- Email: [email protected]
Esophageal resection for recurrent achalasia
322
CORRESPONDENCE
Ann Thorac Surg 1996;62:317-24
volume inside the sphere in terms of the circumference's rate of change, dV C~dC .dV C~dC d~h = ~ ~ and ~ = 2~ 2 dt~
(3)
where subscripts w and h refer to the muscle wrap and heart respectively; dV/dt is the rate of volume change; and dC/dt, as the rate of change of the sphere's circumference, is the shortening velocity of the sphere's surface. Thus, the rate of volume change inside a contracting sphere is function of not only the velocity Of its contracting surface but also its circumference. By equation (3), the greater the circumference, the greater the volume change, even if shortening velocity is held constant. Because dV dV dt~ - dth
(4)
then by substitution equation 3 yields
2 dC
2dC
c 4 ~ = Ch~
(S)
Cw> Ch
(6)
In addition, because
then, by equation (5), dC dC < dt~ dth
(7)
Thus, in DCM, the shortening velocity of the LD muscle wrap must be less than that of the heart, because the circumference of the wrap is greater than that of the heart. If Tang and Hooper are referring to the time for wrap excitation-contraction, the time between neural stimulation and crossbridge activity, we agree that this is a factor; however, it is not the only one. A reduction in transmural myocardial pressure (Pt) will occur if the LD applies a net pressure against the epicardium. In other words, the LD must be loaded. Whether this occurs is a complex function of the excitation-contraction times of the wrap and the cardiomyopathic heart, the wrap's initial tension, the rate of volume change inside the wrap, and the fundamental force-velocity properties of both the wrap and the cardiomyopathic heart. Which factor is the most important is unclear at this time. Using untransformed muscle, our results suggest that DCM benefits the myocardium, in part at least, by reducing transmural myocardial pressure. There is an ongoing controversy regarding the primary mechanism of DCM, and some reports have shown no systolic augmentation. At the same time, there have also been many case reports and studies detailing augmented stroke volume and aortic pressure when directly comparing on beats with off beats in cardiomyoplasty using transformed LD muscle [1-3]. That can only happen if systolic "squeeze" assist occurred, and therefore reduced transmural myocardial pressure. Furthermore, although we know transformed muscle is slower than untransformed muscle, we also know empirically that it is not so slow that zero tension is developed within the time period of a typical cardiac cycle. This means that, properly wrapped, the transformed LD will exert a pressure on the epicardium and reduce the average Pt over the cardiac cycle. We strongly believe that if its experimental limitations are understood and appreciated, untransformed muscle does have a role in DCM research. The point of research is not only to understand the clinical status quo but also to show future directions of the field. Given that new training methods preserving © 1996 by The Society of Thoracic Surgeons Published by Elsevier Science Inc
muscle strength and mass are currently being developed [4], the performance of untransformed mUscle represents the goal of transformed muscle. Because we used a balloon, our model was not, strictly speaking, cardiomyoplasty. This does not mean, however, that our results do not have anything to offer on this subject. The point of our study was to introduce a method of calculating Pt, show that, despite hemodynamics that remained statistically the same, a considerable reduction in P~ occurred, and postulate that such results suggest a mechanism for DCM. Of course, to truly represent clinical cardiomyoplasty, the best animal model would use transformed muscle applied to a dilated cardiomyopathic heart (whose myocardium would contract markedly differently than healthy myocardium); however, if one were to say all models other than this were misleading, then essentially all past experimental work in the field would be invalid.
Frederick Y. Chen, PhD Lishan Aklog, MD Brian J. deGuzman, MD Rita G. Laurence, BS Gregory S. Couper, MD Lawrence H. Cohn, MD Thomas A. McMahon, PhD Division of Applied Sciences Harvard University Cambridge, MA 02138 and Division of Cardiac Surgery Brigham and Women's Hospital Harvard Medical School 75 Francis St Boston, MA 02115
References 1. Chacques JC, Grandjean PA, Schwartz K, et al. Effects of latissimus dorsi dynamic cardiomyoplasty on ventricular function. Circulation 1988;78(Suppl 3):203-16. 2. Chagas ACP, Moreira LFP, Da Luz PL, et al. Stimulated preconditioned skeletal muscle cardiomyoplasty: an effective means of cardiac assist, Circulation 1989;80(Suppl 3):202-8. 3. Kao RL, Christlieb IY, Magovern GJ, Park SP, Magovern GJ Jr. The importance of skeletal muscle fiber orientation for dynamic cardiomyoplasty. J Thorac Cardiovasc Surg 1990;99: 134-40. 4. Fritzsche D, Krakor R, Asmussen G, et al. Anabolic steroids (metanolene) improve muscle performance and hemodynamic characteristics in cardiomyoplasty. Ann Thorac Surg 1995;59:961-70.
