, Ogden DA. Mechanisms ofhemodynamic actions of furosemide: differentiation of vascular and isosorbide dinitrate infusion is that it was not very renal effects on blood pressure in functionally anephric hypertensive effective at reducing sympathetic drive, perhaps because of patients. Am Heart J 1981; 101: 313–18.
prolonged vasodilatation and hence relative hypotension.
Pickkers P, Dormans T, Smits P. Direct vasoactivity of frusemide.
Lancet 1996; 347: 1338–39.
As with many other studies, all patients in the Cotter Northridge D. Frusemide or nitrates for acute heart failure? Lancet study received 40 mg furosemide (along with oxygen and 1996; 347: 667–68.
morphine) intravenously before randomisation; local Lal S, Murtagh JG, Pollock AM, Fletcher E, Binnion PF. Acute ethical considerations also dictated the use of low-dose haemodynamic effects of frusemide in patients with normal and raised
left atrial pressures. Br Heart J 1969; 31: 711–17.
infusion of isosorbide dinitrate as adjunctive therapy in the Gammage MD, Murray RG, Littler WA. Isosorbide-5-mononitrate in furosemide group. In effect, therefore, this study compares the treatment of acute left ventricular failure following acute low-dose furosemide plus bolus isosorbide dinitrate myocardial infarction. Eur J Clin Pharmacol 1986; 29: 639–43.
against high-dose furosemide plus low-dose isosorbide Bosc E, Bertinchant JP, Hertault J. Utilisation de la trinitrine injectable(bolus de 3 mg) dans le traitement de l’edeme pulmonaire dinitrate infusion. Unlike most other studies, data were cardiogenique. Ann Cardiol Angiol 1982; 31: 477–80.
10 Morrison RA, Weigand UW, Jahnchem E, et al. Isosorbide dinitrate haemodynamic and oxygen-consumption benefits are kinetics and dynamics after intravenous, sublingual and percutaneous inferred rather than demonstrated. In addition, the dosing in angina. Clin Pharmacol Ther 1983; 33: 747–56.
11 Sporl-Radun S, Betzein G, Kaufmann B, Liede V, Abshagen U. Effect conclusions are further limited by the need to exclude and pharmacokinetics of isosorbide dinitrate in normal man. Eur Clin J certain categories of patients—those on chronic nitrate or Pharmacol 1980; 18: 237–44.
diuretic therapy or with blood pressure lower than 110/70 12 Taylor T, Chasseaud LF, Doyle E. Pharmacokinetics of isosorbide mm Hg on admission. This latter exclusion may not (in dinitrate after intravenous infusion in human subjects. Biopharm Drugs
1980; 1: 149–56.
retrospect) have been necessary since mean arterial 13 Down WH, Chasseaud LF, Grundy RK. Biotransformation of pressure fell by similar amounts in both groups (132 [SD isosorbide dinitrate in humans. J Pharm Sci 1974; 63: 1147–49.
14] to 107 [15] mm Hg with isosorbide dinitrate and 124[24] to 103 [19] mm Hg with furosemide).
Intravenous isosorbide dinitrate has a rapid onset of action, with peak vasodilatation at 5 min,10–12 but the short elimination half-life (0·6 h) requires frequent repeat dosing when given by bolus. Isosorbide-5-mononitrate Genetic deafness is common, with an estimated prevalence shares the pharmacological actions of the dinitrate and is of 1 per 2000 births. Writing in 1853, before the laws of the main active metabolite formed after administration of mendelian inheritance had even been promulgated, Sir isosorbide dinitrate,13 but it has a much longer half-life William Wilde recognised that the pattern of transmission (5·1 h). The mononitrate therefore seems to represent a of deafness varied from family to family, and he clearly better long-acting nitrate for intravenous bolus use in identified autosomal dominant, autosomal recessive, and X-linked forms.1 Latterly, attempts by researchers to symptomatic and haemodynamic benefits in an open identify homogeneous families on the basis of associated study of acute pulmonary oedema,8 but no randomised, clinical features have led to the recognition of the clinically prospective comparison has been made with furosemide, distinct syndromic forms of deafness, which have formed and no intravenous preparation is yet available.
