Case presentation

An active 73-year-old woman, who enjoyed good health with only a history of hypertension, hyperlipidemia, and osteoporosis, presented to the hospital emergency department on a Saturday night with a prolonged episode of rest angina. She became pain-free after administration of 325 mg of aspirin, subcutaneous enoxaparin, and sublingual nitrates. The initially-normal electrocardiogram evolved T-wave inversions on subsequent studies and troponin peaked at 0.52 ng/mL. She was diagnosed with a non-ST segment elevation myocardial infarction and remained pain-free on enoxaparin (1 mg/kg administered subcutaneously twice a day) and 325 mg of aspirin administered each day over the weekend with catheterization planned for Monday morning.

Catheterization

Left venticulography revealed mild anterior hypokinesis with preserved ejection fraction. Coronary angiography found no evidence of obstructive disease in the right or left circumflex coronary arteries. Severe atherosclerotic narrowing of the proximal segment of the left anterior descending artery was likely the explanation for her acute coronary syndrome (Figures 30-1, 30-2 and Videos 30-1, 30-2). Atherosclerosis also involved the first diagonal branch and the midsegment of the left anterior descending artery, but these lesions were felt to be nonobstructive. The lesion in the proximal segment of the left anterior descending artery was treated with balloon angioplasty followed by placement of a everolimus-eluting stent (2.5 mm diameter by 15 mm long) with an excellent angiographic result (Figure 30-3 and Video 30-3), and intravascular ultrasound confirmed stent apposition. The dose of enoxaparin planned for the morning of the procedure was held (last dose greater than 12 hours from catheterization) and procedural anticoagulation consisted of bivalirudin (33 mg intravenous bolus followed by an intravenous infusion of 1.7 mg/kg/hr) and 600 mg of clopidogrel administered orally at the time of the intervention. Hemostasis was achieved with a femoral artery closure device and she returned to a telemetry unit feeling well with no complaints.

FIGURE 30-1 Coronary angiography performed in a right anterior oblique projection with cranial angulation showing a severe stenosis in the proximal left anterior descending artery (arrow).

FIGURE 30-2 This is another view of the left anterior descending artery in the right anterior oblique view, showing the lesion in the proximal left anterior descending artery.

FIGURE 30-3 Angiogram obtained after placement of a stent in the proximal left anterior descending artery.

Postprocedural course

The patient remained symptom-free overnight, with discharge planned for the next day. However, the morning after her procedure, she reported the acute onset of headache, vertigo, and unsteady gait. An emergency noncontrast head CT scan was performed and showed a right cerebellar hemorrhage. She was transferred to the neuro intensive care unit for further evaluation and management. A brain magnetic resonance imaging study revealed an acute intraparenchymal hemorrhage centered in the right cerebellar hemisphere with mass effect upon the fourth ventricle and no evidence of hydrocephalus. In addition, there was no evidence of tumor or vascular malformation. Scattered, discrete small supratentorial white matter signal abnormalities were noted and were felt to represent chronic small vessel ischemic changes.

After consultation with cardiology, the aspirin and clopidogrel were held for 5 days, and the patient was monitored continuously in the intensive care unit. Fortunately, she remained neurologically stable with improvement in her vertigo and headache and no change in the size of the intracranial bleed on subsequent imaging. Blood pressure remained well-controlled on lisinopril and aspirin, and clopidogrel resumed on the fifth day. She remained stable for 3 additional days and was discharged with only mild gait instability.

Discussion

Cerebrovascular accidents are a rare but dreaded complication of percutaneous cardiovascular procedures, occurring in 0.2% to 0.4% of procedures and associated with a high mortality.^1,2 Most of these events are caused by atheroembolism or clot. Despite the liberal use of procedural anticoagulation, intracranial hemorrhage is, fortunately, very rare. In large series of patients treated with bivalirudin, the risk of intracranial hemorrhage was exceedingly low (one event out of 2993 patients or 0.03%)³; the rate of intracranial hemorrhage when the more powerful glycoprotein IIb/IIIa inhibitors are used is similarly very small at only 0.07%.³ Following intervention, anticoagulation is maintained using dual antiplatelet therapy with the risk of hemorrhagic stroke from the combination of aspirin and clopidogrel of only 0.1% with no difference from aspirin alone.⁴

Management of an intracranial bleed occurring soon after deployment of a coronary stent is a genuine medical catch-22. The same is true for any other major life-threatening bleed such as a serious gastrointestinal or genitourinary hemorrhage. On one hand, the anticoagulants must be stopped to staunch the life-threatening bleed; on the other hand, cessation of anticoagulants might cause acute stent thrombosis and a potentially fatal acute myocardial infarction. The decisions to stop, continue, or hold and reinstitute anticoagulants in the setting of a freshly-deployed stent should not be made in a cavalier fashion. Extensive discussions regarding the risks and benefits of each strategy should occur with the consultant expert as well as the patient and family, with a coherent plan in place to anticipate and treat any potential adverse outcome. In the present case, the serious nature of intracranial hemorrhage led to the wise decision to hold anticoagulation, thus preventing further bleeding and, fortunately, resulting in a favorable outcome.