1372
Brief
Communications
American
November 1992 Heari Jwrnal
Percutaneous balloon angioplasty through an anomalous left main coronary artery Joel K. Kahn,
MD Ann Arbor,
Mich.
Percutaneous transluminal coronary angioplasty (PTCA) has been used to revascularize stenotic coronary arteries in several million patients over the last 15 years. Important advances in technique, equipment, and adjunctive pharmacologic t.reatment have led to routine procedural success rates that are well over 90ei. Although congenital coronary anomalies are observed in as many as 1.5% of patients who undergo coronary angiography,1,2 there are few reports of PTCA in patients with these anomalies. We report the details of PTCA in a patient with a rare anomaly of the left main coronary artery arising from the right sinus of Valsalva. An 82-year-old woman experienced episodic angina over a &week period, which culminated in admission to the hospital with a non-Q-wave anterior myocardial infarction. She continued to have angina in spite of administration of diltiazem and isosorbide dinit.rate, and a cardiac catheterization was performed. The right femoral approach was used with 6F catheters. Left ventriculography demonstrated mild hypokinesis of the anterior wall. A left Judkins catheter did not identify the left main coronary artery (LMCA). The dominant right coronary artery was selectively injected with a Judkins catheter and was determined to be normal. An aortogram demonstrated the origin of the LMCA in the right sinus of Valsalva. A right Amplatz 1 catheter (Becton Dickinson Vascular Access Div.. Sandy, Utah) was used to select the origin of the anomalous left main artery. A pulmonary artery catheter was placed transvenously, and angiography in the left lateral projection demonstrated that the anomalous LMCA coursed in a retroaortic position (Fig. 1). Injections demonstrated a 80?; discrete stenosis of the proximal left anterior descending artery (Fig. 2). After the patient had additional episodes of angina, PTCA was performed. An 8F right Amplatz 1 guide (Schneider Inc., Minneapolis, Minn.) was used to select the anomalous LMCA. An 0.014 inch Hi-Torque Floppy guide wire (Advanced Cardiovascular Systems, Santa Clara, Calif.) and a 2.5 mm Spectrum balloon catheter (Advanced Cardiovascular Systems) were used to cross and dilate the stenotic proximal LAD three times to a maximum of 14 atm for 90 seconds (Fig. 3). Final injections demonstrated a final residual stenosis of less than 20 Y (Fig. 4). After discharge from the hospital, the patient has remained free of angina for 6 months. From Ann Arbor Cardiology Consultants, lar Institute, Ann Arbor, Mich. Reprint requests: bm. MI 48106. ‘Ll4l40533
Joel K. Kahn,
MD,
P.C., Michigan 5333 McAuley,
Hean
and Vascu-
Suite 3009, Ann Ar-
Fig. 1. A selective coronary arteriogram in the left lateral projection. The pulmonary artery Octrge arrow) and the aorta (small arrow) are identified with diagnostic catheters. The anomalous left main coronary artery [open arrow) arises from the right sinus of Valsalva and courses posterior to the aorta.
Fig. 2. In a right anterior oblique projection with cranial angulation a discrete area of narrowing is identified in the proximal left anterior descending artery (arrow). Anomalous origin of the LMCA is a rare anomaly that may be of clinical significance in two ways.’ The LMCA may course between the aorta and pulmonary trunk and may lead to myocardial ischemia and sudden death in the first 2 decades of life.’ Alternatively, t.he LMCA may course
Volume 124 Number
Brief Communications
5
1373
Fig. 3. A 2.5 mm balloon catheter and an 0.014 inch guide wire are positioned across the narrowing during balloon inflat.ion.
