Practical Cardiovascular Medicine. Elias B. Hanna

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(SWEDEHEART) showed an ischemic and bleeding risk identical to UFH.77 Also, bivalirudin may be associated with a higher risk of acute stent thrombosis than UFH, which is reduced by 1-4 hours of high-dose bivalirudin post-PCI. Except for this optional brief infusion of bivalirudin, anticoagulants are stopped after PCI.GPI, in conjunction with either UFH or bivalirudin, is reserved for bailout use during PCI (large thrombus burden, thrombotic complications, or no reflow) (class IIa).78 In contemporary trials, ~15% of STEMI patients require the use of GPI.

      B. Antithrombotic therapies in patients treated with fibrinolytics (started upon presentation)

      1 Aspirin 325 mg.

      2 Clopidogrel 300 mg load if patient is <75 years old, or 75 mg if >75 years old (300 mg rather than 600 mg is the dose studied with fibrinolytics, even in pharmacoinvasive trials; 75 mg is the only dose studied with fibrinolytics in elderly patients).79,80

      3 UFH IV bolus 60 units/kg (not more than 4000 units), followed immediately by heparin drip 12 units/kg/h, adjusted Q6h to keep the PTT 1.5–2.0× the control.

      If the patient is going to have fibrinolytic reperfusion rather than PCI reperfusion, and if PCI is not expected in the next 24 hours, enoxaparin SQ or fondaparinux SQ may be used instead of UFH. In the patient receiving primary fibrinolytic reperfusion, enoxaparin or fondaparinux has a more favorable effect on reinfarction risk than UFH, with less major bleeding with fondaparinux, vs. more major bleeding with enoxaparin.81,82 Patients undergoing standalone fibrinolytic therapy should receive anticoagulants for at least 48 hours and preferably for the duration of the hospitalization. Regimens other than UFH are preferred for anticoagulation >48 hours, because UFH is of no proven benefit beyond 48 hours.

       Dosage of enoxaparin: initial 30 mg IV dose, followed 15 minutes later by 1 mg/kg SQ Q12hFor patients >75 years old, avoid IV dose and administer 0.75 mg/kg Q12hIf GFR <30 ml/min, administer 1 mg/kg SQ Q24h

       Dosage of fondaparinux: 2.5 mg IV initially, then 2.5 mg SQ Qday. Avoid if GFR <30 ml/min.

      Clopidogrel 600 mg load, prasugrel, and 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

      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.

      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

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