Bulletin 2001

	AMS BULLETIN AUTUMN 2001 EDITORS COLUMN We hope that this bulletin being on the website will be more accessible to a wider audience and at the same time reduce the expenses to the Society. We have been having an active and exciting time in Insurance Medicine during the past year. REPORTS FROM MEETINGS: XXth ICLAM This conference was held in Sydney in April and was enjoyed greatly by the participants and guests, many having booked the visit of a lifetime to parts of Australia either before or after the conference. My wife and I went to Hawaii, New Zealand, Sydney, Melbourne, Perth and Singapore. Our Australian colleagues laid on a superb scientific programme with afternoon workshops and a CD Rom to bring home with all the data of the presentations. This has been most useful in underwriting and also an excellent source of continuing medical education. Congratulations to Detloff Rump, his organising and scientific committee and also the back up team. We are very grateful to Dr. Fabrice Chouty for allowing us to use his address to ICAM for this bulletin on a subject difficult to underwrite for the non-specialist. CEECLAM The first joint Hungarian/Polish Central Eastern European meeting took place at Lake Balaton on May1/2 and was so successful that a second meeting is planned in Warsaw on November 12-14 2002. Co-ordination of these meetings between MENBOT (Hungary) and PAIM (Poland) is delegated to the executive of each Society under the heading of CEECLAM. Further details w available through this website when unavailable. ROYAL SOCIETY OF MEDICINE This full day meeting on the 6th July was well attended and covered many interesting and challenging topics. There was an overview of some life products and their underwriting as well as the interface between insurance medicine and a more occupational insurance interface with discussions of Office stress, chronic fatigue and also the Diploma in Disability Assessment Medicine. (DDAM) AMERICAN ACADEMY OF INSURANCE MEDICINE The American Academy meeting this year had a joint meeting with the Canadians in Ottawa on 6-10th October. There was a full programme under the chairmanship of Ross Mackenzie. It seemed a perfect opportunity to keep track of recent changes in North America and a report will appear here soon. FUTURE INTERNATIONAL MEETINGS: ACADEMY OF INSURANCE MEDICINE OF ASIA AIMA IV will be held in Ho Chi Minh City, Vietnam. Further information can be obtained from The Secretary via email. ICLAM 2004 This is planned for April 19-24th 2004 in Venice . It promises to be an interesting programme that should stimulate lively discussion. Registration can be done via: Email: iclam2004@galactica.it. Post: ICLAM 2004 congress Secretariat. Via Selve 2, 31021 Mogliano, Veneto, Italy Over the time that I have been editor of the Bulletin, I have made no secret of the view that we need to widen our parish and welcome insurance related professionals from differing spheres of Insurance. Now that we have this web presence we would welcome the views of the members on how the Society should evolve in the future. Views can easily be expressed via the feedback page on this website. Suggestions on topics that could be discussed at meetings are always welcome and can also be forwarded to Council via the feedback page. THE PRESIDENTS COLUMN The Terrible events in the USA on September 11th with the appalling unanticipated destruction and loss of life in New York and Washington with the subsequent uncertainty have altered life for everyone. Even at a distance the immediacy of television and radio has brought us all together in feelings of sorrow and disbelief. Many of us had friends, colleagues or family working nearby. We send our special condolences to those who were personally affected. I am not aware of any members of the American Academy of Insurance Medicine who were involved, but we certainly send our messages of sympathy and concern to them. It is good to know that their annual meeting in Ottawa proceeded with little change to the programme or numbers attending. Early estimates suggest that Insurers worldwide are expected to payout between 30 and 40 billion dollars, making it their biggest loss of all time. The hardest hit are those shouldering property losses and unquantifiable liability losses. The outlook for life insurers seems better and although some face a large unexpected payout it will not substantially affect their mortality forecasts. Some companies are already seeing stronger demand for life insurance, an interesting quote from an agent for North Western Life Mutual saying ‘we are not being proactive, but it heightens people’ awareness about their own mortality.’ Life insurers face a bill for up to 5 billion overall out of a totals yearly payout in death benefits of 45 billion. Many payouts have already been made and the US industry insurers’ official leader hastened to reassure President Bush that insurers will pay all claims regardless of any ‘act of war’ or terrorism exclusion clauses. However, they are pressing for Government to cap future losses similar to the UK where all contribute to Pool Re which has the backing of the Government as e underwriter of last resort. At our last council meeting on June 6th, there was a lively debate following the finance report, partly as we could see that subscription income particularly corporate subscriptions together with investment income was likely to fall. This led on to a wider discussion of the fundamental aims and activities of the Society. It was agreed that a sub-committee be formed to draw up a discussion paper on the future of the Assurance Medical Society. The working Party has had one meeting already and after a further meeting a paper will be brought to council in \|November. It is hoped that all members will then have the opportunity to comment before the AGM in February 2002. Naturally we would be pleased to have any views of members at any time. The setting up of the website and email address provides ready access. Genetics and insurance continues to ‘rumble’ on, the Human Genetics Commission (HCG) producing its first annual report with Government response expected at the end of October possibly with views on a the new moratorium. The UK Forum for Genetics and Insurance (UKFGI) has its next meeting on Tuesday November 6th the day before our November meeting. The Association of British Insurers (ABI) has been collating numbers of genetic tests used in insurance in 1999 and year 2000, more than half the tests were for Huntington’s Disease, nearly a quarter were BRCA ½, none fore Alzheimer’s from a total of just under 200 test results in year 2000. More than 60% of the test results were negative; approximately two-thirds played a part in the decision process. The detailed results will be made available on the ABI website and to individual companies in due course. Meanwhile the HCG now questions the use of family history in underwriting. Clinical medicine has always regarded family history of considerable importance especially in the way it shapes individuals attitudes towards actual or [potential disease problems but it is right that we should have to re-examine the evidence base for FH and indeed all the parameters in underwriting. Critical illness definitions in the light of medical advances e.g. the earlier and increased diagnosis of prostate cancer from screening and the use of troponins in acute coronary syndromes which is likely to increase substantially the number of patients diagnosed with myocardial infarction present a challenge on all fronts. It may be difficult or impossible to get precise epidemiological data for pricing actuaries, nevertheless, for the consumer there are important advantages in having a standardised definition of the core critical illnesses. The ABI is continuing negotiations with the BMA over fee schedules for General Practice Reports (GPR) and Medical Examination Reports (MER). It is hoped that an agreement will be reached early next year. In the meantime let me reiterate that we are keen to have any comments from any of our members. Use this website not least for the excellent links to the Societies and information sources PROGNOSIS OF CARDIAC ARRHYTHMIAS AND NEW TREATMENT Fabrice Chouty, MD C.M.O. – Hannover-Life-Re (Paris) A.M.C.A.P. General Secretary Cardiovascular disease remains the single largest categorical cause of natural death in Europe and North-America, 50% of which being sudden and unexpected ; and most of them being caused by an acute fatal arrhythmia (at least 65% and probably more). This points out the importance of a careful assessment of the arrhythmia and treatment optimisation in patients with an increased risk of cardiac arrhythmia’s. It is now well known and statistically demonstrated that the two major prognostic factors for sudden cardiac death in patients with an organic heart disease are: ü The left