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Left Main Coronary Artery Spasm: Medical Versus Surgical Management
CASE REPORTS
Left Main Coronary Artery Spasm: Medical Versus Surgical Management Michael G. Fitzsimons, MD, FCCP,* Jennifer Walker, MD,† Ignacio Inglessis, MD,‡ and Charles Boucher, MD‡
V
ASOSPASM OF THE left main coronary artery (LMCA) is a rare condition with potentially devastating consequences. Medical therapy is the initial strategy for management of coronary vasospasm. LMCA spasm may warrant a more aggressive surgical approach.1 Therefore, a case of coronary artery bypass grafting for recurrent LMCA spasm in the face of maximal medical management is reported. CASE REPORT
A 50-year-old man with a history of hypertension, dyslipidemia, and nephrolithiasis was in his usual state of health until 1 week before admission to this hospital when he presented to an outside institution with chest pain and dyspnea. His electrocardiogram showed T-wave inversions in leads II, III, aVF, and V3-V6. He was treated with sublingual nitroglycerin (NTG) with dramatic resolution of his symptoms and electrocardiographic changes. Serum creatine phosphokinase and troponin levels were within normal limits. Cardiac catheterization revealed a 30% LMCA lesion and a 50% to 70% ostial left circumflex (LCx) lesion. He was discharged to home on aspirin, 325 mg, atenolol, 50 mg, and clopidogrel, 75 mg, daily. The patient subsequently underwent an outpatient stress test. After the administration of adenosine, he became hypotensive with inferior ST-segment depressions and ST-segment elevations in leads I, aVL, and V2-V4. Systolic blood pressure was noted to be 70 mmHg, and his heart rate was in the range of 40 beats/min. His symptoms resolved with rest and intravenous fluid administration. He was transferred to this institution for further management. Further review of his history revealed that he had a prior cataract excision. His family history was significant for the death of a brother at age 48 of a myocardial infarction. He denied the use of alcohol, tobacco, or illicit drugs. His height was 165 cm (65 in), and his weight was 77 kg (170 lb) A presumptive diagnosis of coronary artery vasospasm was made on the basis of his recurrent symptoms in the setting of minimal coronary artery disease. A plan to taper his atenolol was made. Review of his catheterization data from the outside hospital suggested a significant ostial LCx stenosis. He underwent a repeat cardiac catheterization with the intention of intervening on that lesion. Catheterization confirmed a 30% LMCA stenosis and revealed a focal 50% LCx ostial stenosis.
From the Departments of *Anesthesia and Critical Care, †Cardiac Surgery, and ‡Cardiology, Massachusetts General Hospital, Harvard Medical School, Boston, MA. Address reprint requests to Michael G. Fitzsimons, MD, FCCP, Division of Cardiac Anesthesia, Department of Anesthesia and Critical Care, Massachusetts General Hospital, 55 Fruit Street, Boston, MA 02114. E-mail: [email protected] © 2006 Elsevier Inc. All rights reserved. 1053-0770/06/2006-0014$32.00/0 doi:10.1053/j.jvca.2006.04.002 Key words: vasospasm, cardiopulmonary bypass grafting, ischemia, left main coronary artery 834
Intravascular ultrasound revealed an LCx minimal lumen area of 4.7 mm2 (acceptable ⬎4.0 mm2) and an LMCA minimal lumen area of 6.2 mm2 (acceptable ⬎5.9 mm2). Fractional flow reserve was calculated to be greater than 0.75 across both lesions. During the catheterization, the patient developed LMCA spasm, which was treated successfully with intracoronary NTG (Figs 1 and 2). Based on the minimal coronary lumen areas and fractional flow reserve being above the currently accepted cutoff values for hemodynamically significant lesions, the patient’s symptoms were believed to be caused by coronary vasospasm and no percutaneous intervention was made. Intravenous heparin and NTG were continued. Tapering of atenolol was also continued. Approximately 4 AM after his catheterization, he developed chest pain associated with precordial ST-segment elevations (⬎5 mm in V2-V5) and inferior ST-segment depression, hypotension, bradycardia, and, ultimately, asystole. He was successfully resuscitated with chest compressions, atropine, and epinephrine. His cardiac rhythm was a wide-complex tachycardia at 125 beats/min, blood pressure was 93/55 mmHg, and respiratory rate was 16 breaths/min. The rhythm converted spontansously to sinus rhythm. An intra-aortic balloon pump was