ST Segment Elevation Myocardial Infarction

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Chapter 18

St Segment Elevation Myocardial Infarction

1. What are the electrocardiograph (ECG) criteria for the diagnosis of ST segment elevation myocardial infarction (STEMI)?

    Criteria for the diagnosis of STEMI can derive from criteria established for the administration of thrombolytic therapy, which evolved in the late 1980s and 1990s. ECG criteria for suspected coronary artery occlusion include:

image American College of Cardiology Foundation/American Heart Association (ACCF/AHA) criteria for STEMI consist of ST segment elevation greater than 0.1 mV (one small box) in at least two contiguous leads (e.g., leads III and aVF, or leads V2 and V3). The European Society of Cardiology (ESC) STEMI guidelines require 0.2 mV or greater ST elevation when analyzing leads V1 through V3 (but similarly, 0.1 mV elevation for other leads and/or territories). Figure 18.1 demonstrates the ECG finding of ST elevation in a patient with acute myocardial infarction.

image New or presumably new left bundle branch block (LBBB)

2. Is intracoronary thrombus common in STEMI?

    Yes. The majority of STEMI is due to plaque rupture, fissure, or disruption, leading to superimposed thrombus formation and vessel occlusion. Angioscopy demonstrates coronary thrombus in more than 90% of patients with STEMI (as opposed to 35% to 75% of patients with non–ST segment elevation acute coronary syndrome [NSTE-ACS] and 1% of patients with stable angina).

3. What is primary PCI?

    Primary percutaneous coronary intervention (PCI) refers to the strategy of taking a patient who presents with STEMI directly to the cardiac catheterization laboratory to undergo mechanical revascularization using balloon angioplasty, coronary stents, aspiration thrombectomy, and other measures. Patients are not treated with thrombolytic therapy in the emergency room (or ambulance) but preferentially taken directly to the cardiac catheterization laboratory for primary PCI. Studies have demonstrated that primary PCI is superior to thrombolytic therapy when it can be performed in a timely manner by a skilled interventional cardiologist with a skilled and experienced catheterization laboratory team.

4. What are considered to be contraindications to thrombolytic therapy?

    Several absolute contraindications to thrombolytic therapy and several relative contraindications (or cautions) must be considered in deciding whether to treat a patient with lytic agents. As would be expected, these are based on the risks and consequences of bleeding resulting from thrombolytic therapy. These contraindications and cautions are given in Box 18-1.

Modified from Antman EM, Anbe DT, Armstrong PW, et al: ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction. J Am Coll Cardiol 44:E1-E211, 2004, and from Van de Werf F, Ardissino D, Betriu A, et al: Management of acute myocardial infarction in patients presenting with ST-segment elevation. The Task Force on the Management of Acute Myocardial Infarction of the European Society of Cardiology. Eur Heart J 24:28-66, 2003.

5. What is door-to-balloon time?

    Door-to-balloon time is a phrase that denotes the time it takes from when a patient with STEMI sets foot in the emergency room until the time that a balloon is inflated in the occluded, culprit coronary artery. More recently, the concept of medical contact-to-balloon time has been emphasized, given that STEMI may first be diagnosed in the transporting ambulance in some cases. Because balloon angioplasty is no longer always the first intervention performed on an occluded artery, the term has further evolved to medical contact-to-device time. The generally accepted medical contact-to-device time goal is 90 minutes or less in cases in which the patient presents or is taken directly to a hospital that performs PCI. In cases in which the patient must be transferred from a hospital that does not perform PCI to a hospital that does perform PCI, the goal is a medical contact-to-device time of no more than 120 minutes.

6. What is door-to-needle time?

    Door-to-needle time is a phrase that denotes the time it takes from when a patient with STEMI sets foot in the emergency room until the beginning of thrombolytic therapy administration. The generally accepted goal for door-to-needle time is 30 minutes or less.