ventricular ejection fraction (echocardiogram). ü The existence of frequent or complex ventricular arrhythmia’s (standard ECG, Holter). ü The existence of any kind of arrhythmia. I. DIFFERENT TYPES OF ARRHYTHMIAS: 1.Atrial Fibrillation (AF) and Flutter: There are different kind of atrial arrhythmia. One should make the difference between patients having an underlying heart disease (Ischaemic heart disease, hypertension with LVH, mitral valve disease with enlargement of the atrium) and patients without any structural heart disease (lone atrial fibrillation). In patients with an underlying organic heart disease, the occurrence of a permanent atrial fibrillation result in an increase up to 2 fold in the death ratio as compared with a group of patients without an atrial arrhythmia. The patients with the “lone atrial fibrillation” may have either permanent or paroxysmal atrial fibrillation. Patients with paroxysmal AF may have either vagally induced AF or catecholamine induced AF. These two forms of arrhythmia’s mediated by the autonomic nervous system are diagnosed upon the results of the Holter monitoring which shows a different pattern in each case: ü Vagally induced PAF are occurring in the evening, during the night or after a meal, when the vagal tone is enhanced and the Holter shows a slowing down of the cardiac rate followed by atrial extrasystoles and by AF that goes on for a few minutes or several hours and then self converts into sinus rhythm. Sometimes one can observe the alternation of atrial fibrillation and atrial flutter which is almost specific and strongly suggests this mechanism of atrial arrhythmia. This arrhythmia is constantly aggravated by the drugs that slow down the sinus rhythm (digoxin, verapamil) except amiodarone possibly associated with class Ic anti-arrhythmic drugs such as flecaïnide. ü Catecholamine induced atrial arrhythmia are occurring during efforts (easy to set off by a stress test or an isuprel infusion). They often do not last more than a few minutes but are very symptomatic and requires b-blockers therapy associated with class I anti-arrhythmic drugs. ü Lone atrial fibrillation, regardless of its mechanism is associated with an increased risk of stroke and death, particularly in patients aged more than 60 years. It is considered that anticoagulation therapy should improve the life and functional prognosis of such patients. The benefit of anti-arrhythmic therapy is currently on assessment by the A.F.F.I.R.M. trial. 2.Junctional Arrhythmia’s: There are different kinds of junctional arrhythmia regarding whether or not its mechanism requires an atrio-ventricular accessory pathway in patients with a WPW syndrome (short PR and wide QRS due to ventricular pre-excitation through the Kent bundle). In some patients, the Kent bundle does not give a WPW (concealed WPW) but it can be involved in reciprocal tachycardia as well. Patients with AV-nodal reciprocating tachycardia due to a dual conduction through the AV node are considered as having a very slightly increased risk of death as compared with the general population. Patients with a Kent bundle should be carefully checked as they can develop several different tachycardias the prognostic of which can be severe: ü Orthodromic reciprocating tachycardia using the AV node the antegrade way and the Kent bundle the retrograde way (either narrow QRS complexes or wide QRS complexes due to a functional bundle branch block): more than 90% of the reciprocal tachycardias related to the WPW syndrome. ü Antidromic reciprocating tachycardia using the Kent bundle the antegrade way and the AV node the retrograde way and simulating a ventricular tachycardia (wide [totally pre-excited] QRS complexes). ü Atrial fibrillation, the prevalence of which is increased in patients with WPW syndrome. This AF can lead to sudden death in patients the Kent bundle of whom has a very short antegrade refractory period allowing for very fast ventricular rates (more than 250bpm) that can result in ventricular fibrillation and sudden death. This is probably these AF in patients with WPW syndrome which explain the extra mortality of the WPW group as compared with the general population. Such patients with the WPW syndrome may consequently be separated in 2 groups: those who have a long Kent bundle refractory period at rest and during effort (stress testing or EP study) the risk of whom is related to the AF risk only and those with a short Kent bundle