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Coronary artery surgery for recurrent ventricular arrhythmias in patients with variant angina
Coronary artery surgery for recurrent ventricular arrhythmias in patients with variant angina Leonard A. Nordstrom, M.D. James P. Lillehei, M.D. Arnold Adicoff, M.D. Yoshio Sako, M.D., Ph.D. Fredarick L. Gobel, M.D. Minneupolis,
Minn.
Serious ventricular arrhythmias in patients with variant angina due to occlusive coronary artery disease may be difficult to control with conventional medical therapy. In patients with such arrhythmias, coronary artery bypass surgery may be indicated as treatment even though chest pain is not severe. The following cases illustrate successful surgical therapy of recurrent ventricular arrhythmias in two patients with Prinzmetal’s variant angina. Medical therapy failed to adequately control the tachyarrhythmia. Coronary arteriography demonstrated severe occlusive vascular disease, and following coronary artery surgery the arrhythmias were abolished. Case reports Case I, A 41-year-old white man was admitted to the hospital complaining of left chest pain of two months’ duration. The pain was described as a pressure sensation radiating to the jaw and left arm and was not related to exercise, food intake, or emotion. On several occasions the pain awakened the patient during the night. The patient smoked two packages of cigaretites daily, despite the presence of bronchial asthma for the previous 17 years. Adult-onset diabetes mellitus had been treated with diet and tolbutamide for five years. One parent suffered a myocardial infarction and both parents had chronic obstructive lung disease. Occasional inspiratory wheezes were detected in both lungs. The heart was of normal size and a fourth heart sound was present. No cardiac murmur was detected. The serum triglycerides were 540 mg. per 100 ml., the From the Veterans Administration Hospital and the Departments of Medicine and Surgery, University of Minnesota, Minneapolis, Minn. Received for publication July 13, 1973. Reprint requests to: Fredarick L. Gobel, M.D., Cardiovascular Section, Veterans Administration Hospital, 54th St. & 48th Ave. So., Minneapolis, Minn. 55417.
236
blood cholesterol was 245 mg. per 100 ml., and the glucose tolerance test was abnormal. Early in the hospital course, three syncopal episodes associated with chest pain occurred but were not monitored by an ECG. Thereafter frequent episodes of chest pain followed by ST elevation, QRS widening, and short runs of ventricular tachycardia occurred (Fig. 1). ST segment elevation was confined to anterior precordial leads. Six of these episodes resulted in ventricular tachycardia and/or ventricular fibrillation which were successfully treated by D.C. shock in four instances and by a bolus of lidocaine in two instances. The patient was treated intensively in the coronary-care unit (CCU1 for 55 days. Quinidine (200 mg. every four hours), Pronestyl (750 mg. every three hours), propranolol (120 mg. daily), Isordil (to tolerance), atropine, and lidocaine (4 to 5 mg. per minute), either alone or in combination, failed to suppress the ventricular arrhythmias. An attempt at suppressing the arrhythmia by increasing the ventricular rate by pacing was unsuccessful. Coronary arteriography demonstrated high-grade obstruction in the left anterior descending coronary artery (LAD) and diffuse disease in the circumflex branch of the left coronary artery (LCX) (Fig. 21. Diffuse disease was also present in the right coronary artery (RCA). While waiting for operation, the patient had another episode of chest pain and syncope. Shortly after induction of anesthesia, the patient developed hypotension which did not respond adequately to pressor agents. The chest was opened and cardiac massage was initiated. A 1.5 mm. probe could not be passed through the lesion in the LAD and, in spite of a mean aortic pressure of 60 mm. Hg, there was no antegrade flow through the LAD, indicating a highly obstructive lesion. Two aorticocoronary saphenous vein bypass grafts (ACSVG) from the ascending aorta were anastomosed, one each to the LAD and to the posterior descending coronary artery (PDA). The flow rate to the LAD was 90 ml. per minute and the flow rate to the PDA was 65 ml. per minute as measured by an electromagnetic flowmeter at the time of operation. The patient had an uneventful postoperative course. Since operation he has had no chest pain, syncopal episodes, or suspected or documented arrhythmias. Coronary arteriography six months postoperatively revealed both ACSVG to be pa-
February,
1975, Vol. 89, No. 2, pp. 236-241
Lead
MCL i
@I
Kg. 1. Patient 1: A MCL I monitor lead tracing demonstrates typical changes that chest pain: (A) normal pattern, (Bl ST segment elevation, (0 short run of ventricular sion to normal rhythm.