the basis of much recent progress.2–5 These advances For intravenous nitrate therapy to displace furosemide represent a triumph for the rigorous clinical discipline of for the management of acute pulmonary oedema, it needs syndrome delineation, and the molecular diagnostic to be effective in a single bolus injection in most cases, applications accruing will be widely valued by geneticists must be safe to use in the presence of moderate and their patients. However, these new investigations are hypotension, and must be effective in patients on chronic likely to be limited in their application by the relative rarity long-acting nitrate or diuretic therapy. Bolus isosorbide of the individual syndromes to which they appertain. Most dinitrate has not yet been shown to fulfil these criteria; deaf patients, even with a family history suggesting a genetic cause, have no associated clinical features and are randomised prospective comparison with furosemide or a said to have non-syndromic hearing loss.
furosemide/isosorbide dinitrate combination is required.
1997 will be seen as a watershed for genetic advances in The evidence so far suggests that intravenous nitrates non-syndromic deafness because of three separate should have the potential to displace furoemide as first- developments. First was the report from Kelsell and line therapy for acute, cardiogenic pulmonary oedema in colleagues6 that mutations in the connexin 26 (Cx 26) gene THE LANCET • Vol 351 • February 7, 1998 caused deafness in families with both autosomal dominant of the G deletion in Cx 26 may also vary in different and recessive patterns of transmission. Second, a mutation populations, as has previously been observed for the in the human homologue of the Drosophila ⌬F508 mutation in the cystic fibrosis gene. Of more diaphanous, was identified in a large Costa Rican family immediate relevance is the challenge that the possibility of with autosomal dominant deafness.7 Finally, the myosin testing for this mutation in deaf individuals and their VIIA gene, already known to be mutated in a subgroup of families poses to clinicians investigating such cases.
patients with Usher’s syndrome, was additionally found to The investigation of the congenitally deaf patient cause both autosomal recessive and autosomal dominant varies widely among paediatricians, otolaryngologists, audiological physicians, and clinical geneticists. This epidemiological significance of mutations in human absence of agreed guidelines probably reflects the different diaphanous and myosin VIIA remains unclear in terms of backgrounds of clinicians investigating deafness. However, their overall contribution to deafness in the general there has also been a reluctance to investigate, on the population, several reports have combined to underline the grounds that a cause that might alter management was importance of the Cx 26 gene with respect to the aetiology unlikely to be identified. The data reported today render of autosomal recessive forms of deafness.11–13 Initial data this view obsolete and should prompt a re-evaluation of suggest that 50–80% of autosomal recessive congenital practice by all concerned, especially since identification of deafness may be due to the Cx 26 mutation and that up to Cx 26 mutation will preclude the need for other 70% of such mutations are due to deletion of a single aetiological investigations, often of a more invasive nature.
nucleotide—loss of a guanine (G), leading, through a To date, the mutations found have all been identified frameshift mechanism, to premature termination of the under the aegis of research. As with so many other developments in molecular genetics, health services must Inherited forms are thought to be responsible for identify avenues by which research discoveries can be approximately half of all cases of congenital deafness. The rapidly incorporated into clinical service. For the UK, commonest inheritance pattern among non-syndromic what better test of the flexibility of the National Health deaf families is autosomal recessive, estimated to account Service in this much heralded anniversary year can there for up to 75% of all such cases. However, in clinical be than to see the development of pertinent research, such practice, autosomal recessive non-syndromic deafness can as Cx 26 mutation and non-syndromic deafness, for be recognised only after the birth of a second affected clinical services, where it clearly has a large part to play in child, because of the clinical non-specificity of congenital deafness as a presenting feature. Consequently, genetic counselling of families with a single deaf child has always Department of Clinical Genetics and Fetal Medicine, Institute of Child had to be along unsatisfactory empirical lines, which would take account of the known chance of recessivity inthe context of clinically indistinguishable deafness of Wilde WR. Practical observations on aural surgery and the nature anddiagnosis of diseases of the ear. London: Churchill, 1853.
