- Email: [email protected]
defibrillator
954
CASE REPORT CHEKANOV ET AL MULTIDEVICE IMPLANTATION FOR CARDIOMYOPATHY
5. Dennstedt FE, Weilbaecher DG. Tophaceous mitral valve. Report of a case. Am J Surg Pathol 1982;6:79– 81. 6. Bunim JJ, McEwen C. Tophus of the mitral valve in gout. Arch Pathol 1940;29:700– 4. 7. Reynolds C, Tazelaar HD, Edwards WD. Calcified amorphous tumor of the heart. Hum Pathol 1997;28:601– 6. 8. Slavin RE, Wen J, Kumar D, Evans EB. Familial tumoral calcinosis. A clinical, histopathologic, and ultrastructural study with an analysis of its calcifying process and pathogenesis. Am J Surg Pathol 1993;17:788 – 802.
Cardiomyoplasty After Implantation of a Pacemaker and Cardioverter/Defibrillator Valeri S. Chekanov, MD, PhD, Sanjay Deshpande, MD, David Francischelli, MS, Paul Werner, MD, Deborah Waller, RN, and Donald H. Schmidt, MD Milwaukee Heart Institute, Milwaukee, Wisconsin
Presently, a combination of two surgical methods improves the survival of patients with advanced ventricular dysfunction: implantable cardioverter/defibrillator implantation (which prevents sudden cardiac death) and cardiomyoplasty (which prevents further dilatation of the heart and provides additional cardiac assistance). We report the clinical course of a patient who had cardiomyoplasty after cardioverter/defibrillator implantation and pacemaker insertion. It is a rare case in which three different devices cardioverter/defibrillator, pacemaker, and cardiomyostimulator) are functioning together without crosstalk. (Ann Thorac Surg 1998;66:954 – 6) © 1998 by The Society of Thoracic Surgeons
E
nd-stage congestive heart failure continues to be a major challenge in health care. Survival of patients with advanced ventricular dysfunction is limited not only by progressive pump dysfunction, but also by the risk of sudden cardiac death [1]. Despite the use of optimal medical therapy with resultant improvement in functional class and a significant reduction in total mortality, sudden death remains a considerable risk in 26% to 28% of these patients [2]. The principal mechanism of sudden cardiac death in this population remains arrhythmia, with ventricular tachycardia that degenerates into ventricular fibrillation being the most common cause [3]. Bradyarrhythmic cardiac arrest and electromechanical dissociation are also well described and may be more common in idiopathic dilated cardiomyopathy [4]. Presently two surgical methods seem to improve the survival of patients with advanced ventricular dysfunction: implantable cardioverter/defibrillator (ICD) implantation (which prevents the sudden cardiac death)
Ann Thorac Surg 1998;66:954 – 6
and cardiomyoplasty (which prevents further dilatation of the heart and provides additional cardiac assistance). Dynamic cardiomyoplasty is emerging as a promising form of surgical therapy for patients with advanced ventricular dysfunction [5]. However, sudden cardiac death remains a major cause of attrition in long-term survival in patients that have had cardiomyoplasty [6]. In contrast to empirical or electrophysiologically guided antiarrhythmic drug therapy, the ICD appears to have the most optimal outcome in sudden death reduction in this population. Sudden cardiac death rates at 5 years after ICD implantation have been reported to be impressively low (about 4.5%) [4]. The ICD therefore appears to be the optimal additional operation in high-risk patients undergoing dynamic cardiomyoplasty. Recently, ICD implantation after cardiomyoplasty has been recommended for prevention of sudden cardiac death in patients with a history of sudden death or episodes of ventricular tachycardia [7, 8]. Several patients have already received an ICD implantation after successful dynamic cardiomyoplasty. Three of these patients are from The Milwaukee Heart Institute of Sinai Samaritan Medical Center in Milwaukee, Wisconsin [9]. The following case report describes the clinical course of a patient who had cardiomyoplasty after ICD implantation and pacemaker insertion. In this patient three different devices (ICD, pacemaker, and cardiomyostimulator) are functioning together without crosstalk (crosstalk is the sensing of the output of one device by another channel in the same or another device). We propose that this combined therapy may improve survival in patients who are deemed to be at high risk for sudden death after cardiomyoplasty. A 38-year-old male patient was hospitalized at Sinai Samaritan Medical Center in Milwaukee, Wisconsin, for worsening shortness of breath and palpitations. He was found to be in monomorphic ventricular tachycardia. During evaluation of his cardiac status, he was found to have idiopathic cardiomyopathy with an ejection fraction of 0.40. He had electrophysiologic studies and subsequent serial drug testing to determine effective therapy for ventricular tachycardia. Unfortunately, despite a trial of three drugs, the ventricular tachycardia remained inducible. Implantation of an ICD (Medtronic PCD, model 7218B; Medtronic, Inc, Minneapolis, MN) was performed on March 11, 1992. The defibrillation threshhold was 18 joules. Three years after ICD implantation, this patient was doing well and had no further episodes of arrhythmias or ICD discharges. Multigated acquisition scans showed an ejection fraction of 0.51. Then, newonset atrial fibrillation developed with a ventricular response of 60 to 70 beats/min. The patient underwent direct-current cardioversion and was converted to sinus rhythm. Six months later, a permanent dual-chamber pacemaker insertion was recommended for treatment of
Accepted for publication April 8, 1998. Address reprint requests to Dr Chekanov, Winter Research Bldg, 836 N 12th St, Milwaukee, WI 53233.