tent (Fig. 3). There were no dyskinetic areas of the left ventricle. The postoperative resting ECG was normal (Fig. 4A 1.An exercise EGG revealed no ST segment changes at a heart rate of 140 beats per minute but was discontinued because the patient complained of leg pain (Fig. 4B 1. Case 2. A 51-year-old white man was admitted to the hospital because of recurrent chest pain described as a pressure sensation in the lower substernal region. Initially the pain occurred in the morning after awakening from sleep but then nocturnal pain developed. There were no episodes of chest pain associated with exertion. The pain had been present for about one month prior to admission to the hospital. The patient denied dyspnea or syncopal episodes. There was no family history of coronary artery disease but the patient’s father had diabetes mellitus. The physical findings and laboratory data were normal. During the hospital course frequent episodes of chest pain associated with ST segment elevation were noted. A 12 lead ECG revealed these changes to be in Leads II, III, and aVF (Fig. 5A). With chest pain, ST segment elevation, and QRS changes, there were often PVC’s and short runs of ventricuiar tachycardia (Fig. 5B). These episodes persisted over a 25 day period of continuous monitoring in the CCIJ despite medical therapy consisting of Pronestyl (250 mg. every four hours), propranolol (80 mg. daily), Isordil (to tolerance), and an infusion of lidocaine at 4
American
FIeart
Jo‘surnrti
occurred during episi:des of tachycardia, and :Di rever-
Fig. 2. Patient :: A rigat antenor obiq~e view ff2ti degreesi of the left coronary artery demonstrates high-grade obstruction in the left anterior descending Gb?l, arrawsJ and diffuse disease in the !eft circumflex coronary artery 8XX.
Nordstrom
et al.
Fig. 3. Patient 1: Right anterior oblique views (60 degrees) demonstrating (left) descending coronary artery (PDA) and (right) a patent graft to the left anterior cate site of anastomosis).
Standing Rest
III
AVR AVL AVF
immediate Post Exercise
Exercise Recovery 3 minute5
i minute
2 minutes
Fig. 4A. Patient 1: Six months bad a normal 12 lead ECG.
postoperatively
the
Recovery 6 minutes
patient
3 to 5 mg. per minute. Coronary arteriography revealed a 90 per cent obstructing lesion in the mid third of the LCX (Fig. 6). The dominant coronary artery was the left. ,There was also diffuse disease in the RCA. Multiple x-ray views of LAD were interpreted to be normal. At operation an ACSVG was inserted from the ascending aorta to the LCX. Flow measurements were not made. The patient’s postoperative course was unremarkable. There were no further episodes of chest pain, ST elevation, or evidence of an operative or immediate postoperative myocardial infarction. Two and a half years have elapsed since
238
a patent graft to the posterior descending (LAD, arrows indi-
4
minutes
minutes
Fig. 48.
exercise Blackburn
AVF Resting
AVF immediate Post Exercise
Six months postoperatively the patient had a normal ECG at a heart rate of 140 beats per minute. A monitor lead system was used.15
February,
1975, Vol. 89, No. 2
Fig. S-4. Patient 2: A 12 lead ECG demonstrating ST segment elevation in Leads II, III, and aV F during an acute episode of chest pain.
Patient 2: A right anterior ob;qtie ~ieri di) degree~i of the left coronary
artery
demonstrates
high-grade
obstruction
in the left circumflex coronary artery !tCX’.
episode of chest pain tern, (B ) ST segment !ar tachycardia.
CI. VI monitor lead tracing during an demonstrates (A 1 patient’s normal patelevation, and (6) short run of ventricu-
operation witnout recurrent chest pain. A recent resting ECG was normal ar,d an exercise ECG was normal at a heart rate of 150 beats per minute (Figs. 7A and 7B.
Prinzmetal’s variant angina is characterized as typical ischemie cardiac pain with the major exception that pain occurs at rest and not during exercise. These episo es tend to be cyclic and may occur at approximately the same time ST elevation, daily. I22 The ECG demonstrates rather than depression, in the distribution of the involved coronary artery.lJ Approximately 50 per een.t of patients with variant angina have ve~t~i~~~a~ arrhythmias and in a few patients
Fig. 7 . Patienr 2: Two and oni: haif year., postoperatively the resting ECG was normal.
