Ann Thorac Surg 2008;85:647-649. doi:10.1016/j.athoracsur.2007.08.015
© 2008 The Society of Thoracic Surgeons
Case Reports
Postoperative Internal Thoracic Artery Spasm After Coronary Artery Bypass Grafting
Ralf E. Harskamp, MS*,
Jeffrey D. McNeil, MD,
Margreet W. van Ginkel, MS,
Renata B. Bastos, MD,
Clinton E. Baisden, MD, FACS,
John H. Calhoon, MD
Division of Cardiothoracic Surgery, Department of Surgery, University of Texas Health Science Center at San Antonio, San Antonio, Texas
Accepted for publication August 7, 2007.
* Address correspondence to Dr Harskamp, Division of Cardiothoracic Surgery, Department of Surgery, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Dr, San Antonio, TX 78229-3900 (Email: r.e.harskamp{at}gmail.com).
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Abstract
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Spasm of the left internal thoracic artery in the perioperative period represents a life-threatening complication after coronary artery bypass grafting. We present a case in which graft spasm was treated with the administration of intra-arterial nitroglycerin and verapamil. Although vasospasm is more often seen in radial artery grafts, this case demonstrates that left internal thoracic artery grafts are also prone to spasm.
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Introduction
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The left internal thoracic artery (LITA) is the superior conduit for coronary artery bypass grafting surgery. Although LITA spasm is an important perioperative complication, the actual incidence is unknown. In this case report we present a patient with perioperative LITA spasm and briefly review the current treatment of arterial graft spasm.
A 57-year-old Hispanic man with hypertension and hyperlipidemia presented to our hospital with substernal chest pain, shortness of breath, and dyspnea on exertion. He was admitted to the cardiology service for further evaluation. He denied alcohol abuse, had quit smoking, and had quit marijuana approximately 1 year prior to presentation. His family history was positive for coronary artery disease within the immediate family. Outpatient medications included metroprolol (100 mg), aspirin (325 mg), and Lipitor (atorvastatin calcium; Pfizer Inc, New York, NY) (20 mg) each once daily.
Admission vital signs were a temperature of 36.3°C, a pulse of 70 bpm, respiration at 18 bpm, and a blood pressure of 140/88 mm Hg. His body mass index was 30.1 and his bovine serum albumin was 1.9. A harsh systolic murmur, heard best at the right upper sternal border, radiated to the carotids.
Laboratory values were notable for normal electrolytes and creatinine, elevated cardiac enzymes with a troponin of 1.72 ng/mL (normal range, 0.01 to 0.78 ng/mL), and low hemoglobin of 9.6 g/dL (13.5 to 17.5 g/dL). Oxygen saturation was 98% on room air.
Transthoracic echocardiogram demonstrated concentric left ventricular hypertrophy with severely calcified aortic leaflets at a peak gradient of 121 mm Hg and a mean gradient of 78 mm Hg. His other valves were normal. A coronary angiography, in anticipation of valve replacement, revealed chronic occlusion of the proximal left anterior descending coronary artery with no other significant coronary disease. His ejection fraction was 60%.
During his hospitalization, he underwent aortic valve replacement and single-vessel coronary artery bypass grafting surgery. Standard cardiopulmonary bypass with moderate hypothermia (32.9°C) was used. Antegrade and retrograde blood cardioplegia were administered. Myocardial ischemic time lasted 105 minutes. A 21-mm Magna Carpentier-Edwards bovine pericardial valve (Edwards Lifesciences, Irvine, CA) was implanted. Left anterior descending coronary artery revascularization was performed using a pedicled, nonskeletonized LITA. Before anastamosis the LITA was wrapped in papaverine-soaked gauze. The left anterior descending coronary artery was approximately 1.25 mm in diameter and was of reasonable quality. The remainder of the intraoperative course was uneventful.
The patient was transported to the intensive care unit in stable condition without any vasoactive drips. He was uneventfully extubated on the night of surgery. In the afternoon of postoperative day 2, he suddenly had respiratory distress, diaphoresis, and angina develop. An electrocardiogram revealed sinus tachycardia, ST-segment elevations in III, aVF and V1–V3. A chest x-ray film showed normal postoperative changes. Laboratory studies at the time were notable for normal electrolytes, with a creatine of 1.1 mg/dL (0.7 to 1.6 mg/dL) and slightly elevated cardiac enzymes with a troponin of 2.25 ng/mL (0.01 to 0.78 ng/mL), and a hemoglobin of 11.3 g/dL (13.5 to 17.5 g/dL). The patient was urgently taken to the cardiac catheterization laboratory. He was given intravenous furosemide for aggressive diureses, with a decrease in wedge pressure from 35 mm Hg to 25 mm Hg. An angiography demonstrated a LITA vasospasm in the proximal portion of the body of the graft with a maximal stenosis of 90% (Fig 1A). The spasm was unresponsive to nitroglycerin (3 x 200 mcg, intracoronary and 1 x 300 mcg, intracoronary LITA graft), but it resolved to 10% with administration of verapamil (ie, L-type calcium channel blocker) (Fig 1B). He was maintained on nitroglycerin infusion in the intensive care unit. On postoperative day 3 he was started on isosorbide mononitrate (20 mg twice a day) and he was weaned off of the nitroglycerin infusion. He did not experience any further vasospasm or cardiovascular symptoms and was discharged home on postoperative day 5. Oral nitrates were discontinued 6 weeks after his surgery. The patient was seen at a 3-month follow-up and he was doing well.
