- Email: [email protected]
Coronary Artery Spasm After Cardiac Transplantation
other forms of disease requires specific testing. With these limitations in mind, however, our findings suggest that exploration of the fractal distribution of ventricular arrhythmias may provide future useful insights into the mechanism and prognosis of disease. 1. Goldberger AL, Findley LJ, Blackburn MR, Mandall AJ. Nonlinear dynamics in heart failure: implications of long-wavelength cardiopulmonary oscillations. Am Heat? J 1984:107:612-615.
Coronary
Artery
Sudhir Kushwaha,
MBBS,
Spasm After MRCP,
2. Glass L. Complex cardiac rhythms. Nature 1987;330:695-696. 3. Mandelbrot BB. The Fractal Geometry of Nature. New York: Freeman, 1983. 4. Grassberger P, Procaccia 1. Measuring the strangeness of strange attractors. Physica 1983,90:189-208. 5. Holmes J, Kubo SH, Cody RJ, Kligfield P. Arrhythmias in ischemic and nonischemic dilated cardiomyopathy: prediction of mortality by ambulatory electrocardiography. Am J Cardiol 1985;55:146-151. 6. Gradman A, Deedwania P, Cody R, Massie B, Packer M, Pitt B, Goldstein S. Predictors of total mortality and sudden death in mild to moderate heart failure. JACC 1989;14:564-570. 7. Low B, Wolf M. Approaches to sudden death from coronary heart disease. Circulation 1971;44:130-142.
Cardiac
Andrew G. Mitchell,
oronary artery spasm has been shown to play a role in exercise-induced angina,’ unstable angina, acute C myocardial infarction and sudden death.2 The exact mechanisms of coronary artery spasm are poorly understood. Humoral, neural4 and endotheliaP mechanisms have been implicated. Cardiac denervation after transplantation coupled with immunologic damage to the endothelium can potentially alter the regulation of coronary vascular tone through loss of direct neural control’ as well as altering the response to humoral factors due to denervation hypersensitivity.8 Although surgical cardiac From the Department of Cardiology and Cardiac Surgical Unit, Hare field Hospital, Harefield, Middlesex, UB9 6JH United Kingdom. Manuscript received December 11, 1989; revised manuscript received and accepted February 20,199O.
MBBS,
Transplantation MRCP,
and Magdi H. Yacoub,
MD
denervation has been proposed as a form of treatment for patients with severe coronary spasm,g the results are variable and coronary spasm has been documented after cardiac transplantation.10-12 The exact causes, frequency and clinical presentation of this phenomenon have not been adequately defined, particularly in relation to accelerated coronary sclerosis and long-term prognosis. To clarify some of these issues, we discuss 4 cardiac transplant recipients with documented severe coronary spasm. From 1980 to 1989, 667 orthotopic cardiac trans plants have been carried out at Harefield Hospital. Annual reinvestigation, including coronary angiography, is routinely performed. Standard angiographic procedures using the Judkins technique have been adopted using 3 to 5 ml per injection of nonionic medium. All patients are maintained on immunosuppression of cyclosporine A,
THE AMERICAN
JOURNAL
OF CARDIOLOGY
JUNE
15.
1990
1515
TABLE
I Relevant
Clinical
Details
and
Patient Patient age, sex and pretransplant diagnosis Donor age (yrs) and sex lschemic time (min) Mode of presentation of coronary spasm Dizziness and/or syncope ST change on exercise test Arrhythmia on 24hour tape Coronary artery narrowed > 75% at angiography RCA LAD LC Coronary spasm by ergonovine provocation Rejection at time of spasm (endomyocardial biopsy) Permanent ECG changes ECG = electrocardngram:
Results
of Investigations
1
Patient 2
Patient 3
Patient 4
14M Diffuse interstital fibrosis 31 F
35M lschemic cardiomyopathy
48M IDC
39M IDC
36M
32M
33M
225
239
80
135
Collapse during exercise test with asystole
Hypotension with ST elevation during coronary angiography +
Inferior T wave changes on exercise testing
0
Chest pain at rest followed by bradycardia, ST elevation and asystole 0
+
+ 0)
+ 0)
0
+ (1)
0
0
0
Sinus bradycardia
+ + 0 0
0 + + +
+ 0 0 0
(Segmental) + spasm) 0 0 + (Right)
0
0
0
0
Q waves
0
0
0
IDC = idiopathic dilated cardiomyopathy;
IAD = left anterior descending coronary artery; LC = left arcumflex coronary artery
the dose of which is adjusted to maintain a blood level of 150 to 250 rig/liter, and azathiopnme, given at a dose of 2 mg;lkg. Four patients had documented severe coronary spasm at angiography as well as clinical and/or electrocardiographic features. Table I lists donor details and results of routine investigations as well as the relevant clinical features in each patient. All patients went on to develop diffuse coronary artery disease affecting the 3 main coronary arteries and their principle branches within 1 year of the diagnosis of spasm. Only 1 of these patients is still alive.