Fig. 4. Selective angiography after balloon angioplasty demonstrates resolution of coronary narrowing (arrow).
across the pulmonary trunk or behind the aorta. Although symptoms or signs of myocardial ischemia may also be found early in life as a result of compression of the LMCA,4 more commonly they manifest later in life if coronary artery disease develops. Our patient is an example of the second phenomenon. In angiographic series, anomalous origin of the LMCA from the right sinus of Valsalva has been observed in 0.02 % of patients.l, Z Few cases of PTCA in a patient with this anomaly have been reported.5s 6 The technical approach to PTCA in a patient with an anomalous coronary artery tends to differ most from the approach used for other patients in guide catheter selection.: Particular attention to the diagnostic study for the site of the ostium, the angle of take-off, and the course of the artery is required. In our patient, the LMCA arose posterior to the right coronary artery with an inferior angulation. Although the diagnostic right Judkins catheter was unable to select the origin, both the diagnostic and guiding catheters with the right Amplatz 1 configuration had sufficient inferior angulation to be seated in the LMCA in a stable manner. If the origin of the anomalous vessel prohibits adequate guide catheter support, another approach that has been used involves positioning one wire down the anomalous artery and one down the normal artery for further stability.a Although fewer than 20 cases have been reported in the literature on PTCA in patients with anomalous origin of coronary arteries,’ it is likely that with the an increasing number of operators expanding use of PTCA,
will encounter these challenging patients. With careful attention to origin and course of the anomalous vessels and adequate selection of equipment that is tailored to the anatomic characteristics of these arteries, excellent angiographic and clinical results can be anticipated. REFERENCES
1. Hobbs R, Milit H, Raghavan P, Moodie D, Sheldon W. Congenital coronary artery anomalies: clinical and therapeutic implications. Cardiovasc Clin 1982;12:43-58. 2. Topaz 0, DeMarchena EJ, Perin E, Sommer LS, Mallon SM, Chahine RA. Anomalous coronary arteries: angiographic findings in 80 patients. International J Cardiol 1992;34:129-38. 3. Barth CI, Roberts W. Left main coronary artery originating from the right sinus of Valsalva and coursing between the aorta and pulmonary trunk. J Am Co11 Cardiol 19867: 366-73. 4. Murphy DA, Roy DL, Sohal M, Chandler BM. Anomalous origin of left main coronary artery from anterior sinus of Valsalva with myocardial infarction. J Thorac Cardiovasc Surg 197&75:282-5. 5. Bass T, Miller A, Rubin M, Stowers S, Perryman R. Transluminal angioplasty of anomalous coronary arteries. AM HEART J 1986:112:610-13. 6. Grenadier E, Beyar R, Amikam S, Markiewicz W. Two-vessel PTCA of single anomalous coronarv arterv. AM HEART J 1992:123:220-5 7. Top& 0, DiSciascio G, Goudreau E, Cowley MJ, Nath A, Kohli RS, Vetrovec GW. Coronarv angioolastv of anomalous coronary arteries: notes on technical aspects. Cathet Cardiovast Diagn 1990;21:106-11. 8. Das GS, Wysham DG. Double wire technique for additional guiding catheter support in anomalous left circumflex coro-
1374
Brief Communications
nary artery angioplasty.
American
Cathet Cardiovasc Diagn 1991%:
102-4.
9. Romo A, Macaya C, Hernandez R, Alfonso I?,Goicolea J, Zarco P. Percutaneous coronary angioplasty in patients with congenital anomalies of the coronary arteries: a technical &allenee. J Invas Cardiol 1991:3:235-40.
