A. Summary Recommendations [1]

1. Acute Coronary Syndromes (ACS) include:
   1. MI with ST segment elevation (STEMI) or new left bundle branch block (LBBB)
   2. Non ST segment MI (that is, ST segment depression or T wave changes, NSTEMI)
   3. "Unstable Angina" - no ST segment elevation, only reversible myocardial damage
2. All MI patients receive aggressive therapy with:
   1. Antiplatelet agent: aspirin (ASA), clopidogrel, platelet glycoprotein 2b3a (GP2b3a) inhibitor
   2. Anticoagulation: unfractionated or low molecular weight (LMW) heparin or fondaparinux [7]
   3. Anti-ischemic agent: ß-adrenergic blockers (as tolerated), intravenous (IV) nitroglycerin
   4. Early revascularization is generally preferred due to survival benefits [2]
3. Revascularization Strategies [2,3,8,35,71]
   1. Percutaneous coronary Intervention (PCI) with stenting is preferred initial modality for STEMI and high risk NSTEMI and possibly in high risk "unstable angina"
   2. Primary angioplasty is more effective and safer than hospital-based thrombolysis [38]
   3. PCI should be used in any patient who is not a candidate for thrombolysis [6]
   4. Thrombolytics should not be given prior to primary PCI for MI as they increase major adverse events [14,15]
   5. Thrombolytics may be as effective as PCI for MI within 2-3 hours and without Q waves, even in STEMI [29]
4. Catherization Laboratory Not Available [71]
   1. Transfer to catheterization laboratory within 2 hours preferable to on-site fibrinolysis [5]
   2. In STEMI presenting within 2-3 hours and no Q waves on ECG, fibrinolysis is at least as good as PCI [29]
   3. Bolus infusion of fibrinolytic agent should be combined with platelet GP 2b/3a inhibitor
   4. Prehospital fibrinolysis may be as effective as primary angioplasty (due to time saved) [4]
   5. PCI with stenting clearly preferred over thrombolysis in STEMI and high risk NSTEMI [35]
5. Chronic therapy and emerging agents in separate outline