The patients described demonstrate that coronary artery spasm may occur after cardiac transplantation and may have an important influence on the clinical course. In patients 1 and 3, severe spasm was observed at angiography and reversed by intracoronary isosorbide dinitrate. It is likely that in patient 1, spasm was responsible for the inferior infarct and cardiac arrest. In patients 2 and 4, coronary spasm was confirmed by intracoronary ergonovine provocation. All 4 patients had dizzy spells or syncope which may have been related to episodes of spontaneous coronary spasm. These symptoms were related to exertion and in 2
FIGURE 3. Eledmadiogram hrinsianetisodeof~coronaw
1516
THE AMERICAN
JOURNAL
OF CARDIOLOGY
VOLUME
65
of patiemt
2
patients, the typical symptoms were followed by collapse on treadmill exercise testing. Sudden death occurred in 3 patients, suggesting that an acute arrhythmia may have been the causative factor even though 24-hour tape monitoring was negative. In the 2 patients in whom an autopsy was available (patients 1 and 4), severe coronary artery disease was demonstrated but coronary thrombus was absent. Patient 2 had fmed coronary narrowing at sites where spasm was observed. There have been previously published case reports of coronary artery spasm after cardiac transplantation,10-12 of which 1 case may have been catheter provoked.13 In all cases of spontaneous spasm in transplant patients, there are common features. Electrocardiographic ST-segment change and syncopal episodes are a consistent feature. Sudden death occurs and there is an association with the development of coronary artery disease that is rapidly progressive. There was histologic evidence at autopsy of chronic rejection in 2 of our cases and also in the patient reported by Cattan,” suggesting that this may be an important association. There are similarities between the coronary artery spasm in these patients and the well characterized spasm recognized in nontransplanted coronary arteries.’ In these cases, there is a well documented association with angina, acute myocardial infarction and sudden death.* In addition, coronary spasm in native coronary arteries may be an antecedent to the later development of fixed coronary artery disease.l4 This relation may apply in cardiac transplant recipients. It has been suggested that coronary artery spasm may be secondary to alpha-adrenergic sympathetic stimulation.15 Surgical denervation and autotransplantation have therefore been used to treat this conditions but the results have been inconsistent and variable suggesting that this is unlikely to play an important role in the pathogenesis of coronary artery spasm. None of our patients had evidence of reinnervation on physiologic testing and this is in keeping with a recent anatomic study con-
eluding that myocardial innervation is unlikely to be restored in transplanted human hearts.16 Local nonspecific hypersensitivity, rather than a specific agonist-receptor interaction, has been suggested as the mechanism of spasm in variant angina.17 In cardiac transplant recipients, denervation may remove the autonomic neural control mechanisms governing coronary tone and vesselsmay therefore be hypersensitive to local vasoconstrictor stimuli. This nonspecific local hypersensitivity may be an important mechanism. However, it is likely that more than 1 mechanism is involved in the pathogenesis of coronary vasoconstriction and spasm.18 We have used ergonovine maleate to provoke spasm as this is the most reliable and consistent inducer of vasospasm in patients with variant angina in whom there appears to be focal hypersensitivity to the drug.19 Early atherosclerotic change in coronary arteries may enhance the segmental vasoconstriction of these arteries in response to ergonovine.’ Ergonovine has been suggested to act by a direct local action*O and may have stimulatory effect on the endothelium with the release of endotheliurn-derived relaxing factor. 21,22In patients with coronary spasm, endothelial dysfunction may result in the lack of release of endothelium-derived relaxing factor with only a vasoconstrictor effect of the drug. The most important question raised by these patients is the possible association of coronary spasm with the development of accelerated coronary sclerosis.23The incidence of accelerated coronary sclerosis in cardiac transplant recipients is as high as 40% by 2.5 years.24 The course of the patients described was poor. The deaths were within 2 years after transplantation and the coronary artery disease was particularly “aggressive” when compared with the incidence and progression of coronary
FIGURE4.AnigbgraphkappearanceofrigMcoru~ryartery inpaUemt3dminganepisodeof demonsbated~sm.
