ography and achieved a sensitivity of 100% when tested with the cough-provocative maneuver. More recently, Pearson et al17 found that there was no difference in the detection of a PFO when comparing transthoracic and transesophageal echocardiography as long as the PFO was not associated with an atrial septal aneurysm. The result of the current study reveals a detected percentage that is similar to that which would be expected based on autopsy studies.18 In the absence of overt angiographic coronary artery disease, a variety of causes for myocardial infarction exist. In this study, there was no increased prevalence of PFO in patients with myocardial infarction and normal coronary arteries. This suggests that paradoxical embolism through this intra-atrial passage is an uncommon cause for this syndrome. 1. Arnett EN, Roberts WC. Acute myocardial infarction and angiographically normal coronary arteries: an unproven combination. Circulation 1976;53:395– 400. 2. Pasternack RC, Braunwald E, Sobel BE. Acute myocardial infarction. Heart Disease, 3rd ed. Philadelphia: WB Saunders, 1988:1222–1313. 3. Lechat P, Mas JL, Lascault G, Loron P, Theard M, Klimczac M, Drobinski G, Thomas D, Grosgogeat T. Prevalence of patent foramen ovale in patients with stroke. N Engl J Med 1988;318:1148 –1152. 4. Webster MWI, Chancellor AM, Smith HJ, Swift DL, Sharpe DN, Bass NM, Glasgow GL. Patent foramen ovale in young stroke patients. Lancet 1988;2:11– 12. 5. Roberts WC. Coronary embolism: a review of causes, consequences, and diagnostic considerations. Cardiovasc Med 1978;3:699 –710.
6. Prizel KR, Hutchins GM, Bulkley BH. Coronary artery embolism and myocardial infarction: a clinicopathic study of 55 patients. Ann Intern Med 1978;88: 155–161. 7. Dubourg O, Bourdarias J, Fasrcot J, Gueret P, Terjman M, Ferrier A, Rigaud M, Bardet J. Contrast echocardiographic visualization of cough-induced right to left shunt through a patent foramen ovale. J Am Coll Cardiol 1984;4:587–594. 8. Vincent GM, Anderson JL, Marshall HW. Coronary spasm producing coronary thrombosis and myocardial infarction. N Engl J Med 1983;309:220 –223. 9. Conti CR. Coronary-artery spasm and myocardial infarction. N Engl J Med 1983;309:238 –239. 10. Howard RE, Hueter DC, Davis GJ. Acute myocardial infarction following cocaine abuse in a young woman with normal coronary arteries. JAMA 1985; 254:95–96. 11. Chandraratna AN, Nimalasuriya A, Reid CL, Cohn S, Rahimtoola SH. Left ventricular asynergy in acute myocarditis: simulation of acute myocardial infarction. JAMA 1983;250:1428 –1430. 12. Rapold HJ, Haeberli A, Kuemmerli H, Weiss M, Baur HR, Straub WP. Fibrin formation and platelet activation in patients with myocadial infarction and normal coronary arteries. Eur Heart J 1989;10:323–333. 13. Arnett, EN, Isner JM, Redwood DR, Keny KM, Baker WP, Akerstein H, Roberts WC. Coronary artery narrowing in coronary heart disease: comparison of cineangiographic and necropsy findings. Ann Intern Med 1979;91:350 –356. 14. Roberts WC, Jones AA. Quantification of coronary arterial narrowing at necropsy in acute transmural myocardial infarction. Circulation 1980;61:786 – 790. 15. Feit A, Hazday MS, Reddy CVR, Kipperman R. Bilateral coronary thrombosis in the absence of inducible coronary spasm, thrombocytosis, coagulation abnormalities, or angiographic evidence of coronary artery disease: previously undescribed method of myocardial infarction. Cathet Cardiovasc Diagn 1988; 15:40 – 43. 16. Belkin RN, Pollack BD, Ruggiero ML, Alas LL, Tatini U. Comparison of transesophageal and transthoracic echocardiography with contrast and color flow Doppler in the detection of patent foramen ovale. Am Heart J 1994;128:520 –525. 17. Pearson AC, Labovitz AJ, Tatineni S, Gomez CR. Superiority of transesophageal echocardiography in detecting cardiac source of embolism in patients with cerebral ischemia of uncertain etiology. J Am Coll Cardiol 1991;17:66 –72. 18. Haget PT, Scholz DG, Edwards WD. Incidence and size of patent foramen ovale during the first 10 decades of life: an autopsy study of 965 normal hearts. Mayo Clin Proc 1984;59:17–20.
