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Ann Thorac Surg 1998;66:2056-2062
© 1998 The Society of Thoracic Surgeons

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Original Articles

Steal phenomenon from mammary side branches: when does it occur?

^a Cardiac Surgery, Catholic University, Rome, Italy
^b Angiology, Catholic University, Rome, Italy
^c Nuclear Medicine, Catholic University, Rome, Italy
^d Cardiology, Catholic University, Rome, Italy

Accepted for publication June 25, 1998.

Address reprint requests to Dr Gaudino, Divisione di Cardiochirurgia, Policlinico A. Gemelli, Largo A. Gemelli 8, 00168 Rome, Italy

	Abstract

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Background. The hemodynamic significance of patent mammary graft side branches is still controversial. This study was designed to evaluate the potential for flow steal of patent mammary side branches in different hemodynamic conditions.

Methods. Echo-Doppler measurement of mammary graft flow was performed at rest and after dipyridamole-induced coronary vasodilatation in 10 patients with angiographic demonstration of evident mammary graft side branches (study group) and in 10 matched control patients (control group). Concomitant thallium-201 myocardial scintigraphy was performed to assess the adequacy of mammary flow to the myocardial oxygen demand. Patients of the study group were also submitted to flow evaluation in condition of selective muscular or combined systemic and coronary relaxation.

Results. No difference in mammary flow and adequacy to myocardial oxygen demand was detected between patients of the study and control groups both at rest and after dipyridamole infusion. In patients with patent side branches the systolic-to-diastolic flow ratio was maintained in case of combined coronary and peripheral vasodilatation, whereas selective muscular relaxation led to an increase in the systolic and a reduction in the diastolic flow.

Conclusions. Flow steal from patent mammary graft side branches is possible only in case of selective muscular vasodilatation. As this situation is unlikely to occur in the clinical setting, the potential for flow steal of mammary side branches in cardiac surgery patients seems to be minimal.

	Introduction

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The possibility of a steal phenomenon from patent internal mammary artery (IMA) graft side branches is still controversial. Although some investigators have anecdotally reported clinical and instrumental evidence of myocardial ischemia that regressed after IMA side branch embolization or ligature [1–4], angiographic data and intravascular Doppler studies have minimized the hemodynamic importance of IMA side branches [5–8]. Moreover, the published studies have all focused on the possibility of flow steal at rest or in case of selective coronary vasodilatation and no investigation has verified the hemodynamic role of mammary side branches in condition of muscular or combined peripheral and coronary relaxation (as usually occurs during physical exercise).

This study protocol was designed to elucidate the hemodynamic role of IMA graft side branches in condition of systemic and coronary vasodilatation by analyzing the echo-Doppler measurements of mammary flow in two groups of patients: one with and one without undivided IMA graft side branches.

	Materials and methods

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Patient populations
This study protocol involved 10 patients with angiographic demonstration of evident IMA graft side branches (study group) and 10 comparable patients in whom postoperative angiography revealed an IMA graft without side branches (control group).

The 10 components of the study group were selected among the 51 patients who underwent minimally invasive myocardial revascularization at our department from January 1995 to December 1996. Patients undergoing minimally invasive myocardial revascularization during this period were chosen because at that time no dedicated chest retractor for minimally invasive procedure was available at our institution, therefore, in these patients the left IMA was harvested only for a short length of its distal tract and all the proximal side branches were left patent [9]. All 51 patients underwent postoperative angiographic control; selection for enrollment in this investigation was based on the angiographic demonstration of normofunctioning left IMA-to-left anterior descending (LAD) anastomosis with clear evidence of patent left IMA side branches (at least three proximal side branches with diameter greater than or equal to 0.5 mm or a single large branch greater than or equal to 1.5 mm in diameter; see Fig 1 ) and on the willingness of the patient to undergo a new scintigraphic and echo-Doppler control.

View larger version (154K): [in this window] [in a new window]   Fig 1. Postoperative angiographic control in a patient of the study group. Patent mammary graft side branches are particularly evident.

Angiographic characteristics of patients of both groups were measured using a computerized system (Cathex CCIP-310 Heart System; Cathex Co, Tokyo, Japan). All patients did not take any vasoactive medication for 2 days before each test.

