only one SQ dose was given, add 0.3 mg/kg IV during PCI; if enoxaparin was used >12h ago, give 0.5–0.75mg/kg IV bolus)
Note: Avoid switching between UFH and enoxaparin. The switch to bivalirudin is, however, appropriate.
1 β -Blocker, such as oral metoprolol, is administered at a dose of 25 mg Q8–12 h and titrated to 50 mg Q8–12 h if tolerated. In the COMMIT-CCS trial, the initiation of β-blockers on the first day of ACS (mainly STEMI) was associated with an increased risk of cardiogenic shock during that first day, the benefit from β-blockers on reinfarction and VF emerging gradually beyond the second day.73 Overall, β-blockers significantly reduced the endpoint of death/MI/cardiac arrest between day 2 and day 15, but increased this endpoint in the first day and in unstable patients, making the overall β-blocker effect neutral. Therefore, β-blockers should be avoided on the first day if there are any HF signs or features predictive of cardiogenic shock: SBP < 120 mmHg, heart rate > 110 bpm, or age > 70 years.* Counterintuitively, β-blockers are avoided in sinus tachycardia, which is often a pre-shock state. Moreover, intravenous β-blockers are preferably avoided in all patients, as this was the formulation used in COMMIT-CCS on the first day, but may still be used in a patient with active ischemia and none of the previous features (IV metoprolol, 5 mg Q10 min up to 3 times).
2 ACE-Is or ARBs are recommended in ACS patients with HF, LV dysfunction, hypertension, or diabetes (class I indication). They may also be used in ACS patients who do not have these features (class IIa indication). They are avoided in acute renal failure or when SBP is < 100 mmHg or 30 mmHg below baseline.
3 Statin therapy should be started during ACS hospitalization regardless of the baseline LDL. Statin’s benefit is not usually immediate but may become evident within 1 month.74 A more immediate benefit is seen in patients undergoing PCI, as high-dose statin reduces peri-PCI MI.74 The high doses used in secondary prevention trials, such as atorvastatin 80 mg in the PROVE-IT trial, are preferred as they further reduce cardiovascular events (including death/MI) and peri-PCI MI, possibly through superior stabilization of vulnerable plaques. Note that, for patients receiving chronic statin therapy, the harm from statin withdrawal is immediate, with an early cardiac risk that is higher than that of statin non-users.75
4 Nitroglycerin (NTG) is administered sublingually for chest pain (as needed, Q5 min up to three times if tolerated). NTG should be avoided if SBP < 100 mmHg or 30 mmHg below baseline, or bradycardia < 50 bpm. Acutely in ACS, one can give NTG at a lower BP level than one can give β-blockers. Later on, in case of borderline BP, the priority is given to β-blocker administration.IV NTG is indicated for frequently recurrent angina, ongoing angina, or ischemia associated with hypertension or HF. Angina that is not relieved by 400 mcg of sublingual NTG may not be relieved by the smaller infusion dose of IV NTG (10–200 mcg/min); the latter may however be tried, in conjunction with β-blockers and antithrombotic therapy. IV NTG is initiated at 10 mcg/min and increased by 10 mcg/min every 3–5 minutes until symptoms are relieved or a limiting reduction of SBP < 100–110 mmHg occurs. Oral or topical nitrates (patch, paste) are acceptable alternatives in the absence of ongoing angina. After stabilization, IV NTG may be converted to an oral or topical nitrate, with a dosing that prevents tolerance and leaves a 12-hour nitrate-free interval (e.g., isosorbide dinitrate 10–40 mg or nitropaste 0.5–2 inches at 8 a.m., 2 p.m. and 8 p.m.).
5 Morphine may be given for angina that is refractory to the above after a decision is made as to whether emergent revascularization will be performed or not. Thus, morphine should not be used to mask “refractory angina,” and resolution of a true angina only after morphine administration should not defer the emergent performance of coronary angiography ± PCI.
