526
antibiotic prophylaxis for cardiac patients may not be cost-effective. This conclusion should be viewed in the light of prevailing medical practice in the Netherlands. The low compliance rate of 17% in a medically advanced society is a cause for concern and does not accord with other surveys with current regimens.1o The cost of widespread adoption of chemoprophylaxis has not been compared with the cost of treating an established case, and effects on the quality of life have not been defined. Another important issue in the aetiology of infective endocarditis is the dental health of the population; in countries that are less fortunate than the Netherlands in this respect the risk of endocarditis is likely to be higher. The biological properties of the causal pathogens are likewise important in any discussion of the efficacy of chemoprophylaxis for infective endocarditis. Bacteraemia is common in healthy people, whether or not they have cardiovascular abnormalities. Adherence to endocardial surfaces is an important attribute of many isolates responsible for infective endocarditis; among oral streptococci, dextranpositive strains are found more commonly among endocarditis isolates.11 The distribution of these organisms in the population at risk is another factor to be taken into account. Most expert groups have shied away from suggesting prospective controlled studies of the efficacy of chemoprophylaxis on the argument that it would require an impractically large population. Surely it is time for this negative view to be reassessed. The EC, with its 330 million inhabitants and advanced health care systems, might take the matter in hand. The doctrine of faith, hope, and charity may be a philosophy for life: it is no basis for perpetuating costly and possibly ineffective medical practices. Oakley CM. Controversies in the prophylaxis of infective endocarditis: a cardiological view. J Antimicrob Chemother 1987; 20 (suppl A): 99-104. 2. McGowan DA. A dental view of controversies in the prophylaxis of infective endocarditis. J Antimicrob Chemother 1987; 20 (suppl A): 1.
105-09. 3. Glauser MP, Francioli P. Relevance of animal models to the prophylaxis of infective endocarditis. J Antimicrob Chemother 1987; 20 (suppl A): 87-93. 4. Brooks SL. Survey of compliance with American Heart Association guidelines for prevention of bacterial endocarditis. J Am Dent Assoc 1980; 101: 41-43. 5. Finch R. Chemoprophylaxis of infective endocarditis. Scand J Infect Dis 1990; 70 (suppl): 102-10. 6. Editorial. Prophylaxis of bacterial endocarditis: faith, hope, and charitable interpretations. Lancet 1976; i: 519-20. 7. Durack DT. Prophylaxis of endocarditis. In: Mandell GL, Douglas RG, Bennett JE, eds. Principles and practice of infectious diseases. 3rd ed. New York: Churchill Livingstone, 1990: 716-21. 8. van der Meer JTM, van Wijk W, Vandenbroucke JP, Valkenburg HA,
Michel MF. Efficacy of antibiotic prophylaxis for prevention of native-valve endocarditis: nationwide case-control study in the Netherlands. Lancet 1992; 339: 135-39. 9. Bayliss R, Clarke C, Oakley CM, Somerville W, Whitfield AGW, Young SEJ. The microbiology and pathogenesis of infective endocarditis. Br Heart J 1983; 50: 513-19. 10. Shanson DC. Antibiotic prophylaxis of infective endocarditis in the United Kingdom and Europe. J Antimicrob Chemother 1987; 20 (suppl A): 119-31. 11. Parker MT, Ball LC. Streptococci and aerococci associated with systemic infection in man. J Med Microbiol 1976; 9: 275-302.