Nordstrom
et al.
1.2 minutes MPH Grade
3.4 14%
Exercise
Imediate Rest
3 minutes 1.5 MPH 5% Grade
6 minutes 1.7 MPH 10% Grade
2 minutes Recovery
9 minutes MPH 12% Grade
2.5
Fig. 78. Two minute.
and
one half
years
postoperatively
an exercise
Although it has been suggested that variant angina may be associated with an isolated lesion in a single coronary artery, a few autopsy studies have demonstrated diffuse coronary artery disease in addition to the high-grade obstructing lesion. 1,13Both patients reported had significant lesions obstructing more than 50 per cent of the lumen in at least two vessels. Patient 1 had disease involving all three coronary arteries. The ST segment shifts and arrhythmias, however, are thought to be a consequence of a single highgrade obstructing lesion.le3The hope that patients with variant angina might represent the ideal surgical candidate having an isolated solitary lesion in one coronary artery is not borne out in some instances. It has long been recognized that ischemia predisposes to ventricular irritability. Recently, experimental studies have helped to delineate possible underlying mechanisms. Han demonstrated that the fibrillatory threshold in the ventricle is decreased during ischemia.s Additional studies have demonstrated that ventricular impulses are propagated very slowly through ischemic areas and emerge into normal repolarized areas as re-entrant beats.g Such a reentrant process may continue to produce multi-
240
ECG
was normal
at heart
rate
of 150 beats
per
ple extrasystoles or tachycardia in the ventricle. Although difficult to prove, it would seem that a re-entrant mechanism secondary to ischemia may have been the basis for recurrent ventricular tachyarrhythmias in these two patients. Patients with recurrent ventricular tachycardia due to myocardial ischemia may note cessation of the arrhythmia after suffering a myocardial infarction. Myocardial infarctions are common following saphenous vein bypass surgery.lOThat such is not the situation in the patients reported here, and that the relief from the arrhythmia was subsequent to relief of the ischemia by operation, is supported by the normal postoperative ECG’s in both patients and by the patent saphenous vein grafts in the first patient. The surgical approach for variant angina and ventricular arrhythmias is supported by the cases reported here and by several recent reports of patients with ischemic heart disease (not variant angina1 and recurrent tachyarrhythmias who have noted abolition or arrhythmias following coronary artery surgery.“J2J4 It would appear that coronary artery bypass surgery may be of benefit to patients who suffer from recurrent tachyarrhythmias which are secondary to
February,
1975, Vol. 89, No. 2
iscbermic hearz. disease a medical. therapy by a rea men.
which are resistant to nable outpatient regib.
ents with
Prinzmetal’s variant angina of resting chest pain, ST segment elevation, RS widening, ventricular tachycardia, and ventricular fibrillation. These episodes were unresponsive to medical therapy ing lidocaine, procaine amide, and quinidine sulfate. Coronary arteriography revealed severe obstructive coronary artery disease, involving more than one coronary artery, in both patients Aorticocoronary saphenous vein grafts were utilized to bypass significant disease in each patient. En one patient blood flow through the grafts was measured at 90 and 65 ml per minute, respectively, at operation and patent grafts were demonstrated six months postoperatively. Neither patient has had recurrence of chest pain or evidence of ventricular tachycardia at one year or 2% years ~ostoperative~y~ Postoperative resting and maximal exercise EGG’s are normal. Coronary artery surgery may be an effective method of therapy for ischemic ventricular tachycardia when medica? therapy fails.
z
Prinzmetal. M., Kennamer, R., Merliss, R., Wada, T., and Naci, B.: Angina pectoris. I. A variant form of angina pectoris, Am. J. Med. 27:3’75, 1959. 2. Prinzmetal, M.,. Ekmekci, A., Kennamer, R., Kwoczynski, J. K., Shubin, H., and Toyoshima, II.: Variant form of angina pectoris, J. A. M. A. 174:1794, ?36Q. 3. Prinzmetal, M., Ekmekci, A., Toyoshima, H., and Kwoczynski, J.: Angina pectoris. III. Demonstration of
5.
J.
7
3. 3>”
13.
Il.
12.
13. 14.
:_5.