6 Calcium channel blockers. Dihydropyridines (DHPs) are vasodilators (nifedipine, amlodipine). Non-dihydropyridines are vasodilators that also have negative ino- and chronotropic effects (verapamil, diltiazem). Short-acting DHPs, such as nifedipine, lead to reflex tachycardia and should be avoided in ACS; long-acting DHPs may be used in ACS in combination with β-blockers. Non-DHPs may be used in ACS if β-blockers are contraindicated and LV systolic function is normal; as opposed to DHPs, they should generally not be combined with β-blockers.
7 Aldosterone antagonist reduces short-term (30 days) and long-term mortality when initiated in MI patients with EF<40%, at 3-7 days (EPHESUS trial). However, its acute initiation in the emergency department in MI with EF>40% was not beneficial (ALBATROSS trial).76
V. General procedural management after coronary angiography: PCI, CABG, or medical therapy only
After coronary angiography, a decision is made for PCI vs. CABG vs. continuing medical therapy alone, as dictated by the coronary anatomy. If a decision is made to proceed with CABG, hold clopidogrel and ticagrelor for 5 days before surgery, if possible, and hold enoxaparin for 12–24 hours and eptifibatide for 4 hours before surgery.
A. CABG indications
Left main disease
Three-vessel CAD or complex two-vessel CAD involving the LAD (especially proximal LAD), particularly if angiographic SYNTAX score ≥ 23 (SYNTAX trial) or diabetes (FREEDOM trial).77
B. PCI indications
One- or two-vessel disease (≥50%)
PCI is an alternative to CABG in three-vessel CAD or complex two-vessel CAD involving the LAD with a SYNTAX score ≤ 22 and no diabetes.76 Multivessel PCI (including proximal LAD PCI) compares favorably with CABG if the stenoses’ morphology and location are technically amenable to PCI and if full functional revascularization can be achieved with PCI.78 The presence of a chronic total occlusion, one or more technically difficult or long lesions, or diabetes, should favor CABG, especially because CABG provides a more complete revascularization.
NSTEMI with multivessel CAD: single-stage multivessel PCI vs. culprit-only PCI:
When multiple complex lesions are seen in NSTEMI, the culprit artery may not be clearly identified and multivessel intervention is justified. According to a MRI analysis, the culprit artery is misidentified by catheterization in 35% of patients.79 The SMILE trial randomized NSTEMI patients with multivessel disease to multivessel PCI in one stage vs. multiple stages (2nd procedure 3-7 days later). Despite a similarly complete revascularization with only a few days difference, single-stage PCI was associated with significantly less repeat revascularizations at 1 year and a strong trend toward less deaths.80 Large registry analyzes are concordant with SMILE findings.81,82 As such, ESC recommends complete revascularization in NSTEMI with multivessel CAD, but allows flexible timing (class IIa).4
Somewhat similarly, in STEMI, multivessel PCI is to be performed; yet it does not have to be performed in the same setting and may await few days or weeks (COMPLETE, DANAMI-PRIMULTI trials).83,84
C. Among patients with high-risk ACS managed invasively, ~25–30% do not undergo any revascularization after coronary angiography
There are two types of patients within this group:
1 About 10% of patients presenting with a picture of type 1 MI have normal coronary arteries or insignificant CAD (<50% obstructive), this prevalence being higher among women and younger patients (15% of women) (MINOCA).17-25 Half of these patients have a completely normal angiographic appearance of the coronary arteries. MINOCA may be due to: (a) overlooked or recanalized plaque rupture (even at an angiographically normal site), (b) vasospasm, (c) myocarditis or (d) takotsubo. In a meta-analysis of all comers with MINOCA, MRI established the diagnosis in most of the patients (three main diagnoses: myocarditis 38%, infarction from plaque rupture or vasospasm 24%, and takotsubo 16%) (see Section I.E).19,26,27 IVUS and