The presence of cardiovascular symptoms secondary to the existence of a large branch of the internal mammary artery before its anastomosis to the anterior descending artery is controversial. Sutherland and Desai described the presence of the lateral costal artery in their series of 103 patients. Thirty-one patients had evidence of the branch vessel on the right or left internal mammary artery system. The authors suggest early recurrence of angina due to this under-recognized vessel.1 Coil embolization of these vessels has been achieved with variable results.2 Larger studies demonstrate the overall incidence of a large internal mammary artery branch to be 9%, which may account for early recurrence of anginal symptoms in patients receiving left internal mammary-coronary bypass grafts.3 The flow through this vessel is often significant due to the relative low vascular resistance of the systemic branch as compared to the higher resistance coronary system.4 Seminal work by Gould et al. in 1974 has allowed cardiologists to gel together anatomic information obtained by coronary angiography with physiologic information obtained by measuring coronary flow reserve.5 Angiographic assessment of lesion severity is often under-estimated and does not represent the actual physiologic function of the delicate balance of myocardial oxygen supply and demand.6 In this manner, further assessment of angiographically indeterminate lesions may be made through the use of coronary blood flow velocities.7 Coronary flow reserve has been defined as hyperemic flow velocity, divided by basal mean flow velocity. A hemodynamically significant lesion is associated with an absolute coronary flow reserve of less than 2.0.8 Hyperemia can be achieved by intracoronary injection of adenosine (safest, most common) and papaverine.9 Since the early 1990s, the use of coronary flow reserve and other techniques has been validated and well-established.10 This case report describes a novel application of coronary flow reserve techniques. Clinical presentation. A 48-year-old white male presented to the Tulane University Hospital with a past medical history significant for coronary artery disease (CAD) requiring surgical revascularization 36 previously. He also had Acquired Immunodeficiency Syndrome, diabetes mellitus type 2, hypertension, and dyslipidemia. The patient’s chief complaint was intermittent chest pressure during the preceeding 3 months. The substernal pressure was elicited with physical exertion and emotional distress. Associated symptoms included dyspnea, diaphoresis, and occasional nausea. These episodes lasted 5 minutes and were relieved by rest and 1 tablet of sublingual nitroglycerin (0.4 mg). The patient realized that the episodes were occurring more frequently and were similar to his previous pattern of angina. The patient was scheduled for cardiac catheterization due to this presentation. The patient initially presented 3 years prior to admission with unstable angina and was found to have a non-ST segment elevation myocardial infarction. Cardiac catheterization at that time revealed significant stenosis of the proximal left anterior descending artery (LAD), the mid-portion of the right coronary artery (RCA), and the mid-portion of the left circumflex artery (LCX). The patient received coronary artery bypass grafting (CABG) with left internal mammary artery (LIMA) to the LAD, and vein grafts to the LCX and RCA.Treatment of risk factors was optimized in the perioperative period. Attention was focused on the patient’s fasting lipid profile due to disturbance of cholesterol metabolism by the prescribed protease inhibitors for the management of HIV infection. Cardiac catheterization revealed hypokinesis of the anterolateral region of the left ventricle and a left ventricular ejection fraction of 35%. This was consistent with recently measured ejection fraction and wall motion by echocardiography. Patent grafts to the RCA, LAD, and LCX, with only minimal luminal irregularities, were observed upon selective coronary angiography. The native coronary arteries showed only minor progression of disease, with the exception of the proximal LAD, which demonstrated 100% occlusion. The left subclavian was free of lesions. The LIMA graft was easily visualized angiographically and demonstrated no visible disease at the ostium, body or anastomosis. A large thoracic branch was noted at the proximal to mid-portion of the LIMA (Figure 1). Owing to the presence of typical symptoms, theabsence of significant lesions in the grafts or native vessels and the large size of this branch, a potential “steal phenomenon” was postulated. We proceeded with a functional investigation through the use of coronary flow wire techniques. The LIMA was selectively engaged through the existing right femoral artery 6 Fr introducer sheath, using a 6 Fr Z2 (Medtronic, Minneapolis, Minnesota) internal mammary artery guide catheter. A Jomed (Abbott Labs, Abbott Park, Illinois) coronary flow wire was advanced to the LIMA. Baseline coronary flow was measured at the proximal LIMA, thoracic branch, and distal LIMA (Table 1). The flow wire was then placed in the distal LIMA. Coronary flow reserve (CFR) was then measured at the distal LIMA using intra-arterial injection of 24 mg of adenosine, yielding a CFR of 1.8. A Choice PT Floppy 0.014 inch wire (Boston Scientific, Natick, Massachusetts) was advanced into the thoracic branch. A 2.5 mm x 15 mm Maverick (Boston Scientific) coronary angioplasty balloon was advanced into the mid-portion of the branch. Occlusion, as documented by angiography, was achieved by inflating the balloon to 3.5 atmospheres. The CFR was measured again under balloon occlusion of the branch. The CFR at the distal LIMA increased to 3.9, achieving normal values. Due to the large difference in the CFR between baseline and the balloon-occlusion result, coil embolization of the LIMA