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Management of a Patient with ST-Segment Elevation Myocardial Infarction Immediately After Successful Coiling of a Basilar Tip An
March 2004
Case Report. We present the case of a 52-year-old male with a history of hypertension who presented to the Emergency Room (ER) of a community hospital with a 2-month history of progressively worsening exertional chest pressure. While in the ER, the patient had sudden onset of severe headache and lost consciousness. A stat CT scan of the head was performed, which revealed a subarachnoid hemorrhage with evidence of hydrocephalus. He was emergently transferred to a tertiary medical care center, where he was found to be unresponsive but with spontaneous movement of all extremities. Urgent cerebral angiography was performed, which revealed a basilar tip aneurysm. He underwent successful coiling of a basilar tip aneurysm and a placement of a right frontal external ventricular drain. Approximately 6 hours after the procedure, while in the neurosurgery intensive care unit, the patient was found to have new 2 mm ST-segment elevation by 12-lead electrocardiography in the inferior leads with an elevated troponin. He was taken emergently to the cardiac catheterization laboratory. The patient was then sedated and intubated; his blood pressure was 120/74 mmHg, his heart rate was 77 beats/minute, and his respiratory rate was 20 breaths/minute. He had a regular rate and rhythm, and a normal S1 and S2. There were no S3 or S4 or murmurs appreciated. He had clear lung fields without rales or wheezes. The distal pulses were full and equal, and there was no peripheral edema. His laboratory examination revealed a BUN of 12 mg/dL and creatinine of 0.9 mg/dL with a normal hemoglobin and platelet count.
Coronary angiography demonstrated a co-dominant circulation with the following findings: The left main was normal. The proximal left anterior descending artery (LAD) was completely occluded and the distal LAD was a small vessel that was supplied by collaterals. The proximal circumflex artery had a discrete 95% lesion (Figure 1). The right coronary artery (RCA) had a 100% lesion in distal portion (Figure 2). Left ventriculography revealed normal left ventricular function with an estimated ejection fraction of 53% with mild anterolateral hypokinesis, and severe posterobasal and diaphragmatic hypokinesis.
Patient management. After consultation with the neurosurgeon, the decision was made to proceed with percutaneous coronary intervention. Due to the recent placement of a right frontal external ventricular drain, and the coiling of the basilar tip aneurysm for the subarachnoid hemorrhage, the optimal anticoagulation strategy was discussed at length. Use of a glycoprotein IIb/IIIa inhibitor was deemed to be relatively contraindicated due to the risk for intracerebral bleeding, and the consensus was to utilize bivalirudin (60.7 mg bolus followed by 1.75 mg/kg/hour maintenance infusion) for the coronary intervention. The patient was pre-treated with a loading dose of aspirin and clopidogrel. A 6 French (Fr) EBU Launcher (Medtronic Inc., Minneapolis, Minnesota) was used to cannulate the left coronary artery and a short BMW wire (Guidant Corporation, Temecula, California) was used to cross the lesion in the circumflex artery. The patient underwent direct stenting of the lesion in the proximal circumflex artery using a Penta 4.0 x 13 mm device (Guidant Corporation). After stent placement, there was note of a linear dissection at the distal edge of the stent, and a Penta 3.0 x 8 device (Guidant Corporation) was placed across the dissection overlapping the distal edge of the previously placed stent. Final angiography showed no residual stenosis with TIMI III flow (Figure 3). A 6 Fr JR5 Launcher (Medtronic Inc.) was used to cannulate the RCA and a short BMW wire (Guidant Corporation) was used to cross the total occlusion. Balloon angioplasty was performed across the lesion and along the distal RCA and right posterior descending artery using a Maverick OTW 2.5 x 20 mm device (Boston Scientific). A Pixel 2.5 x 18 mm stent (Guidant Corporation) was placed in the distal RCA and a Pixel 2.5 x 13 mm stent (Guidant Corporation) was placed across the site of the total occlusion the mid RCA. Final angiography of the RCA showed no residual stenosis with TIMI III flow (Figure 4). The patient transferred to the neurointensive care unit in stable condition. He subsequently regained full neurological function and underwent successful physical and occupational therapy. He was discharged on aspirin, clopidogrel, extended release lopressor, and altace.
How Would you Manage this Case?