3 ehemma: origm oi ST tiev~aciori ,i’A .I .a.sidi,, ar1gina petcoris, its variant form, early myocardnai infarction, and some non-cardiac conditions, Am, J. Cardiol. 3276, 1959. Gillilan, R. E., IIawley, R., and Warbasse, J. R.: Seconci degree heart block occurring in a patient with Prinzmetal’s variant angina, ATvl H%E?T J 77:380. 1969. Botti, R. E.: A variant form of angina pectoris with recurrent transient complete heart block, Am. J. Cardiol. 17:443, 1966. Whiting; R. B,, Klein, M.D., VanderVter, J., and Lawn, 5.: Variant angina pectoris, N. 1970. Silverman, M. E., and Plamm, M,D: Variant an@na pectoris. Anatomic findings a:ld prognostic implrcations, Ann. Intern, Med. 751339, 1971, !Ian, J.: Ventricular vulnerabi nary occlusion, Am. J. Cardiol. Han, J., Goel, B., and Banson, S : Re-ectrant beats he ventricle during coronary ocdusion, AM :778,1970. H., Jr., Tresch, D. D,, co, E. H., and Lange, R. L.: Incidence, mqrtality rate and sequela of myocardial infarction immediately after coronary artery bypass surgery, - Lab. Clin. Med, 78:802, 1971. ,, Morse, D. P., Wichois, Is. T., and Nakhjavan, F. Goldberg, II.: Emergency aortocoronsry bypass: Treatment of ventricular tacbycardia due i,o ischemic heart disease, J. A. M. A. 21 Massan. N.. Escamilla. H. A.. and C?ark. J. G.: Acute corona& ins&icier-q and life threateriing cardiac acrhythmias eight months after tri$e, heart valve replacement, Surg. C&n. North Am. Peretz, D. I.: Variant angina pectoris of Prinzmetai, Can. Med. Assoc. J, 85:llOl. 1961. Ecker, R. R., Mullins, C. B., Grammer, J. C., Rea, W. J., and Atkins, J. M.: Control of intractable ye~tri~~~~ tachycardia by coronary revascdamk~attnn, Circulation :666, 1971. Blackburn, II., Taylor, II. I+ Cfkomcto. N., et al.: Standardization of the exercise e~e~~ro~~~d~~~~~arn. A systematic comparison of chest lead ~o~~~~r~t~o~s employed for monitoring during exercise, in Karvonen, Barry, A. J., editors: Physical activity and the heart Proceedings of a S~rn~os~~~~ FIeIsinki, Finland) Springfield, Ill., 1964, Charles C Timmas, Publisher, Chap. 9.
Minn.
Serious ventricular arrhythmias in patients with variant angina due to occlusive coronary artery disease may be difficult to control with conventional medical therapy. In patients with such arrhythmias, coronary artery bypass surgery may be indicated as treatment even though chest pain is not severe. The following cases illustrate successful surgical therapy of recurrent ventricular arrhythmias in two patients with Prinzmetal’s variant angina. Medical therapy failed to adequately control the tachyarrhythmia. Coronary arteriography demonstrated severe occlusive vascular disease, and following coronary artery surgery the arrhythmias were abolished. Case reports Case I, A 41-year-old white man was admitted to the hospital complaining of left chest pain of two months’ duration. The pain was described as a pressure sensation radiating to the jaw and left arm and was not related to exercise, food intake, or emotion. On several occasions the pain awakened the patient during the night. The patient smoked two packages of cigaretites daily, despite the presence of bronchial asthma for the previous 17 years. Adult-onset diabetes mellitus had been treated with diet and tolbutamide for five years. One parent suffered a myocardial infarction and both parents had chronic obstructive lung disease. Occasional inspiratory wheezes were detected in both lungs. The heart was of normal size and a fourth heart sound was present. No cardiac murmur was detected. The serum triglycerides were 540 mg. per 100 ml., the From the Veterans Administration Hospital and the Departments of Medicine and Surgery, University of Minnesota, Minneapolis, Minn. Received for publication July 13, 1973. Reprint requests to: Fredarick L. Gobel, M.D., Cardiovascular Section, Veterans Administration Hospital, 54th St. & 48th Ave. So., Minneapolis, Minn. 55417.