Evaluation of mammary artery flow reserve and adequacy to myocardial oxygen demand
Echo-Doppler evaluation of mammary artery flow reserve and adequacy to increased myocardial oxygen demand was performed using a described protocol [10]. The following parameters were calculated both at rest and after intravenous administration of dipyridamole 0.84 mg/kg (Persantin; Boehringer Mannheim, Berlin, Germany): peak systolic velocity (meters per second); end-systolic velocity (meters per second); peak diastolic velocity (meters per second); end-diastolic velocity (meters per second); time average mean velocity (meters per second); resistance index; pulsatility index; systolic-to-diastolic peak velocity ratio. The time average mean velocity was defined as the area between the line traced on the Doppler wave and the baseline. The diameter of the IMA was calculated using internal electronic calipers on frozen frame images from the B-mode recording. Flow (F) was obtained using the formula: F (millimeters per minute) = time average mean velocity (centimeters per second) x (r² x 60) where r is half the internal diameter of the IMA expressed in centimeters.

Thallium-201 myocardial scintigraphy was performed in all patients immediately after the dipyridamole test. The ischemia index (difference between the scintigraphic score after dipyridamole infusion and at rest) [10] was used to quantify the degree of inducible ischemia in the LAD region.

Vasodilatory protocol
On a different day the patients of the study group were submitted to IMA flow evaluation at rest and in condition of selective muscular or combined coronary and peripheral vasodilatation.

Muscular vasodilatation was achieved in 7 patients by the intravenous administration of 500 mg of xantinole nicotinate (Complamin; Italchimici, Rome, Italy), an almost selective peripheral vasodilator widely used in Europe to increase blood flow to ischemic muscles in case of peripheral arterial disease [11]. After xantinole nicotinate infusion the patients were kept supine and immobile and the heart rate was continuously monitored for 15 minutes to identify and exclude patients in whom the administration of this drug led to excessive reflex tachycardia (defined as an increase of more than 10 beats per minute of the baseline frequency) with consequent coronary vasodilatation (an event that occurred in 2 patients).

Combined coronary and systemic vasodilatation was obtained in 10 patients using either 20 mg of sublingual nifedipine (Adalat; Bayer, Hamburg, Germany) or forced ventilation for 2 minutes (which was supposed to increase the flow in the intercostal muscles served by the IMA and to induce reflex tachycardia and coronary relaxation).

Statistical analysis
Data are expressed as mean ± standard deviation. The unpaired Student’s t test was used to compare the hemodynamic characteristics of IMA flow at rest and after systemic or coronary vasodilatation. Two-factor analysis of variance for repeated measures was used to evaluate differences between the study and control groups and the different vasodilator agents. Post hoc comparison with Newman-Keuls test was used to analyze single factors. A p value less than 0.05 was considered significant.

	Results

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Dipyridamole test
Detailed results of the echo-Doppler measurement at rest and after dipyridamole infusion in the two groups are shown in Table 2. No statistical difference in peak systolic velocity, peak diastolic velocity, and flow was found between the study and control groups at rest and after dipyridamole administration. In both groups IMA flow after dipyridamole infusion was significantly superior than at baseline (p < 0.01 for both) with the maximal increase recorded in the peak diastolic velocity (Fig 2 ).

View larger version (108K): [in this window] [in a new window]   Fig 2. Echo-Doppler evaluation of left internal mammary artery flow at rest (A) and after diypyridamole infusion (B) in a patient of the study group. Increase in diastolic peak velocity (V3) is superior to increase in systolic peak velocity (V1). (V2 = end-systolic velocity, V4 = end-diastolic velocity.)

	Comment

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On the other hand, patent IMA side branches constitute a quite common finding at postoperative angiography and their association with reduced coronary perfusion or IMA malfunction has been denied in at least two large angiographic studies [5, 6]. Moreover, Kern and colleagues [7], using an intravascular Doppler-tipped flowmeter inserted in an IMA graft and in a large pectoralis branch, demonstrated minimal flow diversion in the side branch either at rest and during adenosine-induced coronary hyperemia. More recently Luise and coworkers [8] using a similar technique demonstrated lack of significant difference in the flow characteristics between patients with and without patent IMA graft side branches at rest and after intracoronary adenosine infusion.