© 1998 by The Society of Thoracic Surgeons Published by Elsevier Science Inc
David Francischelli is an employee of Medtronic, Inc.
0003-4975/98/$19.00 PII S0003-4975(98)00568-2
Ann Thorac Surg 1998;66:954 – 6
symptomatic sinus bradycardia and complete atrioventricular block. A Medtronic pulse generator, model 7950, was implanted and programmed in a DDDR mode. After pacemaker implantation, no interaction between the ICD and the pacemaker was noted during evaluation of the ICD, both in paced rhythm and during induced ventricular fibrillation. The pacemaker was programmed to DDDR mode with a lower rate of 60 beats/min and an upper rate of 120 beats/min. Over the 5 years after the first examination (March 1992), this patient’s cardiac status progressively declined. He reverted to atrial fibrillation and had development of nocturnal dyspnea and pedal edema. Medications were amiodarone, 200 mg daily; enalapril, 15 mg daily; synthroid, 0.0375 mg daily; digoxin, 0.125 mg daily; warfarin, 4 mg daily; furosemide, 40 mg twice a day; and potassium chloride (K-Dur; Key Pharmaceuticals, Kenilworth, NJ) 20 mEq twice a day. Cardiac catheterization revealed normal coronary arteries, a severely, diffusely reduced ejection fraction calculated at 0.20, and no mitral regurgitation. The right ventricular pressure was 50/25 mm Hg, pulmonary artery pressure was 51/30 mm Hg, and the pulmonary capillary wedge pressure mean was 31 mm Hg. On February 10, 1997, dynamic cardiomyoplasty was performed using the left latissimus dorsi posterior muscle wrap. A Medtronic cardiomyostimulator model 4710 was implanted. Two weeks later, the ICD generator was replaced (because of battery depletion). Interaction between the pacemaker, ICD, and cardiomyostimulator was evaluated at implantation. No evidence of crosstalk was exhibited. Simultaneously, electrical training (via cardiomyostimulator) of the latissimus dorsi muscle wrap was started per protocol. Two days later, polymorphic sustained ventricular tachycardia developed, resulting in four ICD discharges (related to hypokalemia and hypomagnesemia). This ventricular tachyarrhythmia was promptly detected and no crosstalk was evident. With supplementation of potassium and magnesium, the ventricular tachycardia resolved and the ICD did not discharge again. The patient was discharged home, being paced by his defibrillator in a VVI mode. His pacemaker was effectively inactive, because its low rate was less than that of the ICD’s VVI system. During the following 3 months, this patient improved clinically. He progressed from a New York Heart Association class III to a class II level of functioning. His diuretic and corresponding potassium and magnesium supplementation declined. His quality of life improved remarkably. Concomitantly during these same 3 months, his cardiomyostimulator settings were changing per protocol. With each cardiomyostimulator programming, the defibrillator was also interrogated and both devices were checked for crosstalk. As the cardiomyostimulator train of impulses was increased, the pacing pulse of the ICD was intermittently sensed by the cardiomyostimulator. This was most likely caused by changes in threshold and amplitude as the cardiomyoplasty sensing leads matured within the myocardium. Three remedies were considered: (1) reduction of the amplitude or pulse width of the ICD pacing pulse, (2) reduction of the sensitivity of the
CASE REPORT CHEKANOV ET AL MULTIDEVICE IMPLANTATION FOR CARDIOMYOPATHY
955
cardiomyostimulator, or (3) VVI pacing via the cardiomyostimulator. However, the patient’s clinical condition had improved to the point that the decision was made to give him the benefit of VVIR pacing. His existing permanent pacemaker was activated 4 months after cardiomyoplasty. Again, no interaction was demonstrable between the three functioning devices in follow-up. He has continued to improve and is now functioning in New York Heart Association class I.