placed. Intravenous NTG, diltiazem, and heparin were started for treatment of coronary vasospasm. His beta-blocker was discontinued. His troponin-T peaked at 0.56 ng/mL (normal 0.00-0.09 ng/mL). He continued to have recurrent symptoms over the subsequent 48 hours seemingly precipitated by stress and anxiety, despite intravenous NTG titrated as high as 1,000 g/min and intravenous diltiazem to 25 mg/h. Given his persistent symptoms in the setting of aggressive medical management and the area of myocardium that was at risk, the decision was made to treat his condition surgically. The cardiac surgical service was consulted, and he was taken to the operating room for coronary artery bypass graft (CABG) surgery. Intravenous NTG was continued at 1,000 g/min and diltiazem at 25 mg/h. Large-bore peripheral intravenous access was established, and after premedication with midazolam, 2 mg, arterial and central catheters were placed. Anesthesia was induced with midazolam, 5 mg, fentanyl, 750 g, and cisatracurium, 20 mg. His airway was easily intubated, and anesthesia was maintained with isoflurane and an infusion of cisatracurium. Vasoconstrictors were avoided, and crystalloid was administered to maintain blood pressure. Heparin was administered and cardiopulmonary bypass (CPB) initiated. The heart was arrested with warm continuous blood cardioplegia. The body was passively cooled to 35°C. Two-vessel CABG surgery was performed with saphenous vein grafts to the left anterior descending (LAD) and the obtuse marginal arteries. The grafts were sprayed with papaverine to prevent spasm. Diltiazem was restarted at 25 mg/h and NTG at 50 g/min. A spontaneous rhythm returned on removal of the aortic cross-clamp. The atrium and ventricle were paced to a rate of 80 beats/min. Norepinephrine was initiated at 2 g/min. Separation from CPB was uneventful. Total CPB time was 47 minutes with an aortic cross-clamp time of 34 minutes. The patient was taken to the cardiac surgical intensive care unit and extubated within several hours of surgery. He remained hemodynamically stable with no further episodes of ischemia and was discharged to home on the fourth postoperative day on a medical regimen of aspirin, 325 mg, atorvastatin, 20 mg, lisinopril, 5 mg, isosorbide mononitrate, 30 mg, and diltiazem, 360 mg, daily.
Journal of Cardiothoracic and Vascular Anesthesia, Vol 20, No 6 (December), 2006: pp 834-836
LEFT MAIN CORONARY ARTERY SPASM
Fig 1. Left anterior oblique, cranial view. Vasospasm of the LMCA (arrow).
Five months after his procedure, he underwent gated coronary artery computed tomography. Global left ventricular function was noted to be qualitatively normal with normal thickening in all segments of the left ventricle. The grafts to the LAD and obtuse marginal were patent, but the LMCA was completely occluded. He continues to remain asymptomatic. DISCUSSION
Coronary vasospasm is defined as a decrease in the caliber of the coronary arteries with evidence of ischemia, commonly known as variant or Prinzmetal’s angina. This degree of ischemia may be significant enough even in patients with normal coronaries to produce myocardial damage as indicated by elevated cardiac troponin I and cardiac arrest.2,3 Variant angina typically occurs during rest or at night. Cigarette smoking is the major risk factor for coronary vasospasm.4 Additional factors implicated in vasospasm include hypocalcemia,5 sotalol,6 pseudoephedrine,7 hyperventilation,8 ephedrine administration during spinal anesthesia,9 and cocaine use.10 This particular patient had no known risk factors for coronary spasm. Coronary blood flow is primarily regulated by local metabolic requirements, but the vessels are subject to some neurologic control. The mechanism for spasm of the coronary arteries involves both the parasympathetic and sympathetic nervous systems. Yasue et al11 studied 10 patients with variant angina. The cholinergic agonist methacholine precipitated attacks of angina. The anticholinergic drug atropine successfully suppressed the attack. The beta-blocker propranolol was not effective in suppressing the attacks. The parasympathetic agent acetylcholine directly vasodilates the coronary arteries. It also has an indirect action on the release of norepinephrine from the cardiac postganglionic nerve terminals in the heart. Excessive parasympathetic tone can result in the release of large amounts of norepinephrine resulting in coronary spasm. The final pathway of spasm is thus alpha-adrenergic vasoconstriction.
