transtelephonic monitoring so that the parents can send rhythm strips over the telephone if they detect any slight change in the patient’s degree of well being. In this way, it is hoped that important ventricular dysrhythmias will not be missed. The title of the article is also somewhat confusing in that it lumps ventricular tachycardia and accelerated ventricular rhythm but then focuseson ventricular rhythm. If one were only to read the abstract it is possible to believe that ventricular tachycardia should not be treated as well as accelerated ventricular rhythm. I believe that ventricular tachycardia should not only be treated but should be treated vigorously and abolished in infants. Paul C. Gillette, MD
Charleston, South Carolina 26 April
1991
1. Zeigler VL, Gillette PC, Crawford FA, Wiles HB, Fyfe DA. New approaches to treatment of incessant ventricular tachycardia in the very young. J Am Co11Cardiol 1990;16:681-685.
We appreciate Dr. Gillette’s comments concerning our paper. We would start by pointing out that of 10 neonates with accelerated ventricular rhythm available for follow-up, 5 were “successfully” treated, although the indications for treatment were quite marginal. All 10 were completely asymptomatic and the fastest heart rate was 200 beats/min. The outcomes were similar in the treated and nontreated groups in that all patients are alive and well without arrhythmia and the time to resolution was similar in the groups. Clearly these data would not support a conclusion that antiarrhythmic therapy in this group is of benefit. While we agree that the number of patients is small, it represents our center’s 22-year experience with an arrhythmia that is rare in neonates. Considering the well-recognized benign nature of accelerated ventricular rhythm in children and adults as well as the increasingly well-recognized risks of proarrhythmia associated with the use of antiarrhythmic agents, we do not feel that our recommendation to withhold therapy in neonates is so “sweeping.” REPLY:
Concerning the issue of echocardiography, we perhaps did not supply sufficient details. All infants were thought to have structurally normal hearts on physical examination, chest roentgenogram and, in 10 patients, by the most advanced echocardiography available at the time. Infants 1 and 2, presenting in 1972 and 1974, did not have echocardiograms; however, they died of unrelated conditions. To put it more precisely, echocardiograms were normal in the 10 patients available for follow-up. All 10 have had follow-up to the present and are still considered to have structurally normal hearts. The reason for the use of digoxin in the neonate with long QT syndrome is readily explained. In 1968, he was referred from another hospital where he had been successfully treated with digoxin for whathad been diagnosed as supraventricular tachycardia but was actually polymorphous ventricular tachycardia. Conventional wisdom dictated against the use of digoxin in ventricular tachycardia, consequently it was discontinued when he was transferred to UCSF. His arrhythmia recurred and required cardioversion. Therapeutic trials with several other agents including propanalol proved unsuccessful and the patient required multiple cardioversions. In desperation, digoxin was reinstituted with complete control of the arrhythmia. In contrast, the reason for the use of digoxin in 3 patients with accelerated ventricular rhythm was not always clear from the record. In 1, there were associated premature atria1 contractions. In another, the diagnosis was initially thought to be junctional tachycardia, but the correct diagnosis was established when clear fusion complexes were seen. In a third, the diagnosis was known to be acceleratedventricular rhythm, and the attending cardiologist chose digoxin. Dr. Gillette’s careful approach to neonateswith accelerated ventricular rhythm is similar to ours. The principle difference seemsto be Dr. Gillette’s greater concern about possible progression to true ventricular tachycardia. We have not observedsuch a progression in our 22-
year experience, but our hospital was not a major referral center for pediatric arrhythmias during the period of the study. The purpose of our article was to report our total long-term experiencewith ventricular dysrhythmias presenting in neonates and to contrast the differences between ventricular tachycardia and accelerated ventricular rhythm in this age group. It is unfortunate that there was some confusion about the recommendations made concerning treatment. Perhapsthis is due to the emphasis on the benign nature of accelerated ventricular rhythm and only brief comments about the treatment of ventricular tachycardia. We never meant to suggestthat ventricular tachycardia should be left untreated. The final sentenceof the abstract and the final paragraph of the article both clearly refer to withholding treatment in accelerated ventricular rhythm. This recommendation does not apply to true ventricular tachycardia in neonates, which should be treated vigorously. George F. Van Hare, MO San Francisco, California
24 June 1991
Mechanical Failure of a St. Jude Medical Prosthesis
