Appendix A.
Definitions
Chest pain with ischemic profile: chest tightness or anterior chest at rest or exercise radiating to the neck, left arm, or both during >1 min with or without adrenergic manifestations.
Chest pain with non-typical ischemic profile: does not meet the criteria of pain with ischemic profile, however suggesting myocardial ischemia as tightness in lower jaw, anterior neck, epigastrium, etc.
Previous angina: chest pain with ischemic profile, characteristic or not, or equivalent prior to current index event.
Equivalent of ischemia: this kind of ischemia clinical expression has different age-related variations. Ventricular arrhythmias, first event of heart failure without a clear etiology, sudden pulmonary edema, dyspnea at rest or exercise, syncope, mental confusion, asthenia, adynamia, anorexia associated with objective evidence of ischemia, micro, macronecrosis or both (Appendix B).12
Electrocardiogram
Nonspecific: ST depression <0.05 mV or negative asymmetrical T wave <0.2 mV, ventricular hypertrophy, pacemaker rhythm.13-15
ST depression: depression >0.05 mV in two underlying leads or negative symmetrical T wave >0.2 mV.13,16
Transient ST elevation: J point positive slope (>0.2 mV in V1-V3 and >0.1 mV in other leads) in two underlying leads with ST normalization or residual negative deep T wave, spontaneously or secondary therapeutic action.13,16
Persistent ST elevation: positive slope at J point (>0.2 mV in V1-V3 and >0.1 mV in other leads) in two underlying leads.13,16
Electrocardiographic criteria of infarction and left bundle branch block
According to the Mexican electrocardiography school in the context of a left bundle branch block bundle the presence of Q wave in DI, aVL, V5 or V6 leads this suggests a septal infarction; loss of QRS voltage with Q wave in V4, V5 and V6 may correspond to an anteroseptal infarction. The presence of RS or rs with negative T wave (intracavitary lead) in V4-V6 could translate a left ventricular transmural infarction. In Appendix C criteria of Sodi Pallares and Sgarbossa can be observed.14,15
J point moving in the opposite direction to the predominant QRS deflection (negative in the presence of R wave, positive in the presence of S wave) with a magnitude of displacement up to 5 mm is required. The ST and T wave will show the same polarity, behaving as a single pathophysiological entity. A ST elevation in an acute myocardial infarction associated with this conduction disturbance is divided into concordant and discordant. ST elevation ≥0.1 mV (1 mm) in leads with R wave or ST negative slope ≥0.1 mV in leads V1-V3 (with dominant S wave) is called concordant. ST elevation 0.5 mV (5 mm) in leads with S wave is called discordant.15
Acute coronary syndromes groups according to ECG
a) Normal or nonspecific
b) Negative ST depression
c) Transient ST elevation
d) Persistent ST elevation
ST elevation myocardial infarction
a) History of chest pain or discomfort with ischemic profile or not, ≥20 min.
a. Equivalent associated with persistent ST elevation and abnormal biomarkers.
b) ECG with persistent ST elevation >1 mm in at least two underlying leads or left bundle branch block or tall R wave (40 ms) in V1 and V2 leads associated with ST depression V1-V3 and right leads.
c) Elevation of cardiac biomarkers serum levels (preferably troponin) with at least one value above the upper reference limit of 99th percentile.
d) Two-dimensional echocardiogram demonstrating new or presumably new abnormality of regional or global mobility.
Ischemia evidence: Demonstration and objective documentation of myocardial ischemia by echocardiography or nuclear medicine.13,16
Myocardial infarction clinical classification
Uncomplicated: normal blood pressure without left ventricular dysfunction signs, EF >40%, brain natriuretic peptide type-B (BNP) <100 pg/dL, or both.
Complicated with left ventricular dysfunction without clinical manifestations: normal blood pressure or lower limits, no third left ventricular heart sound, EF <40%, or both, BNP >100 pg/dL, or both.
Complicated with ventricular dysfunction with clinical manifestations: acute pulmonary edema or pre-cardiogenic shock suspicion (borderline blood pressure, hypotension, or both, clinical expression of -renin-angiotensin-aldosteronevasopressin system activity, oliguria, delayed capillary refill, lower lobes crackling rales, EF <30%, BNP >600 pg/dL.
