Catheterization and Cardiovascular Diagnosis 23:107-110 (1991)
Case Reports Accordion Effect in Tortuous Right Coronary Arteries During Percutaneous Transluminal Coronary Angioplasty R. Andrew Rauh, MD, Robert W. Ninneman, MD, David Joseph, MBBS, Vinod K. Gupta, MD, Dale G. Senior, MD, and William P. Miller, MD Coronary spasm and intimal dissection are well-known complications of coronary angioplasty with potentially serious consequences. Their treatments are different and need to be instituted quickly to prevent vessel closure. We report two cases of mechanical deformation caused by the angioplasty hardware masquerading as dissection or spasm during coronary angioplasty of tortuous native right coronary arteries. Key words: intimal dissection, vascular spasm, PTCA complication
INTRODUCTION
Vascular spasm and endothelial dissection are common, well-known complications of percutaneous transluminal coronary angioplasty (PTCA). Both of these entities can adversely affect PTCA outcome and need to be treated differently and quickly. Spasm can usually be reversed with intracoronary nitroglycerin [ 11 (IC NTG), but may occasionally require intracoronary calcium channel blockade [2]. Intimal dissection, on the other hand, requires mechanical intervention with either a prolonged balloon inflation to “tack up” the dissection, atherectomy device to remove the dissection, or laser balloon to “weld” the dissection in an effort to prevent total occlusion of the vessel. We report two patients who both developed focal, proximal lesions during PTCA of tortuous, native right coronary arteries (RCA). The lesions were unchanged by IC NTG, but resolved once the guide wire and balloon catheter were withdrawn. We believe that mechanical straightening of the RCA secondary to angioplasty hardware occurred, creating an “accordion” effect that might be confused with coronary artery spasm or intimal dissection. Appropriate treatment requires recognition of this previously unreported entity.
CASE REPORTS Patient 1
A 49-yr-old male presented with an acute inferior wall myocardial infarction (MI). He was given intravenous streptokinase with clinical evidence for reperfusion. His hospital course was uncomplicated and he underwent low-level exercise testing with thallium scintigraphy on the seventh day post-MI. There was no evidence of ex0 1991 Wiley-Liss, Inc.
ercise induced ischemia. He remained asymptomatic for 6 wk at which time he underwent maximal exercise testing with thallium scintigraphy which revealed a reversible inferior wall perfusion defect consistent with ischemia in the territory of the RCA. On subsequent cardiac catheterization, ventriculography revealed a hypokinetic inferior wall. The coronary arteriogram revealed a tortuous RCA with a symmetrical 90% stenosis in the midright coronary artery (Fig. 1-arrow indicates target lesion). There was nonocclusive disease in the left coronary system. The patient subsequently underwent PTCA. Prior to the procedure, he was premedicated with diltiazem (60 mg p.0.) and aspirin (325 mg p.0.). At the time of the procedure, he was given intravenous heparin (10,000 units), atropine (0.6 mg), and dextran (300 cc). An 8-F four-bend Judkin’s guide catheter was used to cannulate the RCA and a 0.014 flexible steerable guide wire (USCI Billerica, MA) was used to cross the lesion. Balloon inflations were performed with a 2.75-mm Sprint balloon catheter (USCI). Three inflations were performed (6 atm for 60 sec, 8 atm for 90 sec and 120 sec) , Angiography performed after balloon deflation showed marked straightening of the proximal RCA with a proximal, symmetric filling defect and narrowing of the vessel (not present on scout views) but without en-
From the Cardiology Section, Department of Medicine, University of Wisconsin, Madison. Received September 12, 1990; revision accepted December 21, 1990. Address reprint requests to R. A. Rauh, MD, Cardiology Section, H6/349, University of Wisconsin Hospital and Clinics, 600 Highland Avenue, Madison, WI 53792.