However, none of the published studies investigated the possibility of flow steal from the IMA branches in condition of peripheral (or combined systemic and coronary) vasodilatation. If the possibility of blood steal from the IMA side branches exists, it seems conceivable that flow diversion occurs in condition of systemic (and not coronary) relaxation. Instead, the intracoronary infusion of adenosine produces a selective amelioration of IMA coronary run-off, nonphysiologically increasing the difference between the high resistance muscular and the low resistance coronary beds and thus minimizing the possibility of flow steal from the side branches.

The use of transthoracic echo-Doppler for the assessment of IMA patency is widely accepted in clinical practice [12, 13]. The recent validation of this method for the study of IMA flow variations in response to vasoactive substances or in stress conditions [14, 15] led us to choose this technique for the investigation of the IMA-to-side branches steal phenomenon.

In our series no difference in left IMA flow was detected between patients with and without patent IMA branches either at rest and after dipyridamole-induced coronary vasodilatation. The increase in IMA flow was always able to meet the myocardial oxygen demand and no scintigraphically evident flow steal could be demonstrated in patients of the study group.

Assuming that in the left IMA of patients of the study group systolic blood flow is mainly directed to the side branches and diastolic flow is essentially to the LAD, as hypothesized by Kern and coworkers [7], it is possible to extrapolate from our data the relative hemodynamic importance of IMA branches and LAD vascular bed in different conditions.

At rest most of the IMA graft flow occurs in diastole; this systolic-to-diastolic flow ratio obviously decreases in condition of selective coronary relaxation (Fig 2) and remains almost unchanged in case of simultaneous coronary and systemic vasodilatation (as is in the case of nifedipine administration or forced ventilation) (Figs 3 and 4 ).

View larger version (107K): [in this window] [in a new window]   Fig 3. Echo-Doppler evaluation of left internal mammary artery flow at rest (A) and after 2 minutes of forced ventilation (B) in a patient of the study group. There is an increase in both the peak systolic velocity (V1) and the peak diastolic velocity (V3). (V2 = end-systolic velocity, V4 = end-diastolic velocity.)

View larger version (103K): [in this window] [in a new window]   Fig 4. Echo-Doppler evaluation of left internal mammary artery flow at rest (A) and after nifedipine administration (B) in a patient of the study group. There is an increase in both the peak systolic velocity (V1) and the peak diastolic velocity (V3). (V2 = end- systolic velocity, V4 = end-diastolic velocity.)

View larger version (95K): [in this window] [in a new window]   Fig 5. Echo-Doppler evaluation of left internal mammary artery flow at rest (A) and after xantinole nicotinate infusion (B) in a patient of the study group. There is an increase in the peak systolic velocity (V1) and a decrease in peak diastolic velocity (V3). (V2 = end-systolic velocity, V4 = end-diastolic velocity.)

On the basis of the reported observations it is our impression that, when the IMA-to-coronary artery anastomosis is well constructed and the coronary artery has a good caliber and length, diversion of blood flow from the coronary system to the side branches is a remote possibility. However, if technical imperfections (anastomotic stenosis) or anatomic factors (small quality and diameter of the distal IMA or the target vessel) reduce the IMA run-off, flow can probably be diverted into large side branches with lower resistance.

In support of this theory, in at least two of the published cases of flow steal an anastomotic stenosis was associated with the persistence of mammary side branches [4, 16]; in both patients clinical improvement and increase of IMA diameter were achieved after percutaneous dilatation of the anastomosis, even in the absence of complete side branch occlusion. It is conceivable that in these patients the resolution of the anastomotic stenosis has led to a significant amelioration of the IMA run-off, restoring the normal ratio between mammary graft and side branch resistances and thus, minimizing flow diversion in the IMA branches.