Clifford J. Berger, MD and Alice K. Jacobs, MD
Boston University Medical Center
Boston, Massachusetts
The authors present a 52-year-old hypertensive male with an acute inferior myocardial infarction (MI) in the setting of an acute subarachnoid hemorrhage complicated by hydrocephalus. On arrival at the tertiary care center, the patient was unresponsive and underwent coiling of a basilar tip aneurysm and placement of a ventricular drain. Six hours later, he was found to have new inferior ST-segment elevation on electrocardiogram.
This is a very challenging and difficult treatment dilemma that we encounter occasionally, more commonly in the post-operative setting when a patient who has just had a surgical procedure is found to be having an acute MI. In these cases, the risks of intervening must be carefully balanced against the expected benefits. The authors chose to intervene on two of three diseased coronary vessels and obtained an excellent angiographic and procedural result.
We would have tried to avoid taking this patient with an acute and life-threatening central nervous system bleed six hours earlier to the cardiac catheterization laboratory. He was hemodynamically stable with an inferior myocardial infarction that is associated with an acceptably low mortality, particularly in a young patient. The risks of any anticoagulation, including heparin or bivalirudin, or antiplatelet agents such as aspirin or clopidogrel, are clearly not quantifiable from available data in the literature. One can logically presume that this risk is not trivial and that the consequences could be permanent brain damage or death. We would have tried to initially manage this patient conservatively to avoid the potential risks associated with anticoagulation that would have been required to perform percutaneous intervention.
However, once the decision was made to perform emergency percutaneous coronary intervention, a few points are worthy of comment. The choice of bivalirudin instead of unfractionated heparin is a reasonable one. In the Bivalirudin Angioplasty Trial and in the subgroup of the REPLACE-1 trial that did not receive glycoprotein IIb/IIIa inhibitors, bivalirudin was associated with lower rates of major bleeding compared with unfractionated heparin. However, patients with acute ST-segment elevation myocardial infarction were excluded from these trials.
In this setting, we would have tried to avoid placement of a coronary stent if possible. The stent obligates this patient to both aspirin and clopidogrel in the acute setting. An adequate balloon angioplasty result would have accomplished the acute goal of restoring flow to salvage myocardium. The higher rate of restenosis associated with balloon angioplasty in comparison to a stent would have been less of an acute concern than the increased risk of bleeding associated with the addition of clopidogrel. Furthermore, a Hepacoat stent could have been considered to treat a suboptimal balloon angioplasty result since there are some data to suggest that the subacute stent thrombosis rate is acceptable with this stent in the absence of clopidogrel.
Finally, it is unclear why the lesion in the non-infarct related artery was treated. Percutaneous coronary intervention of a non “culprit” lesion during primary angioplasty is considered a Class III indication in the ACC/AHA Guidelines for Percutaneous Coronary Intervention. It seems as though “less” would be better in this situation, and it would be helpful to understand the author’s procedural strategy.
Luis M. de la Fuente, MD
Instituto Argentina de Diagnòstico y Tratamiento
Buenos Aires, Argentina
First of all, we would like to congratulate the authors of this work for the therapeutic success achieved, bearing in mind the complex and difficult situation with which this patient arrived to the ER. In response to the clinical management of the patient presented in this paper, although we share the authors’ therapeutic approach, we would like to point out a few things that differ in the procedure we would had followed, given that case.
The patient presented to the ER with a two-month history of progressively worsening exertional chest pressure; the patient then suddenly lost consciousness. Considering this background, we might have chosen to study the coronary circulation, in the same procedure, immediately after the neuro-intervention had finalized. The angiogram would allow us to have a clear picture of the coronary anatomy and left ventricle, thereby letting us anticipate the treatment of his coronary artery disease, if convenient.
As far as the anticoagulation strategy is concerned in patients with a high bleeding risk, bivalirudin has been shown to be superior to and safer than heparin; therefore, it was the logical anticoagulant of choice in this patient. However, in centers where the bivalirudin is not available, heparin should be used.
The coronary angiogram performed approximately 6 hours later demonstrated complete occlusion of the proximal LAD with distal collateral fillings. The proximal Cx had a 95% obstruction, and the RCA was totally occluded in the distal portion. The left ventriculogram showed a severe posterobasal and diaphragmatic hypokinesis and mild antero-lateral hypokinesis. It would have been very useful to analyze the origin of the collateral circulation to the LAD. Regarding the angioplasty procedure itself, it is no question that this was a high-risk patient.
