Ann Thorac Surg 2002;73:297-300
© 2002 The Society of Thoracic Surgeons
Case report
Coronary artery spasm and ventricular fibrillation after off-pump coronary surgery
Hartmuth B. Bittner, MD*a
a Department of Surgery, Division of Cardiovascular and Thoracic Surgery, University of Minnesota, Minneapolis, Minnesota, USA
Accepted for publication April 19, 2001.
* Address reprint requests to Dr Bittner, Division of Cardiovascular and Thoracic Surgery, Box 207 Mayo, 420 Delaware St, Minneapolis, MN 55455, USA
e-mail: bittn006{at}tc.umn.edu
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Abstract
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Native coronary artery or bypass graft spasm is a rare cause of acute myocardial infarction after coronary artery bypass grafting. This report presents angiographic documentation of native coronary artery spasm following successful multivessel off-pump coronary revascularization, which caused myocardial ischemia leading to inferior wall myocardial infarction and ventricular fibrillatory arrest.
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Introduction
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The incidence of sustained tachycardia or ventricular fibrillation after cardiac surgery ranges from 0.4% to 1.4% [1]. These potentially lethal arrhythmias often are unexpected and may occur at any time after coronary revascularization. Predisposing factors include myocardial ischemia, low cardiac output, metabolic derangements, drug interactions, and severe left ventricular dysfunction. Development of ventricular arrhythmias should prompt evaluation for ongoing myocardial ischemia, and the etiology for the event should be immediately investigated. Possible causes include incomplete myocardial protection, incomplete revascularization, atheromatous emboli from the aorta, air embolism, thrombosis of either a native vessel or a new graft, and vasospasm.
A 63-year-old man with a 4-month history of exertional chest pain was admitted for elective coronary artery bypass grafting. The patient’s risk factors for coronary artery disease and comorbidity included history of several previous myocardial infarctions, recent percutaneous transluminal coronary angioplasty and stenting of the left circumflex artery, hypertension, adult onset diabetes mellitus, obesity, chronic obstructive pulmonary disease associated with a 150 pack-history of tobacco abuse. Cardiac catheterization revealed three-vessel coronary artery disease (Fig 1)
with a totally occluded right coronary artery, filling retrogradely into a large right posterior descending artery (PDA, Fig 2),
significant flow limiting lesions in the proximal left circumflex system and left anterior descending artery (LAD). The left ventriculogram showed a decreased ejection fraction of 40%.
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Fig 1. The right anterior oblique (RAO) projection and left coronary artery injection revealed severe three-vessel coronary artery disease. The right coronary artery was chronically occluded and filled retrogradely from the left anterior descending (LAD) into a large posterior descending artery (PDA). The size 8 French angiography catheter (Cath) allows esti mating of the diameter of the coronary arteries. (D = diagonal branch; OM = obtuse marginal branch.)
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Fig 2. The LAO projection and left coronary artery injection (LAD = left anterior descending artery; OM = obtuse marginal branch; PDA = posterior descending artery.)
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While the greater saphenous vein was harvested, a median sternotomy was performed and the left internal thoracic artery (LITA) dissected and mobilized over its entire length. Heparin 300 U/kg was administered intravenously 3 minutes prior to distal transsection of the LITA, which was a very large conduit with excellent flow characteristics.
In preparation for off-pump coronary revascularization, the right side of the sternum was elevated by 30 to 35 degrees, the right-sided pericardial-pleural structures were vertically incised at the level of the inferior vena cava under protection of the right phrenic nerve, and the operating table was tilted to the right. Tension on the previously placed deep pericardial sutures rotated the entire heart toward the surgeon’s side with the LAD, its diagonal and the first obtuse marginal artery (OM1) becoming near midline structures. Tension on the deepest pericardial sutures led to elevation of the cardiac apex and herniation through the open chest allowing full exposure of the PDA selected to be the fourth distal target. The distal anastomoses were constructed first in the following sequence: saphenous vein grafts (SVG) to OM1, Diagonal, PDA, and LITA to distal LAD, using a 7-0 monofilament running suture technique. Immediately following the construction of each distal SVG anastomosis, the proximal SVG site was connected to a cannula, which was inserted at the ascending aorta for immediate arterial blood flow through the grafts. The three proximal anastomoses were constructed last using a 6-0 monofilament running suture technique after a partial aortic occlusion clamp was applied. Throughout, the online monitored hemodynamics were very stable with venous O2-saturation greater than 73%, cardiac index of greater than 2.0 L/min, and systolic artery pressure greater than 110 mm Hg. Only for heart positioning and construction of the OM1 distal anastomosis, norepinephrine IV infusion was started when the systolic blood pressure decreased to 90 mm Hg. Patency of the distal anastomoses and conduit flow were assessed by probing the anastomosis with vascular microdilators and qualitatively with an Ultrasonic Doppler Flow Detector (model 812; Parks Medical Electronics, Inc, Aloha, OR). Furthermore, back-bleeding was noted from the proximal ends of the Diagonal and OM1 branch SVG conduits while the proximal anastomoses were constructed. The activated clotting time (ACT) was kept above 300 seconds and the heparin effect fully reversed with protamine at the end of the operation.