Coronary Interventional Procedures in Pediatric Heart Transplant Recipients With Cardiac Allograft Vasculopathy Robert E. Shaddy,
James A Revenaugh, MD, Garth S. Orsmond, Lloyd Y. Tani, MD
ardiac allograft vasculopathy (CAV) is the main limiting factor to long-term survival after pediatric C heart transplantation. Although the exact incidence of 1
CAV after pediatric heart transplantation is unknown, reported incidences have ranged from 3% to 43%.2– 4 Treatment options have been very limited, but some centers have advocated early listing for retransplantation as soon as the diagnosis of CAV is made because of risks of rapid deterioration and sudden death.5 In adult heart transplant recipients, coronary interventions including balloon and laser angioplasty, stenting, atherectomy, and bypass surgery have met with limited success.6 –11 There is virtually no reported experience with coronary interventional procedures in pediatric heart transplant recipients.4 This report From the University of Utah, Primary Children’s Medical Center, and LDS Hospital, Salt Lake City, Utah. Dr. Shaddy’s address is: Cardiology, Suite 1500, Primary Children’s Medical Center, 100 North Medical Drive, Salt Lake City, Utah 84113. Manuscript received August 6, 1999; revised manuscript received and accepted December 16, 1999.
©2000 by Excerpta Medica, Inc. All rights reserved. The American Journal of Cardiology Vol. 85 June 1, 2000
reviews our experience with coronary interventional procedures in 3 pediatric heart transplant recipients. •••
Of the 47 pediatric heart transplant recipients followed by our institution who are aged ⬎1 year from transplantation, we identified 3 who underwent coronary artery interventions as treatment for CAV. The age at the time of initial transplant was 5, 12, and 16 years, respectively. The time from transplant to development of angiographically documented CAV was 7, 6, and 2 years, respectively. Two patients (nos. 1 and 3) had cytomegalovirus (CMV)-positive serologies, and patient 2 was CMV negative. No patient had significant hypercholesterolemia or hypertension. Left ventricular systolic function was normal in all patients at the time of coronary intervention, and right ventricular endomyocardial biopsy demonstrated no rejection. Weight at the time of coronary intervention was 52, 75, and 37 kg, respectively. Indications for coronary interventions were severe stenosis of ⬎80% in all 0002-9149/00/$–see front matter PII S0002-9149(99)00773-6
patients, angina with strongly positive stress test in 1 patient, and left ventricular diastolic dysfunction in another patient. Coronary interventions were performed in an adult cardiac catheterization laboratory by an interventional cardiologist with consultation from the pediatric heart transplant team. Eight of 10 coronary lesions were treated with rotational atherectomy (either de novo or restenotic lesions), and intracoronary stents were used in 3 lesions (in 1, after rotational atherectomy). Stented vessels were 2.5 mm in 1 lesion (in which a Cook Gianturco-Rubin 2 stent, 2.5 ⫻ 25 mm, was used) and 3.0 mm in 2 lesions (in both of which AVE Micro stents [Medtronic, Mounds View, Minnesota], one 12 mm and one 18 mm, were used). Intracoronary ultrasound was used in 1 patient to assess etiology of abrupt no reflow in 1 patient after rotational atherectomy. The procedural success rate was 100% and no clinically evident complications were experienced. The mean preprocedural angiographic diameter stenosis was 91 ⫾ 4.2%. The mean postprocedural angiographic stenosis was 8.6 ⫾ 4.6%. Patient 1 underwent heart transplantation at 5 years of age because of idiopathic dilated cardiomyopathy. He did very well after transplantation, with only 2 episodes of mild allograft rejection requiring outpatient treatment. Routine annual angiography 6 years after transplant demonstrated 40% stenosis of the left anterior descending coronary artery. Dobutamine stress echocardiography was normal. Repeat angiography 6 months later showed no progression of the lesion, although angiography 12 months later showed an 80% stenosis of the left anterior descending artery. Repeat dobutamine stress echocardiography was again normal. He underwent successful stenting of the left anterior descending artery with excellent initial and follow-up angiographic results. He is currently listed for and awaiting retransplantation. Patient 2 underwent heart transplantation at 12 years of age for complex single ventricle anatomy with mild pulmonary hypertension unsuitable for other palliative procedures. She did very well until she presented with congestive heart failure, decreased ventricular function, and hemodynamic instability 6 years after transplant. She was diagnosed with rejection, and coronary angiography at that time demonstrated 40% stenosis of her left circumflex coronary artery. After several weeks of pressor support and augmented immunosuppression, her echocardiographic ventricular function at baseline and with dobutamine were normal. Five months later, she presented with angina and a strongly positive exercise treadmill test. Repeat coronary angiography demonstrated 85% stenosis of the left anterior descending coronary artery, 80% stenosis of a second diagonal artery, and subtotal stenosis of the left circumflex artery. In a staged procedure, she underwent rotational atherectomy of the left anterior descending artery and diagonal lesion, and 2 weeks later rotational atherectomy followed by intravascular ultrasound-guided stenting of the circumflex artery. These interventions immediately resulted in wide patency of all 3 vessels,
