CASE REPORTS
Creation of Pseudo Narrowing Coronary Angioplasty
During
Alan N. Tenanlia, MD. James E. Tcheng, MD, Harry R. Phillips, Ill, MD, and Richard s. Stack, MD ince the initial description of percutaneoustransluminal coroS nary angioplasty (PTCA) by Gruentzig et al,t the application of PTCA has expanded dramatically, exceeding 300,000 cases annually. Along with this growth, patients with increasingly complex coronary arterial anatomy and lesions are being treated. Technologic advances,coupled with operator experience,have reduced acute procedural risk to an acceptable, although not negligible, level.2 During the performance of PTCA, the interventional cardiologist must quickly recognize and appropriately manage any complication that arises.In addition, the operator must be able to differentiate true complications from pseudocomplications; that is, the operator must recognize the artifactual nature of an apparent complication that is not necessarilywhat it appearsto be. For instance, Espluges et al3 reported the appearanceof persistent staining by contrast material of the arterial wall, suggesting significant dissection during PTCA while using a new monorail balloon catheter. The artifact disappearedwith balloon deflation.3 We report a patient in whom straightening of a tortuous coronary artery by a PTCA guidewire created the false impressionof 2 new narrowings during PTCA. A 65-year-old man, who had had an acute myocardial infarction 6 days earlier, had an uncomplicated course and did not receive thrombolytic therapy. Cardiac catheterization revealed 95% narrowing in diameter of a single coronary vessel in a tortuous proximal right corory artery (Figure I). PTCA was performed by standard technique through the right femoral artery with an 8Fr Judkins right coronary guide catheter (Baxter Healthcare, From the Duke University Medical Center, Box 3275, Durham, North Carolina 27710. Manuscript received August 14, 1990; revised manuscript received and accepted November 21, 1990.
658
Santa Anna, Caltfornia), an 0.018”guidewire (Hi Torque FloppyTM, Advanced Cardiovascular Systems, Santa Clara, California), and a 2.5mm PTCA balloon catheter (Skinny .O1aTM,SciMed, Maple Grove, Minnesota). The narrowing was crossed without difficulty and dilated to 10 atm for 3 minutes and to 11 atm for 2 minutes. Intracoronary nitroglycerin was given (200 ug) and (with the guidewire still across the lesion) arteriography repeated. In addition to a residual 500% stenosis at the initial narrowing, 2 new narrowings proximal to the target stenosis were now angiographically revealed (Figure
2). The Skinny .018TMPTCA catheter was removed and exchanged for a 3.0-mm PinkertonTM (Advanced Cardiovascular Systems) PTCA catheter, and the original lesion dilated once again. Administration of additional intracoronary nitroglycerin failed to relieve the new proximal narrowings. A decision was made not to treat the new narrowings with angioplasty but to remove the balloon and guidewire systems instead and assess the results. Arteriography, immediately repeated after removal of the PTCA systems, demonstrated a residual 25% diameter narrowing at the original PTCA site,
FIGURE 3. Rnal angiogram after angioplasty demonstrating a 25% residual stenosis at the original angioptasty site (arrow) and a normal vessel proximally. The initial target lesion was redilated with a 3.0-mm balloon angioplasty catheter, and the balloon catheter and guidewire removed before this tine sequence.
FIGURE 1. Angiogram before angioplasty revealing lesion (arrow) in torbrous right coronary artery.
r
FIGURE 2. Interim angiogram after dilation of the right coronary artery stenosis with a 2.5mm balloon angioplasty catheter, with the guidewire across the lesion, demonstrating a residual 50% stenosis at the site of the initial dilation (large arrow) and the angiographic appearance of 2 new stenoses proximal to the target lesion (small arrows).
FIGURE 4. Proposed mechanism for creation of pseudo narrowings by straightening of the coronary artery by a coronary guidewire. Gecause the overall length of the vessel wall must be maintained as the segment is straightened, the wall invaginates at 2 locations to accommodate the extra wall length. gee text for details.