Extubation in the operating room failed due to severe agitation associated with sudden hypoxia, sustained superventricular tachycardia (SVT), and systemic hypotension. Several boluses of phenylephrine were given to stabilize the systemic systolic blood pressure. Subsequent bronchoscopy cleared a right bronchial mucous plug enabling the collapsed right upper lobe to expand and resolving the hypoxia. Approximately 1 hour after arrival in the intensive care unit and 2 hours after operation, the patient developed inferior wall ischemia, which progressed into sustained cardiac arrest due to ventricular fibrillation. The patient was resuscitated with direct-current electrocardioversion. There were no electrolyte or metabolic abnormalities. An electrocardiogram was consistent with acute inferior myocardial infarction. Immediate coronary angiography revealed patent LITA and vein graft conduits with severe narrowing of the LITA graft, and the native and bypassed coronary artery branches (Figs 3–5).
The diagnosis of coronary artery vasospasm was made. High dose intraconduit and coronary artery infusion of nitroglycerin was initiated and subsequently continued intravenously, which led to restabilization of hemodynamics, venous O2-saturation, and systemic blood pressure.
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Fig 3. Severe native coronary artery spasm of the posterior descending artery. Saphenous vein graft (SVG) bypass to posterior descending artery. (Cath = catheter.)
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Fig 4. Severe native coronary artery spasm of the obtuse marginal branch. Saphenous vein graft (SVG) bypass to obtuse marginal branch.
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Fig 5. Severe native coronary artery and conduit spasm of the left anterior descending artery (LAD). Left internal thoracic artery (LITA) bypass to LAD.
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Comment
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The few previously reported cases of perioperative coronary artery spasms with immediate angiographic documentation have demonstrated either diffuse nonocclusive spasm in all native coronary arteries or spasm localized to a nongrafted right coronary artery [2]. The causes of coronary artery spasm after coronary artery bypass grafting are not fully understood. Several factors thought to provoke spasm may interact in the postoperative period including high endogenous catecholamine levels, manipulation of coronary arteries during dissection for placement of a bypass graft, hypothermia, small coronary arteries, and underlying atherosclerotic disease [2, 3]. In the patient of this report, angiographic evidence was obtained of primarily native coronary artery spasm probably caused by the catecholamine surge and sympathetic nervous system response with awakening in the operating room, the stress reaction of the failed extubation in combination with high doses of administered alpha-receptor agonists. A high suspicion of vasospasm is necessary prompting early coronary angiography and recognition allowing effective therapy with coronary vasodilators [4, 5]. This procedure could be lifesaving as demonstrated in the present report. Could the sequence of distal grafting have been altered to improve the outcome? This is difficult to answer, however, it is preferable to graft posterolateral circumflex artery branches first in beating heart coronary revascularization to prevent any tension on the LITA to LAD anastomosis with the required heart rotation toward the right chest. Despite the fact that norepinephrine has the least coronary artery vasoconstrictive effect compared with other commonly used vasopressors, its constant administration to support a low blood pressure during off-pump coronary surgery should lower the threshold for conversion to cardiopulmonary bypass assisted coronary artery bypass grafting. In order to avoid additional catecholamine release, stress responses, and hypoxemia-induced hemodynamic compromise with awakening in the operating room, operating table extubation should not have been considered in this patient, which in combination with high doses of intravenous phenylephrine could have led to the unexpected catastrophic event of coronary artery vasoconstriction.
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References
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Zeff R.H., Iannone L.A., Kongtahworn C., et al. Coronary artery spasm following coronary artery revascularization. Ann Thorac Surg 1982;34:196-200.[Abstract]
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Abstract
Introduction