Killip and Kimball classification
I: without left ventricular dysfunction signs
II: left ventricular third heart sound, basal crackling rales, or both
III: acute pulmonary edema
IV: cardiogenic shock
Pulmonary edema: increased work of breathing with or without severe desaturation (saturation <90%), left ventricular gallop or tachycardia, crackling rales or wheezes >50% in lung fields. Chest X-ray with interstitial, alveolar, or mixed pulmonary edema.
Cardiogenic shock: (1) systolic blood pressure <90 mmHg without support of vasoactive substances or 100 mmHg with vasopressors use; (2) clinical, radiographic expression of pulmonary venocapillary hypertension, or both; (3) signs of peripheral vascular hypoperfusion; (4) metabolic acidosis; (5) cardiac index <2.2 L/min/m2; (6) pulmonary capillary pressure >18 mmHg; and (7) arteriovenous oxygen difference >5.5 ml/dL.
Risk stratification in ACS without ST elevation
Variables predictors of poor in-hospital outcome according to odds ratio (OR) and confidence intervals (CI) were selected from RENASICA II3 multivariate analysis: diabetes (OR 3.1, CI 1.94-5.06, and p < 0.0001); ischemic chest pain >20 min (OR 2.3, CI 1.43-3.69, and p 0.0006); heart failure history (OR 2.2, CI 1.16-4.23, and p 0.01); age >65 years old (OR 1.8, CI 1.27-2.67, and p 0.001); positive troponin (OR 1.7, CI 1.05-0.97, and p 0.02); and ST depression >3 leads (OR 1.6, CI 1.08-2.61, and p 0.02).
Effectiveness
Percutaneous coronary intervention
Angiographic: antegrade reperfusion of culprit artery with TIMI III flow and adequate myocardial perfusion.13
Electrocardiographic: ST decreased >70% in the most meaningful leads in an ECG taken 90 min after angiographic reperfusion regarding index event ECG.13
After pharmacological reperfusion
Electrocardiographic: ST decreased >70% in the most meaningful leads in an ECG taken 90 min after pharmacological fibrinolysis the fibrinolytic regarding index event ECG.13
Security
Major bleeding: Fatal bleeding, documented retroperitoneal, intracranial, or intraocular bleeding, bleeding resulting in hemodynamic compromise requiring specific treatment, bleeding requiring surgical intervention or decompression of a closed space to control the event, any transfusion >1 unit red packed cells or whole blood or a hemoglobin drop >3 g/dL or more or hematocrit >10%.17
Minor bleeding: microscopic hematuria not associated with trauma by ureteral procedures. Prolonged or recurrent epistaxis requires plugging or intervention; gastrointestinal or subconjunctival bleeding or hemoptysis. Hematoma >5 cm related with length in-hospital stay or new hospitalization. Bleeding decreasing hemoglobin drop <3 g/dL or considering duration requires protamine sulfate.17
Fibrinolysis inducing hypotension: Blood pressure ≤90/60 mmHg during or at the end of the fibrinolytic infusion without other apparent reason.
Percutaneous coronary intervention
Primary angioplasty: with or without stent; without prior or concomitant fibrinolytic therapy or glycoprotein IIb/IIIa use.13
Rescue angioplasty: coronary intervention in patients after unsuccessful fibrinolytic therapy (persistent chest pain, ST elevation or decrease <70%, or both on an ECG at 90 min).
Percutaneous coronary intervention
Residual lesion: ≤30% and epicardial TIMI flow 3.
Suboptimal: Residual lesion: >30% and epicardial TIMI flow 2.