835
Medical management of coronary spasm primarily consists of nitrates and calcium channel blockers. Beta-blockers are usually considered detrimental when used alone because betablockade may result in unopposed alpha-adrenergic stimulation and an increase in coronary vascular tone.12 Nitrates may be administered intravenously, orally, topically, or sublingually with relief in the majority of patients.13 Intracoronary infusion of nitrates has also been successfully used to treat spasm after percutaneous transluminal angioplasty.14 Calcium channel blockers have been used successfully in combination with nitrates and beta-blockers15 and as monotherapy.16 Surgical management of coronary spasm is rarely indicated. This patient had moderate coronary atheroma, but the lesions were not determined to be of hemodynamic significance based on fractional flow reserves ⬎0.75 (ratio of maximal achievable coronary flow in a stenotic vessel/normal maximal coronary flow) and minimal luminal areas greater than accepted cutoff; thus, medical management was initially planned.17,18 CABG surgery has been advocated for the management of vasospasm refractory to medical management.13 Results have been found to be variable, however, with recurrent angina and graft thrombosis being the major problem.19 Some authors have advocated surgical coronary angioplasty with sympathetic plexectomy20 in an attempt to prevent the activation of alpha-adrenergic stimulation. Bertrand et al21 have suggested that complete sympathetic plexectomy in combination with CABG surgery may improve survival and decrease symptoms. The present patient suffered from spasm of the LMCA, a condition that rarely has been reported1,19 and that carries with it potentially devastating consequences. A case of recurrent LMCA spasm, which was successfully treated with medical management alone, has been reported previously. The authors of that report suggested persisting with medical therapy for at
Fig 2. Right anterior oblique, caudal view. Resolution of LMCA spasm after treatment with intracoronary nitroglycerin.
836
FITZSIMONS ET AL
least 8 weeks before considering surgical intervention.19 However, this patient showed recurrent spasm despite aggressive medical management. In this setting, the decision was made to proceed with surgical therapy, recognizing the risks of postoperative spasm and graft thrombosis because of preferential flow through the native, widely patent coronary arteries. The anesthetic plan focused on avoiding excessive sympathetic stimulation because anxiety was believed to be a precipitating factor, minimize alpha-adrenergic stimulation (norepinephrine), and treat hypotension with fluid administration. Diltiazem and NTG were continued until CPB was initiated. A saphenous vein graft to the LAD was used in lieu of the left internal mammary artery (LIMA) to avoid the risk of LIMA spasm and because the LIMA tends not to mature to areas with competitive flow. Berger at al22 showed that grafting the LIMA to native vessels with ⬍50% stenosis resulted in a higher rate of
stenosis of the arterial conduit than if the native stenosis was greater. Separation from CPB was uneventful except for slight hypotension treated with fluids and low-dose norepinephrine. His recovery was uneventful. The computed tomography performed 5 months after his procedure showed good flow through the vein grafts but complete occlusion of the LMCA. The LMCA occlusion was believed to be caused by either progression of the atherosclerosis or preferential blood flow through the grafts. LMCA spasm is an uncommon, potentially lethal condition. The limitations of a single case report must be recognized, and this is not meant to imply that surgical treatment should be the first line of treatment. Medical management of an LMCA spasm should be attempted at the outset with expeditious progression to surgical therapy only if symptoms continue to recur despite maximum therapy.