B. Overview of Therapies [1]

1. These therapies should be given based excellent evidence for clinical benefit
   1. Oxygen - all patients
   2. ß-Adrenergic Blockers - as tolerated by blood pressure and heart rate; avoid early use in patients with signs of cardiogenic shock [64]
   3. Aspirin (ASA) - all patients without strong contraindications
   4. Clopidogrel added to ASA improves patency, reduces ischemic complications [9] and significantly reduces death, reinfarction and stroke [65]
   5. Clopidogrel 300-600mg loading dose then 75mg po qd (with ASA) should be used in all STEMI patients prior to PCI, even those treated with thrombolytics or abcixiamb [34,54]
   6. Reperfusion: PCI (usually with stenting), thrombolysis, or CABG [2,3,17]
   7. Heparin: low molecular weight heparins and/or fondaparinux generally preferred, particularly in combination with thrombolytics [7]
   8. Fondaparinux (Arixtra®), a Factor Xa inhibitor used in STEMI [22] or ACS [23], reduces mortality, reinfarction even when added to heparin without increasing bleeding or stroke
   9. GP2b3a inhibitor - with all PCI, particularly in patients with elevated troponins [24,34]
   10. ACE Inhibitor (ACE-I) or AT2 receptor blocker (ARB) - begin within 1-3 days of infarction
   11. Early aggressive statin use to reduce cholesterol is clearly beneficial
   12. Nitrates - clearly provide symptomatic anginal relief, minimal effects on mortality
   13. Calcium blockers - some of these agents are safe and may be beneficial in MI
   14. No benefit to supplemental L-arginine (nitric oxide donor) in acute MI [66]
2. Key EARLY decision is medical (thrombolysis) versus invasive strategies [2,3]
   1. Invasive stragies are PCI (usually with stenting) or bypass surgery (CABG)
   2. High risk patients most likely to benefit from timely invasive therapy
   3. Left main disease and diffuse disease likely best treated with CABG or PCI with stenting
   4. PCI with stenting (bare or drug eluting) is very effective and safe [24,68]
   5. Early invasive strategy for STEMI and probably high risk NSTEMI recommended [3]
   6. PCI after 3 days in persistent coronary occlusion is not beneficial; may be harmful [40]
3. Therapies that may be useful in selected patients
   1. Lidocaine, intravenous - only for patients with post-MI ventricular arrhythmias
   2. Amiodarone (particularly with depressed LV function) - for ventrikcular arrythymias
   3. Magnesium, intravenous - benefits certain arrhythmias, not routine use [19]
   4. Diltiazem use typically in patients intolerant to ß-adrenergic blockers
   5. Prophylactic implantable cardioverter defibrillator (ICD) after MI of no overall benefit [26]
4. Therapies should generally be avoided
   1. Prophylactic lidocaine in absence of ventricular arrhythmias
   2. Most calcium channel blockers, particularly short-acting nifedipine
   3. Type I anti-arrhythmic agents (such as procainamide, quinidine)
   4. Type III anti-arrhythmic agents - routine use provides no overall benefit
   5. Do not give thrombolytics to patients who are likely to undergo angioplasty ± stenting
   6. Glucose-insulin-potassium associated with slighly increased death at 3 days []
5. Monitoring Patients and Risk Stratification
   1. Echocardiography (or perfusion imaging) evaluation of ventricular and valvular function
   2. Critical to rapidly triage patients for thrombolysis or angioplasty
   3. Patients with clear evidence of MI should be admitted to an intensive care unit
   4. Patients on thrombolytic therapy should be monitored for reperfusion; those who have no evidence of reperfusion will benefit from rescue angioplasty [44]
   5. Patients without complications for initial 24 hours may be moved to monitored floor
   6. Consider discharge in 4-5 days for patients with uncomplicated MI
   7. Left Ventricular (LV) function should be assessed in all patients prior to discharge
   8. Screening for risk factors and interventions should be done prior to discharge
6. No differences in 30-day mortality found in women versus men with acute MI [10]
7. Overall mortality 3-10% at one year, lower mortality with early revascularization in STEMI [2]

