Throughout her stay, the patient was continuously monitored, but no evidence of arrhythmia or atrial fibrillation was found. Upon discharge, the neurologist recommended the patient receive clopidogrel and aspirin therapy for 3 months with subsequent aspirin monotherapy afterward. The patient was discharged after 10 days in the hospital.
Discussion
Although she had an MI, the patient presented here did not experience any chest pain. Her chief complaint in the ED was paresthesias related to her concomitant stroke, and only on further probing did she describe the additional symptoms of fatigability and vomiting.
Since heart disease and stroke share common risk factors and pathophysiology, acute cerebral ischemic events may happen concurrently with MIs. In a review of studies that included approximately 2,900 patients who had an acute stroke, Kerr et al1 found that 20% had elevated troponin levels within 7 days of the stroke. In 2013, the American Heart Association and American Stroke Association published guidelines advising that all patients who present with acute cerebral ischemia have an emergent ECG and baseline troponin level.2 This was in response to evidence that even low positive troponin levels have been associated with an increased risk of mortality.3 Positive troponin levels are especially important because fatal and nonfatal stroke post-MI events have been found to be increasing in frequency for women, even though there has been a significant overall reduction in post-MI mortality.4 Patients who have an ischemic stroke concurrently with an acute MI or soon after have an overall poorer clinical prognosis.5
For emergency physicians (EPs), this is a “chicken or the egg” scenario. It is difficult to determine which came first: the MI or the cerebral ischemia. Similar risk factors can result in an acute embolic event from revascularization, atrial fibrillation without proper anticoagulation, or a poorly functioning left ventricle.6 It is important to remember that regardless of the order of occurrence, the incidence of ischemic stroke is markedly increased in conjunction with an acute MI.7 Several theories have been advanced regarding the relationship between ischemic stroke and acute MI. One theory proposes that elevated troponin levels could be related to a large catecholamine release after a cerebral ischemic stroke, resulting in subsequent myocardial injury or cardiomyopathy.7 However, this theory remains controversial.
Management
The major consideration for the EP is whether or not to give thrombolytics to a patient who presents with concomitant acute MI and ischemic stroke. An acute MI within the 3 months preceding an acute stroke is considered a relative contraindication for intravenous tissue plasminogen activator (tPA).8 It has also been found, albeit rarely, that there is an increased risk of cardiac rupture or tamponade due to the breakdown of the fibrin clot within the necrotic cardiac tissue.8
How should patients with stroke complicated by acute cardiac compromise be managed in the ED? One acute vascular event cannot be ignored while addressing the other. There are no evidence-based guidelines for the management of patients who present with this picture.8 In addition, no published clinical studies have focused on the decision-making process for these patients.8
Immediate percutaneous coronary intervention for the MI performed on such patients would prevent the use of tPA for the acute stroke. Though any anticoagulation increases the risk for postischemic cerebral hemorrhage, heparin is necessary to prevent the formation of a left ventricle thrombus.7 Alternately, mechanical thrombectomy and cardiac catheterization may be combined as emergent treatments for these patients, but performing these two procedures simultaneously is not widely available.
For a patient who presents to the ED within both the cardiac and stroke treatment windows, tPA might be a viable option, and the only one readily valuable.8 However, the EP must be mindful of the varying dosages of tPA and means of administration for different thrombosis sites. Also, care must be taken when treating a patient with dual or triple antiplatelet therapy because of the increased risk of hemorrhage.9 Currently, no safe standardized regimens have been established, and further trials need to be performed.10
If the patient in this case report had presented at our ED with only signs and symptoms of an MI, typically she would have been treated with heparin, aspirin, and an urgent cardiac catheterization. If she had presented with only signs and symptoms of a stroke, she would have been treated with full-dose aspirin and worked up from a neurological perspective. Because she had signs and symptoms of both, she presented a dilemma. She was initially treated with heparin to prevent a thrombus formation, but then later changed to only clopidogrel and aspirin to prevent further episodes of coffee ground emesis or worsening hemorrhagic conversion.