refractory period and a very high risk for sudden death and may be treated by catheter ablation. The evaluation of the Kent bundle refractory period is something serious and requires: ü Either an electrophysiologic study (EPS) testing the Kent bundle refractory period at basal status and after isuprel infusion. ü And/or a stress test during which AF is triggered through a transoesophagial catheter; the refractory period of the Kent bundle being approached as near to the shortest RR interval during AF. Patients who have underwent successful catheter ablation (as checked by EP study) are probably close to a normal risk as it is shown that the prevalence of AF in such patient was then comparable to the standard group and there is no more reciprocating tachycardia and “malignant” AF neither. Further studies should confirm this hypothesis relying on clinical impression. 3.Ventricular Arrhythmia’s: The ventricular arrhythmia’s includes ventricular extrasystoles, ventricular runs (salvos) and ventricular tachycardia. The prognosis of ventricular arrhythmia’s is often considered as worrying, specially in patients with an underlying organic heart disease, a fortiori in those into whom a sustained ventricular tachycardia (VT) in inducible during an electrophysiologic testing. As a matter of fact it has been recently (BUXTON, NEJM, 2000; 342: 1937-45) demonstrated that: ü Patients with ventricular arrhythmia’s and coronary heart disease or congestive heart failure, and low left ventricular ejection fraction (<40%) have an increased risk of death (sudden death and overall mortality). ü This risk is even higher in a group of patients into whom a VT is inducible during the EPS (S1S2S3 protocol). Consequently, although being invasive, EPS is a relevant tool for differentiating patients with a higher risk. Another recent study concerning 6101 patients checked between 1967 and 1972 and followed up over a mean period of 23 years shown that exercise induced ventricular arrhythmia’s were associated with a significantly higher death ratio. Patients were divided in 3 groups regarding the existence or not of premature ventricular complexes (PVC’s) on the rest ECG: ü Group I: frequent PVC’s (more than 10% of the QRS complexes on any strip of 30sec) ü Group II: rare PVC’s (less than 10%) ü Group III: no PVC’s The death ratio (all causes) among patients of group I was obviously higher (41%) than for group II (27.9%) or III (26%). Patients with PVC’s induced during a standard stress test were significantly different as well: ü Overall mortality of group I vs/II+III : p<0.001 ü Overall mortality of group II vs/III : p=NS. ü Cardiovascular mortality of group I vs/II+III : p<0.001 ü Cardiovascular mortality of group II vs/III : p=NS These results concerns any type of VPB’s occurring during exercise or during the recovery period. The relative risk is similar to that associated with a positive exercise test (Jouven et al. NEJM 2000, 343:826-33) Ventricular arrhythmia’s may sometimes be associated to some specific genetic pattern such as ü The Long-QT syndrome ü The Brugada’s syndrome ü The Idiopathic (fascicular, focal) VT (Parkinson & Papp syndrome) ü The Right ventricular dysplasia ü The Hypertrophic cardiomyopathy. 3.1.The long QT syndrome: This is a hereditary disease associating a prolonged QT interval (sometimes transient or fluctuating), syncope or epilepsy related to paroxysmal episodes of torsades de pointes that may degenerates into ventricular fibrillation (Jervell Lange Nielsen or Romano Ward syndrome). A familial history of sudden cardiac death is almost always found. The prevalence is #1/10 000. The only treatment is the automatic implantable cardioverter defibrillator (AICD). 3.2.The Brugada syndrome: Described in the early 90ies by P.Brugada, this is a hereditary disease related to a genetic alteration of the gene SCN5A coding for a sodium channel. This family disease is more frequent in Japan, Thaïland, Far-east countries. Its prevalence in Europe is close to 0.1%. The risk for sudden death is probably very high so these patients do stand for the implantation of an AICD. The typical ECG feature of the Brugada Syndrome includes a right bundle branch block and a ST segment elevation in leads V1, V2, V3: typically with a “cove form” (70%) but sometimes “saddle” or subnormal form (30%) that can be unmasked (or enhanced) with Ajmaline, Procainamide or flecaïnide acetate infusion. 