November 1992 Hewl Journal
Sian slice reconstruction was performed to generate ‘rota tional” views of the heart as l-pixel thick slices. These views consisted of a series of individual slices through the long axis of the heart, which were obtained sequentially every 15 degrees over a 180-degree arc. With this method. a total of 12 slices (single cuts through the horizontal and vertical long-axis planes, as well as 10 additional cuts ohlique to these planes) were obtained. One hour later. a maximal exercise treadmill test was performed (modified Bruce protocol; starting stage: 1.7 miles per hour and 5(, grade). Technetium 99m sestamibi (22 mCi) was given I minute before the peak exercise level was reached. The patient exercised for a total of 230 seconds. Maximum heart rate was 163 beats/min, and blood pressure response was appropriate. At peak exercise level the patient experienced his usual chest pain, and an additional 2.0 mm of horizontal ST-segment depression over baseline was seen in the anterolateral precordial leads. Ninety seconds after exercise was stopped the patient experienced VT (Fig. l), which persisted for 30 seconds and resolved spontaneously. The patient was free of symptoms during this episode, and the arrhythmia did not recur. Single photon emission coniputed tomography was repeated 45 minutes after the end of the exercise test. Myocardial perfusion images (Fig. 2) revealed left ventricular dilation, persist,ent defects that involved the posterior wall and basal portion of the inferior wall, and transient defecm of the inferinr and apical segments. Case 2. The patient was a 61-year-old man who was referred for exercise testing for evaluation of functional status. Medical history was remarkable for an acute myocardial infarction 3 months before presentation, which was complicated by mild congestive heart failure. At the time of the exercise test the patient was free of symptoms. Medications at. the time of the test were digoxin and captopril. A two-dimensional echocardiogram, which was performed immediately before treadmill testing, showed akinesis of the septum and dyskinesis of the apex. The baseline ECG showed normal sinus rhythm, a maximum QRS width of 0.08 seconds, Q waves in leads Vi, Vs, and V:,. and nonspecific ST-segment abnormalities in leads Vs and VG. Technetium 99m sestamibi imaging with single photon emission computed tomography was performed with the protocol described previously. The patient exercised for 162 seconds (Bruce protocol). The heart rate increased t,o 156 beats/min at. peak exercise Ievel, and blood pressure response was ap propriate. At peak exercise level, t,he patient had chest pain, up to 1.5 mm horizontal and downsloping STsegment depression in the inferior leads, and VT at a rate of 250 beats/min for 6 seconds (Fig. 3). The test was stopped immediately, and no recurrence of the arrhythmia was seen. Technetium 99m sestamibi images showed left ventricular dilation; persistent perfusion defects that involved the anterior, apical, and inferior segments; and a transient defect of the septum (Fig. 4). Subsequent core nary angiography demonstrated triple-vessel CAD. Comments. Exercise-induced ventricular arrhythmias are often seen in patients who are referred for exercise stress testing. In a review of 3351 patients who were -1
Myocardial imaging with technetium 99m sestamibi after exercise-induced ventricular tachycardia Henry G. Stratmann, James L. Littlefield, St. Louis, MO.
MD, Michael Flynn, MD, MD, and Mark D. Wittry, MD
Development of ventricular tachycardia (VT) is an uncommon occurrence during routine exercise treadmill testing.le4 Although this arrhythmia may occur in patients who do not have clinically overt heart disease, it is more often associated with the presence of concomitant coronary artery disease (CAD) or left ventricular systolic dysfunction.l,z, 4 Technetium 99m sestamibi is a new myocardial perfusion agent that can be used to assess the presence of CAD and exercise-induced myocardial ischemia.‘. s In this report, t,he results of tomographic imaging with gamTc sestamibi in two patients who experienced exercise-induced VT are presented. Case 2. A 58-year-old man was referred for exercise testing to evaluate the efficacy of medical therapy for CAD. Significant history included coronary artery bypass surgery 9 and 5 years before presentation and an acute myocardial infarction that was complicated by congestive heart failure 3 months before exercise testing. Cardiac catheterization at the time of myocardial infarction showed severe triplevessel CAD, occlusion of all bypass grafts except for an internal mammary graft to the left anterior descending coronary artery, and a calculated left ventricular ejection fraction of 0.21. At the time of the stress test, the patient had stable, infrequent chest pain (New York Heart Association class II) and no symptoms of congestive heart failure. Medications that were being taken at the time of the test were digoxin, captopril, and isosorbide dinitrate. The preexercise 12-lead ECG showed normal sinus rhythm, a maximum QRS width of 0.09 seconds, nonspecific ST abnormalities, and no Q waves that were consistent with prior myocardial infarction. Single photon emission computed tomography was first performed at rest and then at 45 minutes after injection of 8 mCi of ggmTc sestamibi Cate-
From the Departments of Cardiology and Nuclear Medicine, St. Louis Veterans Administration Medical Center and St. Louis University, St. Louis. Reprint requests: Henry Stratmam, MD, Department of Cardiology, 11 IA-JC, St. Louis Veterans Administration Medical Center. St. Louis, MO G3lX5. 4/4/40667
-~
Brief
Communications
American
November 1992 Heari Jwrnal
Percutaneous balloon angioplasty through an anomalous left main coronary artery Joel K. Kahn,
MD Ann Arbor,
Mich.
