thrombosis or resting pain is accompanied by a troponin rise. Unstable angina is, thus, a vanishing entity. 32
The patient either has non-cardiac pain, stable angina (sometimes severe), or true ACS with positive troponin. The negative troponin, truly “unstable angina” is rare and is more in the realm of severe or progressive stable angina than unstable CAD with plaque rupture.
G. Additional notes: definition of reinfarction, type 3 MI, post-PCI MI (type 4 MI), and post-CABG MI (type 5 MI)
In patients with a recent infarction (a few days earlier), the diagnosis of reinfarction relies on:
CK or CK-MB re-elevation, as they normalize faster than troponin, or
Change in the downward trend of troponin (re-increase > 20% above the nadir)1
Type 3 MI is defined as sudden death with preceding clinical and ECG features suggestive of MI, such as VF.
In the post-PCI context, MI is diagnosed by a troponin elevation > 5× normal, along with ischemic ST changes or Q waves, new wall motion abnormality, or angiographic evidence of procedural complications.1 In patients with elevated baseline cardiac markers that are stable or falling, post-PCI MI is diagnosed by > 20% reincrease of the downward trending troponin to a value >5x normal, along with the other features (most studies use a 50% rather than a 20% cutoff in the post-PCI context). Note that spontaneous NSTEMI carries a much stronger prognostic value than post-PCI NSTEMI, despite the often mild biomarker elevation in the former (threefold higher mortality).33,34 In fact, in spontaneous NSTEMI, the adverse outcome is related not just to the minor myocardial injury but to the ruptured plaques that carry a high future risk of large infarctions. This is not the case in the controlled post-PCI MI. Along with data suggesting that only marked CK-MB elevation carries a prognostic value after PCI, an expert document has proposed the use of CK-MB ≥ 10× normal or troponin ≥70x normal to define post-PCI MI, rather than the mild troponin rise.34
In the post-CABG context, MI is diagnosed by a troponin elevation > 10× normal, associated with new Q waves or new wall motion abnormality.1
Additional note: importance of LVEDP
The determination of LVEDP is critical in patients with ACS and insignificant CAD. Elevated LVEDP from acute diastolic dysfunction or severe HTN is a common cause of mild troponin elevation in patients with normal coronary arteries. Microvascular coronary flow is driven by the gradient between diastolic blood pressure and LVEDP; thus, microvascular flow is impeded by an elevated LVEDP. In fact, a gradient of 40 mmHg between diastolic blood pressure and CVP, or by extrapolation, LVEDP, is a zero-flow gradient, as at least 40 mmHg is required to overcome the microvascular resistance.35
II. Clinical features, ECG, cardiac biomarkers, and echocardiography in ACS
A. Assess the clinical features of chest pain (Table 1.2)
The relief of chest pain with sublingual nitroglycerin does not reliably predict ACS. Similarly, the relief of chest pain with “GI cocktail” does not predict the absence of ACS.36
Chest pain lasting over 30-60 min with consistently negative markers usually implies a low ACS likelihood. A prolonged pain is usually one of 2 extremes, an infarct or a non-cardiac pain.
B. ECG
The following ECG findings are diagnostic of non-ST elevation ischemia:
ST depression ≥ 0.5 mm, especially if transient, dynamic, not secondary to LVH, and occurring during the episode of chest pain.
Deep T-wave inversion ≥ 3 mm (T inversion < 3 mm is non-specific).
Transient ST elevation (lasting < 20 minutes). This corresponds to a thrombus that occludes the lumen off and on, an unstable plaque with vasospasm, or, less commonly, a stable plaque with vasospasm.
ST depression in ≥6 leads with ST elevation in aVR or V1 suggests left main or 3-vessel CAD
On the other hand, LVH and bundle branch blocks are not specific for ischemia and make the ECG less interpretable. They do predict an intermediate risk of in-hospital complications (vs. high risk for dynamic ST depression).4,39 As per ESC guidelines: “hemodynamically stable patients presenting with chest pain and LBBB only have a slightly higher risk of MI compared to patients without LBBB.“
Only 50% of patients with non-ST elevation ACS have an ischemic ECG,40 and 20% of NSTEMIs have an absolutely normal ECG.41,42 Yet, patients with ischemic ECG are higher-risk patients and most often have LAD or multivessel involvement.
ECG performed during active chest pain has a higher sensitivity and specificity for detection of ischemia. However, even when performed during active ischemia, the ECG may not be diagnostic, particularly in left circumflex ischemia. In fact, up to 40% of acute LCx total occlusions and 10% of LAD or RCA occlusions are not associated with significant ST-T abnormalities, for various reasons: (i) the vessel may occlude progressively, allowing the development of robust collaterals that prevent ST elevation or even ST depression upon coronary occlusion; (ii) the ischemic area may not be well seen on the standard leads (especially posterior or lateral area); (iii) underlying LVH or bundle branch blocks may obscure new findings; a comparison with old ECGs is valuable. In general, ~15–20% of NSTEMIs are due to acute coronary occlusion, frequently LCx occlusion, and may be, pathophysiologically, STEMI-equivalents missed by the ECG and potentially evolving into Q waves.43 NSTEMI patients with acute coronary occlusion have a higher 30-day mortality than patients without an occluded culprit artery, probably related to delayed revascularization of a STEMI-equivalent.44
To improve the diagnostic yield of the ECG:
In a patient with persistent typical angina and non-diagnostic ECG, record the ECG in leads V7–V9. ST elevation is seen in those leads in > 80% of LCx occlusions, many of which are missed on the 12-lead ECG.
Repeat the ECG at 10–30-minute intervals in a patient with persistent typical angina.
Perform urgent coronary angiography in a patient with persistent distress and a high suspicion of ACS, even if ECG is non-diagnostic and troponin has not risen yet.
ECG should be repeated during each recurrence of pain, when the diagnostic yield is highest. ECG should also be repeated a few hours after pain resolution (e.g., 3–9 hours) and next day, looking for post-ischemic T-wave inversion and Q waves, even if the initial ECG is non-diagnostic. The post-ischemic T waves may appear a few hours after chest pain resolution.
Table 1.2 Clinical features of chest pain
| Clinical features suggestive of angina Typical angina is reproduced or worsened by exertion. In case of vasospasm, angina may occur only at rest or at night without an exertional component Severe distress, deep fatigue, diaphoresis, jaw radiation, or severe nausea during pain is concerning for angina (the latter symptoms may occur without pain and are called “angina equivalents”) Prior history of CAD or MI with typical angina or symptoms mimicking prior MIa New MR murmurb |
|
Clinical features suggestive of a low angina likelihood (the 3 Ps) Chest pain that is P ositional or reproduced with certain chest/arm movements P leuritic pain (↑ with inspiration or cough: suggests pleural or pericardial pain, or costochondritis) P alpable
|