Esophageal Resection for R e c u r r e n t Achalasia To the Editor: I read with much attention and interest the article by Miller and associates [1]. They reported on 37 patients from whom they removed the esophagus as a remedial operation due to recurrence of symptoms after the initial procedure for the treatment of achalasia. In this group of patients they had two intraoperative deaths (5.4%) and twelve complications (32.4%), including cardiac dysrhythmia, cervical anastomosis leak, transient vocal cord paralysis, pulmonary embolus, and one reexploration for bleeding. I would like to take issue with this type of approach and report our results with a much less aggressive surgical treatment. In a group of 210 patients with advanced achalasia due to Chagas" 0003-4975/96/$15.00
Ann Thorac Surg 1996;62:317-24
disease in whom we performed a cardioplasty with an endoluminal valve, 17 were undergoing reoperations [2]. In this group of patients we had neither mortality nor morbidity [3]. In a collected series of 755 patients who had this type of cardioplasty, as described by Thai in 1965, reported in the Brazilian literature, we found a mortality rate of 0.32%, morbidity of 4.72%, and good to excellent results in 91.2% [4-6]. In our initial report of 450 patients treated for this condition, 40 had the esophagus removed through the chest. In this subset of patients we had a mortality rate of 7.5% and good results in only 75% [4]. In cases of perforation due to pneumatic dilatation the cardioplasty offers the same good results as if performed on elective basis [5]. We realize that of the host of 45 procedures already described to treat this condition none is satisfactory [6]. However, we should never forget that this is a benign disease and its treatment should be kept simple and straightforward, with minimal morbidity and mortality, even in cases of recurrence as described by Miller and associates. I compliment the Mayo group on another complete and most rewarding article about this simple but at times distresssing disease.
Manoel Ximenes III, MD, PhD Thoracic Surgery Unit Hospital de Base of the Distrito Federal Brasilia, DF, Brazil References 1. Miller DL, Alien MS, Trastek VF, Deschamps C, Pairolero PC. Esophageal resection for recurrent achalasia. Ann Thorac Surg 1995;60:922-34. 2. Ximenes M. Chagas' disease of the esophagus. In: Shields TW, ed. General thoracic surgery. Philadelphia: Williams & Wilkins, 1994:1538-69. 3. Ximenes M. Chagas' disease. In: Pearson FG, Deslauriers J, Ginsberg RJ, Hiebert CA, McKneally MF, Urschel HC Jr, eds. Esophageal surgery. New York: Churchill Livingstone, 1995: 443-57. 4. Ximenes M, Silva RO, DeBiase H, et al. Primary surgical treatment of Chagas' megaesophagus. Results of 450 cases. HFA Pub Tec Cient 1987;2:147-61. 5. Ximenes M. Ruptured Chagas' megaesophagus. Surg Gynecol Obstet 1989;168:263-74. 6. Ximenes M. Megaesophagus. Current review of techniques and results. Rev Saude DF 1991;2:207-36.
Reply To the Editor: We thank Dr Ximenes for his comments regarding our article [1]. We recognize his surgical expertise in the treatment of achalasia secondary to Chagas"disease. However, we think he has misinterpreted our article. The basis of our article was to present follow-up information on patients who required esophageal resection as a reoperative procedure for achalasia. We tried to examine which procedures should be performed to minimize operative morbidity and mortality and improve long-term functional results. From our retrospective review, we concluded that transhiatal esophageal resection for recurrent symptoms or complications after initial surgical treatment for achalasia was associated with increased morbidity and mortality. We believe that when esophageal resection is required after initial surgical treatment has failed, direct visualization of the esophagus should be performed transthoracically. In our group of patients who underwent transthoracic esophagectomy, there were no © 1996 by The Society of Thoracic Surgeons Published by Elsevier Science Inc
CORRESPONDENCE
323
operative deaths. Only 8.2% of our patients who required surgical intervention for treatment of their achalasia underwent esophageal resection. None of these resections were done as the initial treatment. Doctor Ximenes and associates [2] reported a mortality rate of 7.5% in 40 patients who underwent primary surgical treatment of achalasia secondary to Chagas' disease. We consider this a high mortality rate for initial therapy of benign disease. We concur with Dr Ximenes that the treatment of these patients should be kept simple; however, when esophageal resection is required as a reoperative procedure it should be performed via a transthoracic approach to minimize complications in this group of patients.