REFERENCES 1. Tzivoni D, Merin G, Milo S, et al: Spasm of the left main coronary artery. Br Heart J 38:104-107, 1976 2. Wang C-H, Kuo L-T, Hung M-J, et al: Coronary vasospasm as a possible cause of elevated cardiac troponin I in patients with acute coronary syndrome and insignificant coronary artery disease. Am Heart J 144:275-281, 2002 3. Weston CF, Tigg A, Griffiths BE: Pre-hospital cardiac arrest associated with coronary artery vasospasm. Int J Cardiol 38:98-100, 1993 4. Nobuyshi M, Abe M, Nosaka H, et al: Statistical analysis of clinical risk factors for coronary artery spasm: Identification of the most important determinant. Am Heart J 124:32-38, 1992 5. Magnus PC, Missri J: Hypocalcemia-associated coronary vasospasm. Conn Med 69:3-7, 2005 6. Muto S, Ashizawa N, Arakawa S, et al: Sotalol-induced coronary spasm in a patient with dilated cardiomyopathy associated with sustained ventricular tachycardia. Intern Med 43:1051-1055, 2004 7. Manini AF, Kabrhel C, Thomsen TW: Acute myocardial infarction after over-the-counter use of pseudoephedrine. Ann Emerg Med 45:213-216, 2005 8. Fangio P, De Jonghe B, Lacherade JC, et al: Coronary spasm in a 59-yr-old woman with hyperventilation. Can J Anaesth 51:850-851, 2004 9. Wahl A, Eberli FR, Thomson DA, et al: Coronary artery spasm and non-Q-wave myocardial infarction following administration. Br J Anaesth 89:519-523, 2002 10. Lange RA, Hillis LD: Cardiovascular complications of cocaine use. N Engl J Med 345:351-358, 2001 11. Yasue H, Touyama M, Shimamoto M, et al: Role of autonomic nervous system in the pathogenesis of Prinzmetal’s variant form of angina. Circulation 50:534-539, 1974
12. Nansa JN, Sutton RB, Alazraki N, et al: Acute myocardial infarction in post infarct patient possibly through beta-blocker-induced coronary artery spasm. Am Heart J 113:388-391, 1987 13. Conti RC: Large-vessel coronary vasospasm: Diagnosis, natural history and treatment. Am J Cardiol 55:41B-49B, 1985 14. Kern KB, Temkin LP, Fenster PE: Continuous intracoronary nitroglycerin infusion for spasm after angioplasty. Clin Cardiol 6:609612, 1983 15. Hugenholtz PG, Serruys PW, Balakumaran K: Drug therapy: How effective is nifedipine for unstable angina? J Cardiovasc Med 7:373-378, 1982 16. Mehta J, Pepine CJ, Day M, et al: Short-term efficacy of oral verapamil in rest angina: A double-blind placebo-controlled trial in CCU Patients. Am J Med 71:977-982, 1981 17. Jasti V, Yalamanchili V, Wongpraparut N, et al: Correlations between fractional flow reserve and intravascular ultrasound in patients with an ambiguous left main coronary stenosis. Circulation 110:28312836, 2004 18. Nishioka T, Amanullah AM, Luo H, et al: Clinical validation of intravascular ultrasound imaging for assessment of coronary stenosis severity: Comparison with stress myocardial perfusion imaging. J Am Coll Cardiol 33:1870-1878, 1999 19. Ng WL, Sim EK, Yeo TC, et al: Surgery for left main spasm. Is it indicated? Int J Cardiol 54:213-216, 1996 20. Sen RC, Hitter E, Ranquin R, et al: Surgical coronary angioplasty for left main vasospasm. Am Heart J 129:399-400, 1995 21. Bertrand ME, Lablanche JM, Rousseau MF, et al: Surgical treatment of variant angina: Use of plexectomy with aortocoronary bypass. Circulation 61:877-882, 1980 22. Berger A, MacCarthy PA, Siebert U, et al: Long-term patency of internal mammary artery bypass grafts: Relationship with preoperative severity of the native coronary artery stenosis. Circulation 110:II-36II-40, 2004 (suppl 2)
Left Main Coronary Artery Spasm: Medical Versus Surgical Management Michael G. Fitzsimons, MD, FCCP,* Jennifer Walker, MD,† Ignacio Inglessis, MD,‡ and Charles Boucher, MD‡
V
ASOSPASM OF THE left main coronary artery (LMCA) is a rare condition with potentially devastating consequences. Medical therapy is the initial strategy for management of coronary vasospasm. LMCA spasm may warrant a more aggressive surgical approach.1 Therefore, a case of coronary artery bypass grafting for recurrent LMCA spasm in the face of maximal medical management is reported. CASE REPORT
