Asian Cardiovasc Thorac Ann 2004;12:133-138
© 2004 Asia Publishing EXchange Ltd
Surgical Treatment of Coronary Artery Fistulas: 15 Years’ Experience
Ufuk Demirkilic, MD,
Ertugrul Ozal, MD,
Hakan Bingol, MD,
Faruk Cingoz, MD,
Celalettin Gunay, MD,
Suat Doganci, MD,
Erkan Kuralay, MD,
Harun Tatar, MD
Department of Cardiovascular Surgery, Gulhane Military Medical Academy, Ankara, Turkey
For reprint information contact: Ufuk Demirkilic, MD Tel: 90 312 304 5206 Fax: 90 312 232 3038 Email: udemirkilic{at}gata.edu.tr Suleyman Bey Sokak. 23/9, Maltepe, Ankara, Turkey 06570.
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ABSTRACT
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We report our experience of surgical treatment of coronary artery fistula and focus on the electrocardiographic changes that may be seen postoperatively. Between 1988 and 2003, cardiac operations were carried out on 9,487 patients, of whom 21 had a coronary artery fistula. The mean age of these 21 patients was 36.8 ± 4.9 years. The fistula originated from the right coronary artery in 9 cases and from the left side in 12. The fistulous connection was to the right ventricle in 5 patients, to the right atrium in 6, to the pulmonary artery in 8, and to the coronary sinus in 2. There was no operative mortality. Two patients (10%) had nonspecific electrocardiographic changes during the postoperative period. Repeat coronary angiography revealed normal coronary anatomy in both, and their electrocardiograms normalized within 2 months. Patients suspected to have myocardial ischemia related to the surgical procedure, with ST segment depression or T wave abnormalities on the electrocardiogram, should undergo repeat angiography to eliminate the possibility of coronary artery damage.
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INTRODUCTION
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Coronary artery fistula (CAF) is quite rare with an incidence of 0.13% to 0.22% in patients undergoing coronary angiography.1,2 Although the majority of such fistulas are congenital, some may be related to chest trauma, cardiac surgery, or coronary angioplasty.2,3 The clinical features are similar in both forms. A CAF is usually asymptomatic but complications may develop. Conduction disorders and rhythm disturbances, especially atrial fibrillation, may be associated with CAF.1,4,5 Coronary angiography is necessary for diagnosis, accurate delineation of the anatomy, and planning of the surgical repair. Color-flow echocardiography may also demonstrate CAF. Transesophageal echocardiography is an additional mode of diagnosis and its superior imaging can guide surgical management, monitor the development of wall motion abnormalities, and confirm fistulous tract ligation.1–6 Transcatheter closure is generally safe and effective with excellent clinical results and an acceptable complications profile.7–11 However, myocardial ischemia may occur after transcatheter or surgical closure due to coronary artery damage.8,9,12 Nonspecific changes in the electrocardiogram (ECG) may be encountered following CAF closure in patients with angiographically normal coronary anatomy.
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PATIENTS AND METHODS
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Between 1988 and 2003, cardiac operations were carried out on 9487 patients in our institute. 21 of these patients had a coronary artery fistula (incidence of CAF, 0.22%), their mean age was 36.8 ± 4.9 years (range, 3–63 years), and 12 were male. 9 patients were asymptomatic but a continuous murmur was detected on physical examination. The most common symptom was effort dyspnea (6 patients, 29%), and 5 patients (23%) presented with angina pectoris. Atrial arrhythmias were frequently found when the fistula originated from the right coronary artery. The fistula originated from the right coronary artery in 9 patients and from the left coronary artery in 12. The location of the fistulous connection was the right ventricle in 5 cases, the right atrium in 6, the pulmonary artery in 8, and the coronary sinus in 2. 4 patients had associated cardiac lesions that required additional surgical procedures.
