Systolic Compression of Bypass Grafts

Myocardial bridging is defined as systolic compression of an epicardial coronary artery segment underlying myocardial tissue.1 On angiography, it is recognized as systolic compression of an epicardial coronary segment resulting in systolic narrowing (milking effect) of that segment.¹ The prevalence of bridging ranges from 5% to 86% in autopsy series and from 0.5–7.5% in coronary angiography series.^1,2 Its detection may be enhanced by operator recognition of the phenomenon.² Myocardial bridging commonly involves the left anterior descending coronary artery (LAD), and to a lesser extent, the right coronary and the left circumflex arteries.¹ It is more prevalent in patients with transplanted hearts3 and hypertrophic obstructive cardiomyopathy.^4,5 Myocardial bridging of epicardial veins have also been observed at autopsy.⁶ To the best of our knowledge, the phenomenon of dynamic compression of bypass grafts supplying native coronary arteries during systole has not been described. Case Reports Case 1. A 76-year-old female was admitted to our hospital in May 2004 with chest tightness and shortness of breath of one day duration. She had a history of coronary artery disease with coronary artery bypass grafting in 1978, and a redo operation in 1983, along with mitral valve repair, congestive heart failure with severe left ventricular dysfunction, atrial fibrillation requiring atrio-ventricular node ablation with placement of a biventricular pacemaker in 2001. She had multiple hospitalizations for congestive heart failure and angina symptoms within the last six months prior to this admission. On admission, her physical examination was notable for a blood pressure of 120/60 and a heart rate of 80 beats per minute. She had a jugular venous pressure of 20 cm of water with prominent v-wave, inspiratory crackles at the right base of the lung, a grade III/VI holosystolic murmur loudest at the left sternal border, and a third heart sound. Her electrocardiogram showed ventricular pacing at 80 beats per minute with left bundle branch block morphology. The patient was treated with aspirin, metoprolol, intravenous heparin, nitrates and diuretics, with prompt resolution of her symptoms in the emergency room. Cardiac markers including troponin I and creatinine kinase were unremarkable. A transthoracic echocardiogram revealed worsening right ventricular function with severely depressed right and left ventricular functions, biatrial enlargement, biventricular dilatation and hypertrophy, severe tricuspid regurgitation, and moderate-to-severe mitral regurgitation. A hybrid adenosine myocardial perfusion/viability study was done using thallium for the rest-redistribution images, and technetium-99 m for the adenosine-stress images showed ischemia and scarring in the distribution of the right coronary artery with myocardial viability in all the vascular territories. The gated SPECT left ventricular ejection fraction was 29% with global hypokinesis. The patient subsequently underwent right and left heart catheterization. The systolic pulmonary artery pressure was 39 mmHg, the mean pulmonary capillary wedge pressure was 26 mmHg, and the systolic right ventricular pressure was 41 mmHg. Left heart catheterization showed severe native triple-vessel disease with patent grafts to the LAD artery and obtuse marginal branch. The saphenous vein graft supplying the right posterior descending artery (PDA) had a mid-70% stenosis with dynamic systolic narrowing (Figure 1). Primary stenting was successfully performed with deployment of a 3.5 x 33 mm Cypher™ stent (Cordis Corporation, Miami, Florida), with 0% residual stenosis and resolution of the dynamic narrowing (Figure 2). She subsequently had an uneventful recovery and remained free of chest pain and shortness of breath. Case 2. A 64-year-old male presented with chest pain at rest. He had coronary artery bypass graft surgery in 1994 and percutaneous intervention to the vein graft to obtuse marginal six months prior to presentation. He also has history of atrial fibrillation, moderate mitral regurgitation and mitral stenosis with a valve area of 1.7, ischemic cardiomyopathy with a left ventricular ejection fraction of 45%, sick sinus syndrome with a dual chamber pacemaker, hyperlipidemia and right carotid endarterectomy in 1995. Two-dimensional echocardiography revealed an enlarged left atrium with left ventricular dilation and mildly depressed left ventricular function. Coronary angiography showed mid-LAD and proximal right coronary artery occlusion and a 40% left circumflex lesion. The vein graft to the PDA was occluded, but the vein graft to the obtuse marginal had a widely patent stent. Angiography of the left internal mammary artery (LIMA) graft to the LAD showed dynamic, systolic compression of the distal segment of the graft with each contraction of the heart (Figure 3). This lesion was treated with a 3.0 x 28 mm Cypher stent, with no complications and no residual lesion (Figure 4). Discussion Systolic compression of coronary vessels other than due to myocardial bridging has been described in the setting of a left ventricular aneurysm.⁷ Two cases of LIMA compression by mediastinal drain in the immediate postoperative period, and one case of LIMA compression by a large LAD pseudoaneurysm have been reported in the literature.^8–10 Dynamic compression of bypass grafts has not been described. We hypothesized that the systolic compression of the vein graft resulted from extrinsic compression of the vein graft by the dilated right atrium during movement and rotation of the heart accentuated by the presence of severe tricuspid regurgitation during systole, and also possibly from enlargement of the other cardiac chambers. As to the LIMA graft, we hypothesized that the LIMA graft was tethered to the sternum due to fibrosis and was compressed by the enlarged left atrium during the systolic movement and rotation of the heart. The vein graft to the right coronary artery usually arises from the aorta anteriorly, courses on top of the right atrium proximally, and then curves down and posterior to the right ventricle before reaching its distal target. The LIMA to the LAD artery usually arises from the left subclavian artery and courses down towards the LAD, passing anterior to the LA before it is anastomosed to the LAD. Other causes of extrinsic compressions, such as mediastinal masses or aneurysms, could not be excluded since we did not perform computed tomography or magnetic resonance imaging of the chest. However, chest X-rays done in both cases did not grossly show any masses, and two-dimensional echocardiography did not show any ventricular aneurysms or pseudoaneurysms. The fact that the grafts were compressed during systole points to a dynamic process of compression which can most plausibly be explained by the systolic motion of the heart, or perhaps aneurysmal arterial structures. The systolic compression of the bypass grafts in our patients was clinically significant in view of resultant angina symptoms in both cases, and ischemia in the right coronary artery distribution and interval decrease in the right ventricular ejection fraction in the case of the saphenous vein graft. Serious manifestations such as myocardial ischemia, infarction and sudden death have been reported in relation to myocardial bridging of native coronary arteries.^1,11–15 Surgical interventions and percutaneous transluminal angioplasty, with or without stent placement, have been used therapeutically for myocardial bridging.^16–19 Haager and Schwarz followed patients with myocardial bridges over LAD arteries for two years and found that all had good clinical outcomes, with a 36% restenosis rate.¹⁸ Conclusion We call attention to the systolic compression of bypass grafts as a potential cause of chest pain and myocardial ischemia, and the utility of percutaneous transluminal angioplasty with stent placement. We suggest this may be an under-recognized and treatable cause of angina and myocardial ischemia in patients who have undergone coronary artery bypass grafting.

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