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Ann Thorac Surg 2007;83:490-494
© 2007 The Society of Thoracic Surgeons
a Department of Cardiology, Catharina Hospital, Eindhoven
b Department of Thoracic Surgery, Catharina Hospital, Eindhoven
c Department of Biomedical Engineering, Eindhoven University of Technology, Eindhoven, The Netherlands
Accepted for publication September 20, 2006.
* Address correspondence to Dr Botman, Department of Cardiology, Catharina Hospital, PO Box 1150, 5602 ZA Eindhoven, The Netherlands. (Email: carcbn{at}cze.nl).
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Abstract |
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METHODS: Coronary angiography, MRI, and fractional flow reserve measurements were performed in 18 patients 8 years after direct surgical angioplasty of the left main coronary artery.
RESULTS: At coronary angiography and MRI, a dilated funnel-shaped left main coronary artery was seen in all 18 patients, but both methods failed to demonstrate a flow-limiting lesion in the distal left main coronary artery in 1 patient. The functional severity was shown by fractional flow reserve measurement, and subsequently, this patient underwent repeated bypass grafting surgery.
CONCLUSIONS: After long-term follow-up, 17 of 18 patients had an excellent result of direct surgical angioplasty of the left main coronary artery. MRI is a safe and noninvasive way to visualize the left main coronary artery after direct surgical angioplasty, but quantitative assessment of a lesion is not reliable. Fractional flow reserve measurements are mandatory to evaluate the hemodynamic properties of the left main coronary artery after direct surgical angioplasty.
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Introduction |
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TopAbstractIntroductionPatients and MethodsResultsCommentReferences |
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The limitations of coronary angiography to assess LMCA stenosis are well recognized; therefore, newer anatomic and physiologic methods, both invasive and noninvasive, have been suggested to evaluate LMCA disease [5–7]. The usefulness of magnetic resonance imaging (MRI) to evaluate the anatomic properties of the LMCA and fractional flow reserve (FFR) measurements to evaluate its physiologic properties are well documented [8, 9].
In some case reports and small studies, anatomic evaluation of the result after LMDSA is reported with coronary angiography, MRI, intravascular ultrasound, spiral computed tomography (CT), or even transesophageal echocardiography [10–13]. In this study, we evaluated the physiologic properties of the LMCA after LMDSA and compared noninvasive MRI with invasive coronary angiography and FFR measurements of the LMCA in 18 patients 8 years after LMDSA.
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Patients and Methods |
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Surgical Technique
The LMCA was approached anteriorly. The incision was started on the anterior aspect of the aortic root and was extended across the left lateral wall towards the LMCA. A curved incision was made into the right lateral aortic wall towards the LMCA, and the pulmonary root was unrolled towards the left by traction sutures to ease exposure. The anterior aspect of the LMCA was incised across the stenosis. A venous onlay patch was used to enlarge the LMCA and the adjacent 2 cm of the aortic incision to give the LMCA ostium a funnel shape, which favors a laminar blood flow [4].
Magnetic Resonance Imaging
MRI was performed on an Intera CV 1.5t system (Philips Medical Systems, Best, The Netherlands, MRI version 10.3) equipped with high-performance gradients (60 mT/m, 150 mT/m per second rise time) and dedicated cardiac imaging software (release 10.3). A phased-array coil and vectorcardiographic monitoring were used. A scout localizer sequence in three orthogonal directions was performed to localize the left coronary artery and to place the navigator as described previously [14]. These scout images were used to define a transverse three-dimensional (3D) imaging volume encompassing the proximal left coronary artery. The navigator was placed vertical through the dome of the right hemidiaphragm.
An end-expiratory 5-mm gating window was used for acceptance of image acquisition data. To define an imaging window in the mid-diastolic part of the cardiac cyc1e, a balanced, turbo fast-field echo cine sequence in a four-chamber plane (defined using real-time interactive imaging) was performed in which the right coronary artery and the circumflex artery were axially transected. This cine run was used to define a mid-diastolic imaging window with minimal cardiac and coronary movement.
Next, coronary MRIs were acquired by using a vectorcardiographic-triggered free-breathing navigator-gated multisection 3D-segmented transverse balanced fast field-echo sequence with fat suppression and T2 preparation prepulses. The imaging parameters were 5.6/2.8 (TRJTE), a 110-degree flip angle, a 270-mm field of view, a 272 x 272 x 20 matrix reconstructed to 512 x 512 x 40 pixels, and a turbo fast field-echo factor (number of shots per heartbeat) of 16, which resulted in an acquired spatial resolution of l x l x 3 mm reconstructed to 0.5 x O.5 x 1.3 mm. The MRI images were acquired during the previously defined mid-diastolic time window of 90 ms. The whole imaging protocol was performed within 15 minutes [15].
Coronary Angiography and Fractional Flow Reserve Measurements
After administration of 5000 units of heparin, a left coronary guiding catheter was advanced in the left coronary ostium, 200 µg of intracoronary nitroglycerin was administered, and coronary angiograms were performed in at least two orthogonal views. Thereafter a 0.014-inch pressure guidewire (Pressure Wire, Radi Medical Systems, Uppsala, Sweden) was advanced to the tip of the guiding catheter, and after equal pressures were confirmed at that location, the wire was advanced across the LMCA. Intravenous adenosine at 140 µm/(kg µ min) was administered through the femoral vein to induce maximum coronary hyperemia [16].