236
blood cholesterol was 245 mg. per 100 ml., and the glucose tolerance test was abnormal. Early in the hospital course, three syncopal episodes associated with chest pain occurred but were not monitored by an ECG. Thereafter frequent episodes of chest pain followed by ST elevation, QRS widening, and short runs of ventricular tachycardia occurred (Fig. 1). ST segment elevation was confined to anterior precordial leads. Six of these episodes resulted in ventricular tachycardia and/or ventricular fibrillation which were successfully treated by D.C. shock in four instances and by a bolus of lidocaine in two instances. The patient was treated intensively in the coronary-care unit (CCU1 for 55 days. Quinidine (200 mg. every four hours), Pronestyl (750 mg. every three hours), propranolol (120 mg. daily), Isordil (to tolerance), atropine, and lidocaine (4 to 5 mg. per minute), either alone or in combination, failed to suppress the ventricular arrhythmias. An attempt at suppressing the arrhythmia by increasing the ventricular rate by pacing was unsuccessful. Coronary arteriography demonstrated high-grade obstruction in the left anterior descending coronary artery (LAD) and diffuse disease in the circumflex branch of the left coronary artery (LCX) (Fig. 21. Diffuse disease was also present in the right coronary artery (RCA). While waiting for operation, the patient had another episode of chest pain and syncope. Shortly after induction of anesthesia, the patient developed hypotension which did not respond adequately to pressor agents. The chest was opened and cardiac massage was initiated. A 1.5 mm. probe could not be passed through the lesion in the LAD and, in spite of a mean aortic pressure of 60 mm. Hg, there was no antegrade flow through the LAD, indicating a highly obstructive lesion. Two aorticocoronary saphenous vein bypass grafts (ACSVG) from the ascending aorta were anastomosed, one each to the LAD and to the posterior descending coronary artery (PDA). The flow rate to the LAD was 90 ml. per minute and the flow rate to the PDA was 65 ml. per minute as measured by an electromagnetic flowmeter at the time of operation. The patient had an uneventful postoperative course. Since operation he has had no chest pain, syncopal episodes, or suspected or documented arrhythmias. Coronary arteriography six months postoperatively revealed both ACSVG to be pa-
February,
1975, Vol. 89, No. 2, pp. 236-241
Lead
MCL i
@I
Kg. 1. Patient 1: A MCL I monitor lead tracing demonstrates typical changes that chest pain: (A) normal pattern, (Bl ST segment elevation, (0 short run of ventricular sion to normal rhythm.
tent (Fig. 3). There were no dyskinetic areas of the left ventricle. The postoperative resting ECG was normal (Fig. 4A 1.An exercise EGG revealed no ST segment changes at a heart rate of 140 beats per minute but was discontinued because the patient complained of leg pain (Fig. 4B 1. Case 2. A 51-year-old white man was admitted to the hospital because of recurrent chest pain described as a pressure sensation in the lower substernal region. Initially the pain occurred in the morning after awakening from sleep but then nocturnal pain developed. There were no episodes of chest pain associated with exertion. The pain had been present for about one month prior to admission to the hospital. The patient denied dyspnea or syncopal episodes. There was no family history of coronary artery disease but the patient’s father had diabetes mellitus. The physical findings and laboratory data were normal. During the hospital course frequent episodes of chest pain associated with ST segment elevation were noted. A 12 lead ECG revealed these changes to be in Leads II, III, and aVF (Fig. 5A). With chest pain, ST segment elevation, and QRS changes, there were often PVC’s and short runs of ventricuiar tachycardia (Fig. 5B). These episodes persisted over a 25 day period of continuous monitoring in the CCIJ despite medical therapy consisting of Pronestyl (250 mg. every four hours), propranolol (80 mg. daily), Isordil (to tolerance), and an infusion of lidocaine at 4
American
FIeart
Jo‘surnrti
occurred during episi:des of tachycardia, and :Di rever-
Fig. 2. Patient :: A rigat antenor obiq~e view ff2ti degreesi of the left coronary artery demonstrates high-grade obstruction in the left anterior descending Gb?l, arrawsJ and diffuse disease in the !eft circumflex coronary artery 8XX.
Nordstrom
et al.
Fig. 3. Patient 1: Right anterior oblique views (60 degrees) demonstrating (left) descending coronary artery (PDA) and (right) a patent graft to the left anterior cate site of anastomosis).
