MEIER, B.

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European Heart Journal (1996) 17, 1612-1613EditorialsCoronary angioplasty of rapidly progressivelesions — nothing to it or just too rare to be recognizedas a problem?See page 1671 for the article to which this EditorialrefersThe paper from the Lille group in this issue''1 estab-lishes a more than reasonable hypothesis only torefute it on the basis of their well documented databank. They surmised that lesions having shown rapidprogression before angioplasty have a higher prepon-derance for restenosis than those that built up moreslowly. This hypothesis is based on data of their owngroup'21 and of others'31, revealing an increased rest-enosis rate in patients undergoing coronary angio-plasty for unstable angina. They carefully avoidconfusion with the high restenosis rate found afterangioplasty for rapidly recurring lesions reportedpreviously with data from the same data bank[4]. Suchlesions are of different structure and pathophysiology(intimal proliferation and constructive remodelling)whereas rapid progression of non-dilated lesions isbased on progressive atherosclerosis and plaque rup-ture with organized thrombi'51. Much to their and mysurprise, the hypothesis fell short when scrutinized intheir prospectively accumulated and carefully main-tained data bank. Did the authors find the truth ordid they fall victim to a type II error?As often in biology, the answer is both 'yes'and 'no' to both questions. One can deduct conclus-ively from the paper that a rapidly progressive denovo lesion that is dilated during an elective pro-cedure yields results comparable with those of lesionsthat have barely changed over the past 7 months.However, these quiescent lesions that have progressedrecently but apparently have not been 'caught in theact' are not the ones we are truly worried about. Ourconcern in terms of acute problems and restenosesfocuses on truly unstable lesions. Even in the groupwith rapid progression, only 20% of the patientswere considered as unstable. This is lower thanmost series of unselected coronary angioplasty pro-cedures. Two factors may account for the low per-centage of unstable clinical presentations in a groupof patients with documented progression of theircoronary artery disease. First, the definition usedfor unstable angina (chest pain with electrocardio-graphic changes within 48 h before an electivecoronary angioplasty) is quite stringent and some-what contradictory. Second, the series is explicitlybased on patients called in for a routine follow-upangiography at about 6 months after an initialsuccessful coronary angioplasty. Through such anarrow window, unstable angina is rare to see. Theauthors then took a closer look at the patients withunstable angina (i.e. nine people) but were unable toconfirm the high tendency of restenosis they haddescribed earlier121. This was a type II error trap ifever there was one.A number of additional points are of note inthe report. The average reference vessel diameter of2-5 mm of a reasonably large cohort (85 patients) ofunselected coronary stenoses is small. This may beintrinsic to the method of quantitative coronary an-giography employed. It may or may not influence theballoon selection. Again, the mean balloon diameterof 2-8 mm is clearly below industry standards. Acertain systematic under-dilation cannot be excludedand may account for the relatively high degree ofstenosis at the end of the procedure (32%) which, inturn, lends to a high categorical percentage of rest-enosis (not given in the paper) and a low late loss(0-3 mm). A low mean late loss will reduce the powerof discrimination. A certain deficiency of the paper isthe absence of data concerning the acute outcome ofangioplasty in the two groups. The authors probablywished to prevent false conclusions based on type I ortype II errors. In groups of only 40 patients, even instentless procedures as the ones described, acuteocclusion has only to be expected in about threepatients per group. Of course, if the rapidly pro-gressing group had only included patients with trulyunstable angina, an increased incidence of acuteproblems could have become apparent. With aprevalence of unstable angina of 20% in the 'high0195-668X/96/111612 + 07 $25.00/0 © 1996 The European Society of CardiologyEditorials 1613risk' group and a mere 5% in the control group acuteevents are likely to have been very rare.It is