Comment Sudden cardiac death remains a significant contributor to mortality in patients with advanced ventricular dysfunction. Although dynamic cardiomyoplasty may provide improvement in hemodynamic status and functional class, the risk of sudden death remains a vexing problem. Antiarrhythmic drug therapy alone does not appear to extend a favorable outcome because of several limitations. It is anticipated that the ICD used in conjunction with dynamic cardiomyoplasty will favorably affect survival by reducing the risk of arrhythmic death in patients with advanced ventricular dysfunction. The timing of ICD implantation in relationship to dynamic cardiomyoplasty needs to be individualized. Cardiomyoplasty may be performed in patients who have already had ICD implantation. Alternatively, ICD implantation may be performed concomitantly or soon after a cardiomyoplasty operation. In some high-risk patients, ventricular tachycardia or cardiac arrest has not recurred after cardiomyoplasty, perhaps as a result of improvement in hemodynamics, ventricular stretch, or autonomic imbalance. However, long-term data are not available and the number of patients reported is small. Implantation of an ICD should not be deferred in these individuals, because the antiarrhythmic effect of cardiomyoplasty cannot be accurately predicted. At the present time, there is little published information about the potential interactions between the ICD and the cardiomyoplasty system. Provided care is taken during implantation to ensure that such interaction does not occur, ongoing follow-up should parallel the results of concomitant ICD and pacemaker implantation.
References 1. Schocken DD, Arrieta MI, Leaverton PE, Ross EA. Prevalence and mortality rate of congestive heart failure in the United States. J Am Coll Cardiol 1991;20:301– 6. 2. Greene HL. Clinical significance and management of arrhythmias in heart failure patient. Clin Cardiol 1992;15(Suppl 1): 13–21. 3. Luu M, Stevenson WG, Baron K, Walden J. Diverse mechanisms of unexpected cardiac arrest in advanced heart failure. Circulation 1989;80:1675– 80. 4. Akhtar M, Avitall B, Jazayeri M, et al. Role of implantable cardioverter-defibrillator therapy in the management of high risk patients. Circulation 1992;85(Suppl 1):1131–9. 5. Chachques JC, Berrebi A, Hernigon A, et al. Study of muscular and ventricular function in dynamic cardiomyoplasty: a ten year follow-up. J Heart Lung Transplant 1997;6:854– 67. 6. Magovern J, Magovern GJ Sr, Maher TD, et al. Operation for
956
CASE REPORT CHEKANOV ET AL MULTIDEVICE IMPLANTATION FOR CARDIOMYOPATHY
congestive heart failure: transplantation, coronary artery bypass, and cardiomyoplasty. Ann Thorac Surg 1993;56:418–25. 7. Thakur RK, Chow LH, Guiraudon GM, et al. Latissimus dorsi dynamic cardiomyoplasty: role of combined ICD implantation. J Card Surg 1995;10:295–7. 8. Francischelli D, Peterson D, Stein P, Gealow K, Grandjean P.
