Successful Treatment with Primary Angioplasty of Acute Myocardial Infarction Occurring During Cerebellar Hemorrhage

Acute myocardial infarction may occur alone or, less frequently, associated with other medical conditions, such as intestinal hemorrhage, trauma, vascular operation and more rarely cerebral hemorrhage.1 We describe a case of a patient in which a myocardial infarction occurred soon after the appearance of a cerebellar hemorrhage related to a hypertensive crisis. Case Report. A 59-year-old Caucasian male presented to the emergency department stuporous with severe hypertension (290/170 mmHg) and bouts of vomiting. Relatives reported that he suddenly became agitated because of occipital headache and dizziness and then slipped into a stuporous state. The patient reported a history of smoking, dyslipidemia, poorly controlled hypertension and obesity (weight, 116 kilograms). A presumptive diagnosis of subtentorial acute lesion was made on the basis of the aforementioned symptoms and the presence of cerebellar signs of ocular bobbing and anisocoria. The CT scan showed acute hydrocephalus secondary to a cerebellar hematoma and the patient was brought to the operating room. The dura mater was opened in a “Y” fashion through a large medial occipital craniectomy. The hematoma was removed and a ventriculostomy was performed via a right paravermian cerebellar approach. An ST segment elevation was observed during the operation; soon after, the patient went into ventricular fibrillation. After D.C. shock, he went into marked bradycardia and hypotension, and was promptly reverted with the implementation of cerebral ventricular drainage, closed chest massage and atropine. The electrocardiogram at that point showed an acute evolving anterolateral myocardial infarction. He was treated with intravenous lignocaine, trinitrine, a bolus of 2,500 IU of heparin and 250 mg of aspirin. At the end of the operation, as the signs of the infarction were still present and the hemodynamic conditions were deteriorating, the patient was brought to the catheterization laboratory. Coronary angiography via the left femoral artery showed a total thrombotic occlusion of the mid-left anterior descending (LAD) coronary artery (Figure 1) and a moderate lesion of the right coronary artery. During the diagnostic procedure, the patient went into atrial fibrillation. A bolus of 0.20 mg/kilogram of body weight of abciximab (ReoPro, Eli Lilly and Company, Indianapolis, Indiana) and 3,000 IU of heparin were given intravenously. The ostium of the main stem was cannulated with an EBU 4, 6 French guiding catheter (Medtronic, Minneapolis, Minnesota), a Wizdom 0.014´´ wire (Cordis Corporation, Miami, Florida) was passed through the obstruction and a 3.0 x 20 mm World Pass balloon (Cordis Corporation) was inflated twice in order to open the entire lesion, at nominal pressure for 30 seconds. Two Carbostents (3.0 x 15 mm and 3.5 x 15 mm) (Sorin, Saluggia, Italy) were then implanted in a retrograde sequence at 14 bar with some overlapping (Figure 2). TIMI 3 flow was soon reestablished with the help of a few intracoronary boluses of 20 µg adenosine. The coronary artery was opened 90 minutes after the occurrence of the infarction. The ST elevation returned almost to baseline in less than 1 hour and the sinus rhythm was restored a few hours after an amiodarone infusion. The CK peak was 816 IU at 8 hours. The patient was maintained on an intravenous abciximab infusion of 0.125 µg/kg for the first day and then 0.0625 µg/kg/m a day for the following 3 days. He was then started on intravenous aspirin 250 mg per day and from the sixth post-operative day on low doses of low molecular weight heparin. When extubated on the 9th postoperative day, he was shifted to oral ticlopidine 250 mg twice daily for 3 weeks and then to daily aspirin 160 mg indefinitely. No hemorrhagic complications occurred during these treatments and the patient made an uneventful cardiac recovery. He was then submitted to a ventricular cisternostomy on the 23rd day (ticlopidine was stopped 4 days before the operation and intravenous aspirin was given at a dose of 250 mg until extubation). The patient was discharged on the 32nd day with electrocardiographic signs of a minimal anteroseptal infarction, while the 2-dimensional echocardiogram showed a localized anteroapical hypo-akinesia. At 6-month follow-up, he was submitted to a control coronary angiography which showed a good result of the LAD stenting with a mild restenosis at the beginning of the proximal stent (Figure 3). A 3.5 x 15 mm Carbostent was directly implanted in the lesion of the distal right coronary artery. At 12-month follow-up, the patient was asymptomatic for dyspnea and angina with mild impairment of balance and slight dysarthria. Discussion. A retrospective study reported myocardial infarction to occur in 0.4% of cases of cerebral and in 5% of cases of subarachnoid hemorrhage.1 The occurrence in cerebellar hemorrhage is unknown. The concomitance of these two conditions is frequently overlooked if an electrocardiogram and serial enzyme studies are not performed or a serious arrhythmia occurs.2 In cerebellar hemorrhage, the cardiac anomalies observed are predominantly due to vagal hypertonus, favored by the elevated intracranial pressure. The puzzling cardiac anomalies — the so called “neurogenic stunned myocardium syndrome” described in cerebral and, mostly, subarachnoid hemorrhages3,4 — are usually absent and therefore our clinical diagnosis was straightforward. In our patient, the hypertensive crisis was probably the initial event favoring the cerebellar hemorrhage and both events triggered a “true” transmural myocardial infarction because the patient likely had important preexisting coronary artery disease. Some have advocated spasm as a possible cause of myocardial infarction in the setting of cerebral hemorrhage.5 The peculiarity of this case is the contemporary occurrence of a highly thrombotic event such as an acute myocardial infarction and a serious bleeding condition such as a brain hemorrhage which poses a stressful therapeutic challenge. Thus, some patients have been treated conservatively,6 while others have been sent to surgery,7 even though a mechanical revascularization has been advocated as the most appropriate treatment.8 This option seemed to be the best for our patient, who had a rapidly deteriorating hemodynamic status. To the best of our knowledge, this is the first reported case of such conditions treated with primary angioplasty. We chose to use coated stents because of the low thrombogenicity documented both experimentally9 and in clinical practice.10,11 The Carbostent is a multi-cell, slotted-tube stent with turbostratic carbon coating.9 The choice of the safest antithrombotic regimen proved to be the most challenging task in this situation. There is hemorrhagic risk with the association between abciximab and heparin.12 Considering the pathophysiology of thrombus formation during AMI and stent implantation, we thought that the use of a IIb/IIIa receptor inhibitor was the safest way to prevent stent thrombosis and at the same time minimize the risk of brain hemorrhage. Therefore, unfractionated heparin at a low dose was given only during the procedure. Heparin alone could have been considered an alternative, but the risk of recurrent myocardial infarction and urgent repeat percutaneous transluminal coronary angioplasty has been shown to be higher with this treatment than with abciximab.13,14 Moreover, the surgical drainage lowered the risk of reaccumulation of blood in the cerebellum. The prolonged infusion of a low dose of abciximab for a few days, chosen empirically, along with the use of coated stents proved to be safe and successful in preventing both acute and subacute stent thrombosis (which we feared most) in a patient in whom the oral absorption of drugs was uneven. It is likely that the same result could have been obtained with stainless-steel stents and the concomitant use of abciximab, given their widespread use in acute myocardial infarction cases in everyday practice.13,14 Primary angioplasty with the judicious use of a platelet glycoprotein IIb/IIIa receptor inhibitor should be considered one of the relatively safe options to treat acute extensive myocardial infarction associated with surgically treated cerebral hemorrhage. Acknowledgment. We wish to acknowledge Dr. Ted Feldman of the Chicago University Hospitals for his thoughtful revision of the paper.

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