In conclusion, our data suggest that, although a minimal flow steal is observable in case of selective muscular vasodilatation, mammary flow diversion in the side branches can occur only to a minimal extent in physiologic conditions. The IMA flow steal from patent side branches is probably the result of a rare combination of unfavorable anatomic and technical conditions, with limited impact in the general population of patients undergoing coronary operations.

	References

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1. Schmid C., Heublein B., Reichelt S., Borst H.G. Steal phenomenon caused by a parallel branch of the internal mammary artery. Ann Thorac Surg 1990;50:463-464.[Abstract]
2. Nakhjavan F.K., Koolpe H.A., Bruss J., Najhi M., Radke T. Transcatheter coil occlusion for treatment of left internal mammary–anterior descending artery steal phenomenon. Cathet Cardiovasc Diagn 1993;28:347-350.[Medline]
3. Ayres R.W., Lu C.T., Benzuly K.H., Hill G.A., Rossen J.D. Transcatheter embolization of an internal mammary artery bypass graft sidebranch causing coronary steal syndrome. Cathet Cardiovasc Diagn 1994;31:301-303.[Medline]
4. Mishkel G.J., Willinsky R. Combined PTCA and microcoil embolization of a left internal mammary artery graft. Cathet Cardiovasc Diagn 1992;27:141-146.[Medline]
5. Ivert T., Huttunen K., Landou C., Björk V.O. Angiographic studies of the internal mammary artery 11 years after coronary artery bypass grafting. J Thorac Cardiovasc Surg 1988;96:1-12.[Abstract]
6. Kuttler H., Hauenstein K.H., Wenz W., Schlosser V. Significance of early angiographic follow-up after internal thoracic artery anastomosis in coronary surgery. Thorac Cardiovasc Surg 1988;36:96-99.[Medline]
7. Kern M.J., Bach R.G., Donohue T.J., Caracciolo E.A., Wolford T., Aguirre F.V. Role of large pectoralis branch artery in flow through a patent left internal mammary artery conduit. Cathet Cardiovasc Diagn 1995;34:240-244.[Medline]
8. Luise R., Teodori G., Di Gianmarco G, et al. Persistence of mammary artery branches and blood supply to the left anterior descending. Ann Thorac Surg 1997;63:1759-1764.[Abstract/Free Full Text]
9. Possati G., Gaudino M., Alessandrini F., Zimarino M., Glieca F., Luciani N. Systematic clinical and angiographic follow-up of patients submitted to minimally invasive coronary artery bypass. J Thorac Cardiovasc Surg 1998;115:785-790.[Abstract/Free Full Text]
10. Gaudino M., Serricchio M., Tondi P., et al. Non-invasive evaluation of mammary artery flow reserve and adequacy to increased myocardial oxygen demand. Eur J Cardiothoracic Surgery 1998;13:404-409.
11. Reynolds J.E.F. Martindale the extrapharmacopeia. London: The Pharmaceutical Press, 1993.
12. Van Son J.A.M., Skotnicki S.H., Peters M.B.M., Pijls N.H.J., Noyez L., van Asten W.N.J.C. Noninvasive hemodynamic assessment of the internal mammary artery in myocardial revascularization. Ann Thorac Surg 1993;55:404-409.[Abstract]
13. Canver C.C., Armstrong V.M., Nichols R.D., Mentzer R.M. Color-flow duplex ultrasound assessment of internal thoracic artery graft after coronary bypass. Ann Thorac Surg 1995;59:389-392.[Abstract/Free Full Text]
14. Takemura H., Kawasuji M., Sakakibara N., Tedoriya T., Ushijima T., Watanabe Y. Internal thoracic artery graft function during exercise assessed by transthoracic Doppler echography. Ann Thorac Surg 1996;61:914-919.[Abstract/Free Full Text]
15. Canver C.C., Armstrong V.M., Cooler S.D., Nichols R.D. Assessment of internal thoracic artery vasoreactivity in response to sublingual nitroglycerin. Ann Thorac Surg 1997;63:1041-1043.[Abstract/Free Full Text]
16. Ishizaka N., Ikari Y., Saeki F., et al. Repeat embolization of the side branch of the internal mammary artery graft by gelatin sponge particles and micro coils. Cathet Cardiovasc Diagnosis 1995;34:245-249.

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