Standing Rest
III
AVR AVL AVF
immediate Post Exercise
Exercise Recovery 3 minute5
i minute
2 minutes
Fig. 4A. Patient 1: Six months bad a normal 12 lead ECG.
postoperatively
the
Recovery 6 minutes
patient
3 to 5 mg. per minute. Coronary arteriography revealed a 90 per cent obstructing lesion in the mid third of the LCX (Fig. 6). The dominant coronary artery was the left. ,There was also diffuse disease in the RCA. Multiple x-ray views of LAD were interpreted to be normal. At operation an ACSVG was inserted from the ascending aorta to the LCX. Flow measurements were not made. The patient’s postoperative course was unremarkable. There were no further episodes of chest pain, ST elevation, or evidence of an operative or immediate postoperative myocardial infarction. Two and a half years have elapsed since
238
a patent graft to the posterior descending (LAD, arrows indi-
4
minutes
minutes
Fig. 48.
exercise Blackburn
AVF Resting
AVF immediate Post Exercise
Six months postoperatively the patient had a normal ECG at a heart rate of 140 beats per minute. A monitor lead system was used.15
February,
1975, Vol. 89, No. 2
Fig. S-4. Patient 2: A 12 lead ECG demonstrating ST segment elevation in Leads II, III, and aV F during an acute episode of chest pain.
Patient 2: A right anterior ob;qtie ~ieri di) degree~i of the left coronary
artery
demonstrates
high-grade
obstruction
in the left circumflex coronary artery !tCX’.
episode of chest pain tern, (B ) ST segment !ar tachycardia.
CI. VI monitor lead tracing during an demonstrates (A 1 patient’s normal patelevation, and (6) short run of ventricu-
operation witnout recurrent chest pain. A recent resting ECG was normal ar,d an exercise ECG was normal at a heart rate of 150 beats per minute (Figs. 7A and 7B.
Prinzmetal’s variant angina is characterized as typical ischemie cardiac pain with the major exception that pain occurs at rest and not during exercise. These episo es tend to be cyclic and may occur at approximately the same time ST elevation, daily. I22 The ECG demonstrates rather than depression, in the distribution of the involved coronary artery.lJ Approximately 50 per een.t of patients with variant angina have ve~t~i~~~a~ arrhythmias and in a few patients
Fig. 7 . Patienr 2: Two and oni: haif year., postoperatively the resting ECG was normal.
Nordstrom
et al.
1.2 minutes MPH Grade
3.4 14%
Exercise
Imediate Rest
3 minutes 1.5 MPH 5% Grade
6 minutes 1.7 MPH 10% Grade
2 minutes Recovery
9 minutes MPH 12% Grade
2.5
Fig. 78. Two minute.
and
one half
years
postoperatively
an exercise
Although it has been suggested that variant angina may be associated with an isolated lesion in a single coronary artery, a few autopsy studies have demonstrated diffuse coronary artery disease in addition to the high-grade obstructing lesion. 1,13Both patients reported had significant lesions obstructing more than 50 per cent of the lumen in at least two vessels. Patient 1 had disease involving all three coronary arteries. The ST segment shifts and arrhythmias, however, are thought to be a consequence of a single highgrade obstructing lesion.le3The hope that patients with variant angina might represent the ideal surgical candidate having an isolated solitary lesion in one coronary artery is not borne out in some instances. It has long been recognized that ischemia predisposes to ventricular irritability. Recently, experimental studies have helped to delineate possible underlying mechanisms. Han demonstrated that the fibrillatory threshold in the ventricle is decreased during ischemia.s Additional studies have demonstrated that ventricular impulses are propagated very slowly through ischemic areas and emerge into normal repolarized areas as re-entrant beats.g Such a reentrant process may continue to produce multi-
240
ECG
was normal
at heart
rate
of 150 beats
per
ple extrasystoles or tachycardia in the ventricle. Although difficult to prove, it would seem that a re-entrant mechanism secondary to ischemia may have been the basis for recurrent ventricular tachyarrhythmias in these two patients. Patients with recurrent ventricular tachycardia due to myocardial ischemia may note cessation of the arrhythmia after suffering a myocardial infarction. Myocardial infarctions are common following saphenous vein bypass surgery.lOThat such is not the situation in the patients reported here, and that the relief from the arrhythmia was subsequent to relief of the ischemia by operation, is supported by the normal postoperative ECG’s in both patients and by the patent saphenous vein grafts in the first patient. The surgical approach for variant angina and ventricular arrhythmias is supported by the cases reported here and by several recent reports of patients with ischemic heart disease (not variant angina1 and recurrent tachyarrhythmias who have noted abolition or arrhythmias following coronary artery surgery.“J2J4 It would appear that coronary artery bypass surgery may be of benefit to patients who suffer from recurrent tachyarrhythmias which are secondary to
February,
1975, Vol. 89, No. 2
iscbermic hearz. disease a medical. therapy by a rea men.