easy to concur with the authors thataccidentally detected lesions that have recentlyprogressed can and should be dilated without asignificantly increased risk of recurrence. Thecommunity of angioplasty operators is grateful forthese data, endorsing a long established practice.However, the paper does not minimize the acuteproblems or increased likelihood of restenosiswhen it comes to plaques dilated at the verymoment of progression. The authors are far tooexperienced not to have conveyed this caveat clearlyin the discussion.B. MEIERUniversity Hospital,Bern, SwitzerlandReferences[1] Bauters C, Passart F, Lablanche J-M, McFadden EP, HamonM, Bertrand ME. Restenosis after coronary angioplasty forrapidly progressive coronary stenosis. Eur Heart J 1996; 17:1671-7.[2] De Groote P, Bauters C, McFadden EP, Lablanche JM, LeroyF, Bertrand ME. Local lesion-related factors and restenosisafter coronary angioplasty: evidence from a quantitativeangiographic study in patients with unstable angina undergoingdouble-vessel angioplasty. Circulation 1995; 91: 968-72.[3] Plokker HWT, Ernst SMPG, Bal ET el al. Percutaneoustransluminal coronary angioplasty in patients with unstableangina pectoris refractory to medical therapy: long-term clini-cal and angiographic results. Cathet Cardiovasc Diagn 1988;14: 15-18.[4] Bauters C, Lablanche JM, McFadden EP, Leroy F, BertrandME. Clinical characteristics and angiographic follow-up ofpatients undergoing early or late repeat dilation for a firstrestenosis. J Am Coll Cardiol 1992; 20; 845-8.[5] Meier B, Ramamurthy S. Plaque sealing by coronaryangioplasty. Cathet Cardiovasc Diagn 1995; 36: 295-7.European Heart Journal (1996) 17, 1613-1614Arrhythmogenic right ventricular disease, dysplasia andcardiomyopathySee page 1717 for the article to which this EditorialrefersThis issue contains an interesting article on long-termchanges in the ECGs of patients with ventriculararrhythmias originating in the right ventricle11'. Theauthors describe their patients as having arrhyth-mogenic right ventricular disease but quote exten-sively references concerning arrhythmogenic rightventricular dysplasia. In fact the term arrhyth-mogenic right ventricular disease refers to a largergroup of patients than the classical arrhythmogenicright ventricular dysplasia, which is clearly identifiedby its specific histological structure rarely available ina common clinical series12'.In addition to the presence of ventriculartachycardia (of unknown origin) the authors' criteriafor inclusion are based on contrast angiography. Thisis also an interesting approach in clinical diagnosissince angiography is strongly dependent on theunderlying anatomical structure and has generallybeen considered as the 'gold standard' for the diagnosisby showing evidence of segmental abnormalities'3'4'.However, in addition to this approach theauthors have included in their selection the so-called'more diffuse forms'. We are concerned that thesemore diffuse forms may confuse the issue. Diffusedilatation of the right ventricle alone is not a signof arrhythmogenic right ventricular dysplasia. Itcould be the result of different forms of idiopathiccardiomyopathy mostly involving the right ventriclewithout replacement of myocardial fibres by fattytissue'51. Even segmental abnormalities could bethe result of a localized form of healed myo-carditis, ischaemia or cardiomyopathy16'. Onlyspecific segmental abnormalities, such as outpouchingbulges, microaneurysms, or deep fissures in theinfundibulum or at the apex are markers of arrhyth-mogenic right ventricular dysplasia. However, suchcomments are not of academic importance since theprognosis of these various subgroups may be differ-ent. For instance, the development of myocarditisrecently demonstrated in a subgroup of cases super-imposed on arrhythmogenic right ventricular dys-plasia could lead to progressive modification of theECG that is not the result of the dysplastic phenom-enon (replacement of right ventricular musculature byadipocytes and fibrous tissue) but a different phenom-enon that could affect both right and left ventricles'71.Therefore, the changes observed in some of the casesmay not be the result of evolution of the basic disease,but the consequence of a different phenomenon acting

Coronary angioplasty of rapidly progressive lesions — nothing to it or just too rare to be recognized as a problem?

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