Daniel L. Miller, MD Division of Cardiothoracic Surgery University of Louisville School of Medicine 201 Abraham Flexner Way, Suite 1200 Louisville, KY 40202 Mark S. Allen, MD Section of Thoracic Surgery Mayo Clinic 200 First St, S W Rochester, M N 55905 References 1. Miller DL, Allen MS, Trastek VF, Deschamps C, Pairolero PC. Esophageal resection for recurrent achalasia. Ann Thorac Surg 1995;60:922-34. 2. Ximenes M. Ruptured Chagas' megaesophagus. Surg Gynecol Obstet 1989;168:263-74. T r a n s m y o c a r d i a l Laser R e v a s c u l a r i z a t i o n a n d Coronary Artery Bypass Grafting Without Cardiopulmonary
Bypass To the Editor: Treatment alternatives for patients with coronary artery disease have become increasingly sophisticated. Direct revascularization involving application of a high-energy CO 2 laser to create transmural cardiac channels may establish blood flow from the ventricular cavity to the myocardial vascular network [1]. In selected cases coronary artery bypass grafting without extracorporeal circulation is technically feasible [2]. In this clinical report, we present a patient in whom these treatment modalities were combined. A 59-year-old man was referred to our institution in February 1996. Previously the patient had undergone coronary artery bypass grafting in 1984. He suffered myocardial infarction in 1990 and 1995. He had experienced periods of unstable angina since April 1995. Cardiac catheterization revealed that the patient's native left anterior descending coronary artery, the right coronary artery, and the grafts to these arteries were occluded. The circumflex artery was highly stenotic, with an open graft. Angiography showed poor distal periphery of the coronary arteries. Left ventricular angiography and echocardiography showed mild apical hypokinesis with an ejection fraction of approximately 0.50. The patient was not a candidate for coronary angioplasty or conventional coronary artery bypass grafting. After assessing the viability of the ischemic ventricular segments, we offered him transmyocardial laser revascularization. The heart was approached through the fourth intercostal space. The adhesions 0003-4975/96l$15.00
CORRESPONDENCE
Ann Thorac Surg 1996;62:317-24
volume inside the sphere in terms of the circumference's rate of change, dV C~dC .dV C~dC d~h = ~ ~ and ~ = 2~ 2 dt~
(3)
where subscripts w and h refer to the muscle wrap and heart respectively; dV/dt is the rate of volume change; and dC/dt, as the rate of change of the sphere's circumference, is the shortening velocity of the sphere's surface. Thus, the rate of volume change inside a contracting sphere is function of not only the velocity Of its contracting surface but also its circumference. By equation (3), the greater the circumference, the greater the volume change, even if shortening velocity is held constant. Because dV dV dt~ - dth
(4)
then by substitution equation 3 yields
2 dC
2dC
c 4 ~ = Ch~
(S)
Cw> Ch
(6)
In addition, because
then, by equation (5), dC dC < dt~ dth
(7)
Thus, in DCM, the shortening velocity of the LD muscle wrap must be less than that of the heart, because the circumference of the wrap is greater than that of the heart. If Tang and Hooper are referring to the time for wrap excitation-contraction, the time between neural stimulation and crossbridge activity, we agree that this is a factor; however, it is not the only one. A reduction in transmural myocardial pressure (Pt) will occur if the LD applies a net pressure against the epicardium. In other words, the LD must be loaded. Whether this occurs is a complex function of the excitation-contraction times of the wrap and the cardiomyopathic heart, the wrap's initial tension, the rate of volume change inside the wrap, and the fundamental force-velocity properties of both the wrap and the cardiomyopathic heart. Which factor is the most important is unclear at this time. Using untransformed muscle, our results suggest that DCM benefits the myocardium, in part at least, by reducing transmural myocardial pressure. There is an ongoing controversy regarding the primary mechanism of DCM, and some reports have shown no systolic augmentation. At the same time, there have also been many case reports and studies detailing augmented stroke volume and aortic pressure when directly comparing on beats with off beats in cardiomyoplasty using transformed LD muscle [1-3]. That can only happen if systolic "squeeze" assist occurred, and therefore reduced transmural myocardial pressure. Furthermore, although we know transformed muscle is slower than untransformed muscle, we also know empirically that it is not so slow that zero tension is developed within the time period of a typical cardiac cycle. This means that, properly wrapped, the transformed LD will exert a pressure on the epicardium and reduce the average Pt over the cardiac cycle. We strongly believe that if its experimental limitations are understood and appreciated, untransformed muscle does have a role in DCM research. The point of research is not only to understand the clinical status quo but also to show future directions of the field. Given that new training methods preserving © 1996 by The Society of Thoracic Surgeons Published by Elsevier Science Inc
muscle strength and mass are currently being developed [4], the performance of untransformed mUscle represents the goal of transformed muscle. Because we used a balloon, our model was not, strictly speaking, cardiomyoplasty. This does not mean, however, that our results do not have anything to offer on this subject. The point of our study was to introduce a method of calculating Pt, show that, despite hemodynamics that remained statistically the same, a considerable reduction in P~ occurred, and postulate that such results suggest a mechanism for DCM. Of course, to truly represent clinical cardiomyoplasty, the best animal model would use transformed muscle applied to a dilated cardiomyopathic heart (whose myocardium would contract markedly differently than healthy myocardium); however, if one were to say all models other than this were misleading, then essentially all past experimental work in the field would be invalid.
