within the preceding 3 months, documented ischemia on stress testing, and one- or two-vessel CAD derived a 70% reduction of cardiovascular events, including cardiac death, with PCI.59
The OAT trial does not apply to a coronary chronic total occlusion (CTO) that has not led to a large transmural infarct, in which case the myocardial contractility is fairly preserved because of the collateral network. A progressive occlusion that allows for an adequate collateral network to develop may not present as MI. It typically presents as chronic angina or a small NSTEMI, not STEMI. Opening a CTO has a beneficial effect on symptoms and, possibly, LV function.
VIII. Angiographic findings, PCI, and cellular reperfusion; multivessel disease in STEMI
A. PCI: microvascular and cellular reperfusion
Approximately 15% of occluded arteries acutely recanalize before the PCI procedure, in the first 4 hours, and achieve TIMI 2 or 3 flow (from spontaneous or antithrombotic-induced lysis). This STEMI is called “transient STEMI”, and may also be called “aborted STEMI” if cardiac biomarkers only rise minimally (CK-MB <2× normal).9 Residual stenosis usually persists.60–62
During PCI, the lesion is dilated with balloon angioplasty then stented. In comparison with standalone balloon angioplasty, stenting reduces the early risk of reocclusion/reinfarction by 50% (to <2%) and the late risk of restenosis, without affecting mortality.61 Drug-eluting stents are used, as they do not increase late stent thrombosis and significantly reduce restenosis.62 A routine initial use of aspiration thrombectomy has not shown superiority to balloon angioplasty in two large trials.63
Following primary PCI, ~95% of patients achieve TIMI 3 flow, while 5% achieve TIMI 0–2 flow despite wide macrovascular patency, also called “no reflow.” The term “no reflow” implies poor microvascular flow and is only used after treating all significant epicardial stenoses. TIMI flow <3 is a predictor of poor outcomes, but TIMI 3 flow does not necessarily imply appropriate microvascular flow. In fact, only ~60% of patients with TIMI 3 flow achieve significant ST-segment resolution (= cellular reperfusion), and only 70% achieve appropriate myocardial blush (= microvascular reperfusion).63,64 “Appropriate myocardial blush,” also called “myocardial blush grade 2 or 3,” is used to describe brisk contrast staining of the myocardium followed by contrast clearance and no residual myocardial stain by the next injection. Impaired coronary flow, impaired myocardial blush, or the lack of ST resolution implies: (i) distal microembolization, (ii) microvascular spasm, or (iii) myocyte injury and swelling from ischemia or reperfusion injury, especially late reperfusion, sometimes irreversible. The best long-term outcomes (survival and LV function) are seen in patients with ST-segment resolution and good myocardial blush, while intermediate outcomes are seen in patients with discordant findings.65
Persistent ST elevation after successful primary or rescue PCI implies microvascular obstruction or cellular injury, and thus worse long-term prognosis. The patient may have mild persistent chest pain. Unlike persistent ST elevation after thrombolysis, persistent ST elevation after a successful PCI does not dictate any further procedure, unless the patient has severe recurrence of pain.
Patients with no-reflow are treated with (i) intracoronary vasodilators, (ii) GPI, or (iii) IABP. After treatment of the epicardial stenosis, IABP improves coronary microvascular flow and relieves ongoing ischemia.
When angiography is performed in patients who have been successfully reperfused with fibrinolytics, data from the pharmacoinva- sive trials suggests that ~15–20% of the infarct-related arteries have a residual stenosis <50% that does not require PCI.30,43,66,67 While most plaques that lead to MI are <50% at baseline, fibrinolytics often partially dissolve the thrombus, not fully, hence the frequent residual obstruction.
B. Multivessel disease in STEMI
Approximately 50–60% of patients presenting with STEMI have multivessel CAD, and up to 40% have multiple complex plaques.45,61,68
The traditional teaching had been to only treat the culprit artery in hemodynamically stable patients, and to concomitantly treat culprit and non-culprit arteries in cardiogenic shock. Evidence now suggests the opposite: stable patients may safely undergo non-culprit PCI acutely, while cardiogenic shock patients with a clear culprit artery have a dramatic 8% absolute increase in mortality if non-culprit PCI is performed acutely (CULPRIT-SHOCK trial, STEMI or NSTEMI).69 Non-culprit PCI increases procedural time and contrast load, leading to more LV volume overload and renal injury and is hazardous in the hemodynamically compromised patient. Also, non-culprit PCI may induce peri-PCI myocardial injury, distal embolization or side branch compromise, unlikely to be tolerated in the tenuous patient.
Outside cardiogenic shock, complete revascularization of non-culprit arteries with stenoses >70%, regardless of the presence of residual symptoms or ischemia, was beneficial and reduced the 3-year risk of future MI, mainly NSTEMI, in comparison to culprit-only PCI, according to the large COMPLETE trial (5.4% vs. 7.9%); of note, mortality was not reduced. Non-culprit PCI was performed during a procedure separate from culprit PCI, within the same hospitalization or up to 45 days after discharge.70 Other trials have suggested the safety of non-culprit PCI in the same setting as culprit PCI (PRAMI, Compare-acute) or separately during the same hospitalization (DANAMI-3 PRIMULTI).71,72 Only COMPLETE has shown a reduction in MI, and thus, non-culprit PCI at a separate setting may be favored, during the same hospitalization (especially if critical stenosis >90%) or soon after it, as long as non-culprit PCI is feasible and the patient is not too sick to tolerate it. Immediate non-culprit PCI may be performed, while accounting for the complexity of PCIs and the total contrast load.
CABG is rarely required acutely in STEMI (~0.2-1%),62,63 but may be more frequently required in patients with cardiogenic shock and severe left main or three-vessel disease. In fact, in the SHOCK trial, 37% of invasively managed patients were emergently revascularized with CABG (a median of 2.7 hours after randomization, 19 hours after MI).73 Acute CABG may also be required after a failed PCI.
If staged CABG is judged necessary for full revascularization of non-culprit arteries after culprit PCI, it is preferred to wait at least 24 hours, and preferably 3–7 days. CABG mortality is increased in the first 3 days after a large MI.74 In patients who developed RV infarct and were not successfully reperfused in the first 6 hours, it is better to delay CABG 4 weeks to let the RV heal (otherwise, there may be severe, intractable RV dilatation upon opening the pericardium during CABG). In a patient with left main or three-vessel disease and RCA-related MI, the RCA is stented and CABG performed 1 month later. If CAD is critical (e.g., > 75% left main stenosis), one may recanalize the RCA with balloon angioplasty and perform CABG sooner, a few days later.
IX. Antithrombotic therapies in STEMI
A. Antithrombotic therapies in conjunction with primary PCI
1 Aspirin 325 mg upon presentation.
2 ADP-receptor antagonist is loaded at the time of PCI, or in the emergency room before catheterization if STEMI diagnosis is certain.75 Even prasugrel may be loaded before catheterization in STEMI. Yet, ATLANTIC trial failed to show a benefit of pre-cath loading vs. loading during PCI.76Ticagrelor and prasugrel are preferred as they further reduce ischemic events compared to clopidogrel, particularly in STEMI.
3 Upstream unfractionated heparin (UFH) in the ED (60 units/kg, up to a maximum dose of 4000 units).
4 During PCI:UFHBivalirudin vs. UFH: initial studies suggested lower bleeding with bivalirudin, but these studies were flawed by an unbalanced GPI use with
