ticagrelor have not been studied within 24 hours of fibrinolytics, and thus are generally avoided during this time frame. Conversely, if delayed PCI is performed >24 hours after fibrinolysis, one of these regimens should be used. For PCI within 24 hours of fibrinolysis, use clopidogrel 300 mg +/– GPI.44–46
X. Other acute therapies
1 β -Blockers (e.g., metoprolol orally 25 mg Q8–12h, titrated to 50 mg Q8–12h). A meta-analysis of old trials addressing β-blockers in acute MI has shown that β-blockers reduce mortality after MI, whether HF is present or not.83 In the COMMIT-CCS trial, the use of β-blockers beyond the first 24–48 hours after MI was beneficial and significantly reduced the risk of recurrent MI and VF at 15 days.84 However, the earlier administration of β-blockers, especially IV β-blockers, increased the risk of cardiogenic shock, particularly in high-risk subgroups, where a net adverse effect was seen. Thus, β-blockers should be acutely avoided in these subgroups:
Killip class ≥ II (any degree of HF); age >70 years.
Sinus tachycardia >110 bpm: The more tachycardic the patient, the less likely he is to acutely benefit from β-blockers. In general, tachycardia reflects a large MI and compensates for a low stroke volume (pre-shock state). Slowing the heart rate precipitates shock.
SBP <120 mmHg or 30 mmHg lower than baseline, or evidence of low output. However, beyond the first 24–48 hours, SBP <90–100 mmHg, rather than 120 mmHg, is the contraindication to β-blocker use.
Also, avoid β-blockers in other classic contraindications: Sinus bradycardia <60 bpm, PR >0.24 s, any second- or third-degree AV block, history of severe asthma, or active bronchospasm.β-Blockers are generally titrated to the maximal tolerated dose before hospital discharge and are expected to have a short- and long-term benefit, for up to one year in patients with normal EF.85-87 In patients with LVEF <40% or patients who developed HF but are now stable, β-blockers are started slowly, later than 24 hours, then titrated in the outpatient setting (e.g., carvedilol is started as 6.25 mg BID in the hospital, 3 days after MI, and uptitrated every 3–10 days, as in the CAPRICORN trial; this regimen reduced late mortality in patients with low EF, with or without HF).88
Oral ACE-Is (or ARBs if cough or angioedema occurs with ACE-I). Wait a few hours before starting an ACE-I to ensure the patient is stable and not evolving into cardiogenic shock. Try to start an ACE-I early, in the first 24 hours. In landmark trials of ACE-inhibition in acute MI, ACE-I was initiated in the first 24 hours of all types of MI, whether anterior or inferior, accompanied by HF or not, and improved early mortality (survival curves start to diverge at day 1 and become significant at 1 week and 6 weeks).89,90 ACE-I therapy is particularly beneficial in LV dysfunction, anterior MI or HF (SAVE trial).91 The benefit is less marked when ACE-I is used unselectively in all MI patients, including those with inferior MI and without HF, but ACE-I is still reasonable for a duration of 6 weeks, as in those trials. ACE-I is avoided in acute renal failure or when SBP <100 mmHg or 30 mmHg below baseline; intravenous ACE-I is avoided in all patients because of the risk of hypotension. A low-dose, short-acting ACE-I may be used in the acute setting in order to verify tolerability. Sacubitril-valsartan did not prove superior to ACE-I in acute MI with low EF (PARADISE-MI trial). Examples of ACE-I dosing:Captopril 6.25 mg TID, to be doubled with each subsequent dosage, until 50 mg TIDor Lisinopril 5 mg Qday, to be increased to 20–40 mg Qday
Nitroglycerin. Administer 0.4 mg of sublingual NTG up to three times during active angina, then start IV drip if tolerated hemodynamically. NTG is useful for chest pain, HTN, or HF concomitant to MI. It may lead to hypotension or vagal shock and should be avoided if SBP<100 mmHg, bradycardia <50 bpm, tachycardia >100 bpm, or if RV infarct is suspected with inferior MI (even if RV infarct is clinically silent).
Morphine. Administer morphine if the pain is severe and uncontrolled despite NTG, provided that reperfusion therapy is underway.
High statin dose (atorvastatin 80 mg, rosuvastatin 20 mg)
Glucose control. In hyperglycemia, with or without prior diabetes, insulin (IV or SQ) is administered to maintain blood glucose≤180 mg/dl during acute MI/ACS. Afterwards, when the patient is less ill, try to achieve normoglycemia.92
Monitoring. The patient is monitored in a coronary care unit for 12–24 hours, then transferred to a step-down unit in the absence of complications. In general, an uncomplicated STEMI is safely discharged after 72 hours of hospitalization (PAMI-II trial), or even 48 hours according to modern data.93-95 Patients qualify for early discharge if they undergo a successful reperfusion with primary PCI, have one- or two-vessel CAD, are younger than 70 years of age without major comorbidities, and have no arrhyth- mias or pump failure.
Echo. Echo should be performed before hospital discharge in all patients, and should be performed or repeated urgently in a patient with shock or suspected mechanical complication.
XI. Risk stratification
A. Killip classification uses clinical features upon presentation to assess STEMI prognosis.
Class I: no HF (30-day mortality = 3%)96
Class II: crackles up to one-third of the lung fields or S3 (= HF, mortality = 13%)
Class III: pulmonary edema (mortality = 27%)
Class IV: cardiogenic shock (mortality = 50–60%)
Note that Killip classification is only applied at presentation. It also has a prognostic value in NSTE-ACS.
B. TIMI risk score for STEMI
Depending on the STEMI TIMI risk score (Table 2.3), the 30-day mortality of fibrinolytic-treated STEMI patients ranges from 1% to 35%.97 The benefit of reperfusion is highest in the higher risk groups.
C.Troponin I peaks at a level of 50–300 ng/ml (at ~24 h), CK typically peaks at 2500–5000 units/l (at 18–24 h). Reperfusion therapy makes these biomarkers peak earlier and often at higher levels; however, the total volume of CK or troponin released is smaller, i.e., the distribution curves over time are narrower and the decline is faster (3–4 days for troponin I). The CK or troponin mass, rather than the CK or troponin peak, correlates with the infarct size and the prognosis. Aborted STEMI, whether aborted spontaneously or with very early reperfusion, is characterized by a biomarker rise that is usually mild (CK-MB <2× normal).
XII. LV remodeling and infarct expansion after MI (see Figure 2.5)
XIII. Discharge, EF improvement, ICD
A. Discharge medications
See Chapter 1, Section VI.
B.EF improves 1–3 months after discharge and justifies follow-up echocardiography for risk assessment. There are two explanations for EF improvement:
LV dysfunction that occurs immediately after MI is partly due to post-ischemic stunning rather than necrosis. When an artery occludes transiently, necrosis occurs in part of the myocardium, while dysfunction without necrosis, called stunning, occurs in other parts. The stunned myocardium recovers over the course of days to weeks after arterial recanalization.
ACE-Is, β-blockers, and aldosterone antagonists reduce LV remodeling and LV size, allowing an increase in EF for the same amount of necrotic myocardium (Figure 2.5). Each one of these drugs allows an EF improvement of up to 5%.
C.