C. Acute Therapy [11,17]

1. Oxygen
2. ASA and Clopidogrel
   1. 325 mg qd short term (80mg qd appears to be insufficient) - may be chewed initially
   2. 325 mg qod long term or 81-160mg po qd long term
   3. Use in combination with nitrates and clot lysing agents
   4. Reduces mortality ~20% in acute MI setting
   5. ASA should be given before arriving in the hospital in high risk patients
   6. In persons with ASA allergy, clopidogrel 75mg po bid a reasonable alternative
   7. ASA should never be withheld during supect MI except for major contraindications
   8. Clopidogrel 300-600mg loading then 75mg po qd should be added to ASA in patients <75 years old with ST segment elevation MI receiving fibrinolytic therapy [9,54]
   9. Clopidogrel 75mg qd added to standard therapy reduces death, reinfarction, stroke [64]
3. Reperfusion Therapy
   1. Percutaneous coronary interventions (PCI), usually angioplasty with stenting, is superior to in-hospital thrombolysis and is first line for most MI's [12]
   2. Thrombolysis is used in hospitals where PCI is not available
   3. Preceding ("facilitating") PCI with either abciximab or retaplase thrombolysis did not improve STEMI outcomes and increased major and minor bleeding risks [75]
   4. Prehospital fibrinolysis associated with improved outcomes compared with in-hospital, and similar outcomes to PCI [4]
   5. Rescue PCI should be available to any patient undergoing thrombolysis [44]
   6. Atrial natriuretic peptide (ANP) infusion (0.025µg/kg/min x3 days) in patients with acute MI and reperfusion reduced total creatine kinase. improved left ventricular function [52]
   7. Thrombus aspiration PCI may appears more beneficial than standard angioplasty [74]
4. Heparin [7,13]
   1. LMW heparin and/or fondaparinux is generally preferred over standard heparin
   2. Heparins potentiate antithrombin action and have direct antithrombin effect
   3. Standard heparin given IV (1000U/hr; initial 5000U bolus) or subcutaneous (10,000U bid)
   4. Weight based dosing is preferred in order to achieve target APTT 50-70 seconds
   5. Dose is 60-70U/kg (max 4000U) bolus iv, then 12-15U/kg/hr continuous (max 1000U/hr)
   6. LMW heparins and fondaparinux dosed on weight basis and do not require APTT monitoring
   7. LMW heparin superior to standard heparin on mortality when combined with TPA [30]
   8. LMW heparin superior to standard heparin for preventing reinfarction in STEMI [67]
   9. Increasing heparin doses is associated with high increased bleeding, little benefit
   10. Enoxaparin (LMW heparin) may be as effective as abciximab when combined with thrombolytic tenecteplase and is easier to administer
   11. Fondaparinux at least as effective, reduced bleeding, compared with enoxparin in ACS and acute MI [22,23]
   12. Bivalirubin has reduced risk of bleeding versus GP2b3a inhibitors + heparin [76]
5. GP2b3a Inhibitors [20]
   1. GP2b3a inhibitors improve blood flow in with PCI for acute STEMI [51]
   2. Abciximab (ReoPro®) reduces whort and long-term mortality in PCI, not thrombolysis [24]
   3. Abciximab reduces 30-day reinfarction rate when used with thrombolysis [24]
   4. Abciximab beneficial after clopidogrel loading in PCI, particularly with troponin elevation [34]
6. Hirudin (Revasc®) - thrombin inhibitor with some benefit over heparin in patients with ACS
7. Bivalirudin (Angiomax®)
   1. Synthetic derivative of hirudin, inhibits free and clot-bound thrombin
   2. FDA approved for high risk angioplasty patients
   3. Bivalirudin alone has reduced risk of bleeding and similar efficacy in STEMI treated with PCI and stenting compared with heparin + gp2b/3a inhibitor [76]
   4. No mortality benefit in unstable angina or MI [18]