FIGURE 5. RighI i~dinitrateafter
THE AMERICAN
coronmyarteryinpatient3afterinfusionol demonaratedspasm.
JOURNAL
OF CARDIOLOGY
JUNE
15, 1990
1517
disease at this institution. By the end of 1989, 12 of 268 patients (4.5%) had significant coronary artery disease and of these, only 1 had died within 2 years (unpublished data). It has been suggested that catheter-induced spasm is related to spontaneous spasm.25 We have noted at least 6 cases of catheter tip spasm in transplant recipients since 1980, but none had significant fxed coronary artery disease. 1. Maseri A, Chierchia S. Coronary artery spasm: demonstration, definition, diagnosis, and consequences. Prog Cardiouasc Dis 1982:25:169-192. 2. Conti RC. Mywardial infarction: thoughts about pathogenesis and the role of coronary artery spasm. Am Heart J 1985;110:187-193. 3. Ginsburg R, Bristow MR. Kantrowitz N, Bairn DS, Harrison DC. Histamine provocation of clinical coronary artery spasm: implications concerning the pathogenesis of variant angina pectoris. Am Heart J 1981;102:819. 4. Yasue H, Touyama M, Shimamoto M, Kato H, Tanaka S, Akiyama F. Role of the autonomic nervous system in the pathogenesis of Prinzmetal’s variant form of angina. Circulation 1974;50:534-539. 5. Shimokawa H, Tomoike H, Nakayama S, Yamamoto H, Arakari H, Nakamura M. Coronary artery spasm induced in atherosclerotic miniature swine. Science 1983:221:560-562. 6. Brasile L, Zerbe T, Rabin B, Clarke J, Abrams A, Cerilli J. Identification of antibody to vascular endothelial cells in patients undergoing cardiac transplantation. Transplantation 1985;40:672-675. 7. Young MA, Vatner SF. Regulation of large coronary arteries. Circ Res 1986:59:579-596. 6. Yusuf SF, Theodoropoulos S, MathiasCJ, Dhalla N, Wittes J, Mitchell A, Yacoub M. Increased sensitivity of the denervatcd transplanted human heart to isoprenaline both before and after beta-adrenergic blockade. Circulation 1987:75:696-704. 9. Bertrand ME, Lablanche JM, Tilmant PY, Ducloux G, Warembaurg H, Soots G. Complete denervation of the heart (autotransplantation) for treatment of severe, refractory coronary spasm. Am J Cardiol 1981:47:1375-1378. 10. Buda AJ, Fowles RE, Schroeder JS, Hunt SA, Cipriano PR, Stinson EB, Harrison DC. Coronary artery spasm in the denervated transplanted human
Transcatheter Occlusion Detachable Balloon
of High Flow Blalocldaussig
Marc Gewillig, MD, Luc Van der Hauwaert,
stenosis and abundant, high velocity, turbulent blood flow-the reported procedures were difficult and cumbersome, and the final result was frequently suboptimal. We evaluated the feasibility and effectiveness of goldvalve detachable balloons for occluding high flow Blalock-Taussig shunts. A modified Blalock-Taussig shunt (4 to 6 cm of 6 mm Gore- Tex) was created in 8 mongrel dogs (weight I8 to 29 kg, mean 22). When reevaluated 4 to 6 weeks after surgery, there was evidence of a significant shunt because thepulsepressure had increasedfrom 30 f 4 to 60 f 8 mm Hg and the left ventricular end-diastolic volume From the Laboratory of Experimental Cardiology, Gasthuisberg University Hospital Leuven, B-3000 Leuven, Belgium. This study was supported in part by the Belgian National Research Foundation, Brussels, and Gore-Tex Belgium, Lii?ge, Belgium. Manuscript received December 18, 1989; revised manuscript received and accepted February 13, 1990.
