Ann Thorac Surg 1997;63:1257-1261
© 1997 The Society of Thoracic Surgeons
Original Article: Cardiovascular
The Internal Mammary Artery Malperfusion Syndrome: Late Angiographic Verification
Mario Gaudino, MD,
Carlo Trani, MD,
Nicola Luciani, MD,
Francesco Alessandrini, MD,
Gianfederico Possati, MD
Departments of Cardiac Surgery and Cardiology, Catholic University, Rome, Italy
Accepted for publication November 6, 1996.
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Abstract
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Background. Here we report our experience with the incidence and the surgical treatment of the internal mammary artery (IMA) malperfusion syndrome, evaluate the predictive role of previously described risk factors for the syndrome, and assess the late patency of IMA grafts in patients in whom an IMA malperfusion syndrome was diagnosed and treated by additional saphenous vein grafting of the left anterior descending coronary artery.
Methods. From June 1992 to November 1995, 969 IMAs were anastomosed to the left anterior descending coronary artery system. In 11 patients, IMA malperfusion syndrome was diagnosed and treated by additional saphenous vein grafting of the LAD. There were 8 men and 3 women with a mean age of 58.9 years. The angiographic and clinical data for each patient were reviewed, and all but 1 surviving patient underwent late angiographic control (mean follow-up, 18 months; range, 4 to 46 months).
Results. One patient died in the hospital. No previously described risk factor was strongly associated with the occurrence of IMA malperfusion syndrome. Late angiography revealed a malfunctioning IMA graft in 7 of the 9 patients. A string sign was observed in 1 patient and a normally functioning IMA anastomosed to a diagonal branch not connected to the LAD, in another. In no patient was a widely patent and normally functioning IMA graft observed.
Conclusions. In our series, a high proportion of IMA grafts were found to be malfunctioning at late angiography. This observation, in contrast to previous reports, suggests that IMA malperfusion syndrome can often be attributable to technical problems in harvesting the IMA or in performing the IMA anastomosis. Functional IMA insufficiency seems to play only a marginal role in determining the IMA malperfusion syndrome.
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Introduction
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The internal mammary artery (IMA) malperfusion syndrome is the clinical expression of an acute discrepancy between the flow of an IMA graft and the myocardial oxygen demand. This syndrome was first fully described independently by von Segesser and colleagues [1] and Sarabu and associates [2] in 1987 and has subsequently been reported by several other groups [3–6]. Its etiology is still controversial: once technical errors have been ruled out, spasm, small size of the mammary artery, persistence of major IMA side branches, intraoperative hypotension, and IMA overstretching have all been suggested as possible causative factors [1, 2, 6–14].
The aim of the present study was to report our experience with regard to the incidence and the surgical treatment of the IMA malperfusion syndrome, to evaluate the predictive role of previously described risk factors for the syndrome, and to assess the late patency of IMA grafts in patients in whom this syndrome was treated by additional saphenous vein grafting.
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Patients and Methods
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In a series of 1,124 consecutive isolated complete myocardial revascularizations performed in the Cardiac Surgery Department of the Catholic University of Rome between June 1992 and November 1995, the left IMA (LIMA) was anastomosed to the left anterior descending coronary artery (LAD) system in 969 patients. Venous or other arterial conduits were used for non-LAD target vessels.
In all instances, the techniques for LIMA harvesting and preparation were the same. Immediately after a median sternotomy, the LIMA was dissected using a low-powered electrocautery to mobilize the artery with its pedicle. Vasodilation of the LIMA was achieved with either topically applied or intraluminal papaverine hydrochloride according to a previously described protocol [15]. The LIMA was used only when, after its dilation with papaverine, the surgeon considered its flow adequate by visual inspection. The anastomoses were performed using 8-0 polypropylene suture during cardioplegic arrest. Until November 1993, we used hypothermic cardiopulmonary bypass and cold crystalloid cardioplegia delivered antegrade and retrograde. Subsequently, we used warm blood cardioplegia given antegrade and retrograde combined with normothermic extracorporeal circulation.