A 50-year-old man with a history of hypertension, dyslipidemia, and nephrolithiasis was in his usual state of health until 1 week before admission to this hospital when he presented to an outside institution with chest pain and dyspnea. His electrocardiogram showed T-wave inversions in leads II, III, aVF, and V3-V6. He was treated with sublingual nitroglycerin (NTG) with dramatic resolution of his symptoms and electrocardiographic changes. Serum creatine phosphokinase and troponin levels were within normal limits. Cardiac catheterization revealed a 30% LMCA lesion and a 50% to 70% ostial left circumflex (LCx) lesion. He was discharged to home on aspirin, 325 mg, atenolol, 50 mg, and clopidogrel, 75 mg, daily. The patient subsequently underwent an outpatient stress test. After the administration of adenosine, he became hypotensive with inferior ST-segment depressions and ST-segment elevations in leads I, aVL, and V2-V4. Systolic blood pressure was noted to be 70 mmHg, and his heart rate was in the range of 40 beats/min. His symptoms resolved with rest and intravenous fluid administration. He was transferred to this institution for further management. Further review of his history revealed that he had a prior cataract excision. His family history was significant for the death of a brother at age 48 of a myocardial infarction. He denied the use of alcohol, tobacco, or illicit drugs. His height was 165 cm (65 in), and his weight was 77 kg (170 lb) A presumptive diagnosis of coronary artery vasospasm was made on the basis of his recurrent symptoms in the setting of minimal coronary artery disease. A plan to taper his atenolol was made. Review of his catheterization data from the outside hospital suggested a significant ostial LCx stenosis. He underwent a repeat cardiac catheterization with the intention of intervening on that lesion. Catheterization confirmed a 30% LMCA stenosis and revealed a focal 50% LCx ostial stenosis.
From the Departments of *Anesthesia and Critical Care, †Cardiac Surgery, and ‡Cardiology, Massachusetts General Hospital, Harvard Medical School, Boston, MA. Address reprint requests to Michael G. Fitzsimons, MD, FCCP, Division of Cardiac Anesthesia, Department of Anesthesia and Critical Care, Massachusetts General Hospital, 55 Fruit Street, Boston, MA 02114. E-mail: [email protected] © 2006 Elsevier Inc. All rights reserved. 1053-0770/06/2006-0014$32.00/0 doi:10.1053/j.jvca.2006.04.002 Key words: vasospasm, cardiopulmonary bypass grafting, ischemia, left main coronary artery 834
Intravascular ultrasound revealed an LCx minimal lumen area of 4.7 mm2 (acceptable ⬎4.0 mm2) and an LMCA minimal lumen area of 6.2 mm2 (acceptable ⬎5.9 mm2). Fractional flow reserve was calculated to be greater than 0.75 across both lesions. During the catheterization, the patient developed LMCA spasm, which was treated successfully with intracoronary NTG (Figs 1 and 2). Based on the minimal coronary lumen areas and fractional flow reserve being above the currently accepted cutoff values for hemodynamically significant lesions, the patient’s symptoms were believed to be caused by coronary vasospasm and no percutaneous intervention was made. Intravenous heparin and NTG were continued. Tapering of atenolol was also continued. Approximately 4 AM after his catheterization, he developed chest pain associated with precordial ST-segment elevations (⬎5 mm in V2-V5) and inferior ST-segment depression, hypotension, bradycardia, and, ultimately, asystole. He was successfully resuscitated with chest compressions, atropine, and epinephrine. His cardiac rhythm was a wide-complex tachycardia at 125 beats/min, blood pressure was 93/55 mmHg, and respiratory rate was 16 breaths/min. The rhythm converted spontansously to sinus rhythm. An intra-aortic balloon pump was placed. Intravenous NTG, diltiazem, and heparin were started for treatment of coronary vasospasm. His beta-blocker was discontinued. His troponin-T peaked at 0.56 ng/mL (normal 0.00-0.09 ng/mL). He continued to have recurrent symptoms over the subsequent 48 hours seemingly precipitated by stress and anxiety, despite intravenous NTG titrated as high as 1,000 g/min and intravenous diltiazem