THE AMERICAN JOURNAL OF CARDIOLOGY VOLUME 67
with complete resolution of the proximal “narrowings” (Figure 3).
Figure 4 illustrates the proposed mechanismby which pseudonarrowings can be created by the straightening of a coronary artery segmentwith an angioplasty guidewire. The top portion of Figure 4 shows the tortuous vessel segment before guidewire placement. Numbered lines mark equidistant points along the artery wall. The lower portion of Figure 4 illustrates the effects of vessel straightening. While the ends of the segmentof the artery are maintained in a static position, the straightening of the segment by the guidewire causes invagination of the central portion of the vessel at 2 points to accommodate the excess in vessel wall length. The numbered lines in this portion of Figure 4 demonstrate that the overall length of the vessel wall is maintained by the folding of the wall into the 2 invaginations. Removal of the guidewire then allows
the vesselto return to its normal tortuous configuration, relaxing the arterial wall, and culminating in resolution of the pseudo narrowings. A more common cause of new narrowing during PTCA is vasospasm secondary to the endothelial trauma that occurs during manipulation of angioplasty devices. This phenomenon is best managed with intracoronary nitroglycerin, sublingual nitroglycerin, or sublingual nifedipine, or a combination of these, along with removal of the irritant stimulus. In our case,persistenceof the new narrowings despiterepeated dosesof intracoronary nitroglycerin and the temporal relation of PTCA system removal to their disappearance supports arterial wall invagination as the mechanismof narrowing. Review of the 2,150 PTCA procedures performed at our institution over the past 2 yearssuggestsan incidence of pseudo narrowing as frequent as 1 in 250 proceduresinvolv-
Myocardial Ischemia-Induced Anterior Conduction Delay
Transient
Constantine A. Hassapoyannes, MD, and William P. Nelson. MD
lthough a trifascicular structure A has been proposed for the left bundle branch, conduction delay in a third fascicle is rarely recognized.*J This may be due to a lack of specific features for diagnosis of anterior conduction delay,3 becauseidentical patterns can be obtained with right ventricular hypertrophy or posterior myocardial infarction.4 We present the stresstest of a patient with critical coronary artery diseasethat exhibited ischemia and transient, complex conduction delay, manifested as prominent anterior forces followed by right bundle branch block (RBBB), with evolution of anteroseptal infarction. An active 72-year-old hypertensive man was referred for treadmill From the Department of Medicine, Division of Cardiology, University of South Carolina School of Medicine and WJB Dorn Veterans Hospital, Garners Ferry Road (Veterans Administration Campus), Columbia, South Carolina 29201. Manuscript received August 6, 1990; revised manuscript received and accepted October 22, 1990.
testing. Cardiac examination was unremarkable (blood pressure 1401 70 mm Hg, heart rate 70 beatslmin). The electrocardiogram was normal. By the end of stage I (Bruce protocol), the QRS widened to 105 ms, from 95 at baseline, with R-wave notching inferolaterally. At 4 minutes and 30 seconds, the patient became mildly dyspneic, the PR interval widened from 160 to 190 ms and the QRS to 120 ms, with concomitant ST elevation in VI and depression inferolaterally (Figure 1). By the end of stage II (6 minutes), the QRS morphology changed, with the 80-ms axis manifesting marked anterior displacement in the horizontal but no change in the frontal plane. In addition, the small Q waves initially present in leads II and V, disappeared. Blood pressure decreased to 88168 mm Hg, pulse rate increased to 130 beatslmin, the patient developed angina, and the test was discontinued. Four seconds into recovery, the QRS duration increased to I60 ms, with widening and rightwardTHE AMERICAN
JOURNAL
ing the right coronary artery, with variable compromiseof anterograde coronary flow. Unusual iatrogenic pseudocomplicationssuch asthoseillustrated by this casemust be distinguished and managedappropriately. Knowledge of this pseudocomplication will help avoid inappropriate treatment, including unnecessary PTCA that could potentially expose the patient to additional risk. 1. Gruentzig AR, Senning A, Siegenthaler WE. Nonoperative dilatation of coronary artery stenosis: percutaneous transluminal coronary angioplasty. N Engl J Med 1979;301:61-68. 2. Detre K, Holubkov R, Kelsey S, Cowley M, Kent K, Williams D, Myler R, Faxon D, Holmes D Jr, Bourassa M, Block P, Gosselin A, Bentivoglio L, Leatherman L, Dorros G, King S III, Galichia J, AlBassam M, Leon M, Robertson T, Passamani E, and the Co-Investigators of the National Heart, Lung, and Blood Institute’s Percutaneous Transluminal Coronary Angioplasty Registry. Percutaneous transluminal coronary angioplasty in 1985-1986 and 1977-1981. N Engl J Med 1988;310:265-270. 3. EsplugesE, Cequier AR, &bate X, Jara F. False coronary dissection with the new Monorail angioplasty balloon catheter. Cathet Cardiovasc Diagn 1990;19:30-33.