Among the 969 patients in whom the LIMA was anastomosed to the LAD system, we retrospectively identified 14 patients (1.4%) whose postoperative course suggested IMA malperfusion syndrome. In all 14, after they were weaned from cardiopulmonary bypass, we observed sudden onset of a low cardiac output syndrome (defined as progressive deterioration of cardiac output with a concomitant rise in pulmonary wedge pressure) associated with anterior ischemic electrocardiographic changes with or without recurrent major ventricular arrhythmias. In all 14 patients, additional saphenous vein grafting of the LAD was performed immediately and led to hemodynamic improvement in 11. The 3 patients in whom low cardiac output persisted after reoperation were excluded from this study.
The preoperative clinical and angiographic data for the 11 patients were reviewed with reference to the previously described risk factors for IMA malperfusion syndrome. We decided not to perform statistical analysis because of the small number of patients in the study. There were 8 men and 3 women with a mean age of 58.9 years (range, 43 to 73 years). Dyslipidemia was present in 6 patients (55%), hypertension and diabetes in 5 (45%), and history of smoking in 3 (27%).
The total number of anastomoses was 30, for a mean of 2.7 anastomoses per patient. In 2 patients, the LIMA was anastomosed to a diagonal branch of the LAD because of the poor quality of the LAD itself. The intraoperative evaluation of LIMA flow was obtained from the operative charts of all 11 patients. In every instance, the flow pattern was judged to be normal. The caliber of each LIMA was also estimated to be adequate (2 to 4 mm).
Figure 1
shows the temporal distribution of the onset of IMA malperfusion syndrome in our series. All but three cases occurred within the first 120 minutes after removal of the aortic cross-clamp, with 45% in the first hour. However, one case occurred 14 hours after the end of the coronary artery bypass grafting procedure.
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Fig 1. . Time of onset of clinical signs of internal mammary artery malperfusion syndrome. Most cases began within the first 2 hours after aortic cross-clamp removal (45% in the first and 27% in the second hour). Mean time of onset was 138.5 minutes (range, 0 to 840 minutes); one case occurred 14 hours after the end of the operation.
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At reoperation, a supplementary saphenous vein graft was interposed between the ascending aorta and the LAD distal to the LIMA anastomosis in 8 patients and proximal and distal to the LIMA anastomosis in 2 patients. In 1 patient, the LIMA anastomosis was disconnected, and two vein grafts were placed to the proximal and distal LAD. In all instances, the LIMA-LAD anastomosis was patent when checked with a 1.5-mm probe inserted from the distal LAD arteriotomy. All the patients were successfully weaned from cardiopulmonary bypass.
All surviving patients were followed regularly at our institution by clinical examination and surface electrocardiogram. Stress test and two-dimensional echocardiography were performed 6 months after operation and then every year. Nine patients underwent late angiographic control at a mean follow-up of 18 months (range, 4 to 46 months). One patient was not scheduled for this procedure because he had a severe reaction to the contrast medium at the time of the preoperative angiogram. Stenoses with 50% reduction or more of the cross-sectional area were considered major, and intracoronary administration of nitroglycerin was routinely done after the first injection of contrast medium to obtain maximal pharmacologic vasodilation. Ejection fraction was calculated by the area-length method.
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Results
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Analysis of Risk Factors
We analyzed the incidence of the previously described risk factors for IMA malperfusion syndrome in our patients.
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PREOPERATIVE EJECTION FRACTION.
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Mean ejection fraction (calculated by the area-length method at preoperative angiography) was 0.55 (range, 0.40 to 0.65). Seventy-two percent of patients had an ejection fraction of 0.60 or higher, and only 1 patient had an ejection fraction lower than 0.40.
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LEFT VENTRICULAR HYPERTROPHY.
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On the basis of echocardiography, left ventricular hypertrophy was identified in 1 patient. Electrocardiographic signs of left ventricular hypertrophy were present in 2 patients (18%).
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ANTERIOR WALL MOTION.
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In 7 patients (64%), there was normal anterior wall contractility. In 2, the anterior wall was hypokinetic and in 2 dyskinetic.
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PREVIOUS CORONARY OPERATION.
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Only 1 patient had had previous coronary artery bypass grafting, and the saphenous vein graft on the LAD had subcritical stenosis.
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SEQUENTIAL LIMA GRAFTING.
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No sequential LIMA graft was associated with the malperfusion syndrome in our series.
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ANGIOGRAPHIC DATA.
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No particular angiographic finding or lesion was clearly associated with IMA malperfusion syndrome. Collateral flow to the LAD from the right coronary artery was present in 36% of our patients. Severe proximal stenosis of the LAD in the presence of a large (>2 mm) distal vessel with high runoff was detected in 55%.