The recent report by Orsinelli and co-authors’ about the fracture of 1 leaflet of a St. Jude Medical prosthesis again raises the problem of mechanical failure of all humanmade devices; some are less prone to these failures than others, but none can be completely free from them. Four years ago, in Johannesburg, I observed the case of a St. Jude Medical prosthesis which, during implantation, had a fracture remarkably similar to that published by Orsinelli et al (Figure 1). The valve had just been implanted by a very senior surgeon who categorically denied that any undue force had been applied. Of importance is that this obviously very delicate prosthesishas weaknesses,one of which appears to be in the longitudinal line, just outside the pivots. It is not unlikely that in the case READERS COMMENTS
841
cells,’ vascular smooth muscle cells (Figure 8b in Reference l), and with myofibroblasts in juvenile xanthogranuloma.2,3 Having used this antibody, Amano et al4 visualized not only macrophages, but also vascular endothelial structures and, most probably, also immature smooth muscle cells. This is evidenced by a presenceof immunoreactive elongated vascular structures incompatible with macrophages in their Figures lb and 2a. In return, the investigators4 raise an extremely important and intriguing question: Why do foam cells disappear successively from the intimal thickening in vein autografts while these cells are present in arterial atherosclerosis? One feels intuitively that this phenomenon must be related to an increase of the intraluminal pressure and, consequently, to an increase of the circumferential tension in aortocoronary bypass vein autografts. Increased circumferential tension results from a passive stretching of the vascular wall or from its active contraction and leads to a formation of compensatory intimal thickening.s Undifferentiated mesenchymal cells migrate into the inti1. Orsinelli DA, Becker RC, Cuenoud ma and, being “stretched,” start to HF, Noran JM. Mechanical failure of a form cytoplasmic myofilaments6 in St. Jude Medical prosthesis. Am J Curorder to compensate the increased diol 1991:67:906-908. circumferential tension. This accelerates their differentiation into smooth muscle cells and shortens Antibody HAMS6 is Not the period during which they are Macrophage-Specific in able to carry out lipid phagocytokin Autografts sis.7In contrast, the arterial intima is protected from stretch by the Antibody HAM56 is not macro- well-adapted media and its cells are phage-specific because it cross-re- not stimulated urgently to build up smooth muscle myofilaments. acts with vascular endothelial reported by Orsinelli et al the valve could have been damaged at the time of implantation. Whatever the case, the leaflets are susceptible to intrinsic or extrinsic strain and can break. This may occur early, as in our case,where the prosthesis could have been explanted immediately-or later, as in Orsinelli’s case, potentially leading to fatal consequences. I have also witnessed the fracture of the disc of a MedtronicHall valve, approximately 6 months after implantation. Neither case was reported in the medical literature but the manufacturers and the Food and Drug Administration were informed of both occurrences, which were the only known examples of mechanical failure among over 2,000 implantations of each one of these 2 devices. Nothing is unbreakable in this world. Prosthetic mechanical valves are obviously not exceptions. It is therefore essential to exercise the utmost care not to affect their integrity durin im lantation. ur. Anhnsr,mD.m University of Coimbra Coimbra, Portugal 14 June 1991
842
THE AMERICAN JOURNAL OF CARDIOLOGY VOLUME 68
SEPTEMBER 15. 1991
Instead, they phagocytize lipids which maintain their intracellular cyclic adenosine monophosphate at a low level7 and induce their transdifferentiation into macrophagelike cells.* JidT.Beramk,m Detroit, Michigan 21 June 1991 1. Gown AM, Tsukada T, Ross R. Human atherosclerosis. II. Immunocytochemical analysis of the cellular composition of human atherosclerotic lesions. Am J Pathof 1986;125:191-207. 2. Janney CG, Hurt MA, Santa Cruz DJ. Deep juvenile xanthogranuloma. Subcutaneous and intramuscular forms. Am J Surg Puthol 1991;15:150-159. 3. Beranek JT. Histogenesis of foam cells in xanthomas. Clin Exp Dermatol; in press. 4. Amano J, Suzuki A, Sunamori M, Tsukada T, Numano F. Cytokinetic study of aortocoronary bypass vein grafts in place for less than six months. Am .I Curdiol 1991;67:1234-1236. 5. Joshita T, Sakata N, Yoshida Y, Ooneda G. Experimental pathological study on arterial wall injury given by elevated intravascular pressure and its repairblood pressure and circumferential tension. In: Reinis Z, Pokomy J, Linhart J, Hild R, Schirger A, eds. Adaptability of Vascular Wall. Prague: Avicenum Czechoslovak Medical Press, 1980:22-24. 6. Gown AM. The mysteries of the myofibroblast (partially) unmasked. Lob Irwest 1990;63:1-3. 7. Smirnov VN, Voyno-Yasenetskaya TA, Antonov AS, Lukashev ME, Shirinsky VP, Tertov VV, Tkachuk VA. Vascular signal transduction. Ann NY Acad Sci 1990;598:167-181. 8. Lipton BH, Bensch KG, Karasek MA. Microvessel endothelial cell transdifferentiation: phenotypic characterization. Differentiation 1991;46:117-133.