   5. Likely more effective than heparin when combined with streptokinase [18]
   6. Strongly consider use in patients with heparin-induced thrombocytopenia or high bleeding risk
8. ß-Adrenergic Blockers [21]
   1. Reduce post-MI arrhythmias and decreases oxygen consumption by cardiac tissue
   2. When used within 24 hours of MI in all patients, reduces arrhythmias and reinfarction but increases risk of cardiogenic shock [64]
   3. When used acutely and chronically, 15-20% reduction in death rate
   4. Recommended in ALL patients post-MI without absolute contraindications but caution in patients with reduced LV ejection fraction
   5. Reduce mortality in patients with pulmonary disease, heart failure (CHF), or diabetes
   6. Increased risk for cardiogenic shock mainly in hemodynamically unstable patients [64]
   7. May be prudent to delay use until hemodynamic condition has stabilized [64]
   8. Esmolol (t1/2 ~ 2 min) - high fluid load but easily titrated for BP and heart rate
   9. Metoprolol IV 2.5-5mg may be given q2-4 hours to control heart rate but caution with use in first 36-48 hours due to increased cardiogenic shock risk [64]
   10. Rapid transition to oral ß1-selective agent (metoprolol, atenolol) recommended
   11. Carvidilol 3-21 days after MI in patients with LV EF <40% reduces mortality [25]
   12. ß-Blockers are very strongly recommended in ALL post-MI cases
   13. Caution with use in inferior MI and Right Ventricular MI where bradycardia is common
9. ACE-I or ARB
   1. ACE-I and ARB reduce LV enlargement, incidence of CHF, and mortality post-MI
   2. Most effective in patients with EF post-MI <40% for prevention of development of CHF
   3. ACE-I or ARB should be started within 6-48 hours of acute MI in most patients
   4. ACE-I are as effective as ß-blockers post-MI in patients with impaired LV function
   5. ARB are generally considered equivalent to ACE-I
10. Nitroglycerin (TNG)
    1. Coronary artery and mainly venous vasodilator
    2. Acutely: Give sublingual (SL) TNG up to 3-5 doses
    3. Active infarction or unstable angina: IV TNG is much preferred over paste or SL
    4. Nitropaste, 1-2 inches every 6 hours (may have 4-6 hour nitrate free interval)
    5. TNG decreases episodes of chest pain and improves symptoms of heart failure
    6. Unlikely that TNG has a substantial effect on MI associated mortality
11. Magnesium (Mg) - reasonable in patients with ventricular arrhythmias, especially Torsade
12. Invasive Therapy (see below) [2]
    1. PCI (percutaneous coronary intervention) usually with stenting [32]
    2. CABG (Coronary Artery Bypass Graft)
    3. Invasive therapy is controversial for treatment of non-Q wave MIs presentin within 2-3 hours (see below)
    4. Thrombolytics should not be given prior to primary PCI for MI as they increase major adverse events [14,15]
    5. Thrombolytics as or more effective than PCI for STEMI without Q waves that presents within 2-3 hours [29]
13. Blood Transfusion [31]
    1. Improve delivery of oxygen to cardiac tissue
    2. Some studies show worsening on outcomes with hematocrits >30-33%
    3. In elderly with MI, transfusion for <31% is probably beneficial
14. Contraindicated in MI
    1. Anti-Arrhythmic Agents for prophylaxis (only use if significant arrhythmias occur)
    2. D-Sotolol increased mortality in patients with reduced LV EF given peri-MI
    3. Calcium Channel Blockers - generally not indicated; consider if ß-blocker not tolerated
    4. Diltiazem is safe in MI and may reduce overall complications of thrombolysis
    5. Nicorandil of no benefit in acute MI treated with reperfusion [52]
    6. Hematocrit elevated with transfusion to excess of 30-32%