The FFR, which is considered the gold standard for physiologic assessment of the coronary artery, was ca1culated by the ratio Pd/Pa at steady-state maximum hyperemia, where Pd is mean coronary pressure distal of the LMCA (recorded by the pressure wire) and Pa is mean aortic pressure (recorded by the guiding catheter) as described before [16, 17]. The FFR measurements where performed twice with the pressure wire, once in the anterior descending artery and once in the circumflex artery. After the second measurement, a pullback curve was performed at sustained hyperemia to localize the pressure drop, if present.
Data Analysis
All quantitative coronary angiography data, FFR, and MRI measurements were stored digitally and analyzed off-line by an independent experienced reviewer. Because of the funnel shape of the LMCA after LMDSA, no reference diameter for quantitative coronary angiography and MRI measurements were available; therefore, the results of these methods are expressed as minimal lumen diameter and minimal square area.
FFR is expressed as usual by a number between 0 and 1, expressing the achieved maximum blood flow as a fraction of the normal maximum blood flow if no LMCA disease would be present at all. All data are expressed as mean ± standard deviation with ranges.
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Results |
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Clinical Follow-Up
After 8 years of clinical follow-up, 16 of the 18 patients were in angina class I according to the Canadian Cardiovascular Society and 2 were in angina class II. No additional interventions or repeated surgery had been necessary in any of these patients up to the moment of the invasive and noninvasive investigations. The baseline characteristics of these patients are presented in Table 1.
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At coronary pressure measurement, the FFR was 0.93 ± 0.09 (range, 0.66 to 1.00). In one patient, the FFR of the LMCA was below 0.75, considered as the threshold for a significant stenosis, and this patient underwent repeated CABG surgery. The patient with a stenosis in the distal left anterior descending artery underwent a percutaneous coronary intervention. The clinical follow-up, angiographic, and physiologic data are presented in Table 2.
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Comment |
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TopAbstractIntroductionPatients and MethodsResultsCommentReferences |
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The most common cause of LMCA stenosis is arteriosclerosis affecting particularly the mid part and distal bifurcation, often associated with two-vessel or three-vessel disease. LMCA stenosis is present in 9% of the patients undergoing bypass surgery. CABG is an excellent treatment of LMCA stenosis but with some potential limitations that include complete graft-depending perfusion owing to progressive occlusion of the LMCA and the risk of arteriosclerotic changes or occlusion of bypass grafts [20, 21]. It has also been suggested that perfusion of a large area of the myocardium retrograde would be suboptimal [22].
Direct surgical angioplasty of the LMCA was suggested as a good alternative by restoring the native antegrade flow and allowing PCI of more peripheral lesions as coronary artery disease progresses [23]. The two technical methods described to get access to the LMCA are the posterior and anterior approach. The anterior approach was used in the present study [4, 23].
Different methods have been used to evaluate the result of LMDSA but not on a regular basis or systematically in follow-up studies. Most reports have used coronary angiography, intravascular ultrasound, MRI, transesophageal echocardiography, or ultrafast CT and concern one or just a few patients [10–13].
To obtain both anatomic and physiologic information, the techniques we used for evaluating the LMCA after direct surgical angioplasty in our present study were MRI, coronary angiography, and FFR measurements. In our opinion, intravascular ultrasound is suboptimal for evaluating the LMCA after surgical angioplasty. Owing to the wide funnel shape of the LMCA, the intravascular ultrasound catheter cannot be positioned centrally in the LMCA [24].
Previous reports have shown the feasibility of using MRI to evaluate the LMCA after surgical angioplasty [12]. The advantage of MRI over coronary angiography is its noninvasive character and the relatively short time to perform an MRI for evaluating the LMCA. The disadvantage of MRI compared with coronary angiography is the low resolution of MRI (1 to 2 mm2 in the present study), making quantitative assessment of a specific stenosis more difficult, although angiographic determination of degrees of narrowing of the LMCA is also subject to considerable error. The angiographic errors appear to result primarily from the presence of arteriosclerotic plaque in the LMCA and an insufficient number of angiographic projections [5].
The same problem was encountered in our series of 18 patients evaluated 8 years after LMDSA. Angiography, although projections were made from different angles, and MRI both failed to give specific information about the distal LMCA with respect to the functional severity of a lesion in the distal LMCA in 1 patient. This lesion appeared nonsignificant on angiography and could not be seen on MRI, although both methods provided a good anatomic view of the LMCA.
The problem of anatomic evaluation of a stenosed LMCA is the poor correlation with the physiologic properties of the same stenosed LMCA, as we showed in previous work [9]. This emphasizes the general problem that anatomic evaluation of the LMCA often poorly corresponds with the physiologic severity of an eventual stenosis, a problem not only present in classic coronary angiography but also inherent to any anatomic method used to evaluate the LMCA.
So far, no information was available about the hemodynamic and physiologic properties of the LMCA after direct surgical angioplasty. An average FFR of 0.93 ± 0.09 indicates that a good functional operative result was present in most patients 8 years after LMDSA. Only in 1 patient was a significant pressure drop present at the distal LMCA, which was not recognized either by coronary angiography or MRI (Fig 1). This patient underwent repeated CABG surgery. The remaining 17 patients showed a FFR exceeding 0.90 in the LMCA, indicating there was no significant hyperemic pressure drop in the LMCA even after 8 years of follow-up. This ruled out any flow obstruction in the LMCA after LMDSA, regardless of its funnel-shaped morphology. In this cohort, 17 of 18 patients had an excellent functional result of direct surgical angioplasty after long-term follow-up.
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  R. A.E. Dion Invited commentary Ann. Thorac. Surg., February 1, 2007; 83(2): 494 - 495. [Full Text] [PDF]
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