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Eur J Cardiothorac Surg 1999;15:251-254
© 1999 Elsevier Science NL


Do internal mammary artery side-branches have the potential for haemodynamically significant flow steal?

Mario Gaudino, Michele Serricchio, Paolo Tondi, Franco Glieca, Piergiorgio Bruno, Gianfederico Possati, Paolo Pola

Department of Cardiac Surgery and Angiology, Catholic University, Rome, Italy

Received 2 June 1998; received in revised form 6 January 1999; accepted 12 January 1999.

Corresponding author. Divisione di Cardiochirurgia, Policlinico A. Gemelli, Largo A. Gemelli 8, 00168 Rome, Italy. Tel.: +39-6-3058181; fax: +39-6-3055-535; e-mail: mgaudino@pelagus.it


    Abstract
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 Abstract
 Introduction
 Methods
 Results
 Discussion
 References
 
Objective: To evaluate the potential for flow steal of the internal mammary artery (IMA) side-branches at rest and in case of dilatation of their vascular bed (as probably occurs during physical exercise). Methods: Transthoracic echo-Doppler evaluation of IMA flow was performed preoperatively in 40 patients undergoing myocardial revascularization. IMA flow was measured at rest and in condition of peripheral vasodilatation (obtained using forced ventilation for 2 min, dypiridamole 0.84 mg/kg endovenous (e.v.), xantinole nicotinate 500 mg e.v., nifedipine 20 mg sublingual (s.l.)). Results: IMA mean peak systolic velocity increased 23% after forced ventilation (from 67 to 83 cm/s), 6% after dypiridamole (from 75 to 80 cm/s), 30% after xantinole infusion (from 62 to 81 cm/s) and 23% after nifedipine administration (from 60 to 74 cm/s). IMA flow increased 17.7% after forced ventilation (from 39.5 to 46.5 ml/min), 4.8% after dypiridamole (from 39.2 to 41.1 ml/min), 20.2% after xantinole infusion (from 41.4 to 49.8 ml/min) and 16.5% after nifedipine administration (from 41.6 to 48.5 ml/min). Conclusions: The limited functional flow reserve of the in situ IMA, even after pure muscular vasodilatation, seems to minimize the possibility of significant flow steal from patent IMA graft collaterals.

Key Words: Mammary artery • Collaterals • Flow steal


    Introduction
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 Abstract
 Introduction
 Methods
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Although cases of flow steal from patent internal mammary artery graft side branches (IMASB) have been anedoctally reported (and careful identification and legation of all the IMASB recommended) [1] [2] [3] [4] [5], to date the haemodynamic importance of IMASB at rest and after pharmacological or exercise-induced dilatation has received only limited attention, so that the effective potential of these vessels to induce a clinically significant flow steal in patients submitted to coronary bypass procedures is still controversial.

The volume capacity of IMASB and, more notably, its variations in the different physiological situations is the major determinant of this potentiality as, if only limited amount of blood can be diverted in the mammary side branches, flow steal from the larger coronary bed would seem unlikely.

This report was conceived to provide an estimation of the IMASB haemodynamic importance at rest and after pharmacological or exercise-induced vasodilatation by using a transthoracic echo-Doppler method.


    Methods
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 Abstract
 Introduction
 Methods
 Results
 Discussion
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Patients population
This study protocol involved 40 patients selected among the 361 coronary artery bypass cases referred at the Department of Cardiac Surgery of the Catholic University of Rome between September 1997 and February 1998.

The main preoperative clinical characteristics of these patients are summarized in Table 1.


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Table 1. Preoperative characteristics

 
Selection was based on the willingness of the patients to undergo the echo-Doppler investigation. The evaluation was performed in the preoperative period (at a mean interval of 1.5±2.0 days before surgery) and informed consent to the procedure was provided by all patients.

Evaluation of mammary artery flow reserve
Evaluation of mammary artery flow reserve was performed following a described protocol [6].

The left IMA was usually detected in the third intercostal space in parasternal position. Colour-Doppler imaging was obtained using a constant angle of 60° between the ultrasound beam and the long axis of the vessel. Under Colour-Doppler guidance, a pulsed Doppler evaluation of the flow velocity in the IMA using a sample volume of 1 mm3, and taking into consideration the angle between the ultrasound beam and the axis of the vessel, was performed.