3.3.The focal idiopathic ventricular tachycardia: The ECG pattern of these focal ventricular tachycardias is very specific, especially those arising from the right ventricle outflow tract that are “rather” narrow (although the QRS complexes are wide) with a right axis and a left bundle branch block pattern. They are usually catecholamine sensitive and almost always benign. The b-blockers are usually efficacious on such arrhythmia’s. Some of them have a different ECG pattern with left axis and right bundle branch block pattern. They are benign as well as the other form but an organic heart disease should absolutely be excluded by echocardiogram and (if necessary) cardiac catheterization. These arrhythmia are usually Calcium-blockers sensitive (Verapamil). 3.4.The arrhtyhmogenic Right Ventricular Dysplasia This is due to a progressive fibro-fatty replacement of the RV free wall (enlargement of the RV (echo) associated with recurrent ventricular tachycardias due to multiple re-entrant circuits through these dysplastic zones. The Prevalence is 1/5000 (3 men/1 woman). Amazingly, this disease is often diagnosed in young patients doing a lot of sports. This is an evolutive disease with a constant and progressive aggravation. These patients with recurrent episodes of sustained ventricular tachycardias require efficacious treatment associating Catheter ablation (at the beginning of the disease) with Drug therapy (Sotalol, amiodarone, Nadolol, propafenone) and even AICD if the arrhythmia is not well controlled. 3.5 The ventricular arrhythmias of the Hypertrophic Cardiomyopathy (hcm) This is a primary and familial disorder, probably the most common genetically transmitted cardiovascular disease currently known. Its prevalence is 0.2% (autosomal/dominant). Sudden death may be the first manifestation of HCM and different arrhythmias may complicate the evolution of the disease such as atrial arrhythmias (thrombo-embolism risk, cardiac failure), Ventricular tachycardia and even bitachycardia, Conduction troubles and combinations. II. TREATMENT OF ARRHYTHMIAS: 1.The tools: ü Anti-arrhythmic drugs (class I, class III and IV) ü b-blockers (Class II) : Nadolol. ü Drug combinations. ü Digoxin ü Catheter ablation techniques ü AICD 2.Atrial arrhythmias: ü Vagally induced PAF requires Flecainide and or Amiodarone. ü Catecholamine induced PAF requires b-blockers and class I anti-arrhythmic agents. ü Permanent AF may require Digoxin or verapamil for heart rate control. ü Aspirin or Warfarin should be associated to anti-arrhythmic therapy. Patients with highly symptomatic paroxysmal atrial arrhythmia may be proposed for catheter ablation in some cases such as when Atrial flutter and Atrial fibrillation are related to a triggering zone firing rapidly from the pulmonary veins (often young patients). In some cases, catheter ablation can also be used for ablating the His bundle in association –in the same time-with the implantation of a permanent pacemaker. [No incidence on the long term survival.] 2.Junctional arrhythmias: Drug therapy is often disappointing in the treatment of these patients. The drug should be efficacious on both the triggering extrasystole (atrial or ventricular) and the conduction properties of the pathways used by the re-entrant wavefront such as: ü Drugs that slow down the intra-nodal conduction (verapamil, digoxin, ß-blockers) ü Drugs that slow down the conduction through an accessory pathway (flecaïnide). ü Drug combinations. Catheter ablation is often successful and amazingly efficacious on both re-entrant tachycardias and atrial fibrillation in the patients with the WPW syndrome so that it is likely that such patients are very close to a normal risk after successful ablation procedure. The main purpose of the procedure is to ablate either one of the two pathways in the case of AVNRT (mainly the fast pathway) or the Kent bundle itself for the WPW syndrome. 