D. Thrombolytics in MI: Overview [33]

1. Indications
   1. Chest pain consistent with acute MI
   2. ECG Changes consistent with MI
   3. Symptom onset within 12-18 hours (24 hours in some cases)
   4. Age is a relative risk for bleeding risk only
   5. Strongly consider pre-hospital thrombolysis in appropriate settings [4]
   6. Do not give thrombolytics prior to primary PCI [14,15]
2. ECG Changes
   1. ST segment elevation >1mm (0.1mV) in at least 2 contiguous leads
   2. New or presumed new Left BBB
   3. ST-segment depression with prominent R in V2 and V3 (thought to be posterior-MI)
   4. Presence of LBBB makes ECG diagnosis and location of MI very insensitive
   5. In patients with LBBB and coronary symptoms, strongly consider thrombolytics or PCI
   6. ST segment deviation present in the ECG lead showing initial maximal deviation at 90 min after thrombolysis predicts mortality [36]
   7. Presence of Q waves in STEMI is a poor prognostic finding and suggests PCI [29]
3. Time to Symptom Onset
   1. Indicated definitely <6-12 (18) hours
   2. Much lower benefit 18-24 hours
   3. Do not use if >24 hours unless pain is stuttering (angiography is preferred)
   4. Most effective when used within 2 hours (up to 44% 35 day mortality reduction)
   5. When used within 2 hours, saves 1 life out of every ~20 treated patients
4. Age
   1. Definite benefit with low risks in <75 year olds
   2. >75 year olds has fewer clear benefits with higher bleeding risk
   3. In persons >65 years old, PTCA had somewhat better outcomes than thrombolysis
   4. In >65 year olds who were good thrombolysis candidates, outcomes were similar
5. Women versus Men
   1. Women were ~7 years older than men in GUSTO-1 thrombolytic trial
   2. Women have overall higher mortality rates than men peri-MI
   3. Women had more diabetes, hypertension, and tobacco abuse than men in that trial
   4. Women who received thrombolytics had more fatal and non-fatal complications
   5. Women had better mortality reduction (11.1% women, 10.3% men) than men
6. Assessment of Reperfusion after Thrombolysis [39]
   1. Thrombolysis should begin in <40 minutes and be maximal at ~120 minutes
   2. Coronary angiography is the gold-standard to assess patency of infarct-related vessel
   3. No biochemical marker for reperfusion has been found
   4. However, newer cardiac enzyme monitoring (such as troponins) may be helpful
   5. Clinically, several noninvasive parameters are used but are not always accurate
   6. Reduction of chest pain in 30-120 minutes
   7. Resolution of ST segment elevations is associated with reperfusion
   8. "Reperfusion arrhythmias" such as accellerated idioventricular rhythm (AIVR) are associated with reperfusion
   9. Recurrent angina and/or ECG ischemic changes indicate failed reperfusion
   10. Routine invasive strategy within 24 hours of thrombolysis may be superior to recurrent ischemia guided approach [28]
7. Failed Thrombolysis [39]
   1. Overall failed opening of infarct related vessel occurs in 15-30% of cases
   2. Flow through coronary arteries is graded TIMI 0 (occlusion) to TIMI 3 (normal flow)
   3. TIMI 3 flow is required for optimal response to thrombolysis, preservation of heart
   4. TIMI 3 flow is obtained in ~50% of patients with TPA, ~30% with SK
   5. In addition, poor perfusion of microvascular bed occurs in ~30% of TIMI 3 flow cases
   6. Poor perfusion of microvascular bed (by PET scan) may be due to clots and/or damage
   7. Oxygen radical and other reactive oxygen species (ROS) at time of reperfusion also contributes to lack of reflow
   8. PCI (with stenting; see below) is recommended for failed thrombolysis [44]
   9. This "rescue angioplasty" is superior to repeat thrombolysis or conservative treatment [44]
   10. GP2b3a inhibitors improve flow after thrombolysis or PCI [20,24]
   11. PCI for perisistent coronary occlusion not beneficial, may be harmful [40]
8. Contraindications to Thrombolysis
   1. High risk for cerebral hemorrhage with BP >175mm systolic
   2. Recent Major Surgery
   3. Recent Cerebrovascular Accident
   4. Prolonged cardiopulmonary resuscitation
   5. Bleeding Diathesis
   6. Cerebral Metastases
   7. Menstruation is not a contraindication (benefits outweigh risks)
   8. PCI with stenting should be strongly considered when thrombolysis contraindicated [6]
9. Substantial myocardial stunning with subsequent improvement occurs after reperfusion
10. Mortality Reduction from Thrombolytics
    1. Overall, ~25% reduction overall due to thrombolytic therapy [41]
    2. No clear benefit for unstable angina or non-q wave MI
    3. For systolic BP >175mmHg, increased brain hemorrhage outways benefit
11. Risk of cerebral hemorrhage with thrombolytics is 0.6% for standard, 0.8% for bolus [42]