7. In patients treated with thrombolytic therapy, how long should antithrombin therapy be continued?

    Patients who are treated with unfractionated heparin (UFH) should be treated for 48 hours. Studies of low-molecular-weight heparins (EXTRACT, CREATE) and of direct thrombin inhibitors (OASIS-6) have suggested that patients treated with these agents should be treated throughout their hospitalizations, up to 8 days maximum. Guidelines for adjunctive antiplatelet and antithrombin therapy in patients treated with thrombolytic therapy are given in Table 18-1.

8. Which patients with STEMI should undergo cardiac catheterization?

    Patients with STEMI who should undergo immediate coronary angiography include those who are candidates for primary PCI, those with severe heart failure or cardiogenic shock (if they are suitable candidates for revascularization), and many of those with moderate to large areas of myocardium at risk and evidence of failed fibrinolysis. Cardiac catheterization is reasonable in hemodynamically stable patients with evidence of successful fibrinolysis. Recommendations from the 2011 ACCF/AHA/ Society for Cardiovascular Angiography and Interventions (SCAI) Guidelines on PCI regarding coronary angiography in patients with STEMI are given in Table 18-2.

TABLE 18-2

RECOMMENDATIONS FROM THE 2011 ACCF/AHA/SCAI GUIDELINES ON PCI REGARDING CORONARY ANGIOGRAPHY IN PATIENTS WITH STEMI

image

ACCF, American College of Cardiology Foundation; AHA, American Heart Association; COR, class of recommendation; LOE, level of evidence; PCI, percutaneous coronary intervention; SCAI, Society for Cardiovascular Angiography and Interventions; STEMI, ST segment elevation myocardial infarction.

Modified from Levine GN, Bates ER, Blankenship JC, et al. 2011 ACCF/AHA/SCAI Guideline for Percutaneous Coronary Intervention. A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines and the Society for Cardiovascular Angiography and Interventions. J Am Coll Cardiol 58:e44-e122, 2011.

9. Which patients with STEMI should undergo primary PCI?

    Primary PCI should be performed in patients with STEMI who present within 12 hours of symptom onset, in patients with severe heart failure or cardiogenic shock, and in those with contraindications to fibrinolytic therapy. PCI can also be considered in those who have clinical evidence for fibrinolytic failure or infarct artery reocclusion after fibrinolytic failure, as well as those treated with likely successful fibrinolytic failure. Recommendations from the 2011 ACCF/AHA/SCAI Guidelines on PCI regarding PCI in patients with STEMI are given in Table 18-3.

TABLE 18-3

RECOMMENDATIONS FROM THE 2011 ACCF/AHA/SCAI GUIDELINES ON PCI REGARDING PCI IN PATIENTS WITH STEMI

Indications COR LOE
Primary PCI I A
STEMI symptoms within 12 hours I B
Severe heart failure or cardiogenic shock I B
Contraindications to fibrinolytic therapy with ischemic symptoms <12 hours I B
Asymptomatic patient presenting between 12 and 24 hours after symptoms onset and higher risk IIB C
Noninfarct artery PCI at the time of primary PCI in patients without hemodynamic compromise III: Harm B
Delayed or elective PCI in patients with STEMI (i.e., nonprimary PCI)    
Clinical evidence for fibrinolytic failure or infarct artery reocclusion IIA B
Patient infarct artery 3 to 24 hours after fibrinolytic therapy IIA B
Ischemia on noninvasive testing IIA B
Hemodynamically significant stenosis in a patient infarct artery >24 hours after STEMI 11B B
Totally occluded infarct artery >24 hours after STEMI in a hemodynamically stable asymptomatic patient without evidence of severe ischemia III: No benefit B

ACCF, American College of Cardiology Foundation; AHA, American Heart Association; COR, class of recommendation; LOE, level of evidence; PCI, percutaneous coronary intervention; SCAI, Society for Cardiovascular Angiography and Interventions; STEMI, ST segment elevation myocardial infarction.