anterior direction of the terminal QRSforces consistent with superimposed RBBB. At 4 minutes, the QRS duration narrowed to I20 ms with rsR’s’ morphology in VI and evidence of transmural injury current in VI, VZ and V3. At 6 minutes and 3 seconds, the QRS duration shortened to 105 ms and the prominent anterior forces abated in VI; the anterior injury current resolved, but ST depression persisted inferolaterally. At 1.5 minutes, the electrocardiogram manifested hyperacute anteroseptal infarction. Despite thrombolysis, creatine phosphokinase MB-subunit increased to 54 IU/liter. Angiography, 3 days later, revealed anterior wall hypokinesia, and ostial occlusion of the right coronary artery, which was receiving extensive collateral flow from a proximally and subtotally occluded left anterior descending artery. After revascularization, the patient is in excellent condition.
Exercise-inducedST elevation, in the absence of a myocardial scar, suggestscritical coronary artery disease or spasm. Furthermore, transient, ischemia-induced RBBB during stresstesting has been observed with, but is not limited to, high-grade OF CARDIOLOGY
MARCH
15. 1991
659
Creation of Pseudo Narrowing Coronary Angioplasty
During
Alan N. Tenanlia, MD. James E. Tcheng, MD, Harry R. Phillips, Ill, MD, and Richard s. Stack, MD ince the initial description of percutaneoustransluminal coroS nary angioplasty (PTCA) by Gruentzig et al,t the application of PTCA has expanded dramatically, exceeding 300,000 cases annually. Along with this growth, patients with increasingly complex coronary arterial anatomy and lesions are being treated. Technologic advances,coupled with operator experience,have reduced acute procedural risk to an acceptable, although not negligible, level.2 During the performance of PTCA, the interventional cardiologist must quickly recognize and appropriately manage any complication that arises.In addition, the operator must be able to differentiate true complications from pseudocomplications; that is, the operator must recognize the artifactual nature of an apparent complication that is not necessarilywhat it appearsto be. For instance, Espluges et al3 reported the appearanceof persistent staining by contrast material of the arterial wall, suggesting significant dissection during PTCA while using a new monorail balloon catheter. The artifact disappearedwith balloon deflation.3 We report a patient in whom straightening of a tortuous coronary artery by a PTCA guidewire created the false impressionof 2 new narrowings during PTCA. A 65-year-old man, who had had an acute myocardial infarction 6 days earlier, had an uncomplicated course and did not receive thrombolytic therapy. Cardiac catheterization revealed 95% narrowing in diameter of a single coronary vessel in a tortuous proximal right corory artery (Figure I). PTCA was performed by standard technique through the right femoral artery with an 8Fr Judkins right coronary guide catheter (Baxter Healthcare, From the Duke University Medical Center, Box 3275, Durham, North Carolina 27710. Manuscript received August 14, 1990; revised manuscript received and accepted November 21, 1990.