A median sternotomy was performed in all patients. Cardiopulmonary bypass (CPB) with moderate hypothermia was used in 15 patients (71%) in whom a dual approach for closure of the CAF was preferred. The fistulous communication was directly ligated epicardially, the patient was placed on CPB, and the cardiac chamber was drained and opened. The endocardial orifice of the fistula was inspected and closed from the inside. In the other patients, the fistula was easily identified and inspected on the epicardium after opening the pericardium, it was closed by suture ligation without CPB. This technique was used in 7 cases including one (Case 7) with concomitant coronary artery stenosis; after CAF ligation, CPB was established and the left anterior descending coronary artery lesion was bypassed with a left internal mammary artery graft under cardioplegic arrest. Following epicardial suture ligation, the feeding coronary artery adjacent to the fistulous connection was closed by placing ligatures around it. After several minutes of trial occlusion to confirm that there was no change on the ECG, the suture was tied down. (Figure 1A
). Endocardial closure was undertaken when the fistulous connection could not be explored on the surface of the heart (5 cases). The chamber into which the fistula drained was opened under CPB. One patient with associated mitral stenosis and a history of bacterial endocarditis underwent mitral valve replacement with a 27-mm mechanical prothesis in addition to endocardial closure of the fistula. Combined epicardial and endocardial closure was carried out in 7 cases (Figure 1B). 2 of the 5 fistulas draining into the right ventricle were closed transatrially with simple sutures. The adequacy of closure was tested by infusion of cardioplegic solution into the aortic root, and additional pledgetted mattress sutures were placed if a shunt persisted. Transarterial closure was performed under CPB in 2 patients (Case 1 & 11) whose CAF caused coronary artery dilatation and tortuosity. The most prominent dilatation was located just above the fistulous connection. The aneurysm was incised longitudinally and the fistulous connection was closed by direct suturing with 7/0 polypropylene. The distal part of the coronary artery is usually thin in such patients, so distal run-off patency was checked with a probe. The data of all patients are summarized on Table 1. Case 1, there was a large aneurysm of the circumflex artery and the fistulous connection was to the right ventricle after the aneurysm (Figure 2). The fistulous connection was closed through the aneurysm with 7/0 polypropylene sutures. Aneurysmorrhaphy was performed after redundant aneurysmal tissue was removed (Figure 3). Patient in case 2 had an ostium secundum type atrialseptal defect and a fistulous connection between the circumflex artery and the coronary sinus. The CAF was closed endocardially through the coronary sinus, and the atrialseptal defect was closed by direct suturing.
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Figure 1. Closure of coronary artery fistulas. (A) Epicardial suture ligation of a coronary artery fistula. (B) Dual approach for closure of a fistula between the left anterior descending artery and the pulmonary artery. The fistula is ligated epicardially, the drainage site is opened, and the orifice is closed endocardially with a simple suture.
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Figure 2. Coronary angiogram demonstrating a fistula between circumflex artery and the right ventricle (single white arrow), associated with a coronary artery aneurysm (2 black arrows).
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Preoperatively, nonspecific ECG changes were found in 16 patients. The other 5 patients had specific changes that could be attributed to myocardial ischemia. The most prominent ECG changes were ST segment and T wave alterations. In Case 1, prominent Q-waves were found in leads V3–V6. Severe ischemic changes were observed in the anterior leads in Case 7. Two patients (Case 6 & 15) had atrial fibrillation. Right bundle branch block was detected in one patient (Case 4). After the period of continuous monitoring postoperatively, the first 9 patients had daily ECG recordings. Subsequently, the ECG protocol was changed to use of a telemetric system.
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RESULTS
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There was no operative or hospital mortality. Overall, the mean CPB time was 32 ± 12 min. An aortic crossclamp was used in 9 patients with a mean crossclamp time of 23 minutes and CPB time of 32 ± 8 min. Fistulas that drained into the pulmonary artery could be repaired under CPB without crossclamping (except in Case 8). The pulmonary artery was opened and the fistulous connection was easily identified and sutured; the mean CPB time in this subgroup was 32 ± 3.2 min. 4 patients required inotropic support postoperatively. During a mean follow-up of 6.1 ± 3.2 years, all patients were asymptomatic and in New York Heart Association functional class I.
2 patients with a CAF to the pulmonary artery showed nonspecific ECG changes after surgery. One of them (Case 8) had a fistula originating from the first diagonal artery (Figure 4), and the other had a fistula from the left anterior descending coronary artery (Case 9). Early postoperative continuous ECG monitoring was normal in these 2 patients, but inferior and lateral ischemic ECG changes were noted on the daily routine ECG recordings on postoperative day 7 (Figure 5). Repeat coronary angiography was performed in both patients and the coronary arteries were found to be normal (Figure 6). There was no hemodynamic problem in either of these patients, and the ECG returned to normal 2 months after surgery.
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Figure 4. Preoperative coronary angiogram demonstrating a fistula between the first diagonal artery and the pulmonary artery (white arrow).
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Figure 6. Postoperative coronary angiogram of patient in Case 8, showing normal coronary arteries. The black arrow indicates the left anterior descending artery, the white arrow indicates the diagonal artery. There is no residual fistula.
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DISCUSSION
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Most patients with CAF are asymptomatic in infancy and childhood but may need treatment later in life because of the onset of fistula-related complications such as congestive heart failure, pulmonary hypertension, dyspnea, fatigue, angina pectoris or chest pain due to coronary steal syndrome which causes myocardial ischemia or, less frequently, myocardial infarction, subacute endocarditis, or aneurysm formation with embolization or rupture.5,6,10,13 Ozeki and colleagues13 reported a rare case of chronic pericardial effusion due to aneurysmal rupture of a CAF. Lowe and colleagues4 found that 45% of CAF were asymptomatic and the diagnosis could frequently be suspected from a continuous murmur or ECG findings of right or left ventricular overload or ischemia. Similarly, 43% of patients in our series were asymptomatic and the diagnosis was due to a murmur detected on physical examination.