to 25 mg/h. Given his persistent symptoms in the setting of aggressive medical management and the area of myocardium that was at risk, the decision was made to treat his condition surgically. The cardiac surgical service was consulted, and he was taken to the operating room for coronary artery bypass graft (CABG) surgery. Intravenous NTG was continued at 1,000 g/min and diltiazem at 25 mg/h. Large-bore peripheral intravenous access was established, and after premedication with midazolam, 2 mg, arterial and central catheters were placed. Anesthesia was induced with midazolam, 5 mg, fentanyl, 750 g, and cisatracurium, 20 mg. His airway was easily intubated, and anesthesia was maintained with isoflurane and an infusion of cisatracurium. Vasoconstrictors were avoided, and crystalloid was administered to maintain blood pressure. Heparin was administered and cardiopulmonary bypass (CPB) initiated. The heart was arrested with warm continuous blood cardioplegia. The body was passively cooled to 35°C. Two-vessel CABG surgery was performed with saphenous vein grafts to the left anterior descending (LAD) and the obtuse marginal arteries. The grafts were sprayed with papaverine to prevent spasm. Diltiazem was restarted at 25 mg/h and NTG at 50 g/min. A spontaneous rhythm returned on removal of the aortic cross-clamp. The atrium and ventricle were paced to a rate of 80 beats/min. Norepinephrine was initiated at 2 g/min. Separation from CPB was uneventful. Total CPB time was 47 minutes with an aortic cross-clamp time of 34 minutes. The patient was taken to the cardiac surgical intensive care unit and extubated within several hours of surgery. He remained hemodynamically stable with no further episodes of ischemia and was discharged to home on the fourth postoperative day on a medical regimen of aspirin, 325 mg, atorvastatin, 20 mg, lisinopril, 5 mg, isosorbide mononitrate, 30 mg, and diltiazem, 360 mg, daily.
Journal of Cardiothoracic and Vascular Anesthesia, Vol 20, No 6 (December), 2006: pp 834-836
LEFT MAIN CORONARY ARTERY SPASM
Fig 1. Left anterior oblique, cranial view. Vasospasm of the LMCA (arrow).
Five months after his procedure, he underwent gated coronary artery computed tomography. Global left ventricular function was noted to be qualitatively normal with normal thickening in all segments of the left ventricle. The grafts to the LAD and obtuse marginal were patent, but the LMCA was completely occluded. He continues to remain asymptomatic. DISCUSSION
Coronary vasospasm is defined as a decrease in the caliber of the coronary arteries with evidence of ischemia, commonly known as variant or Prinzmetal’s angina. This degree of ischemia may be significant enough even in patients with normal coronaries to produce myocardial damage as indicated by elevated cardiac troponin I and cardiac arrest.2,3 Variant angina typically occurs during rest or at night. Cigarette smoking is the major risk factor for coronary vasospasm.4 Additional factors implicated in vasospasm include hypocalcemia,5 sotalol,6 pseudoephedrine,7 hyperventilation,8 ephedrine administration during spinal anesthesia,9 and cocaine use.10 This particular patient had no known risk factors for coronary spasm. Coronary blood flow is primarily regulated by local metabolic requirements, but the vessels are subject to some neurologic control. The mechanism for spasm of the coronary arteries involves both the parasympathetic and sympathetic nervous systems. Yasue et al11 studied 10 patients with variant angina. The cholinergic agonist methacholine precipitated attacks of angina. The anticholinergic drug atropine successfully suppressed the attack. The beta-blocker propranolol was not effective in suppressing the attacks. The parasympathetic agent acetylcholine directly vasodilates the coronary arteries. It also has an indirect action on the release of norepinephrine from the cardiac postganglionic nerve terminals in the heart. Excessive parasympathetic tone can result in the release of large amounts of norepinephrine resulting in coronary spasm. The final pathway of spasm is thus alpha-adrenergic vasoconstriction.