and she clinically improved with no further complaints of angina. The patient was listed for retransplantation. Repeat angiography 3 months later demonstrated restenosis of both the stented circumflex artery and the left anterior descending artery distal to the diagonal branch, as well as development of new lesions in the proximal segment of a large first diagonal branch. All lesions were treated with rotational atherectomy with a good angiographic result. Finally, 13 months after her initial angiographic diagnosis of graft vasculopathy and 8 months after her initial coronary intervention, she underwent successful retransplantation and is doing well. Patient 3 underwent heart transplantation at 16 years of age because of severe left ventricular dysfunction after having undergone multiple operations to correct a ventricular septal defect with subaortic stenosis. After transplantation, she had multiple episodes of rejection and chronic left ventricular diastolic dysfunction. She was first diagnosed with CAV 2 years after transplantation with a 90% stenosis of her right coronary artery and truncation of her left coronary arterial vessels without discrete stenoses. At this time, she underwent a stent placement into her right coronary artery with immediate evidence of total relief of obstruction, although she had persistent biventricular dysfunction. She underwent successful retransplantation 4 months after initial presentation and coronary intervention, and is currently doing well. Pathologic findings in the explanted hearts of the 2 patients who underwent retransplantation demonstrated moderate to severe luminal narrowing with intimal thickening and smooth muscle cell proliferation in the large epicardial coronary arteries and no evidence of acute rejection. •••
This report demonstrates that pediatric heart transplant recipients can safely undergo coronary interventional procedures for palliation of CAV. Our experience suggests that coronary interventional procedures are not a long-term solution in the treatment of CAV. However, there may be short-term hemodynamic effects that are valuable. For example, in the second patient in our series, coronary stenting and rotational atherectomy resulted in the disappearance of her anginal symptoms. It is still speculative as to whether coronary interventional procedures actually reduce the risk of sudden death in this situation. However, achieving patency of discrete coronary artery stenoses may allow pediatric heart transplant recipients with CAV to await retransplantation more safely and with less symptoms. Our experience demonstrates the benefits of a close collaboration between pediatric heart transplant programs and adult coronary interventional cardiologists for the appropriate diagnosis and management of these patients. Procedures should probably be limited to patients who have discrete stenoses without angiographic distal arteriopathy.6 Studies in adult heart transplant recipients have suggested that balloon angioplasty may be effective palliative therapy in selected patients.6,7 The use of intracoronary stents has BRIEF REPORTS
also been found to be effective and potentially superior to balloon angioplasty in terms of immediate luminal dimension gain.8,9 Unfortunately, both procedures have a restenosis rate at least as high as native lesions in the adult coronary artery disease population. Limited published experience with the use of coronary atherectomy in heart transplant recipients with CAV suggests possible advantages of this procedure over other types of intervention.11 The intimal fibrosis and cellular intimal thickening seen in CAV may be similar to those seen in restenosis of native coronary vessels.12 There is thus at least a theoretical advantage to debulking these lesions as opposed to performing balloon angioplasty alone. The rapidity with which restenosis and new lesions developed suggests that close clinical and angiographic follow-up is warranted once the diagnosis of CAV is made, regardless of revascularization strategy. Our findings are in agreement with other investigators that pediatric heart transplant recipients who show progression of their CAV should be considered for early listing for retransplantation. However, because of the potentially long waiting times and the significant risks of rapid deterioration and sudden death, there may be a role for coronary interventional procedures in selected patients. We conclude that pediatric heart transplant recipients can safely undergo coronary interventional procedures for palliation of CAV and that