The Cx artery has a proximal subtotal obstruction, and the LAD and the RCA are totally occluded. The first question would be: which one is the culprit artery? I would believe that it is the RCA. Our approach would be to first treat the total occlusion of the RCA to improve the circulation to the ischemic inferior wall and the posterior septum of the LV.
If we are successful with the RCA, we may improve also the collateral circulation to the LA, and reduce somewhat the risk of any complication when we treat the Cx artery.
Our next step would be dilatation and stenting of the Cx artery lesion. We would first predilate the lesion with a balloon in order to minimize any difficulty in delivering the stent across the lesion. The predilatation of the lesion will not only facilitate the delivery of the stent, but also give us some information about the characteristic of the atherosclerotic plaque and the absence or presence of an intimal dissection. This information will allow us to choose the diameter and length of the stent. We would definitely use a drug-eluting stent, if available. This very interesting and complicated case demonstrates how fast and well the percutaneous endovascular therapeutic is evolving.
Nicolas W. Shammas, MS, MD, FACC
Davenport, Iowa
Acute myocardial infarction (AMI) following a hemorrhagic stroke or a neurosurgical procedure poses an exceptionally difficult dilemma to the interventional cardiologist. In general, these patients are treated conservatively to avoid the use of anticoagulants during the angioplasty procedure. When a decision is made to proceed with primary angioplasty in these patients, the risks and benefits should be weighed carefully. A patient with a large infarct and unstable hemodynamics warrants emergent intervention. In this case report, the patient had an inferior AMI with no indication of decompensation or heart failure. Although mortality and morbidity are increased from the AMI, the risk of death from an intracerebral bleed secondary to anticoagulation remains excessively high. A case for conservative management could have been made in this patient.
In the event that primary coronary intervention becomes necessary due to a large infarct and an unstable patient, a short-acting anticoagulant with predictable pharmacokinetics and less demonstrable major bleeding complications might be the “ideal” agent. Bivalirudin, a direct thrombin inhibitor, has been shown to be more effective and with less major bleeding complications than unfractionated heparin during percutaneous coronary interventions.1–3 Furthermore, its anticoagulant effect is predictable and has a short half-life in patients with normal renal function. The choice of bivalirudin over heparin following surgical intervention is theoretically advantageous when there is a need for systemic anticoagulation. One disadvantage of bivalirudin, however, would be the inability to reverse its anticoagulation process if this becomes necessary. This disadvantage, however, is at least partially offset by the very short half-life of the drug. Patients with recent surgical procedures and strokes have been traditionally excluded from interventional trials using bivalirudin and, therefore, safety data of bivalirudin in these patients is not available. In this case report, the interventional outcome was successful and bivalirudin proved to be a successful choice. Further data, however, is needed to clarify the safety of bivalirudin immediately postoperatively and particularly in the neurosurgical patient.
Finally, treatment of the culprit vessel alone (right coronary artery) and staging treatment of the left circumflex artery would have been a likely preferred approach in the management of this patient. The treatment of a non-culprit vessel in the setting of an AMI has been traditionally discouraged. Cessation of all antiplatelets and anticoagulants would have become necessary if intracerebral bleeding occurred during or following the intervention. The presence of several stented vessels would have increased the risk of acute thrombosis and further complicated the management of this patient. Avoiding stenting or using a heparin-bonded stent (Hepacoat) instead of a bare metal stent for the occluded right coronary artery would have been my preferred approach during this intervention. This would have reduced the need for clopidogrel-aspirin combination that caries a higher risk of bleeding than aspirin alone4 and allowed safely the sole use of aspirin post procedure.
1. Bittl JA, Chaitman BR, Feit F, et al. Bivalirudin versus heparin during coronary angioplasty for unstable or postinfarction angina: Final report reanalysis of the Bivalirudin Angioplasty Study. Am Heart J 2001;142:952–959.
2. Lincoff AM, Bittl JA, Harrington RA, et al. Bivalirudin and provisional glycoprotein IIb/IIIa blockade compared with heparin and planned glycoprotein IIb/IIIa during percutaneous coronary intervention; the REPLACE-2 randomized trial. JAMA 2003;289:853–863.
3. Direct Thrombin Inhibitor Trialists’ Collaborative Group. Direct thrombin inhibitors in acute coronary syndromes: Principal results of a meta-analysis based on individual patients’ data. Lancet 2002;359:294–302.
4. The CURE Trial Investigators. Effects of clopidogrel in addition to aspirin in patients with acute coronary syndromes without ST-segment elevation. N Engl J Med 2001;345:494–502.