E. Thrombolytic Agents [33,43]

1. Summary of Agents
   1. Streptokinase (SK; Kabikinase®, Streptase®)
   2. Urokinase (rarely used)
   3. Tissue Plasminogen Activator (TPA, Alteplase®)
   4. Reteplase (Retavase®)
   5. Anistreplase (APSAC; Eminase®)
   6. Tenecteplase (TNKase®)
   7. Lanoteplase
2. TPA (Alteplase®)
   1. Dose100mg iv total infusion (costs ~5X SK)
   2. Usually given "front-loaded" with 15mg bolus, 35mg over 30min, 50mg over 30 min
   3. Front loading regiment required due to short half-life (4 minutes)
   4. Good early (90 minute) vessel patency of >50% (TIMI Grade 3 Flow)
   5. In early studies, mortality with TPA are ~14% less than that with SK
   6. Fonaparinux superior to enoxparin when combined with TPA in large study in ACS [22,23]
   7. Overall event rates, including stroke and death, are about the same with SK and TPA
3. Reteplase (Retavase®)
   1. Reteplase is a derivative of TPA that may work more quickly
   2. As effective as TPA but with less fibrin specificity
   3. Given as two 10U IV boluses 30 minutes apart
   4. Must be given with heparin to prevent early reclosure
   5. With reteplase versus SK, the 35d and 6 month morality rates were simlar
   6. Half-dose reteplase + abciximab 12 hours may be superior to full dose retaplase [36]
   7. Reteplase + abciximab reduced early reinfarction rate but not 1-year mortality [37,46]
   8. Adding reteplase to PCI+abciximab provides no benefit in acute MI [62]
4. Streptokinase (SK, Streptase®) [47]
   1. Reduces MI associated mortality by ~20%, similar to TPA
   2. Early (90 minute) vessel patency 30-35%, less than that seen with TPA
   3. Overall, normal blood flow (TIMI grade III) restored in 50-70% of patients
   4. Specific contraindications to SK: allergy, any previous SK therapy
   5. TPA is generally recommended over SK for patients with large anterior MI
   6. Side effects include hypotension, anaphylactic reactions
   7. Dose: 1.5 million units over one hour, fairly low incidence of bleeds
5. Tenecteplase [48,49]
   1. Triple combination mutant of alteplase (third generation thrombolytic)
   2. Plasma half-life 20 minutes (versus 4 minutes for TPA)
   3. Increased fibrin specificity over TPA and reteplase
   4. More resistant than TPA to inhibition by plasminogen activator inhibitor-1 (PAI-1)
   5. Can be given as single 30-50mg bolus (based on weight)
   6. Equivalent efficacy with minor reduction in bleeding / blood transfusion versus TPA [50]
   7. May be drug of choice in this category (pricing same as TPA and reteplase)
   8. More effective when combined with abciximab or enoxaparin than with heparin
6. Heparin should be started post-infusion of thrombolytic (clear benefit only with TPA)