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Fig 1. (A) Pretreatment angiography shows a proximal area of spasm in the left internal thoracic artery (LITA). (B) Restored flow in LITA after nitroglycerin and verapamil.
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Comment
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The LITA is the preferred conduit for coronary bypass grafting. Although the long-term patency of LITA grafts is superior, spasm of the LITA after coronary artery bypass grafting surgery can be seen as with other arterial grafts [1]. Severe LITA spasm can present with angina, acute hemodynamic collapse, anatomic segmental ST-segment elevation, or ventricular fibrillation, or a combination of these additional factors. Insufficient blood flow through arterial grafts may also cause a "hypoperfusion syndrome" manifested by left ventricular failure, increasing pulmonary wedge pressure, and by cardiac arrest [2].
The mechanism of perioperative vascular spasm is not completely understood. Previous studies have implicated local manipulation, 
-adrenergic activity, high blood pH level, low body temperature, release of vasoconstrictive factors (eg, vasopressin), histamine release, local increased potassium levels, possible rebound vasoconstriction after abrupt withdrawal of calcium-channel blockade, low PaCO2, smoking, and use of the distal section of the LITA [3, 4].
Harvesting techniques have been developed, such as the use of modified pedicled and skeletonized grafts, to minimize manipulation-induced spasm. To prevent vasospasm during or after surgical intervention, and to increase blood flow, some vasodilatory agents are used, including calcium-channel blockers, phosphodiesterase inhibitors, papaverine, and nitroglycerin. Management of perioperative graft spasm varies, because of a lack of well-accepted protocols. In the event of acute refractory hemodynamic collapse in the immediate postoperative period, Sarabu and colleagues [3] have recommended immediate reopening. Spasm can then be treated with topical papaverine and additional grafting. Sarabu and colleagues [3] and Paterson and associates [5] have suggested infusion of intraluminal vasodilators for postoperative LITA vasospasm. The use of angiographic intraluminal injection of vasospasm relieving agents prevents the complications of surgical delay, reoperation, graft manipulation, external graft injection of vasodilators, repeated use of cardiopulmonary bypass, and additional grafting. Sanders and Newman [6] proposed that a high arterial blood pressure should be maintained for LITA and coronary perfusion to prevent vasospasm. It was not determined which inotropic or vasoconstrictive agent is best suited for treatment.
Our patient was successfully treated with nitroglycerin and verapamil injected intraluminally through angiographic catherization. He was continued on oral nitrates rather than verapamil to avoid the combination of verapamil with beta blocker therapy. In our practice, beta blockers are routinely given after cardiac surgery to decrease the incidence of atrial fibrillation. In our search of the English literature, only two reports of internal thoracic artery spasm refractory to angiographic intraluminal injection with nitroglycerin were found [6, 7]. In those cases, intraluminal injection of nitroglycerin was ineffective in reversing the LITA spasm. Based on our results, intraluminal verapamil may be useful in situations in which nitroglycerin is not successful.
Long-term benefits of arterial conduits are being advocated for coronary revascularization. Future studies should investigate the potential for prevention of arterial graft spasm. In addition, more research is required that leads to better understanding of the cause of arterial vasospasm. We are evaluating the use of novel therapies to prevent arterial vasospasm in our laboratory. Information obtained in those studies will potentially be used to develop new treatments or techniques to prevent vasospasm. This approach may help improve long-term outcome of coronary bypass patients in the future by facilitating more widespread use of arterial conduits.
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References
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- Loop FD, Lytle BW, Cosgrove DM, et al. Influence of the internal thoracic artery graft on 10-year survival and other cardiac events N Engl J Med 1986;314:1-6.[Abstract]
- Jones EL, Lattouf OM, Weinstraub WS. Catastrophic consequences of internal thoracic artery hypoperfusion J Thorac Cardiovasc Surg 1989;98:902-907.[Abstract]
- Sarabu MR, McClung JA, Fass A, Reed GE. Early postoperative spasm in left internal thoracic artery bypass grafts Ann Thorac Surg 1987;44:199-200.[Abstract]
- He GW. Contractility of the human internal thoracic artery at the distal section increases toward the endEmphasis on not using the end of the internal thoracic artery for grafting. J Thorac Cardiovasc Surg 1993;106:406-411.[Abstract]
- Paterson HS, Jones MW, Baird DK, Hughes CF. Lethal postoperative coronary artery spasm Ann Thorac Surg 1998;65:1571-1573.[Abstract/Free Full Text]
- Sanders LH, Newman MA. Intractable postoperative internal thoracic artery spasm managed with angiographic intraluminal papaverine J Thorac Cardiovasc Surg 2005;130:938-940.[Free Full Text]
- Kitamura H, Nakayama K, Kitano T. A case of refractory spasm of multiple coronary arteries and left internal thoracic artery graft following off-pump coronary artery bypass grafting surgery Kyobu Geka 2001;54:1103-1106.[Medline]
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Abstract
Introduction