which are resistant to nable outpatient regib.
ents with
Prinzmetal’s variant angina of resting chest pain, ST segment elevation, RS widening, ventricular tachycardia, and ventricular fibrillation. These episodes were unresponsive to medical therapy ing lidocaine, procaine amide, and quinidine sulfate. Coronary arteriography revealed severe obstructive coronary artery disease, involving more than one coronary artery, in both patients Aorticocoronary saphenous vein grafts were utilized to bypass significant disease in each patient. En one patient blood flow through the grafts was measured at 90 and 65 ml per minute, respectively, at operation and patent grafts were demonstrated six months postoperatively. Neither patient has had recurrence of chest pain or evidence of ventricular tachycardia at one year or 2% years ~ostoperative~y~ Postoperative resting and maximal exercise EGG’s are normal. Coronary artery surgery may be an effective method of therapy for ischemic ventricular tachycardia when medica? therapy fails.
z
Prinzmetal. M., Kennamer, R., Merliss, R., Wada, T., and Naci, B.: Angina pectoris. I. A variant form of angina pectoris, Am. J. Med. 27:3’75, 1959. 2. Prinzmetal, M.,. Ekmekci, A., Kennamer, R., Kwoczynski, J. K., Shubin, H., and Toyoshima, II.: Variant form of angina pectoris, J. A. M. A. 174:1794, ?36Q. 3. Prinzmetal, M., Ekmekci, A., Toyoshima, H., and Kwoczynski, J.: Angina pectoris. III. Demonstration of
5.
J.
7
3. 3>”
13.
Il.
12.
13. 14.
:_5.
3 ehemma: origm oi ST tiev~aciori ,i’A .I .a.sidi,, ar1gina petcoris, its variant form, early myocardnai infarction, and some non-cardiac conditions, Am, J. Cardiol. 3276, 1959. Gillilan, R. E., IIawley, R., and Warbasse, J. R.: Seconci degree heart block occurring in a patient with Prinzmetal’s variant angina, ATvl H%E?T J 77:380. 1969. Botti, R. E.: A variant form of angina pectoris with recurrent transient complete heart block, Am. J. Cardiol. 17:443, 1966. Whiting; R. B,, Klein, M.D., VanderVter, J., and Lawn, 5.: Variant angina pectoris, N. 1970. Silverman, M. E., and Plamm, M,D: Variant an@na pectoris. Anatomic findings a:ld prognostic implrcations, Ann. Intern, Med. 751339, 1971, !Ian, J.: Ventricular vulnerabi nary occlusion, Am. J. Cardiol. Han, J., Goel, B., and Banson, S : Re-ectrant beats he ventricle during coronary ocdusion, AM :778,1970. H., Jr., Tresch, D. D,, co, E. H., and Lange, R. L.: Incidence, mqrtality rate and sequela of myocardial infarction immediately after coronary artery bypass surgery, - Lab. Clin. Med, 78:802, 1971. ,, Morse, D. P., Wichois, Is. T., and Nakhjavan, F. Goldberg, II.: Emergency aortocoronsry bypass: Treatment of ventricular tacbycardia due i,o ischemic heart disease, J. A. M. A. 21 Massan. N.. Escamilla. H. A.. and C?ark. J. G.: Acute corona& ins&icier-q and life threateriing cardiac acrhythmias eight months after tri$e, heart valve replacement, Surg. C&n. North Am. Peretz, D. I.: Variant angina pectoris of Prinzmetai, Can. Med. Assoc. J, 85:llOl. 1961. Ecker, R. R., Mullins, C. B., Grammer, J. C., Rea, W. J., and Atkins, J. M.: Control of intractable ye~tri~~~~ tachycardia by coronary revascdamk~attnn, Circulation :666, 1971. Blackburn, II., Taylor, II. I+ Cfkomcto. N., et al.: Standardization of the exercise e~e~~ro~~~d~~~~~arn. A systematic comparison of chest lead ~o~~~~r~t~o~s employed for monitoring during exercise, in Karvonen, Barry, A. J., editors: Physical activity and the heart Proceedings of a S~rn~os~~~~ FIeIsinki, Finland) Springfield, Ill., 1964, Charles C Timmas, Publisher, Chap. 9.