In the OAT trial, patients with MI older than 24 hours (1–28 days old specifically, mainly STEMI/Q-wave MI), who were selected based on the following features did not benefit from PCI and had a trend towards more frequent reinfarctions:53
Totally occluded infarct-related artery (TIMI 0 or 1 flow)
Akinetic or dyskinetic infarcted wall
One- or two-vessel CAD
No recurrent rest or low-threshold angina
No severe ischemia on stress testing
No shock and no persistent functional class III–IV HF
Further analysis showed that PCI was not beneficial even among patients enrolled 1–3 days after MI onset.54 Thus, late PCI of an occluded infarct artery is only indicated in patients with persistent ischemic symptoms, persistent HF, or severe ischemia on stress testing.
On the other hand, data suggest that an infarct artery that is not totally occluded (TIMI 2–3 flow) may benefit from late revasculariza- tion (>24 h) to the same extent that it may benefit from early revascularization, as a patent infarct artery with good collaterals is associated with a more limited MI size and a significant amount of viable myocardium that can be salvaged with revascularization.55-57 Approximately 35% of totally occluded infarct-related arteries spontaneously recanalize in the first 24 hours and may qualify for late revascularization.
Therefore, patients who did not receive emergent reperfusion (late presenters >24 hours) or patients who received fibrinolytics, with or without response, but did not undergo angiography in the first 24 hours after symptom onset may still undergo angiography later than 24 hours (class II):
A non-occluded infarct-related artery may be treated with PCI (class IIb).
Left main disease or three-vessel CAD that largely extends beyond the occluded artery should receive revascularization, typically surgical revascularization, after a post-MI waiting period of at least 3–7 days.
A totally occluded artery should not be treated with PCI unless the patient has a low-threshold angina, severe ischemia on stress testing (class I), or persistent HF after initial therapy (high-risk case with stress test contraindication). If not performed before angiography, the stress test may be performed afterwards, and the patient brought back for PCI once severe ischemia is documented.
If one is unsure that the MI is >24 hours old, PCI may still be performed. While not beneficial, late PCI in the OAT trial was not significantly harmful either, which may justify its use when timing is unclear. Not that ESC uses 48 hours cutoff for avoidance of routine PCI.
Table 2.2 summarizes the PCI timelines. Questions 2, 9,10, and 14 at the end of this chapter illustrate these concepts.
As an alternative to coronary angiography, patients who have not been managed invasively in the first 24 hours of STEMI and who are stable, without persistent HF and angina, may undergo stress testing rather than angiography. In those stable patients, a submaximal stress test (modified Bruce protocol) may be performed 4 days after STEMI onset, and a maximal stress test (symptom-limited Bruce protocol) may be performed 5–14 days later. Severe ischemia or angina on stress testing dictates coronary angiography and revascularization. If no significant residual ischemia is detected, only medical therapy is provided.
As opposed to NSTEMI, where stress testing is avoided even in patients who become free of angina, stress testing is indicated in stable post-STEMI patients free of angina. In NSTEMI, the amount of myocardial necrosis is usually minor and revascularization is needed to salvage a large area of ischemic but non-infarcted myocardium. In non-reperfused STEMI, the myocardium is already largely infarcted and unlikely to benefit from revascularization, unless residual angina or ischemia is shown.
Table 2.2 Revascularization timelines in STEMI.
<12 h after STEMI onset: Emergent primary PCI or fibrinolytic therapy (class I, level of evidence A) 12–24 h: Emergent primary PCI (class IIa). ESC uses 48-h cutoff >24 h: Delayed, non-emergent PCI for: (i) recurrent angina, (ii) severe ischemia on stress testing (class I), (iii) persistent HF. After fibrinolytic therapyDelayed routine PCI 3–24 h later (2-24 h per ESC) (class IIa ACC, class I ESC)Rescue PCI for fibrinolytic failure (class I ESC) If PCI was not performed in the first 24 h, whether the patient received fibrinolytic therapy, with or without success, or did not receive fibrinolytic therapy In the absence of angina recurrence, stress testing is an alternative to coronary angiography. Coronary angiography and late revascularization have the following recommendations:Coronary angiography >24 h after STEMI onset: class IIaPCI of a stenotic but not totally occluded artery: class IIbAvoid PCI of a totally occluded artery >24 h (OAT trial, class III), except in cases of recurrent angina, high-risk stress test (class I), persistent HF with severe functional limitation, or uncertain timing. ESC uses 48-h cutoffCABG if left main or three-vessel CAD extending largely beyond the infarct artery Cardiogenic shock or acute severe HF (massive pulmonary edema = Killip III): emergent PCI regardless of time (class I) |
Ischemia and viability are two different entities, ischemia being the one most definitely improved with revascu-larization (SWISSI-2 trial). Viability implies that at rest, the infarcted territory can uptake significant nuclear agent. Conversely, ischemia implies that at stress, the nuclear defect in the infarcted or peri-infarct territory is significantly more intense or more extensive than at rest; or significant/extensive ST-segment deviations occur. A territory may be viable but non-ischemic, meaning it is already receiving enough perfusion, in which case the benefit of revascularization is less clear. In a substudy of OAT patients who received viability testing, viability did not predict a benefit from late PCI.58 Conversely, in the SWISSI-2 trial, asymptomatic patients who had a STEMI or a NSTEMI 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