The following parameters were calculated: peak systolic velocity (m/s) (PSV); end diastolic velocity (m/s) (EDV); time average mean velocity (m/s) (TAMV) and resistance index (RI). The TAMV was defined as the area between the line traced on the Doppler wave and the base line. The diameter of the IMA was calculated using internal electronic callipers on frozen frame images from the B-mode recording.

Flow (F) was obtained using the formula: F(ml/min)=TAMV (cm/s)x({pi}r2x60) where r is half the internal diameter of the IMA expressed in centimetres.

Vasodilatory protocol
Left IMA flow was evaluated at rest and after (in progressive order).

  1. Forced ventilation for two min (which was supposed to increase the flow in the intercostal muscles served by the mammary artery) (40 patients).
  2. Administration (e.v.) of dypiridamole 0.84 mg/kg (Persantin, Boehringer Mannheim, Germany) (40 patients).
  3. Administration (e.v.) of 500 mg of xantinole nicotinate (Complamin, Italchimici, Italy) (an almost selective peripheral vasodilator) [7] (32 patients).
  4. Administration of nifedipine 20 mg s.l. (Adalat, Bayer, Germany) (29 patients).

Flow evaluation was started immediately after administration of the vasodilator stimulus and continued without interruption for 15 min; measurements were made when the vasodilator effect was judged maximal by the operator. In order to minimize the possible overlapping effects of the various stimuli, a minimal interval of 30 min was allowed between the different tests and the nifedipine administration was performed at last.

Statistical analysis
Data are expressed as mean±standard deviation, minimum and maximum (in parenthesis). The paired Student t-test was used to compare the haemodynamic characteristics of IMA flow at rest and after vasodilatation. A P-value<0.05 was considered significant. Statistical analysis was not applied to flow, as this is a derived measure (as described above).


    Results
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 Abstract
 Introduction
 Methods
 Results
 Discussion
 References
 
Detailed results of the echo-Doppler measurement in the different conditions are shown in Table 2Table 3Table 4Table 5.


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Table 2. Internal mammary artery flow characteristics at rest and after 2 min of forced ventilation

 

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Table 3. Internal mammary artery flow characteristics at rest and after dypiridamole infusion

 

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Table 4. Internal mammary artery flow characteristics at rest and after xantinole nicotinate infusion

 

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Table 5. Internal mammary artery flow characteristics at rest and after nifedipine administration

 
Muscular vasodilatation (achieved either by xantinole nicotinate, forced ventilation or nifedipine) led to a more sustained increase in IMA PSV (+30, +23 and +23%, respectively) although in no case the described increase was superior to the 30% of the baseline value.

As expected, dypiridamole infusion (which has only a limited vasodilator effect on the peripheral vascular system) led to a very limited increase in mammary PSV (+6.6%).

IMA flow increased 17.7% after forced ventilation (from 39.5 to 46.5 ml/min), 4.8% after dypiridamole (from 39.2 to 41.1 ml/min), 20.2% after xantinole infusion (from 41.4 to 49.8 ml/min) and 16.5% after nifedipine administration (from 41.6 to 48.5 ml/min).

IMA diameter varied only slightly (<0.5 mm) following each vasodilator stimulus.


    Discussion
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 Abstract
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 Methods
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 Discussion
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IMASB provide the blood supply for most of the visceral, muscular and osseous components of the anterior chest wall and supero-anterior mediastinum, including the thymus, the sternum and the intercostal muscles [8]. However, it is noteworthy that all the structures served by the IMASB are also supplied by at least one other arterial inflow (in particular the intercostal musculature, who represents by far the most important target of IMASB, is also perfused by the posterior intercostal arteries originating from the descending thoracic aorta), allowing the supposition that the overall flow and the flow reserve of mammary side-branches should be relatively low.

However, as only limited investigation on this subject has been performed until now, to date this supposition could not received an experimental verification.

In clinical practice, angina recurrence associated with patent IMASB has anedoctally been reported by several authors; in most of these cases myocardial ischaemia disappeared after interruption of IMA collaterals, supporting the hypothesis of a significant deviation of mammary blood flow through the IMASB [1] [2] [3] [4] [5].