THE AMERICAN
JOURNAL
OF CARDIOLOGY
Shunts with a
MD, and Wim Daenen, MD
ranscatheter occlusion of Blalock-Taussig shunts T has been reported.1-4 However, because of specific features of these shunts-such as common lack of distal
1518
heart. A clue to underlying mechanisms. Am J Med 198/;70: /144-J 149. 11. Cattan S, Drobinski G, Artigou J-Y, Grogogea Y, Cabrol C. Coronary artery spasm in a transplant patient. Eur Heart J J988,9:557-560. 12. Boffa GM, Faggian G, Buja G. Livi U, Bortolotti U, St&n G, Razzolini R, Stritoni P, Mazzucco A, Thiene G, Chioin R, Gallucci V. Coronary artery spasm in heart transplant recipients. J Heart Tram-plant J989;8:J54~~/58. 13. Goldenberg IF, Levine BT. Coronary artery spasm in a denervated orthotopic transplanted human heart. Cathet Cardioumc Diagn /986;/2:44--47. 14. Marzilli M, Goldstein S, Trivella MA, Palumbo C, Maseri A. Some clinical considerations regarding the relation of coronary vasospasm to coronary atherosclerosis: a hypothetical pathogenesis. Am J Cardiol 1980;45:882-886. 15. Yasue H, Touyama M, Tanaka S, Akiyama F. Prinzmetal’s variant form of angina as a manifestation of alpha-adrenergic receptor mediated coronary artery spasm: documentation by coronary arteriography. Am Heart J 1976:91:148-152. 16. Rowan RA, Billingham ME. Myocardial innervation in long-term heart transplant survivors: a quantitative ultrastructural survey. J Heart Trmsplant J988;7:448-452. 17. Kaski JC, Crea F, Meran D, Rodriguez L, Araujo L, Chierchia S, Davies G, Maseri A. Local coronary supersensitivity to diverse vaswonstrictive stimuli in patients with variant angina. Circulation 1986;74:1255-1265. 16. Maseri A, Kaski JC. Pathogenetic mechanisms of coronary artery spasm. JACC 1989:14:610-612. 19. Schroeder JS, Bolen JL, Quint RA, Clark DA, Hayden WG, Higgins CB, Wexler L. Provocation of coronary spasm with ergonovine maleate. New test with results in 57 patients undergoing coronary arteriography. Am J Cardiol 1977; 40:487-491, 20. Hackett D, Larkin S, Chierchia S, Davies G. Kaski JC, Maseri A. Induction of coronary artery spasm by a direct local action of ergonovine. Circulation J987:75:577-582. 21. Griffith TM, Hughes Edwards D, Lewis MJ, Henderson AH. Ergometrine induced arterial dilatation: an endothelial mediated effect. J Mel Cell Cmdiol 1984;16:479-482. 22. Shimokawa H, Flavahan NA, Shepherd JT, Vanhoutte PM. Endotheliumdependent inhibition of ergonovine induced contraction is impaired in porcine coronary arteries with regenerated endothelium. Circulation J989;80:643-650. 23. Cooper DKC, Boyd ST, Lanza RP, Barnard CN. Factors influencing survival following heart transplantation. Heart Transplant J983;3:86-91. 24. Schroeder JS, Hunt SA. Cardiac transplantation: where arc we? N Engl J Med 1986;3J5:961-963. 25. Roberts DJ, Isner JY, Dcckelbaum LI, Konstam MA, Salem BN. Acute myocardial infarction, normal coronary arteries and catheter-induced spasm. Am J Cardiol 1986;58:360-362.
