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Ann Thorac Surg 1999;68:1065-1066
© 1999 The Society of Thoracic Surgeons
a Cardiothoracic Surgery, Catharina Hospital, Eindhoven, The Netherlands
b Cardiology, Catharina Hospital, Eindhoven, The Netherlands
Address reprint requests to Dr Berreklouw, Department of Cardiothoracic Surgery, Catharina Hospital, Michelangelolaan 2, 5602 ZA Eindhoven, The Netherlands
e-mail: eberr{at}compuserve.com
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| Introduction |
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A 36-year-old female patient with a height of 155 cm and weight of 51 kg (body surface area 1.40 m2), was admitted to the hospital because of progressive right heart failure due to a severe mitral valve stenosis and atrial fibrillation with a rapid ventricular response of 160 to 220 beats per minute. Coronary angiography showed a normal left and right coronary artery. On October 28, 1997, the mitral valve was replaced with a mitral valve prosthesis, and a standard MAZE III procedure [1] was performed. The patient was placed on full normothermic bypass and during the left-sided procedures antegrade and retrograde intermittent warm blood cardioplegia was administered. Six cryolesions were applied, strictly according to the methods described by Cox [1], with 3-mm and 15-mm cryoprobes (Frigitronics; CooperVision Company, Shelton, CT), for 2 minutes at a temperature of -60°C. The operative technique included the described maneuvers to protect the right and left coronary arteries from direct cryogenic trauma. Before going off bypass, a transesophageal echo showed a good contracting left and right ventricle with normal dimensions. The patient was weaned from bypass with the use of low-dose inotropics with a cardiac index of 1.9 L/min/m2. Because the patient showed no spontaneous rhythm, atrial and ventricular pacing by temporary wires was necessary. Shortly after extubation at the first postoperative day, the patient showed no cardiac output and needed to be resuscitated. An intraaortic balloon pump was inserted. A transesophageal echo demonstrated akinesia inferiorly and posteriorly, leading to a poor left ventricular function. The ECG showed pacemaker rhythm. On the coronary angiogram, generalized smaller diameters of the coronary arteries with significant narrowings in the distal circumflex (Fig 1 ) and right coronary arteries were seen. The narrowing inthe circumflex coronary artery was dilated first, with a 3.0-mm angioplasty balloon. When this narrowing was dilated other narrowings developed proximally and distally from this initial point of dilatation. Because these new narrowings did not disappear after intracoronary nitroglycerin, they were also dilated. In total, six dilatations were performed in the circumflex coronary artery. With the same angioplasty balloon, the right coronary artery was dilated. Also in this vessel, new narrowings developed proximally and distally from the location of the first dilatation, without any reaction to intra-coronary nitroglycerin. These new narrowings were dilated as well. In total, three dilatations of the right coronary artery were performed. At the end of the procedure, both coronary arteries were patent again. The patient remained in the hospital for 45 days, but recovered completely. At discharge the echocardiography showed a substantially recovered left ventricular function with hypokinesis in the infero-basal segments. A repeat coronary angiography, 25 days after the PTCAs, no longer showed significant narrowings in the coronary arteries (Fig 2). At 1-year follow-up the patient showed sinus rhythm.
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Also, in our patient, there was an exact match between the sites of coronary narrowings and the localization of the cryolesions. However, in our patient it is likely that the coronary narrowings were not anatomically fixed lesions, and it is our hypothesis that the narrowings were produced by edema in the perivascular epicardial tissues. If direct surgical trauma had been the cause, it would have been apparent when the patient was weaned from cardiopulmonary bypass. On the other hand, if a typical cryolesion of the coronary arteries, as described in the dog model [2], was involved, it would have been likely that the symptoms would occur after a longer delay.
Theoretically, there are several ways to prevent the described complications. The size of a cryolesion depends on the size and shape of the probe, freezing temperatures, duration of freezing, method of thawing, and kind and temperature of the tissues involved [46]. In the MAZE III operation, cryoablation is used on thin (a few millimeters) left and right atrial walls or the connection of these tissues with the valvular annuli, always nearby coronary arteries. For this application it is not necessary that the cryolesion penetrate deeply, especially not in patients with a small body surface area, as was the case in our patient. It is our suggestion to limit the duration of cryoablation in MAZE III procedures to 1 minute for each lesion. Secondly, the cryoablation can be replaced by a radio-frequency catheter that produces only superficial ablation [7]. Thirdly, it can be questioned, as others have done [8], whether cryoablation is essential in the MAZE III procedure as long as, purely by creating the MAZE, the minimum muscular wall substrate to maintain atrial fibrillation is not available anymore.
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