Charleston, South Carolina 26 April
1991
1. Zeigler VL, Gillette PC, Crawford FA, Wiles HB, Fyfe DA. New approaches to treatment of incessant ventricular tachycardia in the very young. J Am Co11Cardiol 1990;16:681-685.
We appreciate Dr. Gillette’s comments concerning our paper. We would start by pointing out that of 10 neonates with accelerated ventricular rhythm available for follow-up, 5 were “successfully” treated, although the indications for treatment were quite marginal. All 10 were completely asymptomatic and the fastest heart rate was 200 beats/min. The outcomes were similar in the treated and nontreated groups in that all patients are alive and well without arrhythmia and the time to resolution was similar in the groups. Clearly these data would not support a conclusion that antiarrhythmic therapy in this group is of benefit. While we agree that the number of patients is small, it represents our center’s 22-year experience with an arrhythmia that is rare in neonates. Considering the well-recognized benign nature of accelerated ventricular rhythm in children and adults as well as the increasingly well-recognized risks of proarrhythmia associated with the use of antiarrhythmic agents, we do not feel that our recommendation to withhold therapy in neonates is so “sweeping.” REPLY:
Concerning the issue of echocardiography, we perhaps did not supply sufficient details. All infants were thought to have structurally normal hearts on physical examination, chest roentgenogram and, in 10 patients, by the most advanced echocardiography available at the time. Infants 1 and 2, presenting in 1972 and 1974, did not have echocardiograms; however, they died of unrelated conditions. To put it more precisely, echocardiograms were normal in the 10 patients available for follow-up. All 10 have had follow-up to the present and are still considered to have structurally normal hearts. The reason for the use of digoxin in the neonate with long QT syndrome is readily explained. In 1968, he was referred from another hospital where he had been successfully treated with digoxin for whathad been diagnosed as supraventricular tachycardia but was actually polymorphous ventricular tachycardia. Conventional wisdom dictated against the use of digoxin in ventricular tachycardia, consequently it was discontinued when he was transferred to UCSF. His arrhythmia recurred and required cardioversion. Therapeutic trials with several other agents including propanalol proved unsuccessful and the patient required multiple cardioversions. In desperation, digoxin was reinstituted with complete control of the arrhythmia. In contrast, the reason for the use of digoxin in 3 patients with accelerated ventricular rhythm was not always clear from the record. In 1, there were associated premature atria1 contractions. In another, the diagnosis was initially thought to be junctional tachycardia, but the correct diagnosis was established when clear fusion complexes were seen. In a third, the diagnosis was known to be acceleratedventricular rhythm, and the attending cardiologist chose digoxin. Dr. Gillette’s careful approach to neonateswith accelerated ventricular rhythm is similar to ours. The principle difference seemsto be Dr. Gillette’s greater concern about possible progression to true ventricular tachycardia. We have not observedsuch a progression in our 22-
year experience, but our hospital was not a major referral center for pediatric arrhythmias during the period of the study. The purpose of our article was to report our total long-term experiencewith ventricular dysrhythmias presenting in neonates and to contrast the differences between ventricular tachycardia and accelerated ventricular rhythm in this age group. It is unfortunate that there was some confusion about the recommendations made concerning treatment. Perhapsthis is due to the emphasis on the benign nature of accelerated ventricular rhythm and only brief comments about the treatment of ventricular tachycardia. We never meant to suggestthat ventricular tachycardia should be left untreated. The final sentenceof the abstract and the final paragraph of the article both clearly refer to withholding treatment in accelerated ventricular rhythm. This recommendation does not apply to true ventricular tachycardia in neonates, which should be treated vigorously. George F. Van Hare, MO San Francisco, California
24 June 1991
Mechanical Failure of a St. Jude Medical Prosthesis
The recent report by Orsinelli and co-authors’ about the fracture of 1 leaflet of a St. Jude Medical prosthesis again raises the problem of mechanical failure of all humanmade devices; some are less prone to these failures than others, but none can be completely free from them. Four years ago, in Johannesburg, I observed the case of a St. Jude Medical prosthesis which, during implantation, had a fracture remarkably similar to that published by Orsinelli et al (Figure 1). The valve had just been implanted by a very senior surgeon who categorically denied that any undue force had been applied. Of importance is that this obviously very delicate prosthesishas weaknesses,one of which appears to be in the longitudinal line, just outside the pivots. It is not unlikely that in the case READERS COMMENTS