VOLUME
65
had increased by 55 f 24%. The shunt was approached from the brachial artery in order to reach it in an obtuse angle. An 8Fr delivery catheter was advanced into the shunt over h previously positioned guidewire. A goldvalve detachable balloon (deflated 2.7 X I .4 mm, fully inflated 14.7 X 7.8 mm, Ingenor) was slipped over a 2.2Fr on a 3Fr carrier catheter, which was previously slid through a 5Fr guiding catheter. The balloon was positionedproximally in the shunt and injlated swifrly with 0.5 ml of diluted (1:2) contrast medium. Slow inflation of the balloon resulted in significant displacement into the pulmonary artery: the 3Fr carrier catheter was very stretchable. The use of a luberculine syringe, however, made nearly instantaneous inflation of the balloon possible. Despite abundant and high velocity (>4 m/s) bloodjlow, the connection between the nozzle and the valve did withstand the turbulent flow in the shunt and accurate posiConing of the balloon was obtained in all dogs. Deflation and repositioning were possible until the balloon was detached with gentle traction on the 3Fr catheter while
Coronary
Artery
Sudhir Kushwaha,
MBBS,
Spasm After MRCP,
2. Glass L. Complex cardiac rhythms. Nature 1987;330:695-696. 3. Mandelbrot BB. The Fractal Geometry of Nature. New York: Freeman, 1983. 4. Grassberger P, Procaccia 1. Measuring the strangeness of strange attractors. Physica 1983,90:189-208. 5. Holmes J, Kubo SH, Cody RJ, Kligfield P. Arrhythmias in ischemic and nonischemic dilated cardiomyopathy: prediction of mortality by ambulatory electrocardiography. Am J Cardiol 1985;55:146-151. 6. Gradman A, Deedwania P, Cody R, Massie B, Packer M, Pitt B, Goldstein S. Predictors of total mortality and sudden death in mild to moderate heart failure. JACC 1989;14:564-570. 7. Low B, Wolf M. Approaches to sudden death from coronary heart disease. Circulation 1971;44:130-142.
Cardiac
Andrew G. Mitchell,
oronary artery spasm has been shown to play a role in exercise-induced angina,’ unstable angina, acute C myocardial infarction and sudden death.2 The exact mechanisms of coronary artery spasm are poorly understood. Humoral, neural4 and endotheliaP mechanisms have been implicated. Cardiac denervation after transplantation coupled with immunologic damage to the endothelium can potentially alter the regulation of coronary vascular tone through loss of direct neural control’ as well as altering the response to humoral factors due to denervation hypersensitivity.8 Although surgical cardiac From the Department of Cardiology and Cardiac Surgical Unit, Hare field Hospital, Harefield, Middlesex, UB9 6JH United Kingdom. Manuscript received December 11, 1989; revised manuscript received and accepted February 20,199O.
MBBS,
Transplantation MRCP,
and Magdi H. Yacoub,
MD
denervation has been proposed as a form of treatment for patients with severe coronary spasm,g the results are variable and coronary spasm has been documented after cardiac transplantation.10-12 The exact causes, frequency and clinical presentation of this phenomenon have not been adequately defined, particularly in relation to accelerated coronary sclerosis and long-term prognosis. To clarify some of these issues, we discuss 4 cardiac transplant recipients with documented severe coronary spasm. From 1980 to 1989, 667 orthotopic cardiac trans plants have been carried out at Harefield Hospital. Annual reinvestigation, including coronary angiography, is routinely performed. Standard angiographic procedures using the Judkins technique have been adopted using 3 to 5 ml per injection of nonionic medium. All patients are maintained on immunosuppression of cyclosporine A,
THE AMERICAN
JOURNAL
OF CARDIOLOGY
JUNE
15.
1990
1515
TABLE
I Relevant
Clinical
Details
and
Patient Patient age, sex and pretransplant diagnosis Donor age (yrs) and sex lschemic time (min) Mode of presentation of coronary spasm Dizziness and/or syncope ST change on exercise test Arrhythmia on 24hour tape Coronary artery narrowed > 75% at angiography RCA LAD LC Coronary spasm by ergonovine provocation Rejection at time of spasm (endomyocardial biopsy) Permanent ECG changes ECG = electrocardngram:
Results
of Investigations
1
Patient 2
Patient 3
Patient 4
14M Diffuse interstital fibrosis 31 F
35M lschemic cardiomyopathy
48M IDC
39M IDC
36M
32M
33M
225
239
80
135
Collapse during exercise test with asystole
Hypotension with ST elevation during coronary angiography +
Inferior T wave changes on exercise testing
0
Chest pain at rest followed by bradycardia, ST elevation and asystole 0
+
+ 0)
+ 0)
0
+ (1)
0
0
0
Sinus bradycardia
+ + 0 0
0 + + +
+ 0 0 0
(Segmental) + spasm) 0 0 + (Right)
0
0
0
0
Q waves
0
0
0
IDC = idiopathic dilated cardiomyopathy;
IAD = left anterior descending coronary artery; LC = left arcumflex coronary artery
the dose of which is adjusted to maintain a blood level of 150 to 250 rig/liter, and azathiopnme, given at a dose of 2 mg;lkg. Four patients had documented severe coronary spasm at angiography as well as clinical and/or electrocardiographic features. Table I lists donor details and results of routine investigations as well as the relevant clinical features in each patient. All patients went on to develop diffuse coronary artery disease affecting the 3 main coronary arteries and their principle branches within 1 year of the diagnosis of spasm. Only 1 of these patients is still alive.