3.Ventricular arrhythmias: It is now clearly demonstrated that the Life prognosis of patients with ventricular arrhythmia’s and an underlying organic heart disease is not improved by class I anti-arrhythmic drugs. (CAST- study). Amiodarone has been shown to be effective whatsoever (18% reduction of the death ratio in CAMIAT study). In another hand it has now been clearly demonstrated that low doses of ß-blockers are improving survival of patients with congestive heart failure They are given at low doses to such patients with an impaired left ventricular function. Normal (or high) doses of b-blockers are effective in patients with catecholamine sensitive arrhythmia’s (as checked by Holter monitoring and stress ECG). Calcium blockers such as Verapamil (or diltiazem, or bepridil) are useful for treating patients with benign (but often highly symptomatic) fascicular VT (probably an arrhythmia to be related to a triggered activity). The main progress in the treatment of ventricular arrhythmia has probably been the improvement of the AICD, introduced in 1980 and since this time becoming smaller and more efficient, currently able to: ü Detect the occurrence of a potentially malignant arrhythmia ü Make the difference between VT and VF. ü Try to stop it by extra-stimulation (S1S2S3) or overdriving in case of VT. ü Try to stop it by DC shock in case of failure or when a VF is detected. ü In case of AV or SA block: Do some pacing. ü Record the arrhythmia and its termination (Holter) for further analysis by physician. Many studies performed during the past 10 years try to evaluate the AICD vs drug therapy on mortality of patients: AICD for Primary prevention of sudden death: 1. CABG-patch trial enrolled patients with coronary heart disease and low LV ejection fraction (<.36) and Late potentials. This study (probably by a bias in patients recruitment) shown no significant difference in the anti-arrhythmic drug group vs AICD. 2. MADIT trial including patients with CAD, myocardial infarction and low LVEF (<.36) and an inducible sustained VT as shown by EP study gave some more interesting results as the AICD group mortality was reduced by 59% vs Anti arrhythmic drugs group. 3. MUSTT trial selected the patients on the same criteria as MADIT with an optimisation of anti-arrhythmic treatment by EP testing. Nevertheless, the AICD group mortality was found reduced by 50% vs AA group. AICD for secondary prevention of sudden death: ü AVID trial selected patients with a sudden death documented as related to a malignant ventricular arrhythmia. After a 3 years follow up the survival ratio in patients treated with anti-arrhythmic drugs was 76% versus 84% among the patients in whom an AICD was implanted. ü CIDS trial selected patients with spontaneous sustained VT or VF and an inducible VT, lasting more than 10 sec. during EP testing. Amiodarone has been tested versus AICD and even though the overall mortality appeared to be reduced by 20% (and the arrhythmogenic mortality by 33%), this was not statistically significant but… ü CASH trial has shown that finally the AICD had better results in terms of mortality than the b-blockers or the amiodarone. The main problem remains the high price of the device so, the main question remains “what are the indications now for the AICD” ? Dividing the patients in 3 groups, it has been proposed by the European Society of Cardiology the following recommendation: 1.Class I patients into whom usefulness, benefit and efficacy of the AICD has been demonstrated or is considered as evident by a consensus. They should definitely be treated by the cardioverter: ü Cardiac arrest due to VT, VF. ü Sustained VT with underlying organic heart disease. ü Patients with low LVEF, spontaneous unsustained VT and inducible sustained VT/VF in spite of drug therapy. 2. Group II including patients for the group of whom no statistical data is yet available, or when there is some statistical contradiction such as the patients with: ü Genetic disease with high risk of sudden cardiac death and no other known treatment than the AICD (Long QT, Brugada syndrome, HCM…). ü Unexplained syncope with inducible VT, VF during the EP testing. ü Badly tolerated VT in patients waiting for a cardiac transplant. 4.Group III including patients into whom the AICD would likely be useless or would not improve the survival such as those with: ü Unexplained syncope without inducible VT, VF or without any organic heart disease. ü Non life threatening arrhythmia that could be successfully treated by either AAA or Catheter ablation (WPW, fascicular VT). ü VT or VF due to an acute and reversible cause (metabolic, ischaemic…) ü patients into whom AICD would not improve survival. In conclusion, enormous progresses have been done during the past 20 years about our knowledge of cardiac arrhythmia, their significance, their mechanism and their treatment. Careful assessment of the patient status often permits to stratify the risk and to give medical advice about underwriting files of such applicants.