841
cells,’ vascular smooth muscle cells (Figure 8b in Reference l), and with myofibroblasts in juvenile xanthogranuloma.2,3 Having used this antibody, Amano et al4 visualized not only macrophages, but also vascular endothelial structures and, most probably, also immature smooth muscle cells. This is evidenced by a presenceof immunoreactive elongated vascular structures incompatible with macrophages in their Figures lb and 2a. In return, the investigators4 raise an extremely important and intriguing question: Why do foam cells disappear successively from the intimal thickening in vein autografts while these cells are present in arterial atherosclerosis? One feels intuitively that this phenomenon must be related to an increase of the intraluminal pressure and, consequently, to an increase of the circumferential tension in aortocoronary bypass vein autografts. Increased circumferential tension results from a passive stretching of the vascular wall or from its active contraction and leads to a formation of compensatory intimal thickening.s Undifferentiated mesenchymal cells migrate into the inti1. Orsinelli DA, Becker RC, Cuenoud ma and, being “stretched,” start to HF, Noran JM. Mechanical failure of a form cytoplasmic myofilaments6 in St. Jude Medical prosthesis. Am J Curorder to compensate the increased diol 1991:67:906-908. circumferential tension. This accelerates their differentiation into smooth muscle cells and shortens Antibody HAMS6 is Not the period during which they are Macrophage-Specific in able to carry out lipid phagocytokin Autografts sis.7In contrast, the arterial intima is protected from stretch by the Antibody HAM56 is not macro- well-adapted media and its cells are phage-specific because it cross-re- not stimulated urgently to build up smooth muscle myofilaments. acts with vascular endothelial reported by Orsinelli et al the valve could have been damaged at the time of implantation. Whatever the case, the leaflets are susceptible to intrinsic or extrinsic strain and can break. This may occur early, as in our case,where the prosthesis could have been explanted immediately-or later, as in Orsinelli’s case, potentially leading to fatal consequences. I have also witnessed the fracture of the disc of a MedtronicHall valve, approximately 6 months after implantation. Neither case was reported in the medical literature but the manufacturers and the Food and Drug Administration were informed of both occurrences, which were the only known examples of mechanical failure among over 2,000 implantations of each one of these 2 devices. Nothing is unbreakable in this world. Prosthetic mechanical valves are obviously not exceptions. It is therefore essential to exercise the utmost care not to affect their integrity durin im lantation. ur. Anhnsr,mD.m University of Coimbra Coimbra, Portugal 14 June 1991
842
THE AMERICAN JOURNAL OF CARDIOLOGY VOLUME 68
SEPTEMBER 15. 1991
Instead, they phagocytize lipids which maintain their intracellular cyclic adenosine monophosphate at a low level7 and induce their transdifferentiation into macrophagelike cells.* JidT.Beramk,m Detroit, Michigan 21 June 1991 1. Gown AM, Tsukada T, Ross R. Human atherosclerosis. II. Immunocytochemical analysis of the cellular composition of human atherosclerotic lesions. Am J Pathof 1986;125:191-207. 2. Janney CG, Hurt MA, Santa Cruz DJ. Deep juvenile xanthogranuloma. Subcutaneous and intramuscular forms. Am J Surg Puthol 1991;15:150-159. 3. Beranek JT. Histogenesis of foam cells in xanthomas. Clin Exp Dermatol; in press. 4. Amano J, Suzuki A, Sunamori M, Tsukada T, Numano F. Cytokinetic study of aortocoronary bypass vein grafts in place for less than six months. Am .I Curdiol 1991;67:1234-1236. 5. Joshita T, Sakata N, Yoshida Y, Ooneda G. Experimental pathological study on arterial wall injury given by elevated intravascular pressure and its repairblood pressure and circumferential tension. In: Reinis Z, Pokomy J, Linhart J, Hild R, Schirger A, eds. Adaptability of Vascular Wall. Prague: Avicenum Czechoslovak Medical Press, 1980:22-24. 6. Gown AM. The mysteries of the myofibroblast (partially) unmasked. Lob Irwest 1990;63:1-3. 7. Smirnov VN, Voyno-Yasenetskaya TA, Antonov AS, Lukashev ME, Shirinsky VP, Tertov VV, Tkachuk VA. Vascular signal transduction. Ann NY Acad Sci 1990;598:167-181. 8. Lipton BH, Bensch KG, Karasek MA. Microvessel endothelial cell transdifferentiation: phenotypic characterization. Differentiation 1991;46:117-133.