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Fig. 1. Patient 1, pre-PTCA (arrowhead denotes target lesion).
dothelial staining or compromised flow (Fig. 2-arrow denotes filling defect). The patient had no chest pain or EKG changes. Administration of 900 p g of IC NTG to relieve possible spasm failed to change the artery’s appearance on repeat angiography . Repeat inflations were performed at the target lesion with a 3.O-miniprofile balloon catheter at 6 atm for 120 sec and at 8 atm for 120 sec. Repeat angiography again revealed no change in the focal lesion in the proximal artery. Since the patient was pain-free without EKG changes, the wire and balloon were withdrawn and arteriography was repeated (Fig. 3). There was return of the original RCA contour with resolution of the proximal focal lesion. The 90% target stenosis was reduced to less than 25%. Serial creatinine kinase (CK) were normal and EKGs were unchanged from baseline. Six months post-PTCA, the patient remains asymptomatic and thallium scintigraphy shows no evidence of inferior ischemia. Patient 2
A 67-yr-old male presented with progressive left lower extremity vascular insufficiency. An arteriogram revealed an occluded superficial femoral artery so the patient was scheduled for surgical revascularization. Preoperative assessment for cardiovascular risk included an exercise multigated bloodpool aquisition (MUGA) scan which revealed an exercise induced regional wall motion abnormality and fall in ejection fraction. Subsequent cardiac catheterization revealed normal resting left ventricular systolic function and a 75-90% symmetrical stenosis in the proximal RCA which demonstrated a “shepherd’s crook” contour (Fig. 4-arrow indicates target lesion.). There was nonocclusive disease in the left coronary system. The patient was premedicated with diltiazem (30 mg) and aspirin (325 mg) and underwent
Fig. 2. Patient 1, immediately post-PTCA with PTCA hardware in place (arrowhead indicates a proximal filling defect). Small dot in mid-right coronary artery is the marker in the middle of the balloon.
Fig. 3. Patient 1, post-PTCA after the wire and balloon have been withdrawn.
PTCA during which he received intravenous heparin (10,000 units), atropine (0.6 mg), and dextran (300 cc). The RCA was successfully cannulated with an 8-F Amplatz left one guiding catheter. A 0.014 flexible steerable, extendable guide wire (USCI) was passed across the stenosis. Dilatations were performed with a 3.0 mm ACX balloon catheter (ACS). The balloon was inflated to 6 atm for 75 sec and 8 atm for 75 sec. There was no chest pain or EKG changes during inflations. Arteriography post-inflation with balloon withdrawn into the guide catheter and wire in place (Fig. 5-arrow indicates filling defect) showed a straightened ‘‘shepherd’s crook” with a focal lesion proximal to the inflation site.
Accordion Effect During PTCA
Fig. 4. Patient 2, pre-PTCA (arrowhead denotes target lesion). Fig. 6.
109
Patient 2, post-PTCA after the wire has been withdrawn.
and different treatments. Recent work by Fischell et al. [l], shows that spasm is nearly a universal consequence of PTCA and can, in their series, be reversed with intravenous or IC NTG. Severe spasm, refractory to IC NTG, can occur but is uncommon, occurring in only 4% of the patients reported by Babbitt et al. [ 2 ] .Unique to these patients was the fact that they all had unstable anginal symptoms as well as unstable lesion morphology as predicted by the criteria of Ambrose et al. [3]. In addition, all of his patients experienced angina and EKG changes during these episodes of severe spasm. In contrast, the patients reported here had stable clinical courses prior to PTCA and their coronary lesions, though severely narrowed, did not have unstable features by Ambrose’s criteria. They also did not experience angina Fig. 5. Patient 2, immediately post-PTCA with wire in place or EKG changes during the procedure. As expected from (arrowheads denote filling defect). the Fischell data, spasm in these patients should readily resolve with IC NTG despite retention of the wire. Subintimal dissection is thought to be one of the mechThe patient received 300 b g IC NTG without change in anisms of successful PTCA [4].Larger dissections likely the appearance of the artery. Because of the experience represent an extreme of this microscopic finding and play with the previously described patient, the wire was withan important role in the 2-10% [ 5 ] incidence of acute drawn and arteriography repeated (Fig. 6). The original vessel closure. Endothelial dissection can occur from the “shepherd’s crook” contour had returned, the focal leguiding catheter, from balloon inflation, or from subinsion had resolved with the vessel lumen being comparatimal passage of the guide wire. We initially suspected ble to pre-PTCA size. The initial stenosis had been redissection in the first patient, but did not dilate this area duced from 75-90% to less than 25%. Serial EKGs and because of the atypical morphology of the lesion. AnCK levels obtained over the next 24 hr were normal. other recent report [6] describes a focal stenosis and slow Four months post-PTCA the patient remained asympflow due to “torsion” of an internal mammary artery tomatic. (IMA) graft during PTCA unresponsive to IC NTG and repeated dilatations. The lesion resolved, however, after DISCUSSION the guide wire and balloon catheter were removed, sugEndothelial dissection and spasm are well-known con- gesting mechanical deformation of the graft. We are unsequences of PTCA with potentially dire consequences aware of any other reports of this phenomenon.