Modified from Levine GN, Bates ER, Blankenship JC, et al. 2011 ACCF/AHA/SCAI Guideline for Percutaneous Coronary Intervention. A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines and the Society for Cardiovascular Angiography and Interventions. J Am Coll Cardiol 58:e44-e122, 2011.

10. What is facilitated PCI?

    Facilitated PCI refers to a strategy of planned PCI immediately or shortly after administration of an initial pharmacologic regimen intended to improve coronary artery patency before the PCI procedure. Such regimens have included full-dose or reduced-dose thrombolytic therapy, glycoprotein IIb/IIIa inhibitors, antithrombin agents, and combinations of agents. The concept is to restore at least some coronary blood flow as the cardiac catheterization laboratory is getting activated and the patient is being transported to the hospital’s catheterization laboratory. Although this strategy is intuitively appealing, studies of such a strategy generally have not demonstrated any advantage of facilitated PCI over primary PCI and it is no longer generally recommended. The term itself is controversial, and there has been a movement to abolish this phrase.

11. What is rescue PCI?

    Rescue PCI is the performance of PCI after thrombolytic therapy has failed in a patient. Studies of rescue PCI versus medical management generally have shown a modest benefit with rescue PCI in appropriately selected patients. The problem with rescue PCI is that clinical and electrocardiographic criteria for predicting which patients have actually failed thrombolytic therapy (have not had successful lysis of coronary thrombosis and restoration of coronary perfusion) are imprecise. Thus, some patients with continued occluded arteries may not be referred for rescue PCI and some patients with successful reperfusion will be referred for unnecessary cardiac catheterization. As with the term facilitated PCI, some have advocated for elimination of the term rescue PCI.

12. Which patients should not be treated with beta-adrenergic blocking agent (β-blocker) therapy?

    β-Blockers have been a mainstay of STEMI therapy for decades. However, in the Clopidogrel and Metoprolol in Myocardial Infarction Trial/Second Chinese Cardiac (COMMIT/CCS-2) study, the potential benefits of β-blocker therapy were offset by an increased incidence of cardiogenic shock and shock-related death with β-blocker therapy. Therefore, in patients with signs of heart failure, evidence of a low-output state, or increased risk for cardiogenic shock, β-blocker therapy should not be initiated. Risk factors for cardiogenic shock include age older than 70 years, systolic blood pressure less than 120 mm Hg, sinus tachycardia greater than 110 beats/min, and heart rate less than 60 beats/min. Other contraindications to initiating β-blocker therapy include PR interval more than 0.24 seconds, second- or third-degree heart block, active asthma, or severe reactive airway disease.

13. Which patients should be treated with nitrate therapy?

    Sublingual (SL) nitroglycerin (0.4 mg) every 5 minutes, up to three doses, should be administered for ongoing ischemic discomfort. Intravenous nitroglycerin is indicated for relief of ongoing ischemic discomfort that responds to nitrate therapy, for control of hypertension, and for management of pulmonary edema. Nitrates should not be administered to patients who have received a phosphodiesterase inhibitor for erectile dysfunction within 24 to 48 hours (depending on the specific agent). Nitrates should also not be administered to those with suspected right ventricular (RV) infarction, systolic blood pressure less than 90 mm Hg (or 30 mm Hg or more below baseline), severe bradycardia (less than 50 beats/min), or tachycardia (more than 100 beats/min) (Box 18-1).

14. Should patients with STEMI be continued on nonselective nonsteroidal antiinflammatory drugs (NSAIDs) (other than aspirin) or COX-2 inhibitors?

    No. Use of these agents has been associated with increased risk of reinfarction, hypertension, heart failure, myocardial rupture, and death. Therefore, such agents should be discontinued at the time of admission.