Pertussis: adults, infants, and herds The diagnosis of pertussis is in serious danger of derailment at a time when its reliability is more important than ever. Despite increasing use of serology, the gold standard for laboratory diagnosis of pertussis is bacterial culture from nasopharyngeal swabs.l Contrary to popular belief, such cultures yield positive results in as many as 80% of cases,l provided specimen collection and laboratory techniques are optimum.2 A Swedish study found an isolation rate of
70%, even though the primary plates were incubated for only 5 days.3 In typical cases of pertussis, clinical diagnosis is usually reliable; not so with milder cases of less than 3 weeks’ duration,4 and especially with adults in whom a severe cough may be the only symptom. Spasmodic cough may be caused by viruses, so laboratory confirmation is necessary. Direct fluorescent antibody testing of nasopharyngeal secretions gives falsepositive results with antigenically related organisms5,6 and cannot be relied own.7 Likewise, the specificity serological tests for pertussis antibody in secretions and serum, used in many countries, averages only 65%.1 Thus only isolation of Bordetella pertussis from individuals with symptoms of whooping cough can be regarded as proof of infection.8 In adults, after the usual catarrhal phase, painful paroxysms of cough, whoop, vomiting and may last for many weeks, although atypical illness with only a persistent cough is more common. The chain of infection usually includes young children, and intervals of 1-3 weeks between dates of onset suggest transmission to or from parent or grandparent or hospital staff. An outbreak in a Wisconsin nursing home for elderly people was typical in that there were no children:9 38 residents and 8 employees were seropositive, but only 4 (all residents) were culturepositive. Better evidence of adult infection came from Sweden, where 174 (5%) of 3488 culture-positive patients were adults (median age 35 years).1° Monthly reports from the Public Health Laboratory Service in Britain have shown a steady incidence of pertussis in adults, although such cases comprise only a small minority of the total isolates from cases of whooping cough. Other reports give little or no evidence of
(Scotland,11 Finland," reliability and the Australia,13 Japan,14 USA15). Widespread silent transmission of pertussis in families was deduced from a small American study of 18 household contacts, only 1 of whom was culture-positive.16 Further alarm comes from the Gambia,i’ with the suggestion that, as the immunity of vaccinated infants wanes, "transmission between young adults is likely to be
diagnostic
intense".
Severe
-
cough (per-tussis), possibly provoked by pertussis toxin, facilitates survival of the host by clearing the airway after the ciliated epithelium has been damaged by other toxins. However, this is not merely a display of microbial compassion: the
527
paroxysms of coughing also promote survival of the microbial species by firing large inocula at a new host. There is little evidence of symptom-free carriers,1&-.20 and, if the microbe cannot be isolated by efficient attempts at swabbing and culture, there must be little risk of dangerous dissemination.5 Pertussis is acquired mainly from cases that are typical clinically.21 Erythromycin, if given for at least 14 days, may have some therapeutic effect before the paroxysmal stage develops,22 but there have been no controlled, blinded studies of erythromycin in prevention of pertussis transmission to exposed contacts.23 All these clues suggest that the incidence of pertussis in adults is low; and infected adults usually take adequate steps to minimise transmission when
coughing.24 If adults were a major reservoir of pertussis, how would the disease have been virtually eliminated in countries that have resorted to a compulsory course of infant vaccination starting at 3 months of age?-countries that were not influenced by the scare about vaccine brain-damage. There is still no evidence of a causal relation between pertussis vaccines and permanent neurological illness;25and confidence in their safety and efficacy is increasing. In Britain, for example, the infant vaccination rate has reached an all-time high of 87%.26 Within a decade, this would give substantial herd immunity to children aged 6 months to 10 years, in whom most pertussis infection occurs; tiny babies would be protected indirectly by the absence of disease in their siblings. However, in this issue (p 507) Booy et al warn of the potential threat to such herd immunity if vaccination starts before 3 months, as now happens in the UK and is recommended by the World Health Organisation in some developing countries. Except, perhaps, for occupational groups such as obstetric and paediatric doctors and nurses, there seems no reason to advise vaccination of adults. In particular, the use of acellular pertussis vaccine can not be justified until trials in millions of vaccinees27 have shown that it is no less safe and effective than the whole-cell vaccine of countries that meet the present recommendations. 1. Cherry JD, Brunell PA, Golden GS, Karzon DT. Report of the Task Force on Pertussis and Pertussis Immunization 1988. Pediatrics 1988; 81: 939-84. 2. Abbott JD, Macaulay ME, Preston NW. Bacteriological diagnosis of whooping cough. Association of Clinical Pathologists: broadsheet 105. London: British Medical Association, 1982. 3. Granström M, Olinder-Nielsen AM, Holmblad P, Mark A, Hanngren K. Specific immunoglobulin for treatment of whooping cough. Lancet 1991; 338: 1230-33. 4. Stott NCH, Davis RH. Pertussis vaccination and pseudo whooping cough. Br Med J 1981; 282: 1871. 5. Preston NW. Pertussis today. In: Wardlaw AC, Parton R, eds. Pathogenesis and immunity in pertussis. Chichester: Wiley, 1988: 1-18. 6. Adamson PC, Wu TC, Meade BD, Rubin M, Manclark CR, Pizzo PA. Pertussis in a previously immunized child with human immunodeficiency virus infection. J Pediatr 1989; 115: 589-92. 7. Centers for Disease Control. Pertussis surveillance: United States, 1986-1988. MMWR 1990; 39: 57-66. 8. Zackrisson G, Taranger J, Trollfors B. History of whooping cough in nonvaccinated Swedish children, related to serum antibodies to pertussis toxin and filamentous hemagglutinin. J Pediatr 1990; 116: 190-94.