110
Rauh et at.
CONCLUSION
REFERENCES
Both of our patients demonstrate mechanical distortion
1. Fischell TA, Derby G , Tse TM, Stadius ML: Coronary artery
of a native RCA presenting angiographically as a focal
vasoconstriction routinely occurs after PTCA-A quantitative arteriographic analysis. Circulation 78: 1323-1333, 1988. Babbitt DG,Perry JM, Forman MB: Intracoronary verapamil for reversal of refractory coronary vasospasm during PTCA. J Am coil Cardiol 12:1377-1381, 1988. Ambrose JA, Hjemdahl-Monsen CE: Arteriographic anatomy and mechanisms of myocardial ischemia in unstable angina. J Am Coll Cardiol 7:1397-1402, 1987. Kohchi K, et al: Arterial changes after PTCA: Results at autopsy. J Am Coll Cardiol 10592-599, 1987. Dorros G , et al: PTCA: Report of complications from the NHLBI PTCA registry. Circulation 67:723-730, 1983. Grewe K, Presti C, Perez JA: Torsion of the internal mammary graft during PTCA: A case report. Cathet Cardiovasc Diagn 19: 195-197, 1990.
lesion consistent with dissection Or spasm‘ The appearante Of spasm unresponsive to IC NTG with PTCA hardware in place in an otherwise stable patient with a tortuous target vessel should alert the operator to the possibility of this “accordion” effect on the artery. This angiographic entity can be treated simply by withdrawing the wire and balloon catheter sparing the patient the risk of inappropriate balloon inflations for an artifactual dissection.
2, 3.
4, 5.
6.
ACKNOWLEDGMENTS
We acknowledge the contributions of Dr. Charles McCauley.
Case Reports Accordion Effect in Tortuous Right Coronary Arteries During Percutaneous Transluminal Coronary Angioplasty R. Andrew Rauh, MD, Robert W. Ninneman, MD, David Joseph, MBBS, Vinod K. Gupta, MD, Dale G. Senior, MD, and William P. Miller, MD Coronary spasm and intimal dissection are well-known complications of coronary angioplasty with potentially serious consequences. Their treatments are different and need to be instituted quickly to prevent vessel closure. We report two cases of mechanical deformation caused by the angioplasty hardware masquerading as dissection or spasm during coronary angioplasty of tortuous native right coronary arteries. Key words: intimal dissection, vascular spasm, PTCA complication
INTRODUCTION
Vascular spasm and endothelial dissection are common, well-known complications of percutaneous transluminal coronary angioplasty (PTCA). Both of these entities can adversely affect PTCA outcome and need to be treated differently and quickly. Spasm can usually be reversed with intracoronary nitroglycerin [ 11 (IC NTG), but may occasionally require intracoronary calcium channel blockade [2]. Intimal dissection, on the other hand, requires mechanical intervention with either a prolonged balloon inflation to “tack up” the dissection, atherectomy device to remove the dissection, or laser balloon to “weld” the dissection in an effort to prevent total occlusion of the vessel. We report two patients who both developed focal, proximal lesions during PTCA of tortuous, native right coronary arteries (RCA). The lesions were unchanged by IC NTG, but resolved once the guide wire and balloon catheter were withdrawn. We believe that mechanical straightening of the RCA secondary to angioplasty hardware occurred, creating an “accordion” effect that might be confused with coronary artery spasm or intimal dissection. Appropriate treatment requires recognition of this previously unreported entity.