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ARTERIAL PRESSURE.
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In 3 patients (27%), the systolic pressure after separation from extracorporeal circulation was 90 mm Hg or lower. At the time of onset of IMA malperfusion syndrome, a systolic pressure of 90 mm Hg or lower was present in only 4 patients (36%).
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CARDIOPULMONARY BYPASS AND MYOCARDIAL PROTECTION.
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The percentage of patients with IMA malperfusion syndrome was similar for the different techniques of cardiopulmonary bypass and myocardial protection (57% with normothermia and 43% with hypothermia).
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DRUG INFUSION AT TIME OF ONSET.
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In 10 patients (91%), nitrates were being administered at the onset of IMA malperfusion syndrome. In 36% of patients, dopamine hydrochloride in inotropic doses was being infused at the time of onset.
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Mortality and Morbidity
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One patient died suddenly on the 15th day after operation, although his condition had seemed to be good. No postmortem examination was performed. Mean stay in the intensive care unit was 3.2 days (range, 2 to 8 days). Ten patients (91%) were discharged from the hospital.
An anterior myocardial infarction (judged on the basis of echocardiographic evidence of anterior hypokinesia, blood, level of myocardial-specific isoenzyme of creatine kinase greater than 4% of the total creatine kinase concentration, and appearance of Q wave on the electrocardiogram) occurred postoperatively in 6 patients. None of the 5 patients who had signs of IMA malperfusion syndrome within the first hour after removal of the aortic cross-clamp sustained a myocardial infarction, whereas the percentage was clearly higher for patients with onset of the syndrome during or after the second hour after cross-clamp removal (Fig 2).
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Fig 2. . Incidence of postoperative myocardial infarction (MI) in relation to time of onset of internal mammary artery malperfusion syndrome. Patients in whom signs of the syndrome developed within the first hour after removal of the aortic cross-clamp had a lower incidence of perioperative MI compared with patients with signs during or after the first 60 minutes (0% versus 100% and 67%, respectively).
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Late Angiographic Study
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Table 1 shows the morphologic status of the LIMA graft and the LAD at the site of the LIMA anastomosis in the 9 patients having late angiographic study. In 4 patients, the LIMA was occluded proximally (proximal occlusion was defined as complete occlusion of the LIMA after the first 2 of 3 cm from the origin). In 2 of these patients, proximal occlusion of the LIMA coexisted with occlusion of the LAD at the level of the LIMA anastomosis (Fig 3). Moderate to severe stenosis of the LIMA-LAD anastomosis was found in 2 patients (Fig 4). In another patient, late angiography revealed retrograde occlusion of the LAD from the level of the LIMA anastomosis. A string sign was found in only 1 patient (Fig 5). A normally functioning LIMA erroneously anastomosed to a diagonal branch not connected to the LAD was found in 1 patient. The saphenous vein grafts were patent in all but 2 patients. In the 6 patients (55%) with a postoperative myocardial infarction, substantial reduction in anterior wall motion was found.
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Fig 3. . (Patient 5.) (A) Late angiography demonstrates a proximally occluded left internal mammary artery (LIMA) graft. (B) Selective visualization of the sequential saphenous vein graft on the proximal and distal left anterior descending coronary artery (LAD) reveals occlusion of the LAD at the level of the LIMA anastomosis.
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Fig 4. . (Patient 7.) Late angiography demonstrates (A) severe stenosis of the left internal mammary artery anastomosis and (B) a normally functioning additional saphenous vein graft.
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Fig 5. . (Patient 2.) At late angiography, selective injection through the left internal mammary artery (LIMA) reveals a string sign, but the entire LAD and the additional saphenous vein graft are visible.
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Comment
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The IMA malperfusion syndrome is the clinical expression of an acute discrepancy between the flow of an IMA graft to the LAD and the myocardial oxygen demand. This syndrome was first reported in 1987 by two groups [1, 2] working independently and then was described by several others [3, 4, 6] in following years. Usually this syndrome occurs at the time of or soon after separation from extracorporeal circulation, when the myocardial oxygen demand abruptly increases, or in the early postoperative period. The syndrome is characterized by reduced cardiac index, severe hypotension, depression of anterior wall contractility, increase in pulmonary wedge pressure, and major arrhythmias, usually making it impossible to wean the patient from cardiopulmonary bypass or making it necessary to immediately restore cardiopulmonary bypass [6]. The treatment of choice for IMA malperfusion syndrome is an additional vein graft to the distal LAD; however, the use of vasodilators (Enoximone), nitroglycerin, Ca2+ antagonists, or topically applied papaverine has also been proposed [16, 17].