9. Addiss DG, Davis JP, Meade BD, et al. A pertussis outbreak in a Wisconsin nursing home. J Infect Dis 1991; 164: 704-10. 10. Trollfors B, Rabo E. Whooping cough in adults. Br Med J 1981; 283: 696-97. 11. MacLean DW. Adults with pertussis. J R Coll Gen Pract 1982; 32: 298-300. 12. Mertsola J, Ruuskanen O, Eerola E, Viljanen MK. Intrafamilial spread of pertussis. J Pediatr 1983; 103: 359-63. 13. Robertson PW, Goldberg H, Jarvie BH, Smith DD, Whybin LR. Bordetella pertussis infection: a cause of persistent cough in adults. Med J Aust 1987; 146: 522-25. 14. Aoyama T, Goto R, Iwai H, Murase Y, Iwata T. Pertussis in the adult. Sixth International Symposium on Pertussis. Bethesda: United States Public Health Service (DHHS Publication no FDA 90-1162), 1990: 249-50 (abstr). 15. Mortimer EA. Pertussis and its prevention: a family affair. J Infect Dis 1990; 161: 473-79 16. Long SS, Welkon CJ, Clark JL. Widespread silent transmission of pertussis in families: antibody correlates of infection and symptomatology. J Infect Dis 1990; 161: 480-86. 17. Mulholland EK. Pertussis vaccine: a time-bomb? Lancet 1990; 335: 1592. 18. Krantz I, Alestig K, Trollfors B, Zackrisson G. The carrier state in pertussis. Scand J Infect Dis 1986; 18: 121-23. 19. Jenkinson D, Pepper JD. A search for subclinical infection during a small outbreak of whooping cough: implications for clinical diagnosis. J R Coll Gen Pract 1986; 36: 547-48. 20. Bass JW. Is there a carrier state in pertussis? Lancet 1987; i: 96. 21. Thomas MG, Lambert HP. From whom do children catch pertussis? Br Med J 1987; 295: 751-52. 22. Bass JW. Erythromycin for pertussis: probable reasons for past failures. Lancet 1985; ii: 147. 23. Health and Welfare Canada. Statement on management of persons exposed to pertussis and pertussis outbreak control. Canada Dis Weekly Rep 1990; 27: 127-30. 24. Williams WO. Whooping cough in adults. Br Med J 1981; 283: 1122. 25. Cherry JD. ’Pertussis vaccine encephalopathy’: it is time to recognize it as the myth that it is. JAMA 1990; 263: 1679-80. 26. White JM, Hobday S, Begg NT. ’COVER’ (Cover of vaccination evaluated rapidly): 19. Comm Dis Rep 1991; 1: R140. 27. Baxter DN, Gibbs ACC. How are the sub-unit pertussis vaccines to be evaluated? Epidemiol Infect 1987; 99: 477-84.