CASE REPORTS Patient 1
A 49-yr-old male presented with an acute inferior wall myocardial infarction (MI). He was given intravenous streptokinase with clinical evidence for reperfusion. His hospital course was uncomplicated and he underwent low-level exercise testing with thallium scintigraphy on the seventh day post-MI. There was no evidence of ex0 1991 Wiley-Liss, Inc.
ercise induced ischemia. He remained asymptomatic for 6 wk at which time he underwent maximal exercise testing with thallium scintigraphy which revealed a reversible inferior wall perfusion defect consistent with ischemia in the territory of the RCA. On subsequent cardiac catheterization, ventriculography revealed a hypokinetic inferior wall. The coronary arteriogram revealed a tortuous RCA with a symmetrical 90% stenosis in the midright coronary artery (Fig. 1-arrow indicates target lesion). There was nonocclusive disease in the left coronary system. The patient subsequently underwent PTCA. Prior to the procedure, he was premedicated with diltiazem (60 mg p.0.) and aspirin (325 mg p.0.). At the time of the procedure, he was given intravenous heparin (10,000 units), atropine (0.6 mg), and dextran (300 cc). An 8-F four-bend Judkin’s guide catheter was used to cannulate the RCA and a 0.014 flexible steerable guide wire (USCI Billerica, MA) was used to cross the lesion. Balloon inflations were performed with a 2.75-mm Sprint balloon catheter (USCI). Three inflations were performed (6 atm for 60 sec, 8 atm for 90 sec and 120 sec) , Angiography performed after balloon deflation showed marked straightening of the proximal RCA with a proximal, symmetric filling defect and narrowing of the vessel (not present on scout views) but without en-
From the Cardiology Section, Department of Medicine, University of Wisconsin, Madison. Received September 12, 1990; revision accepted December 21, 1990. Address reprint requests to R. A. Rauh, MD, Cardiology Section, H6/349, University of Wisconsin Hospital and Clinics, 600 Highland Avenue, Madison, WI 53792.
108
Rauh et al.
Fig. 1. Patient 1, pre-PTCA (arrowhead denotes target lesion).
dothelial staining or compromised flow (Fig. 2-arrow denotes filling defect). The patient had no chest pain or EKG changes. Administration of 900 p g of IC NTG to relieve possible spasm failed to change the artery’s appearance on repeat angiography . Repeat inflations were performed at the target lesion with a 3.O-miniprofile balloon catheter at 6 atm for 120 sec and at 8 atm for 120 sec. Repeat angiography again revealed no change in the focal lesion in the proximal artery. Since the patient was pain-free without EKG changes, the wire and balloon were withdrawn and arteriography was repeated (Fig. 3). There was return of the original RCA contour with resolution of the proximal focal lesion. The 90% target stenosis was reduced to less than 25%. Serial creatinine kinase (CK) were normal and EKGs were unchanged from baseline. Six months post-PTCA, the patient remains asymptomatic and thallium scintigraphy shows no evidence of inferior ischemia. Patient 2
A 67-yr-old male presented with progressive left lower extremity vascular insufficiency. An arteriogram revealed an occluded superficial femoral artery so the patient was scheduled for surgical revascularization. Preoperative assessment for cardiovascular risk included an exercise multigated bloodpool aquisition (MUGA) scan which revealed an exercise induced regional wall motion abnormality and fall in ejection fraction. Subsequent cardiac catheterization revealed normal resting left ventricular systolic function and a 75-90% symmetrical stenosis in the proximal RCA which demonstrated a “shepherd’s crook” contour (Fig. 4-arrow indicates target lesion.). There was nonocclusive disease in the left coronary system. The patient was premedicated with diltiazem (30 mg) and aspirin (325 mg) and underwent
Fig. 2. Patient 1, immediately post-PTCA with PTCA hardware in place (arrowhead indicates a proximal filling defect). Small dot in mid-right coronary artery is the marker in the middle of the balloon.
Fig. 3. Patient 1, post-PTCA after the wire and balloon have been withdrawn.
PTCA during which he received intravenous heparin (10,000 units), atropine (0.6 mg), and dextran (300 cc). The RCA was successfully cannulated with an 8-F Amplatz left one guiding catheter. A 0.014 flexible steerable, extendable guide wire (USCI) was passed across the stenosis. Dilatations were performed with a 3.0 mm ACX balloon catheter (ACS). The balloon was inflated to 6 atm for 75 sec and 8 atm for 75 sec. There was no chest pain or EKG changes during inflations. Arteriography post-inflation with balloon withdrawn into the guide catheter and wire in place (Fig. 5-arrow indicates filling defect) showed a straightened ‘‘shepherd’s crook” with a focal lesion proximal to the inflation site.