Percutaneous transluminal coronary angioplasty (PTCA) has been used to revascularize stenotic coronary arteries in several million patients over the last 15 years. Important advances in technique, equipment, and adjunctive pharmacologic t.reatment have led to routine procedural success rates that are well over 90ei. Although congenital coronary anomalies are observed in as many as 1.5% of patients who undergo coronary angiography,1,2 there are few reports of PTCA in patients with these anomalies. We report the details of PTCA in a patient with a rare anomaly of the left main coronary artery arising from the right sinus of Valsalva. An 82-year-old woman experienced episodic angina over a &week period, which culminated in admission to the hospital with a non-Q-wave anterior myocardial infarction. She continued to have angina in spite of administration of diltiazem and isosorbide dinit.rate, and a cardiac catheterization was performed. The right femoral approach was used with 6F catheters. Left ventriculography demonstrated mild hypokinesis of the anterior wall. A left Judkins catheter did not identify the left main coronary artery (LMCA). The dominant right coronary artery was selectively injected with a Judkins catheter and was determined to be normal. An aortogram demonstrated the origin of the LMCA in the right sinus of Valsalva. A right Amplatz 1 catheter (Becton Dickinson Vascular Access Div.. Sandy, Utah) was used to select the origin of the anomalous left main artery. A pulmonary artery catheter was placed transvenously, and angiography in the left lateral projection demonstrated that the anomalous LMCA coursed in a retroaortic position (Fig. 1). Injections demonstrated a 80?; discrete stenosis of the proximal left anterior descending artery (Fig. 2). After the patient had additional episodes of angina, PTCA was performed. An 8F right Amplatz 1 guide (Schneider Inc., Minneapolis, Minn.) was used to select the anomalous LMCA. An 0.014 inch Hi-Torque Floppy guide wire (Advanced Cardiovascular Systems, Santa Clara, Calif.) and a 2.5 mm Spectrum balloon catheter (Advanced Cardiovascular Systems) were used to cross and dilate the stenotic proximal LAD three times to a maximum of 14 atm for 90 seconds (Fig. 3). Final injections demonstrated a final residual stenosis of less than 20 Y (Fig. 4). After discharge from the hospital, the patient has remained free of angina for 6 months. From Ann Arbor Cardiology Consultants, lar Institute, Ann Arbor, Mich. Reprint requests: bm. MI 48106. ‘Ll4l40533
Joel K. Kahn,
MD,
P.C., Michigan 5333 McAuley,
Hean
and Vascu-
Suite 3009, Ann Ar-
Fig. 1. A selective coronary arteriogram in the left lateral projection. The pulmonary artery Octrge arrow) and the aorta (small arrow) are identified with diagnostic catheters. The anomalous left main coronary artery [open arrow) arises from the right sinus of Valsalva and courses posterior to the aorta.
Fig. 2. In a right anterior oblique projection with cranial angulation a discrete area of narrowing is identified in the proximal left anterior descending artery (arrow). Anomalous origin of the LMCA is a rare anomaly that may be of clinical significance in two ways.’ The LMCA may course between the aorta and pulmonary trunk and may lead to myocardial ischemia and sudden death in the first 2 decades of life.’ Alternatively, t.he LMCA may course
Volume 124 Number
Brief Communications
5
1373
Fig. 3. A 2.5 mm balloon catheter and an 0.014 inch guide wire are positioned across the narrowing during balloon inflat.ion.