835
Medical management of coronary spasm primarily consists of nitrates and calcium channel blockers. Beta-blockers are usually considered detrimental when used alone because betablockade may result in unopposed alpha-adrenergic stimulation and an increase in coronary vascular tone.12 Nitrates may be administered intravenously, orally, topically, or sublingually with relief in the majority of patients.13 Intracoronary infusion of nitrates has also been successfully used to treat spasm after percutaneous transluminal angioplasty.14 Calcium channel blockers have been used successfully in combination with nitrates and beta-blockers15 and as monotherapy.16 Surgical management of coronary spasm is rarely indicated. This patient had moderate coronary atheroma, but the lesions were not determined to be of hemodynamic significance based on fractional flow reserves ⬎0.75 (ratio of maximal achievable coronary flow in a stenotic vessel/normal maximal coronary flow) and minimal luminal areas greater than accepted cutoff; thus, medical management was initially planned.17,18 CABG surgery has been advocated for the management of vasospasm refractory to medical management.13 Results have been found to be variable, however, with recurrent angina and graft thrombosis being the major problem.19 Some authors have advocated surgical coronary angioplasty with sympathetic plexectomy20 in an attempt to prevent the activation of alpha-adrenergic stimulation. Bertrand et al21 have suggested that complete sympathetic plexectomy in combination with CABG surgery may improve survival and decrease symptoms. The present patient suffered from spasm of the LMCA, a condition that rarely has been reported1,19 and that carries with it potentially devastating consequences. A case of recurrent LMCA spasm, which was successfully treated with medical management alone, has been reported previously. The authors of that report suggested persisting with medical therapy for at
Fig 2. Right anterior oblique, caudal view. Resolution of LMCA spasm after treatment with intracoronary nitroglycerin.
836
FITZSIMONS ET AL
least 8 weeks before considering surgical intervention.19 However, this patient showed recurrent spasm despite aggressive medical management. In this setting, the decision was made to proceed with surgical therapy, recognizing the risks of postoperative spasm and graft thrombosis because of preferential flow through the native, widely patent coronary arteries. The anesthetic plan focused on avoiding excessive sympathetic stimulation because anxiety was believed to be a precipitating factor, minimize alpha-adrenergic stimulation (norepinephrine), and treat hypotension with fluid administration. Diltiazem and NTG were continued until CPB was initiated. A saphenous vein graft to the LAD was used in lieu of the left internal mammary artery (LIMA) to avoid the risk of LIMA spasm and because the LIMA tends not to mature to areas with competitive flow. Berger at al22 showed that grafting the LIMA to native vessels with ⬍50% stenosis resulted in a higher rate of
stenosis of the arterial conduit than if the native stenosis was greater. Separation from CPB was uneventful except for slight hypotension treated with fluids and low-dose norepinephrine. His recovery was uneventful. The computed tomography performed 5 months after his procedure showed good flow through the vein grafts but complete occlusion of the LMCA. The LMCA occlusion was believed to be caused by either progression of the atherosclerosis or preferential blood flow through the grafts. LMCA spasm is an uncommon, potentially lethal condition. The limitations of a single case report must be recognized, and this is not meant to imply that surgical treatment should be the first line of treatment. Medical management of an LMCA spasm should be attempted at the outset with expeditious progression to surgical therapy only if symptoms continue to recur despite maximum therapy.