Accordion Effect During PTCA
Fig. 4. Patient 2, pre-PTCA (arrowhead denotes target lesion). Fig. 6.
109
Patient 2, post-PTCA after the wire has been withdrawn.
and different treatments. Recent work by Fischell et al. [l], shows that spasm is nearly a universal consequence of PTCA and can, in their series, be reversed with intravenous or IC NTG. Severe spasm, refractory to IC NTG, can occur but is uncommon, occurring in only 4% of the patients reported by Babbitt et al. [ 2 ] .Unique to these patients was the fact that they all had unstable anginal symptoms as well as unstable lesion morphology as predicted by the criteria of Ambrose et al. [3]. In addition, all of his patients experienced angina and EKG changes during these episodes of severe spasm. In contrast, the patients reported here had stable clinical courses prior to PTCA and their coronary lesions, though severely narrowed, did not have unstable features by Ambrose’s criteria. They also did not experience angina Fig. 5. Patient 2, immediately post-PTCA with wire in place or EKG changes during the procedure. As expected from (arrowheads denote filling defect). the Fischell data, spasm in these patients should readily resolve with IC NTG despite retention of the wire. Subintimal dissection is thought to be one of the mechThe patient received 300 b g IC NTG without change in anisms of successful PTCA [4].Larger dissections likely the appearance of the artery. Because of the experience represent an extreme of this microscopic finding and play with the previously described patient, the wire was withan important role in the 2-10% [ 5 ] incidence of acute drawn and arteriography repeated (Fig. 6). The original vessel closure. Endothelial dissection can occur from the “shepherd’s crook” contour had returned, the focal leguiding catheter, from balloon inflation, or from subinsion had resolved with the vessel lumen being comparatimal passage of the guide wire. We initially suspected ble to pre-PTCA size. The initial stenosis had been redissection in the first patient, but did not dilate this area duced from 75-90% to less than 25%. Serial EKGs and because of the atypical morphology of the lesion. AnCK levels obtained over the next 24 hr were normal. other recent report [6] describes a focal stenosis and slow Four months post-PTCA the patient remained asympflow due to “torsion” of an internal mammary artery tomatic. (IMA) graft during PTCA unresponsive to IC NTG and repeated dilatations. The lesion resolved, however, after DISCUSSION the guide wire and balloon catheter were removed, sugEndothelial dissection and spasm are well-known con- gesting mechanical deformation of the graft. We are unsequences of PTCA with potentially dire consequences aware of any other reports of this phenomenon.
110
Rauh et at.
CONCLUSION
REFERENCES
Both of our patients demonstrate mechanical distortion
1. Fischell TA, Derby G , Tse TM, Stadius ML: Coronary artery
of a native RCA presenting angiographically as a focal
vasoconstriction routinely occurs after PTCA-A quantitative arteriographic analysis. Circulation 78: 1323-1333, 1988. Babbitt DG,Perry JM, Forman MB: Intracoronary verapamil for reversal of refractory coronary vasospasm during PTCA. J Am coil Cardiol 12:1377-1381, 1988. Ambrose JA, Hjemdahl-Monsen CE: Arteriographic anatomy and mechanisms of myocardial ischemia in unstable angina. J Am Coll Cardiol 7:1397-1402, 1987. Kohchi K, et al: Arterial changes after PTCA: Results at autopsy. J Am Coll Cardiol 10592-599, 1987. Dorros G , et al: PTCA: Report of complications from the NHLBI PTCA registry. Circulation 67:723-730, 1983. Grewe K, Presti C, Perez JA: Torsion of the internal mammary graft during PTCA: A case report. Cathet Cardiovasc Diagn 19: 195-197, 1990.
lesion consistent with dissection Or spasm‘ The appearante Of spasm unresponsive to IC NTG with PTCA hardware in place in an otherwise stable patient with a tortuous target vessel should alert the operator to the possibility of this “accordion” effect on the artery. This angiographic entity can be treated simply by withdrawing the wire and balloon catheter sparing the patient the risk of inappropriate balloon inflations for an artifactual dissection.
2, 3.
4, 5.
6.
ACKNOWLEDGMENTS
We acknowledge the contributions of Dr. Charles McCauley.
