Practical Cardiovascular Medicine. Elias B. Hanna

target="_blank" rel="nofollow" href="#ulink_64dc967e-81cc-576b-96f0-9276978d5165">* The GRACE risk score accounts for troponin and ST changes, but also for increasing age, history of HF, tachycardia, hypotension, and renal function.TIMI risk score:1. Age ≥65 years----2. ≥ Three risk factors----3. History of coronary stenosis ≥50%4. ≥ Two episodes of pain in the last 24 hrs----5. Use of aspirin in the prior 7 days (implying aspirin resistance)6. Elevated troponin---- 7. ST deviation ≥0.5 mmA score of 3 or 4 is intermediate risk; 5–7 is high risk. Risk of mortality/MI/urgent revascularization at 14 days: 13% if score = 3; 20% if score = 4; 26% if score = 5; 40% if score = 6/7.

      4 * Also, always avoid β-blockers acutely and chronically in cases of second- or third-degree AV block, PR interval > 240 ms, bradycardia < 55 bpm, or active bronchospasm. Beyond the first day, SBP below 100 mmHg, rather than 120 mmHg, is the contraindication to β-blockers.

2 ST-Segment Elevation Myocardial Infarction

        1. Definition, reperfusion, and general management I. Definition II. Timing of reperfusion III. ECG phases of STEMI IV. STEMI diagnostic tips and clinical vignettes V. Specific case of new or presumably new LBBB VI. Reperfusion strategies: fibrinolytics, primary PCI, and combined fibrinolytics–PCI VII. Coronary angiography and PCI later than 24 hours after presentation-role of stress testing VIII. Angiographic findings, PCI, and cellular reperfusion; multivessel disease in STEMI IX. Antithrombotic therapies in STEMI X. Other acute therapies XI. Risk stratification XII. LV remodeling and infarct expansion after MI XIII. Discharge, EF improvement, ICD

        2. STEMI complications I. Cardiogenic shock II. Mechanical complications III. Recurrent infarction and ischemia IV. Tachyarrhythmias V. Bradyarrhythmias, bundle branch blocks, fascicular blocks VI. LV aneurysm and LV pseudoaneurysm VII. Pericardial complications VIII. LV thrombus and thromboembolic complications IX. Early and late mortality after STEMI

        Appendix 1. Out-of-hospital cardiac arrest: role of early coronary angiography and therapeutic hypothermia

        Questions and answers

1. DEFINITION, REPERFUSION, AND GENERAL MANAGEMENT

      I. Definition

      STEMI is a clinical syndrome of angina or angina equivalent along with:^1–3

       ST-segment elevation ≥2 mm in men or ≥1.5 mm in women in leads V2–V3, or ≥1 mm in two other contiguous chest or limb leads, with a shape consistent with ischemic ST elevation. The shape must be distinguished from early repolarization, pericarditis, or ST-segment elevation secondary to LVH or LBBB; emergent echo or coronary angiography may be performed in case of doubt.

       or:

       Isolated or most prominent ST-segment depression in leads V1–V3 ≥ 0.5 mm, which is reciprocal to posterior ST elevation in leads V7-V9 (true posterior STEMI). In leads V7–V9, the ST-segment elevation cutoff is only 0.5 mm, as the distant location of these leads behind the heart minimizes ST-segment elevation.

      ST-segment elevation below these cut-points may still imply myocardial injury when the clinical setting or the ST-segment morphology suggests ischemia. Emergent reperfusion may still be indicated in these patients, generally with PCI (thrombolysis is not an established therapy for mild degrees of ST elevation, <1 mm).

      Conversely, ST-segment elevation that exceeds these cut-points may not represent STEMI. Careful attention to the morphology of the ST segment and the associated features (Q wave, inverted or ample T wave) is critical.

      STEMI usually evolves into electrocardiographic Q waves (Q-wave MI) and is usually a transmural and large MI. NSTEMI usually evolves into a non-Q-wave MI and is usually a subendocardial, smaller MI. However, there is some overlap: STEMI may not generate Q waves while NSTEMI may generate Q waves.

      Since it takes up to 3 hours for troponin to rise after the onset of infarction, it should not be relied upon for the diagnosis or initiation of emergent therapies.

      Approximately 12.5% of MIs are totally silent and ~12.5% have a mild, atypical presentation (e.g., dyspnea, malaise, nausea).⁴ These cases go unrecognized, and patients may present with HF days or months after acute MI. This presentation is more common in diabetic and elderly patients.

II. Timing of reperfusion

      1 Emergent reperfusion with PCI or fibrinolytics is indicated in patients who present within 12 (24) hours of symptom onset and who have persistent ST elevation in two or more contiguous leads or ST depression that is isolated or most prominent in V1–V3 (class I recommendation for PCI or fibrinolytics at ≤12 h, class IIa for PCI at 12–24 h).¹ This applies even if ischemic symptoms have resolved, as long as ST elevation is persistent and the onset of ischemic symptoms is ≤24 hours.PCI is the preferred strategy, and it should be performed with a door-to-balloon time (DTB) of ≤90 min in patients presenting to PCI- capable hospitals, and ≤120 min in patients transferred from non-PCI-capable to PCI-capable hospitals. If PCI cannot be performed with a DTB of ≤120 min, fibrinolytics should be given to patients presenting within 12 hours of symptom onset (initiated ≤ 10 min from diagnosis).^* Regardless of the setting, the DTB that mitigates PCI’s benefit over fibrinolysis is 120 min (ESC).

      2 Patients presenting >24 hours after symptom onset generally do not have an indication for emergent PCI. Emergent PCI (not fibrinolysis) is selectively indicated in some of these patients, such as patients with persistent ischemic symptoms, cardiogenic shock, acute severe HF with massive pulmonary edema, or when the onset of STEMI is not clearly >24 hours.Otherwise, non-urgent coronary