Antitachycardia devices The first reports of pacing for termination of tachycardia appeared in the 1960s1; and in the early 1980s, with the development of implantable antitachycardia pacemakers, long-term use of antitachycardia pacing became a practicable means of arrhythmia control. Yet, despite these developments, use of the technique was restricted to very small numbers of patients. Why was enthusiasm for long-term antitachycardia pacing so limited? The therapy is invasive and also time-consuming because the device has to be programmed individually. With atrial antitachycardia pacing there was the risk of atrial fibrillation and induction of ventricular fibrillation in patients with accessory pathways.With ventricular tachycardia the risk of heart rate accelerationwas felt to be unacceptable. Long-term efficacy of the technique was limited4 and, because attacks were terminated rather than prevented, symptoms were not always alleviated. For supraventricular arrhythmias introduction of radiofrequency methods for atrioventricular node modification and for ablation of accessory pathways has reduced the use of the technique even further. By contrast, a sharp increase in antitachycardia pacing for ventricular arrhythmias seems likely to occur as a result of the development of implantable cardioverter defibrillators (ICDs) with antitachycardia pacing
antibiotic prophylaxis for cardiac patients may not be cost-effective. This conclusion should be viewed in the light of prevailing medical practice in the Netherlands. The low compliance rate of 17% in a medically advanced society is a cause for concern and does not accord with other surveys with current regimens.1o The cost of widespread adoption of chemoprophylaxis has not been compared with the cost of treating an established case, and effects on the quality of life have not been defined. Another important issue in the aetiology of infective endocarditis is the dental health of the population; in countries that are less fortunate than the Netherlands in this respect the risk of endocarditis is likely to be higher. The biological properties of the causal pathogens are likewise important in any discussion of the efficacy of chemoprophylaxis for infective endocarditis. Bacteraemia is common in healthy people, whether or not they have cardiovascular abnormalities. Adherence to endocardial surfaces is an important attribute of many isolates responsible for infective endocarditis; among oral streptococci, dextranpositive strains are found more commonly among endocarditis isolates.11 The distribution of these organisms in the population at risk is another factor to be taken into account. Most expert groups have shied away from suggesting prospective controlled studies of the efficacy of chemoprophylaxis on the argument that it would require an impractically large population. Surely it is time for this negative view to be reassessed. The EC, with its 330 million inhabitants and advanced health care systems, might take the matter in hand. The doctrine of faith, hope, and charity may be a philosophy for life: it is no basis for perpetuating costly and possibly ineffective medical practices. Oakley CM. Controversies in the prophylaxis of infective endocarditis: a cardiological view. J Antimicrob Chemother 1987; 20 (suppl A): 99-104. 2. McGowan DA. A dental view of controversies in the prophylaxis of infective endocarditis. J Antimicrob Chemother 1987; 20 (suppl A): 1.
105-09. 3. Glauser MP, Francioli P. Relevance of animal models to the prophylaxis of infective endocarditis. J Antimicrob Chemother 1987; 20 (suppl A): 87-93. 4. Brooks SL. Survey of compliance with American Heart Association guidelines for prevention of bacterial endocarditis. J Am Dent Assoc 1980; 101: 41-43. 5. Finch R. Chemoprophylaxis of infective endocarditis. Scand J Infect Dis 1990; 70 (suppl): 102-10. 6. Editorial. Prophylaxis of bacterial endocarditis: faith, hope, and charitable interpretations. Lancet 1976; i: 519-20. 7. Durack DT. Prophylaxis of endocarditis. In: Mandell GL, Douglas RG, Bennett JE, eds. Principles and practice of infectious diseases. 3rd ed. New York: Churchill Livingstone, 1990: 716-21. 8. van der Meer JTM, van Wijk W, Vandenbroucke JP, Valkenburg HA,
Michel MF. Efficacy of antibiotic prophylaxis for prevention of native-valve endocarditis: nationwide case-control study in the Netherlands. Lancet 1992; 339: 135-39. 9. Bayliss R, Clarke C, Oakley CM, Somerville W, Whitfield AGW, Young SEJ. The microbiology and pathogenesis of infective endocarditis. Br Heart J 1983; 50: 513-19. 10. Shanson DC. Antibiotic prophylaxis of infective endocarditis in the United Kingdom and Europe. J Antimicrob Chemother 1987; 20 (suppl A): 119-31. 11. Parker MT, Ball LC. Streptococci and aerococci associated with systemic infection in man. J Med Microbiol 1976; 9: 275-302.