Ann Thorac Surg 1998;66:954 – 6
Cardiomyoplasty and defibrillator: a combined treatment for heart failure. In: Carpentier A, Chachques GC, Grandjean P, eds. Cardiac bioassist. Armonk, NY: Futura, 1997:417–28. 9. Chekanov VS, Deshpande S, Schmidt DH. Cardiomyoplasty combined with implantation of cardioverter-defibrillator. J Thorac Cardiovasc Surg 1997;114:489–91
New Requirements for Recertification in the Year 2001 Diplomates of the American Board of Thoracic Surgery who plan to participate in the recertification process within the next few years should pay particular attention to this notice, because the requirements will change effective in the year 2001. In addition to an active medical license and institutional clinical privileges in thoracic surgery, beginning in 2001, a valid certificate will be an absolute requirement for entrance into the recertification process. If your certificate has expired, the only pathway for renewal of a certificate will be to take and pass the Part I (written) and the Part II (oral) certifying examinations. In 2001, the American Board of Thoracic Surgery will no longer publish the names of individuals who have not recertified. In the past, a designation of “NR” (not See also page 693. recertified) was used in the American Board of Medical Specialties directories if a Diplomate had not recertified. The Diplomate’s name will be published upon successful completion of the recertification process. The CME requirements will also change in 2001. The new CME requirements will be 70 Category I credits in either cardiothoracic surgery or general surgery earned during the 2 years prior to applying for recertification. SESATS and SESAPS will be the only self-instructional material allowed for credit. No Category II credits will be allowed. The Physicians Recognition Award for recertifying in general surgery will not be accepted in fulfillment of the CME requirement for recertification. The preceding information only partially outlines the CME requirements. Interested
© 1998 by The Society of Thoracic Surgeons Published by Elsevier Science Inc
individuals should refer to the 1999 Booklet of Information for a complete description of acceptable CME credits. Diplomates should maintain a documented list of their major cases performed during the year prior to application for recertification. This practice review should consist of 1 year’s consecutive major operative experiences. If more than 100 cases occur in 1 year, only 100 should be listed. Candidates for recertification will be required to complete both the general thoracic and the cardiac portions of the SESATS self-assessment examination. It is not necessary for candidates to purchase SESATS prior to applying for recertification because SESATS will be sent to candidates after their application has been approved. Diplomates may recertify up to 3 years before the expiration of their certificate. Their new certificate will be dated 10 years from the time of expiration of their original certificate or most recent recertification certificate. In other words, recertifying early does not alter the 10-year validation. Recertification is also open to Diplomates with an unlimited certificate and will in no way affect the validity of their original certificate. The deadline for submission of applications for the recertification process is May 1 of each year. A recertification brochure outlining the rules and requirements for recertification in thoracic surgery is available upon request from the American Board of Thoracic Surgery, One Rotary Center, Suite 803, Evanston, IL 60201; telephone number: (847) 475-1520; fax: (847) 475-6240; e-mail: [email protected]..
Ann Thorac Surg 1998;66:956
•
0003-4975/98/$19.00
CASE REPORT CHEKANOV ET AL MULTIDEVICE IMPLANTATION FOR CARDIOMYOPATHY
5. Dennstedt FE, Weilbaecher DG. Tophaceous mitral valve. Report of a case. Am J Surg Pathol 1982;6:79– 81. 6. Bunim JJ, McEwen C. Tophus of the mitral valve in gout. Arch Pathol 1940;29:700– 4. 7. Reynolds C, Tazelaar HD, Edwards WD. Calcified amorphous tumor of the heart. Hum Pathol 1997;28:601– 6. 8. Slavin RE, Wen J, Kumar D, Evans EB. Familial tumoral calcinosis. A clinical, histopathologic, and ultrastructural study with an analysis of its calcifying process and pathogenesis. Am J Surg Pathol 1993;17:788 – 802.
Cardiomyoplasty After Implantation of a Pacemaker and Cardioverter/Defibrillator Valeri S. Chekanov, MD, PhD, Sanjay Deshpande, MD, David Francischelli, MS, Paul Werner, MD, Deborah Waller, RN, and Donald H. Schmidt, MD Milwaukee Heart Institute, Milwaukee, Wisconsin