The etiology of IMA malperfusion syndrome is multifactorial. Possible causative factors include technical problems (as noted here), IMA spasm, subclavian stenosis, low arterial pressure, persistence of major IMA side branches, and IMA overstretching [1, 2, 6–13]. Severe proximal stenosis of the LAD in the presence of a distal artery of good quality (diameter 
2 mm) supplying a large area of normally contracting myocardium, severe ventricular hypertrophy, sequential IMA grafts, use of the terminal part of the IMA, and replacement of a patent saphenous vein graft to the LAD by a new IMA graft have been hypothesized to be risk factors for IMA malperfusion syndrome [3]. In our study, confirming the observation of Jones and colleagues [3], ejection fraction of 0.60 or higher, normal anterior wall contractility, and LAD diameter greater than 2 mm were present in more than half of the patients. However, these factors are common to many of the patients undergoing coronary artery bypass grafting at our institution and do not seem to be highly predictive of the development of IMA malperfusion syndrome. No particular angiographic finding or lesion was clearly associated with the malperfusion syndrome.
Postoperative angiographic studies to assess the patency of IMA grafts in patients with IMA malperfusion syndrome have been performed in only a few of the published series. Vajtai and colleagues [4] in 1992 reported late angiographic results for 3 of 10 patients with postoperative evidence of this syndrome. In 2, the LIMA graft was patent and functioning normally, and in 1, occlusion of the LAD at the level of the LIMA anastomosis was observed. Systematic early and late angiographic studies have been done only by Carrel and coauthors [6]. They restudied 43 patients who had IMA malperfusion syndrome; at late angiography, a widely patent IMA graft and a patent saphenous vein graft were observed in 56% of patients, an IMA graft with a string sign and a patent vein graft in 35%, an occluded IMA graft and normally functioning saphenous vein graft in 7%, and occlusion of both the IMA and saphenous vein grafts in 2.4%.
Our study provides completely different results: at late angiography, no widely patent and normally functioning IMA graft to the LAD could be observed. In all but 1 patient, a technical problem in anastomosing the LIMA to the LAD was the cause of the IMA malperfusion syndrome. In the 1 patient, a patent but narrowed LIMA was observed, but we do not know whether this represents a poor-quality IMA (originally thought to be good) or a string sign induced by competition with the supplementary vein graft. It is interesting that in 3 patients, occlusion of the LAD at the level of the LIMA anastomosis was observed. It is likely that an iatrogenic lesion of the LAD with thrombus accumulation several hours postoperatively resulted in the malperfusion syndrome after the patients were taken from the operating room.
In our series, early reoperation was able to dramatically reduce the incidence of postoperative myocardial infarction: none of the patients who underwent reoperation within 1 hour from the onset of IMA malperfusion syndrome sustained a myocardial infarction, whereas the percentage was much higher for patients who underwent late reoperation. This finding confirms that early diagnosis and emergency additional saphenous vein grafting of the LAD play a key role in limiting the functional consequences of IMA malperfusion syndrome.
In summary, in our experience, late angiography showed that IMA malperfusion syndrome is related to technical factors in the majority of patients (8/9). In the remaining patient, technical problems, although not clearly evident, cannot be excluded. Functional IMA insufficiency or graft spasm were not recognized as causative factors for the malperfusion syndrome. Errors in planning the coronary artery bypass grafting procedure, in harvesting the IMA, or in performing the distal anastomosis can explain most of the cases. The impossibility of identifying any particular risk factor for IMA malperfusion syndrome seems to support this hypothesis. Our report is descriptive, with all the usual limitations of descriptive series. However, this is the second largest angiographic study on IMA malperfusion syndrome, and the striking homogeneity of the results should serve as a warning and lead to the conclusion that angiographic exclusion of a technical problem is mandatory for a correct diagnosis of IMA malperfusion syndrome.
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Footnotes
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Address reprint requests to Dr Possati, Istituto di Cardiochirurgia, Policlinico A. Gemelli, Largo A. Gemelli 8, 00168 Rome, Italy.
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References
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Abstract
Introduction