The patients described demonstrate that coronary artery spasm may occur after cardiac transplantation and may have an important influence on the clinical course. In patients 1 and 3, severe spasm was observed at angiography and reversed by intracoronary isosorbide dinitrate. It is likely that in patient 1, spasm was responsible for the inferior infarct and cardiac arrest. In patients 2 and 4, coronary spasm was confirmed by intracoronary ergonovine provocation. All 4 patients had dizzy spells or syncope which may have been related to episodes of spontaneous coronary spasm. These symptoms were related to exertion and in 2
FIGURE 3. Eledmadiogram hrinsianetisodeof~coronaw
1516
THE AMERICAN
JOURNAL
OF CARDIOLOGY
VOLUME
65
of patiemt
2
patients, the typical symptoms were followed by collapse on treadmill exercise testing. Sudden death occurred in 3 patients, suggesting that an acute arrhythmia may have been the causative factor even though 24-hour tape monitoring was negative. In the 2 patients in whom an autopsy was available (patients 1 and 4), severe coronary artery disease was demonstrated but coronary thrombus was absent. Patient 2 had fmed coronary narrowing at sites where spasm was observed. There have been previously published case reports of coronary artery spasm after cardiac transplantation,10-12 of which 1 case may have been catheter provoked.13 In all cases of spontaneous spasm in transplant patients, there are common features. Electrocardiographic ST-segment change and syncopal episodes are a consistent feature. Sudden death occurs and there is an association with the development of coronary artery disease that is rapidly progressive. There was histologic evidence at autopsy of chronic rejection in 2 of our cases and also in the patient reported by Cattan,” suggesting that this may be an important association. There are similarities between the coronary artery spasm in these patients and the well characterized spasm recognized in nontransplanted coronary arteries.’ In these cases, there is a well documented association with angina, acute myocardial infarction and sudden death.* In addition, coronary spasm in native coronary arteries may be an antecedent to the later development of fixed coronary artery disease.l4 This relation may apply in cardiac transplant recipients. It has been suggested that coronary artery spasm may be secondary to alpha-adrenergic sympathetic stimulation.15 Surgical denervation and autotransplantation have therefore been used to treat this conditions but the results have been inconsistent and variable suggesting that this is unlikely to play an important role in the pathogenesis of coronary artery spasm. None of our patients had evidence of reinnervation on physiologic testing and this is in keeping with a recent anatomic study con-
eluding that myocardial innervation is unlikely to be restored in transplanted human hearts.16 Local nonspecific hypersensitivity, rather than a specific agonist-receptor interaction, has been suggested as the mechanism of spasm in variant angina.17 In cardiac transplant recipients, denervation may remove the autonomic neural control mechanisms governing coronary tone and vesselsmay therefore be hypersensitive to local vasoconstrictor stimuli. This nonspecific local hypersensitivity may be an important mechanism. However, it is likely that more than 1 mechanism is involved in the pathogenesis of coronary vasoconstriction and spasm.18 We have used ergonovine maleate to provoke spasm as this is the most reliable and consistent inducer of vasospasm in patients with variant angina in whom there appears to be focal hypersensitivity to the drug.19 Early atherosclerotic change in coronary arteries may enhance the segmental vasoconstriction of these arteries in response to ergonovine.’ Ergonovine has been suggested to act by a direct local action*O and may have stimulatory effect on the endothelium with the release of endotheliurn-derived relaxing factor. 21,22In patients with coronary spasm, endothelial dysfunction may result in the lack of release of endothelium-derived relaxing factor with only a vasoconstrictor effect of the drug. The most important question raised by these patients is the possible association of coronary spasm with the development of accelerated coronary sclerosis.23The incidence of accelerated coronary sclerosis in cardiac transplant recipients is as high as 40% by 2.5 years.24 The course of the patients described was poor. The deaths were within 2 years after transplantation and the coronary artery disease was particularly “aggressive” when compared with the incidence and progression of coronary
FIGURE4.AnigbgraphkappearanceofrigMcoru~ryartery inpaUemt3dminganepisodeof demonsbated~sm.