Frederick Y. Chen, PhD Lishan Aklog, MD Brian J. deGuzman, MD Rita G. Laurence, BS Gregory S. Couper, MD Lawrence H. Cohn, MD Thomas A. McMahon, PhD Division of Applied Sciences Harvard University Cambridge, MA 02138 and Division of Cardiac Surgery Brigham and Women's Hospital Harvard Medical School 75 Francis St Boston, MA 02115
References 1. Chacques JC, Grandjean PA, Schwartz K, et al. Effects of latissimus dorsi dynamic cardiomyoplasty on ventricular function. Circulation 1988;78(Suppl 3):203-16. 2. Chagas ACP, Moreira LFP, Da Luz PL, et al. Stimulated preconditioned skeletal muscle cardiomyoplasty: an effective means of cardiac assist, Circulation 1989;80(Suppl 3):202-8. 3. Kao RL, Christlieb IY, Magovern GJ, Park SP, Magovern GJ Jr. The importance of skeletal muscle fiber orientation for dynamic cardiomyoplasty. J Thorac Cardiovasc Surg 1990;99: 134-40. 4. Fritzsche D, Krakor R, Asmussen G, et al. Anabolic steroids (metanolene) improve muscle performance and hemodynamic characteristics in cardiomyoplasty. Ann Thorac Surg 1995;59:961-70.
Esophageal Resection for R e c u r r e n t Achalasia To the Editor: I read with much attention and interest the article by Miller and associates [1]. They reported on 37 patients from whom they removed the esophagus as a remedial operation due to recurrence of symptoms after the initial procedure for the treatment of achalasia. In this group of patients they had two intraoperative deaths (5.4%) and twelve complications (32.4%), including cardiac dysrhythmia, cervical anastomosis leak, transient vocal cord paralysis, pulmonary embolus, and one reexploration for bleeding. I would like to take issue with this type of approach and report our results with a much less aggressive surgical treatment. In a group of 210 patients with advanced achalasia due to Chagas" 0003-4975/96/$15.00
Ann Thorac Surg 1996;62:317-24
disease in whom we performed a cardioplasty with an endoluminal valve, 17 were undergoing reoperations [2]. In this group of patients we had neither mortality nor morbidity [3]. In a collected series of 755 patients who had this type of cardioplasty, as described by Thai in 1965, reported in the Brazilian literature, we found a mortality rate of 0.32%, morbidity of 4.72%, and good to excellent results in 91.2% [4-6]. In our initial report of 450 patients treated for this condition, 40 had the esophagus removed through the chest. In this subset of patients we had a mortality rate of 7.5% and good results in only 75% [4]. In cases of perforation due to pneumatic dilatation the cardioplasty offers the same good results as if performed on elective basis [5]. We realize that of the host of 45 procedures already described to treat this condition none is satisfactory [6]. However, we should never forget that this is a benign disease and its treatment should be kept simple and straightforward, with minimal morbidity and mortality, even in cases of recurrence as described by Miller and associates. I compliment the Mayo group on another complete and most rewarding article about this simple but at times distresssing disease.