environmental aetiology, new dominant mutations, and so Abdelkak S, Kalatzis V, Heilig R, et al. A human homologue of the on. In practical terms, couples with one congenitally deaf Drosophila eyes absent gene underlies branchio-oto-renal (BOR) child are counselled a 10% recurrence risk, in the full syndrome and identifies a novel gene family. Nat Genet 1997; 15:
knowledge that, were it possible to identify those families Neyroud N, Tesson F, Denjoy I, et al. A novel mutation in the in which the deafness is autosomal recessive, the potassium channel gene KVLQT1 causes the Jervell and Lange-Nielsen cardioauditory syndrome. Nat Genet 1997; 15: 186–89.
The two related reports in today’s Lancet addressing the Tyson J, Tranebjaerg L, Bellman S, et al. IsK and KvLQT1: mutation ineither of the two subunits of the slow component of the delayed rectifier potassium channel can cause Jervell and Lange-Nielsen syndrome. Hum sporadically occurring deafness are therefore important.
Mol Genet 1997; 6: 2179–85.
Not only do these reports prompt a timely re-evaluation of Everett LA, Glaser B, Beck JC, et al. Pendred syndrome is caused by the appropriate investigation of the congenitally deaf child mutations in a putative sulphate transporter gene (PDS). Nat Genet
1997; 17: 411–22.
but they also serve to alter clinical practice in genetic Kelsell DP, Dunlop J, Stevens HP, et al. Connexin 26 mutations in hereditary non-syndromic sensorineural deafness. Nature 1997; 387:
Xavier Estivill and colleagues show that about 50% of autosomal recessive non-syndromic deafness is due to Cx Lynch ED, Lee MK, Morrow JE, Welcsh PL, Leon PE, King M-C.
Nonsyndromic deafness DFNA1 associated with a mutation of a 26 mutation, consistent with their previously published human homolog of the Drosophila gene diaphanous. Science 1997; 278:
data.11 More importantly, these investigators identified mutations at this locus in 37% of individuals with Liu X-Z, Walsh J, Mburu P, et al. Mutations in the myosin VIIA gene sporadically occurring deafness; almost a third of the cause non-syndromic deafness. Nat Genet 1997; 16: 188–90.
Weil D, Kussel P, Blanchard S, et al. The autosomal recessive isolated mutations were due to homozygosity for the G deletion.
deafness, DFNB2, and the Usher 1B syndrome and allelic defects of the Less striking, but highly significant nonetheless, are the myosin VIIA gene. Nat Genet 1997; 16: 191–93.
data from Nicholas Lench and colleagues suggesting that 10 Liu X-Z, Walsh J, Tamagawa Y, et al. Autosomal dominant non- approximately 10% of patients with sporadically occurring syndromic deafness caused by a mutation in the myosin VIIA gene. Nat
1997; 17: 268–69.
deafness have Cx 26 mutations, and that three of the six 11 Zelante L, Gasparini P, Estivill X, et al. Connexin 26 mutations mutations are homozygous for the G deletion. (It should associated with the most common form of non-syndromic neurosensory be noted that the various contributors to this rapidly autosomal recessive deafness (DFNB1) in Mediterraneans. Hum Mol
1997; 6: 1605–09.
emerging area of research have yet to agree on the 12 Carrasquillo MM, Zlotogora J, Barges S, Chakravarti A. Two different terminology for the G deletion, some referring to 30delG connexin 26 mutations in an inbred kindred segregating non-syndromic and others preferring 35delG.) It remains to be recessive deafness: implications for genetic studies in isolated established, over much larger studies of sporadically populations. Hum Mol Genet 1997; 6: 2163–72.
13 Denoyelle F, Weil D, Maw MA, et al. Prelingual deafness: high occurring, congenital deafness whether the figure of 37% prevalence of a 30delG mutation in the connexin 26 gene. Hum Mol or 10% applies to individual populations. The prevalence Genet 1997; 6: 2173–77.
THE LANCET • Vol 351 • February 7, 1998


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