continued investigation into using these palliative procedures is warranted. 1. Boucek MM, Novick RJ, Bennett LE, Fiol B, Keck BM, Hosenpud JD. The
registry of the International Society of Heart and Lung Transplantation: second official pediatric report –1998. J Heart Lung Transplant 1998;17:1141–1160. 2. Radley-Smith RC, Yacoub MH. Long-term results of pediatric heart transplantation. J Heart Lung Transplant 1992;11:S277–S281. 3. Braunlin EA, Hunter DW, Canter CE, Gutierrez FR, Ring WS, Olivari MT, Titus JL, Spray TL, Bolman RM. Coronary artery disease in pediatric cardiac transplant recipients receiving triple-drug immunosuppression. Circulation 1991; 84(suppl III]:III-303–III-309. 4. Pahl E, Zales VR, Fricker FJ, Addonizzio LJ. Posttransplant coronary artery disease in children. A multicenter national survey. Circulation 1994;90[part 2]:II-56 –II-60. 5. Razzouk AJ, Chinnock RE, Dearani JA, Gundry SR, Bailey LL. Cardiac retransplantation for graft vasculopathy in children: should we continue to do it? Arch Surg 1998;133:881– 885. 6. Halle AA, DiSciascio G, Massin EK, Wilson RF, Johnson MR, Sullivan HJ, Bourge RC, Kleiman NS, Miller LW, Aversano TR, Wray RB, Hunt SA, Weston MW, Davies RA, Rincon G, Crandall CC, Cowley MJ, Kubo SH, Fisher SG, Vetrovec GW. Coronary angioplasty, atherectomy, and bypass surgery in cardiac transplant recipients. J Am Coll Cardiol 1995;26:120 –128. 7. Fiane AE, Klow NE, Simonsen S, Levorstad K, Geiran O. Percutaneous transluminal angioplasty and retransplantation due to transplant coronary artery disease. Scand Cardiovasc J 1997;31:223–227. 8. Heublein B, Pethig K, Maab C, Wahlers T, Haverich A. Coronary artery stenting in cardiac allograft vascular disease. Am Heart J 1997;134:930 –938. 9. Wong PMT, Piamsomboon C, Mathur A, Chastain HD, Singh DJ, Liu MW, Parks JM, Iyer S, Dean LS, Baxley WA, Bourge RC, Roubin GS. Efficacy of coronary artery stenting in the management of cardiac allograft vasculopathy. Am J Cardiol 1998;82:239 –241. 10. Topaz O, Bailey NT, Mohanty PK. Application of solid-state pulsed-wave mid-infrared laser for percutaneous revascularization in heart transplant recipients. J Heart Lung Transplant 1998;17:505–10. 11. Jain SP, Ventura HO, Ramee SR, Collins TJ, Isner JM, White CJ. Directional atherectomy in heart transplant recipients. J Heart Lung Transplant 1993;12: 819 – 823. 12. Liu G, Butany J. Morphology of graft arteriosclerosis in cardiac transplant recipients. Human Pathol 1992;23:768 –773.
Ablation of Right and Left Atrial Premature Beats Following Cardioversion in Patients With Chronic Atrial Fibrillation Refractory to Antiarrhythmic Drugs Andrea Natale, MD, Ennio Pisano´, MD, Salwa Beheiry, RN, Mark Richey, Fabio Leonelli, MD, Raffaele Fanelli, MD, Mimmo Potenza, MD, and Gery Tomassoni, MD ecently, we have become aware that in some patients with paroxysmal atrial fibrillation (AF), R the arrhythmia may be initiated by rapid and repetitive firing of a specific focus.1 We report our experience with mapping and ablation of the atrial tissue responsible for atrial premature complexes in patients with otherwise medically refractory persistent or chronic AF. ••• From the University of Kentucky, Lexington, Kentucky; The Cleveland Clinic Foundation, Cleveland, Ohio; and Casa Sollievo della Sofferenza, San Giovanni Rotondo, Italy. Dr. Natale’s address is: The Cleveland Clinic Foundation, Department of Cardiology/F15, Section of Pacing and Electrophysiology, 9500 Euclid Avenue, Cleveland, Ohio 44195. E-mail: [email protected]
Manuscript received August 6, 1999; revised manuscript received and accepted December 13, 1999.
©2000 by Excerpta Medica, Inc. All rights reserved. The American Journal of Cardiology Vol. 85 June 1, 2000
The study group included 48 patients with symptomatic drug refractory AF. Patients were considered for this study only if they had (1) otherwise persistent or chronic AF that failed ⱖ2 antiarrhythmic medications; (2) left atrial size ⬍4.5 cm, and an ejection fraction ⬎45%; and (3) early recurrence of AF after electrical cardioversion (⬍10 days) clearly precipitated by frequent atrial premature complexes. Each patient had AF requiring electrical cardioversion for restoration of sinus rhythm. Patients discharged from the hospital in sinus rhythm after cardioversion were given a loop recorder and asked to record the heart rhythm with symptom and at least twice every 24 hours. Each patient underwent the procedure after achieving sedation with intravenous fentanyl and midazo0002-9149/00/$–see front matter PII S0002-9149(00)00774-8