It is thought that CAF most commonly originates from the right coronary artery.5,11 However, left coronary arteries were the dominant sites of origin in our series; the fistula arose from the right coronary artery or its branches in 9 (43%) cases, and from the left coronary artery or its branches in 12 (57%). Kamiya and colleagues11 reported a ratio of 104:127 for right and left coronary arteries as the sites of origin of CAF. Three parameters affect hemodynamics: origin, size, and drainage site of the CAF. Approximately 40% of coronary fistulas drain to the right ventricle, 25%–48% to the right atrium, 20%–38% to the pulmonary artery, 7% to coronary sinus, and 8% to the left heart chambers.1–5,10,11 In our series, drainage was to the right ventricle in 24% of cases, to the right atrium in 28%, to the pulmonary artery in 38%, and to the coronary sinus in 10%. Generally, the pulmonary artery and right ventricle are equally common drainage sites.11
The main pathology of fistulas connecting to the right heart chambers is a left-to-right shunt causing volume overload of the right ventricle and pulmonary artery, and subsequently to the left ventricle. Fistulas connecting to the left chambers cause left ventricular volume overload as in aortic insufficiency. The onset of congestive heart failure in patients with CAF may be related to the shunt itself or to the steal phenomenon that occurs because of redirection of coronary blood flow to a low pressure cardiac chamber. Initially, the steal phenomenon causes ischemia in the involved coronary artery area, but global myocardial ischemia may develop later because of collateral circulation via the other coronary arteries. In fistulas that connect to the left ventricle, blood flow is mostly during diastole. This causes an increase in left ventricular end-diastolic pressure, a decrease in perfusion pressure, and myocardial ischemia. Signs of congestive heart failure are common in cases of a fistula draining into the coronary sinus, and arterialization of the coronary sinus is blamed. The increased coronary flow through a fistulous artery adds to the shear stress which causes atherosclerosis.4,5,7,10,14,15
The indication for surgical treatment of small fistulas is unclear. Some surgeons believe that an operation is not indicated if the patient is asymptomatic, and such fistulas may be managed conservatively because they are hemodynamically inconsequential, have a benign long-term prognosis, and may close spontaneously. Although spontaneous closure has been reported, it is uncommon.15,16 Because some fistulas increase in size and produce fistula-related complications, many surgeons recommend transcatheter or surgical treatment.1,4–11,18,19 In view of reports of sudden death and other fistula-related complications, we accept the diagnosis of CAF as an indication for an operation. Complications include thrombosis, distal embolization, and rupture.18,19 In Case 1, although the patient was 3 years old, there was a huge aneurysm of the circumflex artery that was expected to rupture if not surgically excised. Furthermore, the mortality and morbidity of surgical intervention is higher when it is performed after the onset of complications.4,10,11
Little is known about the postoperative nonspecific ECG changes that may be encountered following closure of CAF.1,8,9,12 The changes noted in 2 of our patients did not affect their hemodynamic status, but they forced us to consider the possibility of damage to the coronary arteries during surgical repair. Cheung and colleagues1 performed postoperative cardiac catheterization in 21 patients (51.2%) and found that the native coronary artery either remained dilated and tortuous, or more frequently had thromboses with a short proximal stump, and 4 patients had demonstrable fistula recurrence. Therefore, we performed repeat coronary angiography in our 2 patients with ECG changes. It has been reported that a decrease in sympathetic activation occurs in both the proximal and distal arterial beds in arteriovenous fistulas, and the increase in blood flow following sympathectomy is less than that of the normal vessels in cases of these lesions.20 Sudden closure of a fistulous tract causes a reflex sympathetic hyperactivation and an increase in vascular resistance. Coronary artery resistance was not quantitatively measured, but the slow appearance of the distal coronary run-off on angiography indicated increased resistance. There may also be a sudden drop in the high blood flow of the proximal artery. Increased vascular resistance of the distal artery may contribute to subepicardial ischemia. If ischemic T waves on the ECG following CAF closure were caused by increased vascular resistance, the patient would be expected to be symptomatic, but there was no other sign of ischemia in either of these patients. In view of the normal coronary angiograms and asymptomatic status, these ischemic T waves might be classified as "nonspecific T wave abnormalities" which may be related to disorders such as anxiety, hyperventilation, tachycardia, cold, electrolyte disturbances, cerebrovascular disease, or anemia.
The goal of surgical intervention is to close a fistulous connection while preserving coronary artery anatomy. A coronary fistula may be safely closed without CPB when the lesion is discrete and its location and size are appropriate. When there is a suspicion of coronary ischemia related to a transcatheter or surgical closure procedure, with ECG findings of ST segment depression or T wave abnormalities, repeat coronary angiography should be performed to eliminate the possibility of damage to the coronary artery.
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ABSTRACT
INTRODUCTION