Fig. 4. Selective angiography after balloon angioplasty demonstrates resolution of coronary narrowing (arrow).
across the pulmonary trunk or behind the aorta. Although symptoms or signs of myocardial ischemia may also be found early in life as a result of compression of the LMCA,4 more commonly they manifest later in life if coronary artery disease develops. Our patient is an example of the second phenomenon. In angiographic series, anomalous origin of the LMCA from the right sinus of Valsalva has been observed in 0.02 % of patients.l, Z Few cases of PTCA in a patient with this anomaly have been reported.5s 6 The technical approach to PTCA in a patient with an anomalous coronary artery tends to differ most from the approach used for other patients in guide catheter selection.: Particular attention to the diagnostic study for the site of the ostium, the angle of take-off, and the course of the artery is required. In our patient, the LMCA arose posterior to the right coronary artery with an inferior angulation. Although the diagnostic right Judkins catheter was unable to select the origin, both the diagnostic and guiding catheters with the right Amplatz 1 configuration had sufficient inferior angulation to be seated in the LMCA in a stable manner. If the origin of the anomalous vessel prohibits adequate guide catheter support, another approach that has been used involves positioning one wire down the anomalous artery and one down the normal artery for further stability.a Although fewer than 20 cases have been reported in the literature on PTCA in patients with anomalous origin of coronary arteries,’ it is likely that with the an increasing number of operators expanding use of PTCA,
will encounter these challenging patients. With careful attention to origin and course of the anomalous vessels and adequate selection of equipment that is tailored to the anatomic characteristics of these arteries, excellent angiographic and clinical results can be anticipated. REFERENCES
1. Hobbs R, Milit H, Raghavan P, Moodie D, Sheldon W. Congenital coronary artery anomalies: clinical and therapeutic implications. Cardiovasc Clin 1982;12:43-58. 2. Topaz 0, DeMarchena EJ, Perin E, Sommer LS, Mallon SM, Chahine RA. Anomalous coronary arteries: angiographic findings in 80 patients. International J Cardiol 1992;34:129-38. 3. Barth CI, Roberts W. Left main coronary artery originating from the right sinus of Valsalva and coursing between the aorta and pulmonary trunk. J Am Co11 Cardiol 19867: 366-73. 4. Murphy DA, Roy DL, Sohal M, Chandler BM. Anomalous origin of left main coronary artery from anterior sinus of Valsalva with myocardial infarction. J Thorac Cardiovasc Surg 197&75:282-5. 5. Bass T, Miller A, Rubin M, Stowers S, Perryman R. Transluminal angioplasty of anomalous coronary arteries. AM HEART J 1986:112:610-13. 6. Grenadier E, Beyar R, Amikam S, Markiewicz W. Two-vessel PTCA of single anomalous coronarv arterv. AM HEART J 1992:123:220-5 7. Top& 0, DiSciascio G, Goudreau E, Cowley MJ, Nath A, Kohli RS, Vetrovec GW. Coronarv angioolastv of anomalous coronary arteries: notes on technical aspects. Cathet Cardiovast Diagn 1990;21:106-11. 8. Das GS, Wysham DG. Double wire technique for additional guiding catheter support in anomalous left circumflex coro-
1374
Brief Communications
nary artery angioplasty.
American
Cathet Cardiovasc Diagn 1991%:
102-4.
9. Romo A, Macaya C, Hernandez R, Alfonso I?,Goicolea J, Zarco P. Percutaneous coronary angioplasty in patients with congenital anomalies of the coronary arteries: a technical &allenee. J Invas Cardiol 1991:3:235-40.
