hours old, at a stage where ST elevation is resolving but has not fully resolved yet (close to phase 3). Alternatively, STEMI may be more recent with ongoing or resolving ischemia. This patient does not qualify for fibrinolytics, as ST elevation is <1 mm and the occlusion duration is questionable, but qualifies for emergent PCI if the discomfort is ongoing or if the discomfort occurred within the last 24 hours, even if it is not ongoing.
7. A patient presents with chest pain that has lasted 2–3 hours earlier today and has now resolved. His ECG shows inferior Q waves and T-wave inversion, without any significant ST elevation. Should he undergo emergent reperfusion?
PCI is preferably, but not necessarily, performed emergently. Resolution of ST elevation with appearance of Q waves (phase 3) often implies a late presentation, >12–24 hours, but may also occur after a brief ischemia, e.g., 1–2 hours, as in this case. This patient does not qualify for fibrinolysis (no residual ST elevation). He still qualifies for PCI, not necessarily on an emergent basis.
In general, a patient qualifies for emergent PCI with either of the following two conditions: (i) persistent ST elevation with a presentation less than 24 hours after pain onset (even if pain is not persistent); (ii) persistent pain, even if the patient presents later than 24 hours after pain onset and even if ST elevation has resolved.
V. Specific case of new or presumably new LBBB
Normally, LBBB is associated with ST-segment deviation that is discordant to QRS, i.e., directed opposite to QRS. If a patient has an ischemic presentation and LBBB on the ECG, one cannot tell whether ST elevation is purely secondary to LBBB, if an ischemic injury is partially contributing to the ST elevation, or if there is ischemic ST depression masked by the ST elevation. STEMI is definite if ST abnormality is concordant to QRS, but STEMI or non-ST elevation ischemia is still possible if ST changes are discordant to QRS. This would be the case of a patient with a true anterior injury in V1–V4 or inferior injury, where LBBB’s QRS is negative and where ischemic ST elevation would inherently appear discordant. RBBB, on the other hand, is not associated with significant ST abnormality, and thus ST changes in a patient with RBBB are diagnostic of ischemia. Early thrombolytic trials and their meta-analysis have shown a striking benefit from thrombolytic therapy in patients with any bundle branch block, particularly that a new bundle branch block in STEMI indicates a high-risk STEMI.10 Both types of bundle branch blocks, if secondary to STEMI, represent high-risk categories, but since only LBBB poses a diagnostic challenge, a new or presumably new LBBB has been considered a STEMI equivalent in old ACC guidelines, in order not to miss a high-risk STEMI.
However, STEMI rarely causes left bundle branch infarction, because the left bundle is supplied by both the LAD and RCA and is only affected in extensive infarction. In the GUSTO-1 trial, only ~1% of STEMIs had LBBB on presentation. In fact, a new LBBB often results from a chronic cardiomyopathy, ischemic or non-ischemic, with a dilated or hypertrophied myocardium, rather than an exten- sive acute infarction, and may be first diagnosed in the setting of HF presentation or uncontrolled HTN. 11 A new LBBB may also be rate-related and may have been unveiled by an increase in heart rate.
Evidence has shown that only ~10% of patients with an ischemic presentation and a new LBBB have a STEMI-equivalent (acute coro- nary occlusion on angiography), and <40% have any MI, most commonly NSTEMI.12–15 STEMI is even far less likely when all comers with new LBBB, both atypical or typical presentations, are included (<5%).14 Therefore, in order to make the diagnosis of STEMI, an ischemic presentation is required (ongoing angina, flash pulmonary edema) along with additional ECG features:
Concordant ST-segment depression or elevation of ≥1 mm is >95% specific for the diagnosis of STEMI, but has a limited sensitivity of 20% (Sgarbossa’s concordance). If present, STEMI diagnosis is definite, and emergent reperfusion with fibrinolytics or PCI should be achieved.
Concordant negative T wave or biphasic T wave in multiple leads increases the likelihood of STEMI.
Extreme discordance increases the likelihood of STEMI but has a reduced specificity: discordant ST elevation that exceeds 25% of the QRS height; or upright T wave that exceeds 50% of the QRS height. This discordance ratio is more sensitive and specific than an absolute ST discordance >5 mm, initially suggested by Sgarbossa, but may still be seen in 9% of control patients without MI.16
In the absence of these features, particularly Sgarbossa’s concordance, and in the absence of ongoing typical angina, it is reasonable to urgently perform bedside echocardiography. The presence of a segmental wall motion abnormality without severe thinning, aneurysm, or severe LV dilatation suggests acute ischemia and warrants early angiography; fibrinolytics are preferably avoided since many of these patients have NSTEMI rather than STEMI, and transfer for angiography is preferred even if delays are expected to exceed 120 minutes.12 Abnormal septal motion is universal with LBBB but the anterior and apical contraction is preserved; therefore, anterior and apical akinesis implies ischemia. Global hypokinesis often implies ischemic or non-ischemic cardiomyopathy, such as hypertensive cardiomyopathy, rather than acute ischemia;11 angiography may be needed eventually but is not urgent.
Thus, the 2013 STEMI guidelines state that “new or presumably new LBBB should not be considered diagnostic of acute myo- cardial infarction (MI) in isolation.” 1 The 2020 ESC ACS guidelines state: “hemodynamically stable patients presenting with chest pain and LBBB only have a slightly higher risk of having MI compared to patients without LBBB.”
VI. Reperfusion strategies: fibrinolytics, primary PCI, and combined fibrinolytics–PCI
A. Fibrinolytics (also called thrombolytics): mortality benefit
In the GISSI-1 and ISIS-2 trials and a large meta-analysis, fibrinolytics (mainly streptokinase) have shown:10,17–19
A striking 6.5% absolute mortality reduction and 50% relative mortality reduction in the first hour after STEMI onset, called the golden hour
A 4% absolute mortality reduction in the second hour
A plateau 3% mortality reduction between 3 and 6 hours (relative mortality reduction ~25%)
Absolute mortality reduction of ~2% between 6 and 12 hours. Beyond that, between 12 and 24 hours, the benefit is marginal and questionable.
This time-dependent benefit is due to the fact that very early reperfusion of the occluded coronary artery may lead to full recovery of the ischemic tissue and thus prevent necrosis. In addition, fibrinolytic therapy in the first 2–3 hours is highly efficacious in lysing a fresh thrombus.
The benefit is more striking in high-risk subgroups, such as anterior STEMI, STEMI with bundle branch block, or high STEMI risk score (tachycardia, hypotension). The elderly subgroup is the only high-risk subgroup that, paradoxically, only derives a marginal benefit from fibrinolysis; this is partly because of the high bleeding risk but also because of the more extensive CAD that makes it less likely for fibrinolysis to re-establish perfusion; a half-dose TNK is recommended in patients ≥75 (ESC class IIa).
The mortality benefit is also more striking with the fibrin-specific fibrinolytics (~1% additional mortality reduction).
B. Fibrinolytics: limitations, contraindications, definition of successful response, and definition of TIMI flow (Table 2.1)1,10,20,21
In addition to the classic contraindications, fibrinolysis is contraindicated in a patient with an expected intracranial bleeding risk of >4% (e.g., an elderly [>75] small woman with HTN).20
Consider fibrinolytic therapy successful if: chest pain resolves and