Patients with recurrent ischemic-type chest discom fort after initial reperfusion therapy for STEM

should undergo escalation of medical therapy with nitrates and beta-blockers to decrease myocardial

Figure 34.Algorithm for management of recurrent ischemia/infarction after ST-elevation myocardial infarction (STEMI). IABP = intra- aortic balloon pump; ECG = electrocardiogram; PCI = percutaneous coronary intervention; CABG = coronary artery bypass graft sur- gery. *Ideally within 60 minutes from the onset of recurrent discomfort. Modified with permission from Braunwald et al. Heart Disease: A Textbook of Cardiovascular Medicine. 6th ed. Philadelphia, PA: WB Saunders; 2001:1196 (718).

by guest on April 2, 2018

http://circ.ahajournals.org/

least 30 minutes, usually but not always accompanied by recurrent ST-segment elevation of at least 0.1 mV in at least 2 contiguous ECG leads and re-elevation of CK-MB to more than the upper limit of normal or increased by at least 50% over the previous value (37). Pathological findings of rein- farction show areas of healing myocardium along with the more recent necrosis, usually in the same vascular risk region of myocardial tissue perfused by the original infarct-related artery. Death, severe CHF, and arrhythmias are early compli- cations of reinfarction, and there is an increased incidence of cardiogenic shock or cardiac arrest (25,43,1011). An algo- rithm for diagnosing reinfarction both early and late after fib- rinolytic therapy is shown in Figure 12. In patients with recurrent MI after fibrinolysis, the mortality rate is increased up to 2 years; however, most of the deaths occur early (in the hospital), with little additional risk of death between the index hospitalization and 2 years later (512).

Patients with recurrent ischemic-type chest discomfort should undergo escalation of medical therapy, including beta-blockers (intravenously and then orally) and nitrates (sublingually and then intravenously); consideration should be given to initiation of intravenous anticoagulation if the Class III

Streptokinase should not be readministered to treat recurrent ischemia/infarction in patients who received a non–fibrin-specific fibrinolytic agent more than 5

days previously to treat the acute STEMI event.(Level

of Evidence: C)

It is important to differentiate pain due to pericarditis from pain due to ischemia. The latter is more likely when the chest pain is similar to the initial ischemic-type chest discomfort, occurring at rest or with limited activity during hospitaliza- tion. This may or may not be associated with re-elevation of the CK-MB, ST-segment depression or elevation, or pseudo- normalization of inverted T waves (T-wave inversion on baseline ECG becoming upright during ischemia) (990).

Reinfarction occurs in 4% to 5% of patients who have received fibrinolytic therapy and aspirin (25,43,851,1009,1010). Reinfarction is associated with re- elevation of biomarkers after the initial peak of the index infarction. Diagnosis of reinfarction within 18 hours after initiation of fibrinolytic therapy should be based on recur- rence of severe ischemic-type chest discomfort that lasts at

Figure 35.Algorithm for postreperfusion ischemic stroke treatment. Daily doses of antithrombotic therapy are shown in the algorithm. ASA = aspirin; INR = international normalized ratio; PTA = percutaneous transluminal angioplasty (carotid); CEA = carotid endarterec- tomy. *An INR of 2.0-3.0 is acceptable with tight control, but the lower end of the range is preferable. The combination of antiplatelet therapy and warfarin may be considered in patients aged less than 75 years, with low bleeding risk, and who can be monitored reli- ably.

by guest on April 2, 2018

http://circ.ahajournals.org/

Class IIb

Carotid angioplasty/stenting, 4 to 6 weeks after ischemic stroke, might be considered in STEMI patients who have an acute ischemic stroke attributa- ble to an internal carotid artery–origin stenosis of at least 50% and who have a high surgical risk of

morbidity/mortality early after STEMI. (Level of

Evidence: C)

Acute stroke complicates 0.75% to 1.2% of MIs and is one of the most dreaded outcomes of STEMI (326,1013,1014). Although survival from STEMI has been increasing, mortal- ity from post-STEMI stroke remains over 40% (1013). Prior stroke, hypertension, old age, decreased ejection fraction or multiple ulcerated plaques, and AF are the major risk factors for embolic stroke after STEMI (326,944,1015-1017). Anterior STEMI is often cited as a risk factor, but other infarct locations appear to have similar risk (1015,1018). AF is by far the most important of these risk factors (1019). In the SAVE trial (1017), decreased ejection fraction (18% increased risk per every 5% decrease in ejection fraction) was independently associated with long-term stroke risk in patients with STEMI. Thrombus formation is promoted by extensive wall-motion abnormality, such as anteroapical aki- nesia or dyskinesia, and Killip class III or IV (1020). Embolic stroke after STEMI originates from LV thrombus or from the left atrium in the setting of AF and occurs even in patients treated with fibrinolysis (1015). It does not appear to be useful to test patients with STEMI, even with mural thrombus formation, for prothrombotic syndromes such as factor V Leiden mutation (1021). Several studies in patients with STEMI suggest that aggressive short- and long-term anticoagulation may reduce but not totally prevent mural thrombus formation (744,1022,1023) and occurrence of stroke (1024-1028). Most ischemic cerebral infarctions after fibrinolytic therapy for STEMI occur more than 48 hours after treatment (218,320,322,586). The highest-risk period is the first 28 days after STEMI (1014), but risk is elevated at least to 1 year. In GUSTO-I (1015), Mahaffey et al. found that the risk of ischemic stroke after coronary fibrinolysis may be predicted (1015). Prospective studies are needed to verify this observation. Compared with ICH, patients with ischemic cerebral infarction present more commonly with focal neurological deficits and less commonly with depressed level of consciousness; headache, vomiting, and coma are uncommon (360).

An algorithm for evaluation and antithrombotic therapy for ischemic stroke is shown in Figure 35. If the STEMI patient has sudden onset of a focal neurological deficit and the ini- tial CT scan is negative for blood or mass effect, then ischemic cerebral dysfunction may be presumed in the absence of a severe metabolic disorder, seizures, autoim- mune disease, or cancer. Neurological consultation is recom- mended to assist with planning the neurovascular evaluation and management issues. The location and nature of the ischemic brain lesion should be defined with repeat CT scan or magnetic resonance imaging scan. Vascular lesions should patient is not already therapeutically anticoagulated.

Secondary causes of recurrent ischemia, such as poorly con- trolled heart failure, anemia, and arrhythmias, should be cor- rected (Figure 34) (1012).

With recurrent suspected ischemic-type chest discomfort, coronary arteriography often clarifies the cause of chest dis- comfort with demonstration of a high-grade coronary obstruction. For patients who are considered candidates for revascularization, prompt reperfusion with PCI or CABG is indicated as dictated by the coronary anatomy (Figure 34) (509,515,1012). For patients who are not considered candi- dates for revascularization or for whom coronary angiogra- phy and PCI cannot be implemented rapidly (ideally in less than 60 minutes), readministration of fibrinolytic therapy is reasonable.

Another cause of chest discomfort to consider in patients recovering from STEMI is infarct expansion. This is charac- terized by nonspecific repolarization of abnormalities on the ECG, worsening hemodynamics, but no re-elevation of car- diac biomarkers (43). Management of infarct expansion should focus on diuresis and inhibition of the renin- angiotensin-aldosterone system (see Section 7.4.3).

7.9. Other Complications

7.9.1. Ischemic Stroke

1. Neurological consultation should be obtained in