658
Santa Anna, Caltfornia), an 0.018”guidewire (Hi Torque FloppyTM, Advanced Cardiovascular Systems, Santa Clara, California), and a 2.5mm PTCA balloon catheter (Skinny .O1aTM,SciMed, Maple Grove, Minnesota). The narrowing was crossed without difficulty and dilated to 10 atm for 3 minutes and to 11 atm for 2 minutes. Intracoronary nitroglycerin was given (200 ug) and (with the guidewire still across the lesion) arteriography repeated. In addition to a residual 500% stenosis at the initial narrowing, 2 new narrowings proximal to the target stenosis were now angiographically revealed (Figure
2). The Skinny .018TMPTCA catheter was removed and exchanged for a 3.0-mm PinkertonTM (Advanced Cardiovascular Systems) PTCA catheter, and the original lesion dilated once again. Administration of additional intracoronary nitroglycerin failed to relieve the new proximal narrowings. A decision was made not to treat the new narrowings with angioplasty but to remove the balloon and guidewire systems instead and assess the results. Arteriography, immediately repeated after removal of the PTCA systems, demonstrated a residual 25% diameter narrowing at the original PTCA site,
FIGURE 3. Rnal angiogram after angioplasty demonstrating a 25% residual stenosis at the original angioptasty site (arrow) and a normal vessel proximally. The initial target lesion was redilated with a 3.0-mm balloon angioplasty catheter, and the balloon catheter and guidewire removed before this tine sequence.
FIGURE 1. Angiogram before angioplasty revealing lesion (arrow) in torbrous right coronary artery.
r
FIGURE 2. Interim angiogram after dilation of the right coronary artery stenosis with a 2.5mm balloon angioplasty catheter, with the guidewire across the lesion, demonstrating a residual 50% stenosis at the site of the initial dilation (large arrow) and the angiographic appearance of 2 new stenoses proximal to the target lesion (small arrows).
FIGURE 4. Proposed mechanism for creation of pseudo narrowings by straightening of the coronary artery by a coronary guidewire. Gecause the overall length of the vessel wall must be maintained as the segment is straightened, the wall invaginates at 2 locations to accommodate the extra wall length. gee text for details.
THE AMERICAN JOURNAL OF CARDIOLOGY VOLUME 67
with complete resolution of the proximal “narrowings” (Figure 3).
Figure 4 illustrates the proposed mechanismby which pseudonarrowings can be created by the straightening of a coronary artery segmentwith an angioplasty guidewire. The top portion of Figure 4 shows the tortuous vessel segment before guidewire placement. Numbered lines mark equidistant points along the artery wall. The lower portion of Figure 4 illustrates the effects of vessel straightening. While the ends of the segmentof the artery are maintained in a static position, the straightening of the segment by the guidewire causes invagination of the central portion of the vessel at 2 points to accommodate the excess in vessel wall length. The numbered lines in this portion of Figure 4 demonstrate that the overall length of the vessel wall is maintained by the folding of the wall into the 2 invaginations. Removal of the guidewire then allows
the vesselto return to its normal tortuous configuration, relaxing the arterial wall, and culminating in resolution of the pseudo narrowings. A more common cause of new narrowing during PTCA is vasospasm secondary to the endothelial trauma that occurs during manipulation of angioplasty devices. This phenomenon is best managed with intracoronary nitroglycerin, sublingual nitroglycerin, or sublingual nifedipine, or a combination of these, along with removal of the irritant stimulus. In our case,persistenceof the new narrowings despiterepeated dosesof intracoronary nitroglycerin and the temporal relation of PTCA system removal to their disappearance supports arterial wall invagination as the mechanismof narrowing. Review of the 2,150 PTCA procedures performed at our institution over the past 2 yearssuggestsan incidence of pseudo narrowing as frequent as 1 in 250 proceduresinvolv-
Myocardial Ischemia-Induced Anterior Conduction Delay
Transient
Constantine A. Hassapoyannes, MD, and William P. Nelson. MD
lthough a trifascicular structure A has been proposed for the left bundle branch, conduction delay in a third fascicle is rarely recognized.*J This may be due to a lack of specific features for diagnosis of anterior conduction delay,3 becauseidentical patterns can be obtained with right ventricular hypertrophy or posterior myocardial infarction.4 We present the stresstest of a patient with critical coronary artery diseasethat exhibited ischemia and transient, complex conduction delay, manifested as prominent anterior forces followed by right bundle branch block (RBBB), with evolution of anteroseptal infarction. An active 72-year-old hypertensive man was referred for treadmill From the Department of Medicine, Division of Cardiology, University of South Carolina School of Medicine and WJB Dorn Veterans Hospital, Garners Ferry Road (Veterans Administration Campus), Columbia, South Carolina 29201. Manuscript received August 6, 1990; revised manuscript received and accepted October 22, 1990.
