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Transvenous AV junctional ablation
Volume Number
106 3
G.H.
111-n-77 x1$37
Letters
xl277
X11-7-77 ~~9-77 X/f-M-77 x1/-1377 x//44-77 x11-19-77
1. ECG tracings of G.H., a 53-year-old female.Tracing of March 21 is a normal control record. On December 6, the patient was admitted to hospital with chest pain accompaniedby acute infarction pattern in leadsV, to V,. Enzyme rise indicated the process(CPK 438). On December 9, there wasrecurrent pain with return of ST segment injury in leads V, to V,. This evolved or returned to the control pattern on December 10. No change in enzymes was noted with this episode(CPK 68). On December 13, fresh transmural infarction pattern reappearedwith chest pain, accompaniedby a brisk rise in enzymes (CPK 169). Typical evolution followed from December14 to 19. (ECG recordings were retraced by hand for clarity.)
R.C. x-31-77
x,+77
d-77
to the Editor
x,-;-77
607
l-21-78
Fig.
that ST shifts, a marker of the process, might be found in sequential recordings. Over a 4-month period in 1977, in a study of approximately 120 acute transmural infarcts we found 25 cases with recurrent, transient ST elevation in the leads demonstrating the initial injury. Two examples are provided in Figs. 1 and 2. The typical pattern of an evolving infarction was followed at varying intervals of 1to 5 days by the return of ST segment shifts in precisely the same leads, denoting recurrent injury in the initially involved area. Some patients (Fig. 1) demonstrated as many as five episodes of new ST injury. There was no predictable correlation between the electrical evidence of injury and the clinical picture; some of the patients complained of pain, in others the process was asymptomatic. Both of the examples presented had evidence of further necrosis, hence recurrent infarction; others promptly returned to the control patterns without biochemical evidence of further damage. If the ST segment elevation denotes transmural ischemia,’ then its reappearance after a transmural infarction is cogent evidence for the initial proximal occlusion of the involved vessel being transient spasm. If one insists that the original occlusive event is thrombosis, it is necessary to postulate very rapid lysis in recurrent clot formation at very short intervals of time, i.e., 2 to 3 davs. This seems much less likely than a dvnamic, vasoconstrictive process. A final point should be made; none of these cases was of the Prinzmetal variant form. In fact, the manifestation of acute infarction, if the spasm hypothesis is correct, is a reverse Prinz-
Fig. 2. ECG tracings of R.C., a 69-year-old female. On October 31 the patient was admitted with chest pain. There had been a transient bout one day earlier. Acute anterior infarction pattern is noted in leadsV, through V,. Typical, moderate rise in enzymesaccompaniedthe injury (CPK 459). On November 2, hyperacute injury pattern returned, followed by a marked enzyme rise on November 3 (CPK 1193). Typical evolution followed. (ECG recordings were retraced by hand for clarity.) metal with the original episode resulting in infarction, subsequent ischemic bouts being transient. Goodman Cohen, M.D. 1081 Carling Avenue-Suite 705 Ottawa, Ontario Kl Y 4G2, Canada REFERENCES
1. Dalen JE, Ockene IS, Alpert JS: Coronary spasm, coronary thrombosis, and myocardial infarction: A hypothesis concerning the pathophysiology of acute myocardial infarction. AM HEART J 104:1119, 1982. 2. Maseri A, L’Abbate A, Baroldi G, et al: Coronary vasospasm as a possible cause of myocardial infarction. A conclusion derived from the study of preinfarction angina. N Engl J Med 299:1271, 1978.
TRANSVENOUS AV JUNCTIONAL ABLATION To the Editor:
A new technique for transvenous catheter ablation of the atrioventricular (AV) junction has recently been described.‘,’ At a
608
Letters
September, 1983 American Heart Journal
to the Editor
recent meeting ,of investigators using this technique, it was estimated that approximately 70 patients throughout the world underwent this procedure. In order to assess the efficacy and safety of this procedure, we are in need of follow-up data for these patients. We have therefore instituted a registry to allow for accumulation and analyses of these data. In addition, in order to compare the newer technique with standard cardiac-surgical techniques for His bundle ablation, we plan likewise to accumulate similar data for these patients who have undergone direct surgical attempts at His bundle disruption. If you or your colleagues at your institution have been involved in any of these procedures, please contact Dr. Melvin Scheinman, Room 573 Moffitt Hospital, University of California, San Francisco, CA 94143, telephone (415) 666-1035. The appropriate forms will be sent to you directly to allow for entrance of your data in the registry. Individual patient and institution confidentiality of these data will be strictly enforced. We plan to furnish you with biannual follow-up data from the registry.
Melvin
Scheinman, M.D. Ad hoc Committee on Transvenous AV Junctional Ablation Moffitt Hospital, Room 573 University of California San Francisco, CA 94143
REFERENCES
1. Scheinman MM, Morady F, Hess DS, Gonzalez R: Catheterinduced ablation of the atrioventricular junction to control refractory supraventricular arrhythmias. JAMA 248:851, 1982. 2. Gallagher JJ, Svenson RH, Kasell JH, et al: Catheter technique for closed-chest ablation of the atrioventricular conduction system: A therapeutic alternative for the treatment of refractory supraventricular tachycardia. N Engl J Med 308:194, 1982.