FIGURE 5. RighI i~dinitrateafter
THE AMERICAN
coronmyarteryinpatient3afterinfusionol demonaratedspasm.
JOURNAL
OF CARDIOLOGY
JUNE
15, 1990
1517
disease at this institution. By the end of 1989, 12 of 268 patients (4.5%) had significant coronary artery disease and of these, only 1 had died within 2 years (unpublished data). It has been suggested that catheter-induced spasm is related to spontaneous spasm.25 We have noted at least 6 cases of catheter tip spasm in transplant recipients since 1980, but none had significant fxed coronary artery disease. 1. Maseri A, Chierchia S. Coronary artery spasm: demonstration, definition, diagnosis, and consequences. Prog Cardiouasc Dis 1982:25:169-192. 2. Conti RC. Mywardial infarction: thoughts about pathogenesis and the role of coronary artery spasm. Am Heart J 1985;110:187-193. 3. Ginsburg R, Bristow MR. Kantrowitz N, Bairn DS, Harrison DC. Histamine provocation of clinical coronary artery spasm: implications concerning the pathogenesis of variant angina pectoris. Am Heart J 1981;102:819. 4. Yasue H, Touyama M, Shimamoto M, Kato H, Tanaka S, Akiyama F. Role of the autonomic nervous system in the pathogenesis of Prinzmetal’s variant form of angina. Circulation 1974;50:534-539. 5. Shimokawa H, Tomoike H, Nakayama S, Yamamoto H, Arakari H, Nakamura M. Coronary artery spasm induced in atherosclerotic miniature swine. Science 1983:221:560-562. 6. Brasile L, Zerbe T, Rabin B, Clarke J, Abrams A, Cerilli J. Identification of antibody to vascular endothelial cells in patients undergoing cardiac transplantation. Transplantation 1985;40:672-675. 7. Young MA, Vatner SF. Regulation of large coronary arteries. Circ Res 1986:59:579-596. 6. Yusuf SF, Theodoropoulos S, MathiasCJ, Dhalla N, Wittes J, Mitchell A, Yacoub M. Increased sensitivity of the denervatcd transplanted human heart to isoprenaline both before and after beta-adrenergic blockade. Circulation 1987:75:696-704. 9. Bertrand ME, Lablanche JM, Tilmant PY, Ducloux G, Warembaurg H, Soots G. Complete denervation of the heart (autotransplantation) for treatment of severe, refractory coronary spasm. Am J Cardiol 1981:47:1375-1378. 10. Buda AJ, Fowles RE, Schroeder JS, Hunt SA, Cipriano PR, Stinson EB, Harrison DC. Coronary artery spasm in the denervated transplanted human
Transcatheter Occlusion Detachable Balloon
of High Flow Blalocldaussig
Marc Gewillig, MD, Luc Van der Hauwaert,
stenosis and abundant, high velocity, turbulent blood flow-the reported procedures were difficult and cumbersome, and the final result was frequently suboptimal. We evaluated the feasibility and effectiveness of goldvalve detachable balloons for occluding high flow Blalock-Taussig shunts. A modified Blalock-Taussig shunt (4 to 6 cm of 6 mm Gore- Tex) was created in 8 mongrel dogs (weight I8 to 29 kg, mean 22). When reevaluated 4 to 6 weeks after surgery, there was evidence of a significant shunt because thepulsepressure had increasedfrom 30 f 4 to 60 f 8 mm Hg and the left ventricular end-diastolic volume From the Laboratory of Experimental Cardiology, Gasthuisberg University Hospital Leuven, B-3000 Leuven, Belgium. This study was supported in part by the Belgian National Research Foundation, Brussels, and Gore-Tex Belgium, Lii?ge, Belgium. Manuscript received December 18, 1989; revised manuscript received and accepted February 13, 1990.