November 1992 Hewl Journal
Sian slice reconstruction was performed to generate ‘rota tional” views of the heart as l-pixel thick slices. These views consisted of a series of individual slices through the long axis of the heart, which were obtained sequentially every 15 degrees over a 180-degree arc. With this method. a total of 12 slices (single cuts through the horizontal and vertical long-axis planes, as well as 10 additional cuts ohlique to these planes) were obtained. One hour later. a maximal exercise treadmill test was performed (modified Bruce protocol; starting stage: 1.7 miles per hour and 5(, grade). Technetium 99m sestamibi (22 mCi) was given I minute before the peak exercise level was reached. The patient exercised for a total of 230 seconds. Maximum heart rate was 163 beats/min, and blood pressure response was appropriate. At peak exercise level the patient experienced his usual chest pain, and an additional 2.0 mm of horizontal ST-segment depression over baseline was seen in the anterolateral precordial leads. Ninety seconds after exercise was stopped the patient experienced VT (Fig. l), which persisted for 30 seconds and resolved spontaneously. The patient was free of symptoms during this episode, and the arrhythmia did not recur. Single photon emission coniputed tomography was repeated 45 minutes after the end of the exercise test. Myocardial perfusion images (Fig. 2) revealed left ventricular dilation, persist,ent defects that involved the posterior wall and basal portion of the inferior wall, and transient defecm of the inferinr and apical segments. Case 2. The patient was a 61-year-old man who was referred for exercise testing for evaluation of functional status. Medical history was remarkable for an acute myocardial infarction 3 months before presentation, which was complicated by mild congestive heart failure. At the time of the exercise test the patient was free of symptoms. Medications at. the time of the test were digoxin and captopril. A two-dimensional echocardiogram, which was performed immediately before treadmill testing, showed akinesis of the septum and dyskinesis of the apex. The baseline ECG showed normal sinus rhythm, a maximum QRS width of 0.08 seconds, Q waves in leads Vi, Vs, and V:,. and nonspecific ST-segment abnormalities in leads Vs and VG. Technetium 99m sestamibi imaging with single photon emission computed tomography was performed with the protocol described previously. The patient exercised for 162 seconds (Bruce protocol). The heart rate increased t,o 156 beats/min at. peak exercise Ievel, and blood pressure response was ap propriate. At peak exercise level, t,he patient had chest pain, up to 1.5 mm horizontal and downsloping STsegment depression in the inferior leads, and VT at a rate of 250 beats/min for 6 seconds (Fig. 3). The test was stopped immediately, and no recurrence of the arrhythmia was seen. Technetium 99m sestamibi images showed left ventricular dilation; persistent perfusion defects that involved the anterior, apical, and inferior segments; and a transient defect of the septum (Fig. 4). Subsequent core nary angiography demonstrated triple-vessel CAD. Comments. Exercise-induced ventricular arrhythmias are often seen in patients who are referred for exercise stress testing. In a review of 3351 patients who were -1
Myocardial imaging with technetium 99m sestamibi after exercise-induced ventricular tachycardia Henry G. Stratmann, James L. Littlefield, St. Louis, MO.
MD, Michael Flynn, MD, MD, and Mark D. Wittry, MD
Development of ventricular tachycardia (VT) is an uncommon occurrence during routine exercise treadmill testing.le4 Although this arrhythmia may occur in patients who do not have clinically overt heart disease, it is more often associated with the presence of concomitant coronary artery disease (CAD) or left ventricular systolic dysfunction.l,z, 4 Technetium 99m sestamibi is a new myocardial perfusion agent that can be used to assess the presence of CAD and exercise-induced myocardial ischemia.‘. s In this report, t,he results of tomographic imaging with gamTc sestamibi in two patients who experienced exercise-induced VT are presented. Case 2. A 58-year-old man was referred for exercise testing to evaluate the efficacy of medical therapy for CAD. Significant history included coronary artery bypass surgery 9 and 5 years before presentation and an acute myocardial infarction that was complicated by congestive heart failure 3 months before exercise testing. Cardiac catheterization at the time of myocardial infarction showed severe triplevessel CAD, occlusion of all bypass grafts except for an internal mammary graft to the left anterior descending coronary artery, and a calculated left ventricular ejection fraction of 0.21. At the time of the stress test, the patient had stable, infrequent chest pain (New York Heart Association class II) and no symptoms of congestive heart failure. Medications that were being taken at the time of the test were digoxin, captopril, and isosorbide dinitrate. The preexercise 12-lead ECG showed normal sinus rhythm, a maximum QRS width of 0.09 seconds, nonspecific ST abnormalities, and no Q waves that were consistent with prior myocardial infarction. Single photon emission computed tomography was first performed at rest and then at 45 minutes after injection of 8 mCi of ggmTc sestamibi Cate-
From the Departments of Cardiology and Nuclear Medicine, St. Louis Veterans Administration Medical Center and St. Louis University, St. Louis. Reprint requests: Henry Stratmam, MD, Department of Cardiology, 11 IA-JC, St. Louis Veterans Administration Medical Center. St. Louis, MO G3lX5. 4/4/40667
-~