However, patent IMASB are a common finding at post-operative angiography and their association with angina recurrence has been repeatedly questioned [9] [10]. Moreover, Kern et al. [11] and Luise et al. [12] using intravascular Doppler techniques, demonstrated minimal flow diversion in the mammary collaterals either at rest and during adenosine induced hyperaemia, and similar results have been obtained by our group by means of transthoracic and endovascular evaluation of mammary grafts [13].

The results of the present study demonstrate that at rest, the overall flow in mammary side-branches is low and largely inferior to that reported in the left coronary circulation [14] [15]. Even after muscular vasodilatation (independently from the type of vasodilator stimulus used) the IMASB flow increased only marginally (always less than 20%) confirming the limited haemodynamic importance of IMASB vascular bed, and thus denying the theoretical background for a flow steal from these vessels. Although the increase in PSV and TAMV after various stimuli resulted statistically significant, the absolute increase was always extremely limited, and it seems clear that in this particular context, statistical significance correlates poorly (if at all) with haemodynamic and clinical importance.

Basing on these data it seems unlikely that such a limited vascular bed (who undergo a further dramatic reduction after the surgical preparation of the mammary artery) can be able to compete and steal flow from the larger coronary circulation.

It is our impression that when the IMA-coronary artery anastomosis is well constructed and the target coronary artery has a good calibre and length, diversion of blood flow from the coronary system to the smaller IMASB bed is a remote possibility; the difference in flow pattern between the two districts (diastolic in the coronaries, systolic in the IMASB) makes this diversion even more unlikely.

On the contrary, if technical imperfections (anastomotic stenosis) or anatomic factors (small quality and diameter of the mammary artery or the target vessel) reduce the mammary run-off, flow can probably be diverted to large collaterals with lower resistance.

However, due to the wide inter-individual variability of IMASB anatomy and distribution, extension of our observations to the totality of cardiac surgery patients can be difficult; it is possible that particular anatomic variations of IMASB exist in whom the haemodynamic importance of mammary side-branches is superior to what we have observed.

Despite that, the large number of patients involved in our study and the notable concordance of the echo-Doppler results among the different patients allow us to believe that our observations can be applied to at least the great majority of coronary artery bypass patients.

In conclusion, our investigation testifies that in the majority of patients, the haemodynamic importance of IMASB is small either at rest and in condition of peripheral vasodilatation; this finding minimizes the potential for flow steal of IMASB and underlines the need for further investigation on this controversial subject.


    References
 Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 References
 

  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. Ishizaka N., Ikari Y., Saeki F., Ishizaka Y., Tamura T., Yamaguchi T., Suha H., Ibukuro K. 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.
  6. Gaudino M., Serricchio M., Tondi P., Glieca F., Glordano A., Trahi C., Pola P., Possati G. Non-invasive evaluation of mammary artery flow reserve and adequacy to increased myocardial oxygen demand. Eur J Cardio-thoracic Surg 1998;13:404-409.[Abstract/Free Full Text]
  7. Reynolds J.E.F. Martindale the extrapharmacopeia. London: Pharmaceutical Press, 1993, p. 1313.
  8. Henriquez-Pino J.A., Gomes W.J., Prates J.C., Buffolo E. Surgical anatomy of the internal thoracic artery. Ann Thorac Surg 1997;64:1041-1045.[Abstract/Free Full Text]
  9. Ivert T., Huttunen K., Landou C., Bjork 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]
  10. 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]
  11. 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]
  12. Luise R., Teodori G., Di Gianmarco G., D'Annunzio Z., Paloscia L., Barsotti A., Gallina S., Contini M., Vitolla G., Calafiore A.M. Persistence of mammary artery branches and blood supply to the left anterior descending. Ann Thorac Surg 1997;63:1759-1764.[Abstract/Free Full Text]
  13. Gaudino M, Serricchio M, Glieca F, Bruno P, Tondi P, Giordano A, Trahi C, Calcaghi HL, Pola P, Possati G. Steal phenomenon from mammary side-branches: when does it occur? Ann Thorac Surg 1998;66:2056–2062.
  14. Guyton AC. Textbook of medical physiology. Philadelphia: WB Saunders, 1966, pp. 312–321.
  15. Feigl E.O. Coronary physiology. Physiol Rev 1983;63:1-205.[Abstract/Free Full Text]



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