THE AMERICAN
JOURNAL
OF CARDIOLOGY
Shunts with a
MD, and Wim Daenen, MD
ranscatheter occlusion of Blalock-Taussig shunts T has been reported.1-4 However, because of specific features of these shunts-such as common lack of distal
1518
heart. A clue to underlying mechanisms. Am J Med 198/;70: /144-J 149. 11. Cattan S, Drobinski G, Artigou J-Y, Grogogea Y, Cabrol C. Coronary artery spasm in a transplant patient. Eur Heart J J988,9:557-560. 12. Boffa GM, Faggian G, Buja G. Livi U, Bortolotti U, St&n G, Razzolini R, Stritoni P, Mazzucco A, Thiene G, Chioin R, Gallucci V. Coronary artery spasm in heart transplant recipients. J Heart Tram-plant J989;8:J54~~/58. 13. Goldenberg IF, Levine BT. Coronary artery spasm in a denervated orthotopic transplanted human heart. Cathet Cardioumc Diagn /986;/2:44--47. 14. Marzilli M, Goldstein S, Trivella MA, Palumbo C, Maseri A. Some clinical considerations regarding the relation of coronary vasospasm to coronary atherosclerosis: a hypothetical pathogenesis. Am J Cardiol 1980;45:882-886. 15. Yasue H, Touyama M, Tanaka S, Akiyama F. Prinzmetal’s variant form of angina as a manifestation of alpha-adrenergic receptor mediated coronary artery spasm: documentation by coronary arteriography. Am Heart J 1976:91:148-152. 16. Rowan RA, Billingham ME. Myocardial innervation in long-term heart transplant survivors: a quantitative ultrastructural survey. J Heart Trmsplant J988;7:448-452. 17. Kaski JC, Crea F, Meran D, Rodriguez L, Araujo L, Chierchia S, Davies G, Maseri A. Local coronary supersensitivity to diverse vaswonstrictive stimuli in patients with variant angina. Circulation 1986;74:1255-1265. 16. Maseri A, Kaski JC. Pathogenetic mechanisms of coronary artery spasm. JACC 1989:14:610-612. 19. Schroeder JS, Bolen JL, Quint RA, Clark DA, Hayden WG, Higgins CB, Wexler L. Provocation of coronary spasm with ergonovine maleate. New test with results in 57 patients undergoing coronary arteriography. Am J Cardiol 1977; 40:487-491, 20. Hackett D, Larkin S, Chierchia S, Davies G. Kaski JC, Maseri A. Induction of coronary artery spasm by a direct local action of ergonovine. Circulation J987:75:577-582. 21. Griffith TM, Hughes Edwards D, Lewis MJ, Henderson AH. Ergometrine induced arterial dilatation: an endothelial mediated effect. J Mel Cell Cmdiol 1984;16:479-482. 22. Shimokawa H, Flavahan NA, Shepherd JT, Vanhoutte PM. Endotheliumdependent inhibition of ergonovine induced contraction is impaired in porcine coronary arteries with regenerated endothelium. Circulation J989;80:643-650. 23. Cooper DKC, Boyd ST, Lanza RP, Barnard CN. Factors influencing survival following heart transplantation. Heart Transplant J983;3:86-91. 24. Schroeder JS, Hunt SA. Cardiac transplantation: where arc we? N Engl J Med 1986;3J5:961-963. 25. Roberts DJ, Isner JY, Dcckelbaum LI, Konstam MA, Salem BN. Acute myocardial infarction, normal coronary arteries and catheter-induced spasm. Am J Cardiol 1986;58:360-362.
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had increased by 55 f 24%. The shunt was approached from the brachial artery in order to reach it in an obtuse angle. An 8Fr delivery catheter was advanced into the shunt over h previously positioned guidewire. A goldvalve detachable balloon (deflated 2.7 X I .4 mm, fully inflated 14.7 X 7.8 mm, Ingenor) was slipped over a 2.2Fr on a 3Fr carrier catheter, which was previously slid through a 5Fr guiding catheter. The balloon was positionedproximally in the shunt and injlated swifrly with 0.5 ml of diluted (1:2) contrast medium. Slow inflation of the balloon resulted in significant displacement into the pulmonary artery: the 3Fr carrier catheter was very stretchable. The use of a luberculine syringe, however, made nearly instantaneous inflation of the balloon possible. Despite abundant and high velocity (>4 m/s) bloodjlow, the connection between the nozzle and the valve did withstand the turbulent flow in the shunt and accurate posiConing of the balloon was obtained in all dogs. Deflation and repositioning were possible until the balloon was detached with gentle traction on the 3Fr catheter while