15. What are the main mechanical complications of myocardial infarction?

image Free wall rupture: Acute free wall rupture is almost always fatal. In some cases of subacute free wall rupture, only a small quantity of blood initially reaches the pericardial cavity and begins to cause signs of pericardial tamponade. Emergent echocardiography and immediate surgery are indicated.

image Ventricular septal rupture: A ventricular septal defect (VSD) caused by myocardial infarction and septal rupture occurred in 1% to 2% of all patients with infarction in older series, though the incidence in the fibrinolytic age is 0.2% to 0.3%. Patients may complain of a chest pain somewhat different than their MI pain and will usually develop cardiogenic shock. A new systolic murmur may be audible, often along the left sternal border. Mortality without surgery is 54% in the first week and up to 92% within the first year.

image Papillary muscle rupture: Papillary muscle rupture leads to acute and severe mitral regurgitation. It occurs in approximately 1% of STEMI patients. Because of the abrupt elevation in left atrial pressure, there may not be an audible murmur of mitral regurgitation. Pulmonary edema and cardiogenic shock usually develop. Treatment is urgent or emergent mitral valve replacement (or in rare cases, mitral valve repair).

16. What is the triad of findings suggestive of RV infarction?

    The triad of findings suggestive of RV infarction is hypotension, distended neck veins, and clear lungs. Clinical RV infarction occurs in approximately 30% of inferior MI patients. Because the infarcted right ventricle is dependent on preload, administration of nitroglycerin (or morphine), which leads to venous pooling and decreased blood return to the right ventricle, may lead to profound hypotension. When such hypotension occurs, patients should be placed in reverse Trendelenburg position (legs above chest and head) and treated with extremely aggressive administration of several liters of fluid through large-bore intravenous needles. Those who do not respond to such therapy may require treatment with agents such as dopamine.

    In patients with inferior MI, a right-sided ECG should be obtained. The precordial leads are placed over the right side of the chest in a mirror-image pattern to normal. The finding of 1 mm or greater ST elevation in leads RV4 through RV6 is highly suggestive of RV infarction (Fig. 18-2), although the absence of this often-transient finding should not be used to dismiss a diagnosis of RV infarction made on clinical grounds.

17. Besides plaque rupture and thrombotic occlusion, what are other causes of STEMI?

    Although plaque rupture with subsequent thrombus formation is the most common etiology of STEMI, other causes to consider include:

Bibliography, Suggested Readings, and Websites

1. Antman, E.M. ST-elevation myocardial infarction: management. In Libby P., Bonow R., Mann D., eds.: Braunwald’s heart disease: a textbook of cardiovascular medicine, ed 8, Philadelphia: Saunders, 2008.

2. Antman, E.M., Anbe, D.T., Armstrong, P.W., et al. ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to Revise the 1999 Guidelines for the Management of Patients with Acute Myocardial Infarction). J Am Coll Cardiol. 2004;44:E1–E211.

3. Antman, E.M., Hand, M., Armstrong, P.W., et al. focused update of the ACC/AHA 2004 guidelines for the management of patients with ST-elevation myocardial infarction: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2007;51:210–247. 2008

4. Zafari, A.M. Myocardial infarction. Available at http://emedicine.medscape.com/article/155919-overview. Accessed March 28, 2013

5. Gibson, C.M., Carrozza, J.P., Laham, R.J. Primary PCI versus Fibrinolysis (Thrombolysis) in Acute ST Elevation (Q Wave) Myocardial Infarction: Clinical Trials. Available at http://www.uptodate.com/contents/primary-percutaneous-coronary-intervention-versus-fibrinolysis-in-acute-st-elevation-myocardial-infarction-clinical-trials. Accessed March 28, 2013

6. Reeder, G.S., Kennedy, H.L., Rosenson, R.S. Overview of the Management of Acute ST Elevation (Q Wave) Myocardial Infarction. Available at http://www.uptodate.com/contents/overview-of-the-acute-management-of-st-elevation-myocardial-infarction. Accessed March 28, 2013

7. Van de Werf, F., Ardissino, D., Betriu, A., et al. Management of acute myocardial infarction in patients presenting with ST-segment elevation. The Task Force on the Management of Acute Myocardial Infarction of the European Society of Cardiology. Eur Heart J. 2003;24:28–66.

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