Manoel Ximenes III, MD, PhD Thoracic Surgery Unit Hospital de Base of the Distrito Federal Brasilia, DF, Brazil References 1. Miller DL, Alien MS, Trastek VF, Deschamps C, Pairolero PC. Esophageal resection for recurrent achalasia. Ann Thorac Surg 1995;60:922-34. 2. Ximenes M. Chagas' disease of the esophagus. In: Shields TW, ed. General thoracic surgery. Philadelphia: Williams & Wilkins, 1994:1538-69. 3. Ximenes M. Chagas' disease. In: Pearson FG, Deslauriers J, Ginsberg RJ, Hiebert CA, McKneally MF, Urschel HC Jr, eds. Esophageal surgery. New York: Churchill Livingstone, 1995: 443-57. 4. Ximenes M, Silva RO, DeBiase H, et al. Primary surgical treatment of Chagas' megaesophagus. Results of 450 cases. HFA Pub Tec Cient 1987;2:147-61. 5. Ximenes M. Ruptured Chagas' megaesophagus. Surg Gynecol Obstet 1989;168:263-74. 6. Ximenes M. Megaesophagus. Current review of techniques and results. Rev Saude DF 1991;2:207-36.
Reply To the Editor: We thank Dr Ximenes for his comments regarding our article [1]. We recognize his surgical expertise in the treatment of achalasia secondary to Chagas"disease. However, we think he has misinterpreted our article. The basis of our article was to present follow-up information on patients who required esophageal resection as a reoperative procedure for achalasia. We tried to examine which procedures should be performed to minimize operative morbidity and mortality and improve long-term functional results. From our retrospective review, we concluded that transhiatal esophageal resection for recurrent symptoms or complications after initial surgical treatment for achalasia was associated with increased morbidity and mortality. We believe that when esophageal resection is required after initial surgical treatment has failed, direct visualization of the esophagus should be performed transthoracically. In our group of patients who underwent transthoracic esophagectomy, there were no © 1996 by The Society of Thoracic Surgeons Published by Elsevier Science Inc
CORRESPONDENCE
323
operative deaths. Only 8.2% of our patients who required surgical intervention for treatment of their achalasia underwent esophageal resection. None of these resections were done as the initial treatment. Doctor Ximenes and associates [2] reported a mortality rate of 7.5% in 40 patients who underwent primary surgical treatment of achalasia secondary to Chagas' disease. We consider this a high mortality rate for initial therapy of benign disease. We concur with Dr Ximenes that the treatment of these patients should be kept simple; however, when esophageal resection is required as a reoperative procedure it should be performed via a transthoracic approach to minimize complications in this group of patients.
Daniel L. Miller, MD Division of Cardiothoracic Surgery University of Louisville School of Medicine 201 Abraham Flexner Way, Suite 1200 Louisville, KY 40202 Mark S. Allen, MD Section of Thoracic Surgery Mayo Clinic 200 First St, S W Rochester, M N 55905 References 1. Miller DL, Allen MS, Trastek VF, Deschamps C, Pairolero PC. Esophageal resection for recurrent achalasia. Ann Thorac Surg 1995;60:922-34. 2. Ximenes M. Ruptured Chagas' megaesophagus. Surg Gynecol Obstet 1989;168:263-74. T r a n s m y o c a r d i a l Laser R e v a s c u l a r i z a t i o n a n d Coronary Artery Bypass Grafting Without Cardiopulmonary
Bypass To the Editor: Treatment alternatives for patients with coronary artery disease have become increasingly sophisticated. Direct revascularization involving application of a high-energy CO 2 laser to create transmural cardiac channels may establish blood flow from the ventricular cavity to the myocardial vascular network [1]. In selected cases coronary artery bypass grafting without extracorporeal circulation is technically feasible [2]. In this clinical report, we present a patient in whom these treatment modalities were combined. A 59-year-old man was referred to our institution in February 1996. Previously the patient had undergone coronary artery bypass grafting in 1984. He suffered myocardial infarction in 1990 and 1995. He had experienced periods of unstable angina since April 1995. Cardiac catheterization revealed that the patient's native left anterior descending coronary artery, the right coronary artery, and the grafts to these arteries were occluded. The circumflex artery was highly stenotic, with an open graft. Angiography showed poor distal periphery of the coronary arteries. Left ventricular angiography and echocardiography showed mild apical hypokinesis with an ejection fraction of approximately 0.50. The patient was not a candidate for coronary angioplasty or conventional coronary artery bypass grafting. After assessing the viability of the ischemic ventricular segments, we offered him transmyocardial laser revascularization. The heart was approached through the fourth intercostal space. The adhesions 0003-4975/96l$15.00