Failed: obstructive residual lesion ≥70% and TIMI flow 0-2 or when the guide wire fails through the atherosclerotic lesion.13
TIMI flow before procedure:
TIMI 0: total absence of flow
TIMI 1: slight penetration of the contrast medium without reaching the obstructive lesion or the terminal portion of the vessel
TIMI 2: penetration of the contrast medium reaches the obstructive lesion but not exceeded or the entire artery and typically presents with low flow
TIMI 3: normal coronary flow.13
TIMI flow after procedure:
TIMI 0: total absence of flow
TIMI 1: slight penetration of the contrast medium without reaching the obstructive lesion or the terminal portion of the vessel
TIMI 2: penetration of the contrast medium reaches the obstructive lesion but not exceeded or the entire artery and typically presents with low flow
TIMI 3: normal coronary flow.13
TIMI myocardial perfusion grade (TMPG) before procedure:
TMPG 0: No or minimal blush
TMPG 1: Stain present. Blush persists on next injection
TMPG 2: Dye strongly persistent at end of washout. Gone by next injection
TMPG 3: Normal ground glass appearance of blush. Dye mildly persistent at end of washout.18
TIMI myocardial perfusion grade (TMPG) after procedure:
TMPG 0: No or minimal blush
TMPG 1: Stain present. Blush persists on next injection
TMPG 2: Dye strongly persistent at end of washout. Gone by next injection
TMPG 3: Normal ground glass appearance of blush. Dye mildly persistent at end of washout.18
Major adverse cardiovascular events
Recurrent ischemia: new chest pain episode with ischemic profile (treatment with two antiischemic drugs at least) >5 min, with ST dynamic ECG changes, and without myocardial necrosis.
Reinfarction: Two or more of the following criteria: (1) chest pain with ischemic profile ≥20 min; (2) new ST elevation (>0.1 mV) in two underlying leads or new Q wave; (3) CK-MB new elevation ≥50% normal high upper limit or ≥50% of baseline.
Cardiogenic shock: (1) systolic blood pressure <90 mmHg without support of vasoactive substances, or 100 mmHg with vasopressors; (2) clinical, chest X-ray expression of pulmonary venocapillary hypertension, or both; (3) signs of peripheral vascular hypoperfusion manifested by oligoanuria <1 ml/kg/h; (4) metabolic acidosis; (5) cardiac index <2.2 L/min/m2; (6) pulmonary capillary pressure >18 mmHg; and (7) arteriovenous oxygen difference >5.5 ml/dL.
Cardiovascular death: Secondary to acute coronary ischemic event index or new in-hospital event or during follow-up.
Acute cerebrovascular disease: Loss of neurological function secondary to an ischemic, embolic or bleeding event. Ideally, objective evidence through computerized axial tomography or magnetic resonance must be obtained.
Ventricular fibrillation: Chaotic rhythm with total absence of isoelectric line and total absence of atrial contraction. Ventricular tachycardia: Four or more consecutive ventricular extrasystoles; is considered as not sustained <30 s or sustained >30 s.
Hyperlipidemia: Cholesterol >200 mg/dL or normal levels with treatment.
Previous infarction: Necrosis demonstration by ECG, echocardiography, nuclear medicine or nuclear magnetic resonance.
Mitral insufficiency: Regurgitation murmur radiating to the axilla and objective demonstration by echocardiography and ventriculography.
Renal failure: Serum creatinine >2.0 mg/dL.
Renal dysfunction
Moderate: 50-30 mL/min
Severe: <30 mL/min
Cocroft Gault formula
Serum creatinine clearance = (140 - Age expressed in years) × (Weight expressed in kilograms)
Serum creatinine (mg/dL) × 72
Cardiac arrest: Electromechanical or asystole dissociation.
Pericarditis: Suggestive chest pain with or without pericardial rub and suggestive ECG changes.
Sepsis: Toxi-infectious medical condition characterized by multiple organ failure, incipient or advanced hematological alterations and clinical data of tisular hypoperfusion.
Pulmonary embolism: High risk: sudden dyspnea associated with chest pain or syncope with echocardiographic right ventricular dysfunction, BNP >100 pg/d, or both, dimer D >500, and objective demonstration by radionuclide lung scintigraphy V/P, or pulmonary angiography, or CT angiogram, or magnetic resonance.19
Pulmonary embolism: common risk: sudden dyspnea, tachycardia, pleural pain, without right ventricular dysfunction by ECHO, BNP <100 pg/dL, or both, dimer D >500, and objective demonstration by radionuclide lung scintigraphy V/P, or pulmonary angiography, or CT angiogram, or magnetic resonance.19