Читать книгу Practical Cardiovascular Medicine - Elias B. Hanna - Страница 25

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 pain localized at a fingertip area and fully reproduced with palpationc Pain > 30–60 min with consistently negative troponin Very brief pain < 15 s

^a Traditional CAD risk factors are only weakly predictive of the likelihood of ACS during a given presentation.³⁶ For example, shoulder pain that mainly occurs with shoulder movements is unlikely angina, even in a diabetic patient with prior MI. Once ACS is otherwise diagnosed, diabetes and PAD do predict a higher ACS risk.

^b A new MR murmur in a patient with chest pain is considered ischemic MR until proven otherwise.

^c True angina and PE pain may seem reproducible with palpation, as the chest wall is hypersensitive in those conditions. A combination of multiple low-likelihood features (e.g., reproducible pain that is also positional and sharp), rather than a sole reliance on pain reproducibility, better defines the low-likelihood group.^37,38