thoracic branch was planned. The balloon was removed and a 150 cm Turbo Tracker coil embolization system (Boston Scientific) was chosen to occlude the branch. The coil embolization delivery catheter was advanced over the wire to the mid-portion of the LIMA thoracic branch. Three 2 mm x 3 mm x 22 mm Vortex coils (Boston Scientific) were delivered into the branch. A post-delivery angiogram demonstrated 100% occlusion of the branch vessel. Post-embolization angiograms noted TIMI 3 coronary blood flow within the LIMA graft and distal LAD. Post-delivery CFR was 3.3, significantly higher than baseline (Table 2). The patient tolerated the procedure well and was discharged from the hospital with an observation admission status on the day of the procedure. After six weeks, the patient was seen as an out-patient and he was queried about his initial symptoms. The patient noted a cessation of his angina symptoms since embolization of the branch. He also reported lessened dyspnea on exertion and gradual reduction of the lower extremity edema he was previously experiencing. The patient was attending cardiac rehabilitation and was able to walk approximately one mile. Echocardiography at six weeks post-procedure demonstrated an ejection fraction of 70% and normal wall motion. Discussion. The novel use of coronary flow wire, as described in this case, is reported for the first time. A previous report of the use of coil embolization in an IMA side branch has been published; however, one coil in one case was used, which had subsequent recanalization.2 This adds to the uncertainty about whether these intervened side branches remain occluded and whether the long-term patency of the LIMA graft is affected. The progressive deterioration of this patient’s functional status with progressive angina prompted further evaluation. After the patient’s CABG, and in subsequent resting echocardiograms, his ejection fraction was 55% and he had regional wall motion abnormalities. The admission echocardiography and ventriculography noted a hypokinetic anterior wall, depressed ejection fraction, with angiograms demonstrating intact graft supply to the region. The concept of coronary steal was therefore hypothesized and proven, utilizing coronary flow reserve measurements. This technique is well-suited to determine the hemodynamic significance of fixed coronary lesions.5 The application of the coronary flow wire to other coronary hemodynamic scenarios may demonstrate its continued usefulness. The use of coronary flow reserve and pharmacologic hyperemia in the above situation may not be truly indicative that a thoracic side branch steal exists in all cases, nor that it mimics normal physiologic conditions or exercise hyperemia. Guzon et al. have reported that in three cases evaluating coronary flow velocity during rest, adenosine hyperemia and exercise-induced hyperemia, there was no evidence of thoracic side branch steal.11 In addition, other unknowns remain, such as the rate of recanalization of occluded side branches and whether the long-term patency of the LIMA graft after occlusion of these side branches is affected. In summary, in this symptomatic patient with no other plausible explanation for his clinical presentation, the use of coronary flow wire and coronary flow reserve facilitated the detection of coronary steal. Coil embolization of hemodynamically significant LIMA thoracic branches did improve coronary flow reserve in the LIMA graft, wall motion abnormalities, and left ventricular ejection fraction, as reported in the present communication. Further evaluations are necessary in order to demonstrate reproducibility of these findings. For now, a physiologic evaluation demonstrating the presence of steal is required before attempting an occlusion of the suspected LIMA side branch.
1. Sutherland FW, Desai JB. Incidence and size of lateral costal artery in 103 patients. Ann Thorac Surg 2000;69:1865‚Äì866. 2. Eisenhauer MD, Mego DM, Cambier PA. Coronary steal by IMA bypass graft side-branches: A novel therapeutic use of a new detachable embolization coil. Cathet Cardiovasc Diagn 1998;45:301‚Äì306. 3. Bauer EP, Von Segasser LK, Laske A, Turina MI. Internal mammary artery anomalies. J Thorac Cardiovasc Surg 1990;38:312‚Äì315. 4. Singh RN, Sosa JA. Internal mammary artery-coronary artery anastomosis: Influence of the side-branches on surgical result. J Thorac Cardiovasc Surg 1981;82:909‚Äì914 5. Gould KL, Lipscomb K, Hamilton GW. Physiologic basis for assessing critical coronary stenosis: Instantaneous flow response and regional distribution during coronary hyperemia as measures of coronary flow reserve. Am J Cardiol 1974;33:87‚Äì94. 6. Topol EJ, Nissen SE. Our preoccupation with coronary luminology: The dissociation between clinical and angiographic findings in ischemic heart disease. Circulation 1995;92:2333‚Äì2342. 7. Gould KL, Kirkeeide RL, Buchi M. Coronary flow reserve as a physiologic measure of stenosis severity. J Am Coll Cardiol 1990;15:459‚Äì474. 8. Kern MJ. Curriculum in interventional cardiology: coronary pressure and flow measurements in the cardiac catheterization laboratory. Cathet Cardiovasc Intervent 2001;54:378‚Äì400. 9. Baim DS, Grossman W. Section VI. Special catheter techniques evaluation of myocardial blood flow and metabolism. In: Grossman‚Äôs Cardiac Catheterization, Angiography, and Intervention (6th ed.). Philadelphia: Lippincott, Williams, and Wilkins. 10. Toshihiko N, Amanullah AM, Luo H, et al. Clinical validation of intravascular ultrasound for assessment of coronary stenosis severity. Am J Coll Cardiol 1999;33:1870‚Äì1878. 11. Guzon OJ, Klatte K, Moyer A, et al. Fallacy of thoracic side-branch steal from the internal mammary artery: analysis of left internal mammary artery coronary flow during thoracic side-branch occlusion with pharmacologic and exercise-induced hyperemia. Cathet Cardiovasc Intervent 2004;61:20‚Äì28.