Pertussis: adults, infants, and herds The diagnosis of pertussis is in serious danger of derailment at a time when its reliability is more important than ever. Despite increasing use of serology, the gold standard for laboratory diagnosis of pertussis is bacterial culture from nasopharyngeal swabs.l Contrary to popular belief, such cultures yield positive results in as many as 80% of cases,l provided specimen collection and laboratory techniques are optimum.2 A Swedish study found an isolation rate of
70%, even though the primary plates were incubated for only 5 days.3 In typical cases of pertussis, clinical diagnosis is usually reliable; not so with milder cases of less than 3 weeks’ duration,4 and especially with adults in whom a severe cough may be the only symptom. Spasmodic cough may be caused by viruses, so laboratory confirmation is necessary. Direct fluorescent antibody testing of nasopharyngeal secretions gives falsepositive results with antigenically related organisms5,6 and cannot be relied own.7 Likewise, the specificity serological tests for pertussis antibody in secretions and serum, used in many countries, averages only 65%.1 Thus only isolation of Bordetella pertussis from individuals with symptoms of whooping cough can be regarded as proof of infection.8 In adults, after the usual catarrhal phase, painful paroxysms of cough, whoop, vomiting and may last for many weeks, although atypical illness with only a persistent cough is more common. The chain of infection usually includes young children, and intervals of 1-3 weeks between dates of onset suggest transmission to or from parent or grandparent or hospital staff. An outbreak in a Wisconsin nursing home for elderly people was typical in that there were no children:9 38 residents and 8 employees were seropositive, but only 4 (all residents) were culturepositive. Better evidence of adult infection came from Sweden, where 174 (5%) of 3488 culture-positive patients were adults (median age 35 years).1° Monthly reports from the Public Health Laboratory Service in Britain have shown a steady incidence of pertussis in adults, although such cases comprise only a small minority of the total isolates from cases of whooping cough. Other reports give little or no evidence of
(Scotland,11 Finland," reliability and the Australia,13 Japan,14 USA15). Widespread silent transmission of pertussis in families was deduced from a small American study of 18 household contacts, only 1 of whom was culture-positive.16 Further alarm comes from the Gambia,i’ with the suggestion that, as the immunity of vaccinated infants wanes, "transmission between young adults is likely to be
diagnostic
intense".
Severe
-
cough (per-tussis), possibly provoked by pertussis toxin, facilitates survival of the host by clearing the airway after the ciliated epithelium has been damaged by other toxins. However, this is not merely a display of microbial compassion: the
527
paroxysms of coughing also promote survival of the microbial species by firing large inocula at a new host. There is little evidence of symptom-free carriers,1&-.20 and, if the microbe cannot be isolated by efficient attempts at swabbing and culture, there must be little risk of dangerous dissemination.5 Pertussis is acquired mainly from cases that are typical clinically.21 Erythromycin, if given for at least 14 days, may have some therapeutic effect before the paroxysmal stage develops,22 but there have been no controlled, blinded studies of erythromycin in prevention of pertussis transmission to exposed contacts.23 All these clues suggest that the incidence of pertussis in adults is low; and infected adults usually take adequate steps to minimise transmission when
coughing.24 If adults were a major reservoir of pertussis, how would the disease have been virtually eliminated in countries that have resorted to a compulsory course of infant vaccination starting at 3 months of age?-countries that were not influenced by the scare about vaccine brain-damage. There is still no evidence of a causal relation between pertussis vaccines and permanent neurological illness;25and confidence in their safety and efficacy is increasing. In Britain, for example, the infant vaccination rate has reached an all-time high of 87%.26 Within a decade, this would give substantial herd immunity to children aged 6 months to 10 years, in whom most pertussis infection occurs; tiny babies would be protected indirectly by the absence of disease in their siblings. However, in this issue (p 507) Booy et al warn of the potential threat to such herd immunity if vaccination starts before 3 months, as now happens in the UK and is recommended by the World Health Organisation in some developing countries. Except, perhaps, for occupational groups such as obstetric and paediatric doctors and nurses, there seems no reason to advise vaccination of adults. In particular, the use of acellular pertussis vaccine can not be justified until trials in millions of vaccinees27 have shown that it is no less safe and effective than the whole-cell vaccine of countries that meet the present recommendations. 1. Cherry JD, Brunell PA, Golden GS, Karzon DT. Report of the Task Force on Pertussis and Pertussis Immunization 1988. Pediatrics 1988; 81: 939-84. 2. Abbott JD, Macaulay ME, Preston NW. Bacteriological diagnosis of whooping cough. Association of Clinical Pathologists: broadsheet 105. London: British Medical Association, 1982. 3. Granström M, Olinder-Nielsen AM, Holmblad P, Mark A, Hanngren K. Specific immunoglobulin for treatment of whooping cough. Lancet 1991; 338: 1230-33. 4. Stott NCH, Davis RH. Pertussis vaccination and pseudo whooping cough. Br Med J 1981; 282: 1871. 5. Preston NW. Pertussis today. In: Wardlaw AC, Parton R, eds. Pathogenesis and immunity in pertussis. Chichester: Wiley, 1988: 1-18. 6. Adamson PC, Wu TC, Meade BD, Rubin M, Manclark CR, Pizzo PA. Pertussis in a previously immunized child with human immunodeficiency virus infection. J Pediatr 1989; 115: 589-92. 7. Centers for Disease Control. Pertussis surveillance: United States, 1986-1988. MMWR 1990; 39: 57-66. 8. Zackrisson G, Taranger J, Trollfors B. History of whooping cough in nonvaccinated Swedish children, related to serum antibodies to pertussis toxin and filamentous hemagglutinin. J Pediatr 1990; 116: 190-94.