Presently, a combination of two surgical methods improves the survival of patients with advanced ventricular dysfunction: implantable cardioverter/defibrillator implantation (which prevents sudden cardiac death) and cardiomyoplasty (which prevents further dilatation of the heart and provides additional cardiac assistance). We report the clinical course of a patient who had cardiomyoplasty after cardioverter/defibrillator implantation and pacemaker insertion. It is a rare case in which three different devices cardioverter/defibrillator, pacemaker, and cardiomyostimulator) are functioning together without crosstalk. (Ann Thorac Surg 1998;66:954 – 6) © 1998 by The Society of Thoracic Surgeons
E
nd-stage congestive heart failure continues to be a major challenge in health care. Survival of patients with advanced ventricular dysfunction is limited not only by progressive pump dysfunction, but also by the risk of sudden cardiac death [1]. Despite the use of optimal medical therapy with resultant improvement in functional class and a significant reduction in total mortality, sudden death remains a considerable risk in 26% to 28% of these patients [2]. The principal mechanism of sudden cardiac death in this population remains arrhythmia, with ventricular tachycardia that degenerates into ventricular fibrillation being the most common cause [3]. Bradyarrhythmic cardiac arrest and electromechanical dissociation are also well described and may be more common in idiopathic dilated cardiomyopathy [4]. Presently two surgical methods seem to improve the survival of patients with advanced ventricular dysfunction: implantable cardioverter/defibrillator (ICD) implantation (which prevents the sudden cardiac death)
Ann Thorac Surg 1998;66:954 – 6
and cardiomyoplasty (which prevents further dilatation of the heart and provides additional cardiac assistance). Dynamic cardiomyoplasty is emerging as a promising form of surgical therapy for patients with advanced ventricular dysfunction [5]. However, sudden cardiac death remains a major cause of attrition in long-term survival in patients that have had cardiomyoplasty [6]. In contrast to empirical or electrophysiologically guided antiarrhythmic drug therapy, the ICD appears to have the most optimal outcome in sudden death reduction in this population. Sudden cardiac death rates at 5 years after ICD implantation have been reported to be impressively low (about 4.5%) [4]. The ICD therefore appears to be the optimal additional operation in high-risk patients undergoing dynamic cardiomyoplasty. Recently, ICD implantation after cardiomyoplasty has been recommended for prevention of sudden cardiac death in patients with a history of sudden death or episodes of ventricular tachycardia [7, 8]. Several patients have already received an ICD implantation after successful dynamic cardiomyoplasty. Three of these patients are from The Milwaukee Heart Institute of Sinai Samaritan Medical Center in Milwaukee, Wisconsin [9]. The following case report describes the clinical course of a patient who had cardiomyoplasty after ICD implantation and pacemaker insertion. In this patient three different devices (ICD, pacemaker, and cardiomyostimulator) are functioning together without crosstalk (crosstalk is the sensing of the output of one device by another channel in the same or another device). We propose that this combined therapy may improve survival in patients who are deemed to be at high risk for sudden death after cardiomyoplasty. A 38-year-old male patient was hospitalized at Sinai Samaritan Medical Center in Milwaukee, Wisconsin, for worsening shortness of breath and palpitations. He was found to be in monomorphic ventricular tachycardia. During evaluation of his cardiac status, he was found to have idiopathic cardiomyopathy with an ejection fraction of 0.40. He had electrophysiologic studies and subsequent serial drug testing to determine effective therapy for ventricular tachycardia. Unfortunately, despite a trial of three drugs, the ventricular tachycardia remained inducible. Implantation of an ICD (Medtronic PCD, model 7218B; Medtronic, Inc, Minneapolis, MN) was performed on March 11, 1992. The defibrillation threshhold was 18 joules. Three years after ICD implantation, this patient was doing well and had no further episodes of arrhythmias or ICD discharges. Multigated acquisition scans showed an ejection fraction of 0.51. Then, newonset atrial fibrillation developed with a ventricular response of 60 to 70 beats/min. The patient underwent direct-current cardioversion and was converted to sinus rhythm. Six months later, a permanent dual-chamber pacemaker insertion was recommended for treatment of
Accepted for publication April 8, 1998. Address reprint requests to Dr Chekanov, Winter Research Bldg, 836 N 12th St, Milwaukee, WI 53233.
© 1998 by The Society of Thoracic Surgeons Published by Elsevier Science Inc
David Francischelli is an employee of Medtronic, Inc.