106 3
G.H.
111-n-77 x1$37
Letters
xl277
X11-7-77 ~~9-77 X/f-M-77 x1/-1377 x//44-77 x11-19-77
1. ECG tracings of G.H., a 53-year-old female.Tracing of March 21 is a normal control record. On December 6, the patient was admitted to hospital with chest pain accompaniedby acute infarction pattern in leadsV, to V,. Enzyme rise indicated the process(CPK 438). On December 9, there wasrecurrent pain with return of ST segment injury in leads V, to V,. This evolved or returned to the control pattern on December 10. No change in enzymes was noted with this episode(CPK 68). On December 13, fresh transmural infarction pattern reappearedwith chest pain, accompaniedby a brisk rise in enzymes (CPK 169). Typical evolution followed from December14 to 19. (ECG recordings were retraced by hand for clarity.)
R.C. x-31-77
x,+77
d-77
to the Editor
x,-;-77
607
l-21-78
Fig.
that ST shifts, a marker of the process, might be found in sequential recordings. Over a 4-month period in 1977, in a study of approximately 120 acute transmural infarcts we found 25 cases with recurrent, transient ST elevation in the leads demonstrating the initial injury. Two examples are provided in Figs. 1 and 2. The typical pattern of an evolving infarction was followed at varying intervals of 1to 5 days by the return of ST segment shifts in precisely the same leads, denoting recurrent injury in the initially involved area. Some patients (Fig. 1) demonstrated as many as five episodes of new ST injury. There was no predictable correlation between the electrical evidence of injury and the clinical picture; some of the patients complained of pain, in others the process was asymptomatic. Both of the examples presented had evidence of further necrosis, hence recurrent infarction; others promptly returned to the control patterns without biochemical evidence of further damage. If the ST segment elevation denotes transmural ischemia,’ then its reappearance after a transmural infarction is cogent evidence for the initial proximal occlusion of the involved vessel being transient spasm. If one insists that the original occlusive event is thrombosis, it is necessary to postulate very rapid lysis in recurrent clot formation at very short intervals of time, i.e., 2 to 3 davs. This seems much less likely than a dvnamic, vasoconstrictive process. A final point should be made; none of these cases was of the Prinzmetal variant form. In fact, the manifestation of acute infarction, if the spasm hypothesis is correct, is a reverse Prinz-
Fig. 2. ECG tracings of R.C., a 69-year-old female. On October 31 the patient was admitted with chest pain. There had been a transient bout one day earlier. Acute anterior infarction pattern is noted in leadsV, through V,. Typical, moderate rise in enzymesaccompaniedthe injury (CPK 459). On November 2, hyperacute injury pattern returned, followed by a marked enzyme rise on November 3 (CPK 1193). Typical evolution followed. (ECG recordings were retraced by hand for clarity.) metal with the original episode resulting in infarction, subsequent ischemic bouts being transient. Goodman Cohen, M.D. 1081 Carling Avenue-Suite 705 Ottawa, Ontario Kl Y 4G2, Canada REFERENCES
1. Dalen JE, Ockene IS, Alpert JS: Coronary spasm, coronary thrombosis, and myocardial infarction: A hypothesis concerning the pathophysiology of acute myocardial infarction. AM HEART J 104:1119, 1982. 2. Maseri A, L’Abbate A, Baroldi G, et al: Coronary vasospasm as a possible cause of myocardial infarction. A conclusion derived from the study of preinfarction angina. N Engl J Med 299:1271, 1978.
TRANSVENOUS AV JUNCTIONAL ABLATION To the Editor:
A new technique for transvenous catheter ablation of the atrioventricular (AV) junction has recently been described.‘,’ At a
608
Letters
September, 1983 American Heart Journal
to the Editor
recent meeting ,of investigators using this technique, it was estimated that approximately 70 patients throughout the world underwent this procedure. In order to assess the efficacy and safety of this procedure, we are in need of follow-up data for these patients. We have therefore instituted a registry to allow for accumulation and analyses of these data. In addition, in order to compare the newer technique with standard cardiac-surgical techniques for His bundle ablation, we plan likewise to accumulate similar data for these patients who have undergone direct surgical attempts at His bundle disruption. If you or your colleagues at your institution have been involved in any of these procedures, please contact Dr. Melvin Scheinman, Room 573 Moffitt Hospital, University of California, San Francisco, CA 94143, telephone (415) 666-1035. The appropriate forms will be sent to you directly to allow for entrance of your data in the registry. Individual patient and institution confidentiality of these data will be strictly enforced. We plan to furnish you with biannual follow-up data from the registry.
Melvin
Scheinman, M.D. Ad hoc Committee on Transvenous AV Junctional Ablation Moffitt Hospital, Room 573 University of California San Francisco, CA 94143
REFERENCES
1. Scheinman MM, Morady F, Hess DS, Gonzalez R: Catheterinduced ablation of the atrioventricular junction to control refractory supraventricular arrhythmias. JAMA 248:851, 1982. 2. Gallagher JJ, Svenson RH, Kasell JH, et al: Catheter technique for closed-chest ablation of the atrioventricular conduction system: A therapeutic alternative for the treatment of refractory supraventricular tachycardia. N Engl J Med 308:194, 1982.