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a Department of Cardiac Surgery, Makassed Hospital, Jerusalem, Israel
b Department of Pathology, Makassed Hospital, Jerusalem, Israel
c Department of Cardiology, Makassed Hospital, Jerusalem, Israel
Accepted for publication May 13, 2008.
* Address correspondence to Dr Darwazah, Makassed Hospital, Mount of Olives, PO Box Jerusalem, 19482, Israel (Email: darwaz30{at}hotmail.com).
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Introduction |
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We present a case of moderate atherosclerosis of the left internal mammary artery (LIMA) that developed after repair of coarctation. The artery was used as a conduit to graft the left anterior descending coronary artery (LAD). The behavior of the graft was not as expected. We believe that such conduit should not be used, even in the presence of good blood flow.
A 41-year-old, nondiabetic, nonhypertensive man with previous history of smoking one packet of cigarettes for the last 16 years was admitted for evaluation of chest pain. The pain started 4 months before, associated with gradual decline in his functional capacity. He was unable to walk 100-m uphill.
The patient had undergone a successful repair of aortic coarctation 23 years before, using a Dacron tube graft (Meadox Medical, Oakland, NJ) together with ductal ligation. His blood pressure at the time of operation was 180/130 mm Hg, which dropped to 125/75 mm Hg after surgery. The patient received anti-hypertensive medication in the form of B-blockers (atenolol, 100 mg once daily) for 2 weeks after surgery.
Examination on recent admission revealed a well-built man with a body mass index of 30.4. His blood pressure was 120/75 mm Hg and his heart rate was 70 bpm. Both chest and heart examination were normal. Mild pitting edema was found along both lower extremities and peripheral pulsations were palpable bilaterally.
Laboratory investigations were normal except for hypertriglyceridemia. The level of blood cholesterol was at the upper limit of normal (200 mg/dL), his high density lipoprotein was 24 mg/dL, (normal, 30 to 60), and his low density lipoprotein 129 mg/dL (N, 50 to 155). His chest roentgenogram revealed marked cardiomegaly. Electrocardiography showed normal sinus rhythm with T-wave inversion in leads III and aVF with poor R-wave progression in chest leads. Transthoracic echocardiography showed a moderately dilated left ventricle (left ventricular diastolic diameter, 6.3 cm) with severe apical and mild inferior hypokinesia. Ejection fraction was 0.25. Gradient across the previous repair of coarctation was 30 mm Hg.
Left heart catheterization revealed a totally occluded circumflex and LAD coronary arteries. He had 90% stenosis of the obtuse marginal artery and 99% stenosis of the second diagonal artery. His right coronary artery was normal with retrograde filling of both circumflex and obtuse marginals. His aortogram showed the site of previous repair of coarctation and indirect visualization of a patent with dilated LIMA with no evidence of stenotic lesion.
Surgery was performed on the patient. During dissection of the LIMA, it was found to be enormously dilated, measuring 8 mm in diameter (Fig 1A). After heparinization, the distal end was ligated and a segment of the artery was sent for histopathology. Proximal blood flow was excellent. There was no evidence of calcification along the artery. Routine cannulation of the aorta and the right atrium were done. Due to poor ejection fraction, a beating heart on the pump was used. A saphenous vein was used to graft the obtuse marginal and diagonal arteries, whereas the LIMA was used to graft the LAD, which was small in diameter with a diseased wall. The patient left the operating room and remained hemodynamically stable without any evidence of electrocardiographic changes or enzymatic elevation. Postoperative blood loss was excessive, due to an abnormal coagulation profile. It was corrected by fresh frozen plasma, platelets, and packed red blood cell transfusion.
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Comment |
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Atherosclerosis of the IMA is often a segmental disease. Previous studies [7] showed that it mainly affects proximal segment and lower part close to bifurcation. However, Abad and colleagues [2] found that the distal and bifurcation segments are affected more than the central and proximal parts. Besides the natural development of atherosclerosis of IMA, severe significant lesions have been reported under certain circumstances. Patients with coarctation of the aorta are known to have persistent upper body vascular abnormalities [4]. The development of atherosclerosis of IMA among these patients was reported [3–5].
The degree of affection varies from hypertrophy of the artery [8] to significant obstruction and calcification [4–7]. The cause of atherosclerosis is due to late repair of coarctation and the presence of severe obstructive hypertension [3].
Similarly, our patient had late repair of coarctation when he was 23 years old. Subsequently, we found atherosclerosis of the LIMA. However, the degree of affection was much less than that reported in the previous studies [3–5].
There are two reasons to explain this: (1) the age of our patient at the time of coronary bypass was much younger (ie, he was in his early 40s in comparison with those in their 50s and 60s in the previous reported cases); (2) he did not have persistent hypertension after repair of coarctation. He stopped taking antihypertensive drugs, and his blood pressure was normal when he was admitted for bypass. Among all cases operated previously, IMA was not used for grafting except the case operation of de Caleya and colleagues [8]. In our case we used the LIMA to graft the LAD in spite of the huge dilatation of the artery. Intraoperative evaluation of the LIMA showed no evidence of obstruction or calcification, and the blood flow was satisfactory. Although the LIMA was not directly evaluated during catheterization, it was indirectly visualized during aortogram, which confirmed patency.
For all of the previously mentioned reasons, we decided to use the artery for grafting. Surprisingly, the graft was occluded very early. The exact cause was not clear, but it could be explained by the original poor distal run off of the LAD, the use of fresh frozen plasma, and platelets to control postoperative bleeding, and possibly by the great size mismatch between the huge LIMA and the small LAD.
The possibility of using an alternative arterial graft as radial or gastroepiploic artery was not an option at this stage. We were in no doubt that the quality of the LIMA and the blood flow we have seen intraoperatively justified its use. However, in retrospect, we believe that intraoperative findings were deceiving. It turned out that the LIMA was diseased, which was proved by histopathologic examination and the huge diameter that may have played an important role in early occlusion.
In conclusion, we believe that patients with previous history of coarctation repair will develop atherosclerotic disease of IMA. Therefore, these arteries should not be used for myocardial revascularization, even in the presence of moderate disease with excellent blood flow, as they are liable to undergo early occlusion.
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