F. PCI (PTCA and Stenting) [2,4,16]

1. Primary PCI Versus Thrombolysis [71]
   1. Meta-analysis showed that primary PCI for MI more effective than immediate thrombolysis for reducing 30-day death, reinfarction or stroke [12]
   2. Followup of 5±2 years comparison of PCI versus thrombolysis showed PCI had lower reinfarction, mortality (13% versus 24%), and hospital readmissions [47]
   3. Primary PCI is preferred over thrombolysis in all Q-wave MI, and in STEMI without Q waves presenting >3 hours after onset of symptoms [29]
   4. In a meta-analysis of 8 trials in patients with NSTEMI and USA, invasive strategy had a 20-30% reduction in death, MI and recurrent ACS compared with conservative strategy [78]
   5. In that meta-analysis, high risk women and all men benefit from invasive strategy [78]
   6. Primary PCI is superior to thrombolytic therapy and as safe in centers without on-site cardiac surgery backup [55]
   7. Post-MI stenting+abciximab leads to more viable myocardium than alteplase+abciximab [57]
   8. Adding reteplase to PCI with abciximab does not improve outcomes [62]
   9. Strong support for PCI (especially with stents) over thrombolysis for acute MI
   10. Thrombolytics should not be given prior to primary PCI for MI as they increase major adverse events [14,15]
   11. PCI with sirolimus eluting stents reduced rate of target-vessel revascularization in STEMI but did not affect overall mortality, reinfarction, or stent thrombosis [69]
   12. PCI with paclitaxel-eluting stents reduced incidence of serious adverse cardiac events in STEMI but did not hit statistical significance [70]
2. Indications for PCI in Acute MI
   1. PCI is primary therapy for essentially all patients with MI, particularly in the ~20% of patients in whom thrombolysis is contraindicated [6]
   2. PCI usually indicated for complications of MI including arrhythmias, valve disease, shock
   3. Emergent PCI or CABG reduces mortality in patients with MI and cardiogenic shock [45,63]
   4. Patients with acute MI and cardiogenic shock should always be offered PCI [45,63]
   5. Rescue PCI is recommended in patients with Q-wave MI who fail thrombolysis
   6. Adding GP2b/3a inhibitors to primary PCI improves TIMI grade III flow [51] and mortality [24]
   7. Stents (heparin coated) are preferred over PTCA alone for treatment of acute MI [56]
   8. Stents reduced revascularization versus PTCA at 6 months by >50% in acute MI [56]
   9. Aggressive angioplasty post-MI in the elderly had no benefit versus usual therapy
   10. Early PCI superior to non-invasive strategy in >75 year olds with non-ST segment ACS, but risk of bleeding is increased relative to younger patients [53]
   11. PCI in all patients within 24 hours after thrombolysis reduces 1 year clinical outcomes [28]
   12. PCI post-MI in patients with asymptomatic ischemia and 1-2 vessel CAD superior to anti-ischemic drug therapy on all outcomes [72]
3. PCI in Non-Q Wave MI / NSTEMI (or USA)
   1. In a meta-analysis of 8 trials in patients with NSTEMI and USA, invasive strategy had a 20-30% reduction in death, MI and recurrent ACS compared with conservative strategy [78]
   2. In that meta-analysis, high risk women and all men benefit from invasive strategy [78]
   3. Thrombolysis is at least as good as primary PCI for NSTEMI presenting within 2-3 hours [29]
4. Stenting Vessels with Recurrent Cardiac Ischemia [16]
   1. PCI with stents+abciximab are more effective and at least as safe as thrombolysis for acute MI [57]
   2. Abciximab should always be given prior to PCI/stents for primary MI treatment [58]
   3. Stents more effective than angioplasty alone (including in diabetics)
   4. Stents are less effective in diabetic as compared with non-diabetic patients
5. PCI performed within 1 hour has better outcomes than >1 hour in acute MI [59]
6. Thrombus Aspiration [74]
   1. Usual PCI leads to distal microvascular obstruction due to fragmentation during angioplasty
   2. Thrombus aspiration has been developed to prevent distal embolization during PCI
   3. Aspiration is carried out after guide-wire is placed through target lesion
   4. Thrombus aspiration showed better complete ST segment elevation resolution (56%) versus standard PCI (44%) in patients with STEMI in a single center study [74]
   5. Successful thrombus aspiration occurred in >73%
   6. After 1 year followup, cardiac death 3.6% with thrombus aspiration versus 6.7% without it in a single center study in STEMI [77]
7. Direct atherectomy caused more complications than PTCA in opening vessels

G. Right Ventricular (RV) Infarction [60]

1. High suspicion in patients with MI and:
   1. Hypotension and
   2. Posterior or inferior MI and/or
   3. Bradycardia
   4. Patients with MI but without angina are more likely to have RV involvement [60]
2. ECG changes
   1. Right sided leads are critical for evaluation
   2. Right sided leads can show 0.5-1mm ST elevation in V4 or V5
   3. Consider posterior leads to evaluate for possible circumflex lesion
3. Coronary Angiogaphy and PCI
   1. Coronary angiography is gold standard for diagnosis of RV infarction
   2. Complete reperfusion by PCI is strongly associated with dramatic recovery
   3. With complete reperfusion, RV function almost always returns to baseline [61]
   4. Complete reperfusion with angioplasty also restores cardiac output (mortality 2%)
   5. Failed reperfusion in RV infarction was associated with a 58% mortality rate [61]
   6. PCI is strongly indicated over thrombolysis in RV MI
4. Medical Therapy
   1. Maintain adequate filling pressures (usually >10cm CVP) with volume infusion
   2. Bolus of IV fluids (500-1000cc) frequently needed to maintain blood pressure
   3. Use ß-blockers cautiously as patients are at high risk for hypotension and bradycardia
   4. Dobutamine (? amrinone) is vasopressor of choice for maintaining blood pressure
5. Recommend early PTCA in unstable patients, especially if vasopressors are needed

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