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J Thorac Cardiovasc Surg 1995;110:868-0870
© 1995 Mosby, Inc.


BRIEF COMMUNICATIONS

Enoximone in internal mammary artery hypoperfusion

Mohammad Bashar Izzat, FRCSa, Steve Bolsin, FRCAb, Alan J. Bryan, FRCSc, Gianni D. Angelini, FRCS

Bristol, United Kingdom

Internal mammary artery (IMA) spasm is a recognized cause of left ventricular dysfunction in the early postoperative period and is associated with increased morbidity and mortality.Go Go 1,2 Approaches that have been advocated for the management of severe IMA spasm include immediate reoperation with topical application or intraluminal injection of a vasodilator or the performance of an additional vein graft to the coronary artery involved. We recently reported a study comparing the effect of four systemic vasodilators on IMA flow and showed that enoximone, a phosphodiesterase-III inhibitor, produced a 100% increase in IMA flow, significantly greater than that produced by sodium nitroprusside, dobutamine, or glyceryl trinitrate.Go 3

Recently, a 45-year-old man was admitted to our hospital for coronary artery bypass grafting. Coronary angiography had shown normal left ventricular function and a severe stenosis of the proximal left anterior descending coronary artery (LAD); all other coronary arteries were otherwise normal. Routine transesophageal echocardiography (TEE) was used for intraoperative monitoring. The left IMA was used to graft the LAD, and cardiopulmonary bypass was discontinued with no need for inotropic support. TEE showed good contractility of all segments of the left ventricle. Ten minutes after decannulation and heparin reversal, sudden reduced contractility was noted in the anterior wall of the left ventricle, associated with marked ST segment elevation on the electrocardiogram leads I and II. TEE also showed the depressed contractility of the anteromedial segment of the left ventricle (Fig. 1, A). A diagnosis of IMA hypoperfusion was made, and a bolus of enoximone (500 µg/kg) was given intravenously over 2 to 3 minutes. Within 10 to 15 minutes, the ST segment changes disappeared, and TEE showed return of the anteromedial segment of the left ventricle to its normal contractility (Fig. 1, B). The patient did not have any further intraoperative or postoperative problems, and postoperative electrocardiogram and cardiac enzymes did not show any evidence of myocardial damage.



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Fig. 1. Transesophageal echocardiographic transgastric view of the left ventricle at end-systole. A, Note the bulging anteromedial segment of left ventricle caused by reduced contractility (arrows). B, Eight minutes later, the anteromedial segment of left ventricle has returned to its normal contractility, and left ventricle at end-systole looks symmetrically contractile.

 
This was a case of documented IMA hypoperfusion and its successful treatment with intravenous enoximone, with rapid reversal of the myocardial ischemic changes. It supports our earlier conclusions regarding the benefits of enoximone in treating IMA spasm. Although performing an additional vein graft might have been equally effective, less aggressive measures may, in our opinion, hold the solution to this complication in many cases. We would therefore recommend the systemic use of enoximone to treat IMA hypoperfusion.

Footnotes

From the Departments of Cardiac Surgerya and Anesthesia,b University of Bristol, Bristol, United Kingdom. Back

J THORAC CARDIOVASC SURG 1995;110:868-70 Back

References

  1. Sarabu MR, McClung JA, Fass A, Reed GE. Early postoperative spasm in the left internal mammary artery bypass grafts. Ann Thorac Surg 1987;44:195-200.
  2. Jones EL, Lattouf OM, Weintaub WS. Catastrophic consequences of internal mammary artery hypoperfusion. J THORAC CARDIOVASC SURG1989;98:902-7.
  3. Izzat MB, West RR, Ragoonanan C, Angelini GD. Effect of systemic vasodilators on internal mammary artery flow: implications for postoperative treatment after myocardial revascularization. J THORAC CARDIOVASC SURG 1994;108:82-5.[Abstract/Free Full Text]




This Article
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Alan J. Bryan
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