0003-4975/98/$19.00 PII S0003-4975(98)00568-2
Ann Thorac Surg 1998;66:954 – 6
symptomatic sinus bradycardia and complete atrioventricular block. A Medtronic pulse generator, model 7950, was implanted and programmed in a DDDR mode. After pacemaker implantation, no interaction between the ICD and the pacemaker was noted during evaluation of the ICD, both in paced rhythm and during induced ventricular fibrillation. The pacemaker was programmed to DDDR mode with a lower rate of 60 beats/min and an upper rate of 120 beats/min. Over the 5 years after the first examination (March 1992), this patient’s cardiac status progressively declined. He reverted to atrial fibrillation and had development of nocturnal dyspnea and pedal edema. Medications were amiodarone, 200 mg daily; enalapril, 15 mg daily; synthroid, 0.0375 mg daily; digoxin, 0.125 mg daily; warfarin, 4 mg daily; furosemide, 40 mg twice a day; and potassium chloride (K-Dur; Key Pharmaceuticals, Kenilworth, NJ) 20 mEq twice a day. Cardiac catheterization revealed normal coronary arteries, a severely, diffusely reduced ejection fraction calculated at 0.20, and no mitral regurgitation. The right ventricular pressure was 50/25 mm Hg, pulmonary artery pressure was 51/30 mm Hg, and the pulmonary capillary wedge pressure mean was 31 mm Hg. On February 10, 1997, dynamic cardiomyoplasty was performed using the left latissimus dorsi posterior muscle wrap. A Medtronic cardiomyostimulator model 4710 was implanted. Two weeks later, the ICD generator was replaced (because of battery depletion). Interaction between the pacemaker, ICD, and cardiomyostimulator was evaluated at implantation. No evidence of crosstalk was exhibited. Simultaneously, electrical training (via cardiomyostimulator) of the latissimus dorsi muscle wrap was started per protocol. Two days later, polymorphic sustained ventricular tachycardia developed, resulting in four ICD discharges (related to hypokalemia and hypomagnesemia). This ventricular tachyarrhythmia was promptly detected and no crosstalk was evident. With supplementation of potassium and magnesium, the ventricular tachycardia resolved and the ICD did not discharge again. The patient was discharged home, being paced by his defibrillator in a VVI mode. His pacemaker was effectively inactive, because its low rate was less than that of the ICD’s VVI system. During the following 3 months, this patient improved clinically. He progressed from a New York Heart Association class III to a class II level of functioning. His diuretic and corresponding potassium and magnesium supplementation declined. His quality of life improved remarkably. Concomitantly during these same 3 months, his cardiomyostimulator settings were changing per protocol. With each cardiomyostimulator programming, the defibrillator was also interrogated and both devices were checked for crosstalk. As the cardiomyostimulator train of impulses was increased, the pacing pulse of the ICD was intermittently sensed by the cardiomyostimulator. This was most likely caused by changes in threshold and amplitude as the cardiomyoplasty sensing leads matured within the myocardium. Three remedies were considered: (1) reduction of the amplitude or pulse width of the ICD pacing pulse, (2) reduction of the sensitivity of the
CASE REPORT CHEKANOV ET AL MULTIDEVICE IMPLANTATION FOR CARDIOMYOPATHY
955
cardiomyostimulator, or (3) VVI pacing via the cardiomyostimulator. However, the patient’s clinical condition had improved to the point that the decision was made to give him the benefit of VVIR pacing. His existing permanent pacemaker was activated 4 months after cardiomyoplasty. Again, no interaction was demonstrable between the three functioning devices in follow-up. He has continued to improve and is now functioning in New York Heart Association class I.
Comment Sudden cardiac death remains a significant contributor to mortality in patients with advanced ventricular dysfunction. Although dynamic cardiomyoplasty may provide improvement in hemodynamic status and functional class, the risk of sudden death remains a vexing problem. Antiarrhythmic drug therapy alone does not appear to extend a favorable outcome because of several limitations. It is anticipated that the ICD used in conjunction with dynamic cardiomyoplasty will favorably affect survival by reducing the risk of arrhythmic death in patients with advanced ventricular dysfunction. The timing of ICD implantation in relationship to dynamic cardiomyoplasty needs to be individualized. Cardiomyoplasty may be performed in patients who have already had ICD implantation. Alternatively, ICD implantation may be performed concomitantly or soon after a cardiomyoplasty operation. In some high-risk patients, ventricular tachycardia or cardiac arrest has not recurred after cardiomyoplasty, perhaps as a result of improvement in hemodynamics, ventricular stretch, or autonomic imbalance. However, long-term data are not available and the number of patients reported is small. Implantation of an ICD should not be deferred in these individuals, because the antiarrhythmic effect of cardiomyoplasty cannot be accurately predicted. At the present time, there is little published information about the potential interactions between the ICD and the cardiomyoplasty system. Provided care is taken during implantation to ensure that such interaction does not occur, ongoing follow-up should parallel the results of concomitant ICD and pacemaker implantation.