9. Addiss DG, Davis JP, Meade BD, et al. A pertussis outbreak in a Wisconsin nursing home. J Infect Dis 1991; 164: 704-10. 10. Trollfors B, Rabo E. Whooping cough in adults. Br Med J 1981; 283: 696-97. 11. MacLean DW. Adults with pertussis. J R Coll Gen Pract 1982; 32: 298-300. 12. Mertsola J, Ruuskanen O, Eerola E, Viljanen MK. Intrafamilial spread of pertussis. J Pediatr 1983; 103: 359-63. 13. Robertson PW, Goldberg H, Jarvie BH, Smith DD, Whybin LR. Bordetella pertussis infection: a cause of persistent cough in adults. Med J Aust 1987; 146: 522-25. 14. Aoyama T, Goto R, Iwai H, Murase Y, Iwata T. Pertussis in the adult. Sixth International Symposium on Pertussis. Bethesda: United States Public Health Service (DHHS Publication no FDA 90-1162), 1990: 249-50 (abstr). 15. Mortimer EA. Pertussis and its prevention: a family affair. J Infect Dis 1990; 161: 473-79 16. Long SS, Welkon CJ, Clark JL. Widespread silent transmission of pertussis in families: antibody correlates of infection and symptomatology. J Infect Dis 1990; 161: 480-86. 17. Mulholland EK. Pertussis vaccine: a time-bomb? Lancet 1990; 335: 1592. 18. Krantz I, Alestig K, Trollfors B, Zackrisson G. The carrier state in pertussis. Scand J Infect Dis 1986; 18: 121-23. 19. Jenkinson D, Pepper JD. A search for subclinical infection during a small outbreak of whooping cough: implications for clinical diagnosis. J R Coll Gen Pract 1986; 36: 547-48. 20. Bass JW. Is there a carrier state in pertussis? Lancet 1987; i: 96. 21. Thomas MG, Lambert HP. From whom do children catch pertussis? Br Med J 1987; 295: 751-52. 22. Bass JW. Erythromycin for pertussis: probable reasons for past failures. Lancet 1985; ii: 147. 23. Health and Welfare Canada. Statement on management of persons exposed to pertussis and pertussis outbreak control. Canada Dis Weekly Rep 1990; 27: 127-30. 24. Williams WO. Whooping cough in adults. Br Med J 1981; 283: 1122. 25. Cherry JD. ’Pertussis vaccine encephalopathy’: it is time to recognize it as the myth that it is. JAMA 1990; 263: 1679-80. 26. White JM, Hobday S, Begg NT. ’COVER’ (Cover of vaccination evaluated rapidly): 19. Comm Dis Rep 1991; 1: R140. 27. Baxter DN, Gibbs ACC. How are the sub-unit pertussis vaccines to be evaluated? Epidemiol Infect 1987; 99: 477-84.
Antitachycardia devices The first reports of pacing for termination of tachycardia appeared in the 1960s1; and in the early 1980s, with the development of implantable antitachycardia pacemakers, long-term use of antitachycardia pacing became a practicable means of arrhythmia control. Yet, despite these developments, use of the technique was restricted to very small numbers of patients. Why was enthusiasm for long-term antitachycardia pacing so limited? The therapy is invasive and also time-consuming because the device has to be programmed individually. With atrial antitachycardia pacing there was the risk of atrial fibrillation and induction of ventricular fibrillation in patients with accessory pathways.With ventricular tachycardia the risk of heart rate accelerationwas felt to be unacceptable. Long-term efficacy of the technique was limited4 and, because attacks were terminated rather than prevented, symptoms were not always alleviated. For supraventricular arrhythmias introduction of radiofrequency methods for atrioventricular node modification and for ablation of accessory pathways has reduced the use of the technique even further. By contrast, a sharp increase in antitachycardia pacing for ventricular arrhythmias seems likely to occur as a result of the development of implantable cardioverter defibrillators (ICDs) with antitachycardia pacing
