RESOLVING HEMI’S, INDUCING STEMI’S G. Devany MD, R. Eschete II MS3, J. Godke MD Department of Medicine, Baton Rouge General Medical Center, Baton Rouge, LA INTRODUCTION: Post thrombolysis acute myocardial infarction (AMI) is a rare phenomenon but requires early recognition. Concern for an AMI should not delay or alter the management of acute ischemic stroke. CASE: A 78-year-old man with hypertension, hyperlipidemia, aortic valve replacement, right-sided carotid endarterectomy, and single vessel coronary artery bypass presented with a two-hour history of sudden onset left-sided weakness and left- sided facial droop. Physical exam revealed normal vital signs, a left-sided facial droop, left arm strength of 1/5 and left leg strength of 0/5. The patient’s National Institute of Health Stroke Scale score was 10. The initial Computed Tomography (CT) of the head was normal. The consulting neurologist diagnosed a small vessel distribution infarction causing pure motor deficits. Three hours post-onset, thrombolysis with tissue plasminogen activator (tPA) was initiated. Then the patient complained of chest tightness with substernal pain and he was noted to be diaphoretic and in obvious distress. An EKG showed ST elevations in leads II, III, aVF with ST depressions in leads I and aVL suggestive of posterior/inferior myocardial infarction. The consulting cardiologist confirmed the STEMI diagnosis and advised against any further anticoagulation or percutaneous coronary intervention due to tPA contraindications. The STEMI was medically treated. On the following day, a head-CT revealed a subacute infarction of the right thalamus and posterior limb of the internal capsule. DISCUSSION: Lysis of a thrombus overlying cholesterol containing atherosclerotic plaque may destabilize the plaque. This has been postulated to cause distal vessel cholesterol crystal embolization, not dissolved by thrombolytics. Patients with cerebrovascular and coronary artery disease might experience unintended plaque destabilization in the coronary vascular system following thrombolysis. Another explanation is that thrombolytics cause a disruption of an intracardiac thrombus and subsequent embolization to the distal coronary arteries. One report identified intracardiac thrombus in 26%of patients experiencing transient ischemic attacks by transesophageal echocardiography (TEE). Another study found a cardiac thrombus present in 2.7% of patients who had received tPA for an acute ischemic stroke. In both reports, the presence of intracardiac thrombus was associated with poor prognosis.
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