References 1. Schocken DD, Arrieta MI, Leaverton PE, Ross EA. Prevalence and mortality rate of congestive heart failure in the United States. J Am Coll Cardiol 1991;20:301– 6. 2. Greene HL. Clinical significance and management of arrhythmias in heart failure patient. Clin Cardiol 1992;15(Suppl 1): 13–21. 3. Luu M, Stevenson WG, Baron K, Walden J. Diverse mechanisms of unexpected cardiac arrest in advanced heart failure. Circulation 1989;80:1675– 80. 4. Akhtar M, Avitall B, Jazayeri M, et al. Role of implantable cardioverter-defibrillator therapy in the management of high risk patients. Circulation 1992;85(Suppl 1):1131–9. 5. Chachques JC, Berrebi A, Hernigon A, et al. Study of muscular and ventricular function in dynamic cardiomyoplasty: a ten year follow-up. J Heart Lung Transplant 1997;6:854– 67. 6. Magovern J, Magovern GJ Sr, Maher TD, et al. Operation for
956
CASE REPORT CHEKANOV ET AL MULTIDEVICE IMPLANTATION FOR CARDIOMYOPATHY
congestive heart failure: transplantation, coronary artery bypass, and cardiomyoplasty. Ann Thorac Surg 1993;56:418–25. 7. Thakur RK, Chow LH, Guiraudon GM, et al. Latissimus dorsi dynamic cardiomyoplasty: role of combined ICD implantation. J Card Surg 1995;10:295–7. 8. Francischelli D, Peterson D, Stein P, Gealow K, Grandjean P.
Ann Thorac Surg 1998;66:954 – 6
Cardiomyoplasty and defibrillator: a combined treatment for heart failure. In: Carpentier A, Chachques GC, Grandjean P, eds. Cardiac bioassist. Armonk, NY: Futura, 1997:417–28. 9. Chekanov VS, Deshpande S, Schmidt DH. Cardiomyoplasty combined with implantation of cardioverter-defibrillator. J Thorac Cardiovasc Surg 1997;114:489–91
New Requirements for Recertification in the Year 2001 Diplomates of the American Board of Thoracic Surgery who plan to participate in the recertification process within the next few years should pay particular attention to this notice, because the requirements will change effective in the year 2001. In addition to an active medical license and institutional clinical privileges in thoracic surgery, beginning in 2001, a valid certificate will be an absolute requirement for entrance into the recertification process. If your certificate has expired, the only pathway for renewal of a certificate will be to take and pass the Part I (written) and the Part II (oral) certifying examinations. In 2001, the American Board of Thoracic Surgery will no longer publish the names of individuals who have not recertified. In the past, a designation of “NR” (not See also page 693. recertified) was used in the American Board of Medical Specialties directories if a Diplomate had not recertified. The Diplomate’s name will be published upon successful completion of the recertification process. The CME requirements will also change in 2001. The new CME requirements will be 70 Category I credits in either cardiothoracic surgery or general surgery earned during the 2 years prior to applying for recertification. SESATS and SESAPS will be the only self-instructional material allowed for credit. No Category II credits will be allowed. The Physicians Recognition Award for recertifying in general surgery will not be accepted in fulfillment of the CME requirement for recertification. The preceding information only partially outlines the CME requirements. Interested
© 1998 by The Society of Thoracic Surgeons Published by Elsevier Science Inc
individuals should refer to the 1999 Booklet of Information for a complete description of acceptable CME credits. Diplomates should maintain a documented list of their major cases performed during the year prior to application for recertification. This practice review should consist of 1 year’s consecutive major operative experiences. If more than 100 cases occur in 1 year, only 100 should be listed. Candidates for recertification will be required to complete both the general thoracic and the cardiac portions of the SESATS self-assessment examination. It is not necessary for candidates to purchase SESATS prior to applying for recertification because SESATS will be sent to candidates after their application has been approved. Diplomates may recertify up to 3 years before the expiration of their certificate. Their new certificate will be dated 10 years from the time of expiration of their original certificate or most recent recertification certificate. In other words, recertifying early does not alter the 10-year validation. Recertification is also open to Diplomates with an unlimited certificate and will in no way affect the validity of their original certificate. The deadline for submission of applications for the recertification process is May 1 of each year. A recertification brochure outlining the rules and requirements for recertification in thoracic surgery is available upon request from the American Board of Thoracic Surgery, One Rotary Center, Suite 803, Evanston, IL 60201; telephone number: (847) 475-1520; fax: (847) 475-6240; e-mail: [email protected]..
Ann Thorac Surg 1998;66:956
•
0003-4975/98/$19.00