REFERENCES 1. Tzivoni D, Merin G, Milo S, et al: Spasm of the left main coronary artery. Br Heart J 38:104-107, 1976 2. Wang C-H, Kuo L-T, Hung M-J, et al: Coronary vasospasm as a possible cause of elevated cardiac troponin I in patients with acute coronary syndrome and insignificant coronary artery disease. Am Heart J 144:275-281, 2002 3. Weston CF, Tigg A, Griffiths BE: Pre-hospital cardiac arrest associated with coronary artery vasospasm. Int J Cardiol 38:98-100, 1993 4. Nobuyshi M, Abe M, Nosaka H, et al: Statistical analysis of clinical risk factors for coronary artery spasm: Identification of the most important determinant. Am Heart J 124:32-38, 1992 5. Magnus PC, Missri J: Hypocalcemia-associated coronary vasospasm. Conn Med 69:3-7, 2005 6. Muto S, Ashizawa N, Arakawa S, et al: Sotalol-induced coronary spasm in a patient with dilated cardiomyopathy associated with sustained ventricular tachycardia. Intern Med 43:1051-1055, 2004 7. Manini AF, Kabrhel C, Thomsen TW: Acute myocardial infarction after over-the-counter use of pseudoephedrine. Ann Emerg Med 45:213-216, 2005 8. Fangio P, De Jonghe B, Lacherade JC, et al: Coronary spasm in a 59-yr-old woman with hyperventilation. Can J Anaesth 51:850-851, 2004 9. Wahl A, Eberli FR, Thomson DA, et al: Coronary artery spasm and non-Q-wave myocardial infarction following administration. Br J Anaesth 89:519-523, 2002 10. Lange RA, Hillis LD: Cardiovascular complications of cocaine use. N Engl J Med 345:351-358, 2001 11. Yasue H, Touyama M, Shimamoto M, et al: Role of autonomic nervous system in the pathogenesis of Prinzmetal’s variant form of angina. Circulation 50:534-539, 1974
12. Nansa JN, Sutton RB, Alazraki N, et al: Acute myocardial infarction in post infarct patient possibly through beta-blocker-induced coronary artery spasm. Am Heart J 113:388-391, 1987 13. Conti RC: Large-vessel coronary vasospasm: Diagnosis, natural history and treatment. Am J Cardiol 55:41B-49B, 1985 14. Kern KB, Temkin LP, Fenster PE: Continuous intracoronary nitroglycerin infusion for spasm after angioplasty. Clin Cardiol 6:609612, 1983 15. Hugenholtz PG, Serruys PW, Balakumaran K: Drug therapy: How effective is nifedipine for unstable angina? J Cardiovasc Med 7:373-378, 1982 16. Mehta J, Pepine CJ, Day M, et al: Short-term efficacy of oral verapamil in rest angina: A double-blind placebo-controlled trial in CCU Patients. Am J Med 71:977-982, 1981 17. Jasti V, Yalamanchili V, Wongpraparut N, et al: Correlations between fractional flow reserve and intravascular ultrasound in patients with an ambiguous left main coronary stenosis. Circulation 110:28312836, 2004 18. Nishioka T, Amanullah AM, Luo H, et al: Clinical validation of intravascular ultrasound imaging for assessment of coronary stenosis severity: Comparison with stress myocardial perfusion imaging. J Am Coll Cardiol 33:1870-1878, 1999 19. Ng WL, Sim EK, Yeo TC, et al: Surgery for left main spasm. Is it indicated? Int J Cardiol 54:213-216, 1996 20. Sen RC, Hitter E, Ranquin R, et al: Surgical coronary angioplasty for left main vasospasm. Am Heart J 129:399-400, 1995 21. Bertrand ME, Lablanche JM, Rousseau MF, et al: Surgical treatment of variant angina: Use of plexectomy with aortocoronary bypass. Circulation 61:877-882, 1980 22. Berger A, MacCarthy PA, Siebert U, et al: Long-term patency of internal mammary artery bypass grafts: Relationship with preoperative severity of the native coronary artery stenosis. Circulation 110:II-36II-40, 2004 (suppl 2)