testing. Cardiac examination was unremarkable (blood pressure 1401 70 mm Hg, heart rate 70 beatslmin). The electrocardiogram was normal. By the end of stage I (Bruce protocol), the QRS widened to 105 ms, from 95 at baseline, with R-wave notching inferolaterally. At 4 minutes and 30 seconds, the patient became mildly dyspneic, the PR interval widened from 160 to 190 ms and the QRS to 120 ms, with concomitant ST elevation in VI and depression inferolaterally (Figure 1). By the end of stage II (6 minutes), the QRS morphology changed, with the 80-ms axis manifesting marked anterior displacement in the horizontal but no change in the frontal plane. In addition, the small Q waves initially present in leads II and V, disappeared. Blood pressure decreased to 88168 mm Hg, pulse rate increased to 130 beatslmin, the patient developed angina, and the test was discontinued. Four seconds into recovery, the QRS duration increased to I60 ms, with widening and rightwardTHE AMERICAN
JOURNAL
ing the right coronary artery, with variable compromiseof anterograde coronary flow. Unusual iatrogenic pseudocomplicationssuch asthoseillustrated by this casemust be distinguished and managedappropriately. Knowledge of this pseudocomplication will help avoid inappropriate treatment, including unnecessary PTCA that could potentially expose the patient to additional risk. 1. Gruentzig AR, Senning A, Siegenthaler WE. Nonoperative dilatation of coronary artery stenosis: percutaneous transluminal coronary angioplasty. N Engl J Med 1979;301:61-68. 2. Detre K, Holubkov R, Kelsey S, Cowley M, Kent K, Williams D, Myler R, Faxon D, Holmes D Jr, Bourassa M, Block P, Gosselin A, Bentivoglio L, Leatherman L, Dorros G, King S III, Galichia J, AlBassam M, Leon M, Robertson T, Passamani E, and the Co-Investigators of the National Heart, Lung, and Blood Institute’s Percutaneous Transluminal Coronary Angioplasty Registry. Percutaneous transluminal coronary angioplasty in 1985-1986 and 1977-1981. N Engl J Med 1988;310:265-270. 3. EsplugesE, Cequier AR, &bate X, Jara F. False coronary dissection with the new Monorail angioplasty balloon catheter. Cathet Cardiovasc Diagn 1990;19:30-33.
anterior direction of the terminal QRSforces consistent with superimposed RBBB. At 4 minutes, the QRS duration narrowed to I20 ms with rsR’s’ morphology in VI and evidence of transmural injury current in VI, VZ and V3. At 6 minutes and 3 seconds, the QRS duration shortened to 105 ms and the prominent anterior forces abated in VI; the anterior injury current resolved, but ST depression persisted inferolaterally. At 1.5 minutes, the electrocardiogram manifested hyperacute anteroseptal infarction. Despite thrombolysis, creatine phosphokinase MB-subunit increased to 54 IU/liter. Angiography, 3 days later, revealed anterior wall hypokinesia, and ostial occlusion of the right coronary artery, which was receiving extensive collateral flow from a proximally and subtotally occluded left anterior descending artery. After revascularization, the patient is in excellent condition.
Exercise-inducedST elevation, in the absence of a myocardial scar, suggestscritical coronary artery disease or spasm. Furthermore, transient, ischemia-induced RBBB during stresstesting has been observed with, but is not limited to, high-grade OF CARDIOLOGY
MARCH
15. 1991
659
