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A 62-year-old man presented with acute chest pain that started with mild physical activity and lasted for more than 45 minutes after rest. His past medical history includes advanced coronary artery disease status post coronary artery bypass graft (CABG) surgery 6 years earlier. The grafts included an internal mammary graft to his anterior descending artery and saphenous vein grafts (SVGs) to the marginal branch of the circumflex artery and the posterior descending branch of the right coronary artery. His cardiovascular risk factors included hyperlipidemia, diabetes mellitus, and continued heavy smoking.
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His initial blood work and electrocardiogram revealed elevated cardiac enzymes with ST-segment depression in inferior and lateral leads (II, III, V5, and V6). He was stabilized medically using antiplatelet and anticoagulant therapy before undergoing coronary angiography. Selective bypass graft angiography revealed a subtotal thrombotic occlusion in the body of SVG to the marginal branch of the circumflex artery (Figure 13-1). The lesion was considered the culprit lesion underlying his acute coronary syndrome and was treated percutaneously using a drug-eluting stent. The procedure was uncomplicated, and the patient was discharged the following day with aggressive secondary prevention measures and on dual antiplatelet therapy.
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CLINICAL FEATURES OF SVG FAILURE: HISTORY AND PHYSICAL
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Acute coronary syndrome (ACS) secondary to SVG failure is similar in presentation to native coronary artery failure. Patients most commonly present with angina or pressure-type retrosternal chest pain that typically occurs with exertion but can also occur at rest. Chest pain can radiate to the arms, neck, or jaw with additional symptoms such as diaphoresis, dyspnea, nausea, abdominal pain, or syncope. Typically, although not necessarily, patients with a history of CABG surgery are older with multiple risk factors (eg, diabetes, hypertension, dyslipidemia, and tobacco use) that have resulted in the initial multivessel disease. The physical examination for ACS patients can be unremarkable, but manifestations of cardiogenic shock, acute heart failure (eg, tachycardia, hypotension, and/or elevated venous pressure), or new murmurs carry important diagnostic and prognostic implications.
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Patients with SVG disease can also present with stable ischemic syndromes. SVG lesions can develop insidiously and lead to severe stenosis and even total occlusion over time. Collateral filling from ipsilateral or contralateral vessels can preserve myocardial viability, but it is often inadequate to prevent exertional angina. The clinical significance or degree of angina is determined by the patient’s level of activity, amount of myocardium subtended by the diseased graft, and the efficacy of the collateral circulation providing for that myocardial territory.
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