Acute Coronary Syndrome

ER medical lecture seriesSeptember 21st 2006Dr. Cernik presenting

Slides by Brian A. Romito, DO IM/EM PGY4

Acute Coronary Syndrome (ACS)

● ACS includes spectrum of clinical presentations from common pathophys Myocardial Ischemia/Necrosis;

● Dz Range; continuum from asymptomatic CAD & Stable Angina to unstable angina & STEMI/NSTEM

● ACS/AMI--> Leading cause of death in US

Hx ACS ● Hx; selective coronary arteriography Sones 1959 &

External Cardiac Massage 1960 Kouwenhoven

● Day est 1st Cardiac Arrest team 1960 & 1st CCU 1962 AMI mortality 50%

● 1980s Coronary angiography in AMI showing occlusion in infarct-related artery... Rentrop intracoronary Streptokinase in AMI

● 1980s prehospital portable 12 lead ECG's

ACS- by the Numbers● Ischemic Heart Dz/CAD; leading cause death US 1 million/yr;

160k in 65yrs or younger

● mortality 40yrs; 25% survival AMIsmoking, CTRL lipids, better HTN/DM mngt, resusitation, Cardiac Care

● 6 million US pts/yr Chest Pain eval in ED2 million dx ACS● 2% (120,000) w/ ACS d/c home by ED

● 900,000 AMI/yr; die b/f ED + 30% die in 30 days= 450K● Majority pre-hospital deaths w/in 2hrs of Sx, others disabled● Cost for eval & care pts w/ ACS $100-120 Billion!!!

Spectrum of Dz; Stable Angina

● Transient, episodic chest discomfort via Myocardial Ischemia

● Typically predictable & reproducible w/ frequency of attacks

● Attacks provoked by STRESS; physical, emotional, anemia, environmental, dysrthymias

● Resolves predictable time; spontaneously, w/ Rest, w/ NTG

Canadian Cardiovasc Society Classification

● Class I; No Agina w/ ordinary activity

● Class II; slight limitation ordinary activity ; anina w/ climbing stairs, emotional stress, walking

● Class III; severe limitation of ordinary activity; angina w/ walking 1-2 blocks on level surface, 1 flight steps

● Class IV; inability any physical activity w/o discomfort; anginal symptoms at rest

Unstable aka preinfacrt, accelerating, or cresendo Angina

● Harbinger AMI so Tx Aggressively

● If pt has dx Angina assume Unstable till proven otherwise

● Plaque rupture accompanied by thrombus formation & vasospasm; intraocoronary events... ECG abnormalities; T wave & ST changes.

● Variant aka Prinzmetal's Angina; coronary artery vasospasm at rest w/ min fixed coronary artery lesions; may be relieved by exercise or NTG. ST elevation not possible to discern from AMI

Unstable Angina

● Occurs w/ min exertion or at rest, new onset, worse than prior stable angina ( freq, longer, resists prior meds, starts w/ < stress/exertion)

● Rest Angina; occurs at rest, > 20 minutes, w/in 1 week presentation.

● New Onset Angina; at least Class II, onset w/in 2 months

● Increasing Angina; previous angina more freq, > 20 min despite stopping activity, increase in class w/in 2 months to class III

Acute Myocardial Infarction

● cell death/necrosis myocardium● Typical rise/fall of CK-MB, Trop w/ clinical Sx, ECG changes,

or coronary artery abnormality w/ 1 below:● 1) Ischemic Sx● 2) Dev Q waves● 3) ST elevation or depression● 4) Coronary artery intervention

● Est MI; Dev New pathologic Q's on serial ECGs or Path findings of healed or healing MI

Acute Myocardial Infarction classification

● Old; Transural (transmural process assoc w/ ST elevation) or Non-transmural (subendocarial, ECG changes other than ST elevation-assume smaller infarct size), presumed tissue damage

● Old; Q-wave or Non-Q-wave MI; based on ECG

● Preferred nomenclature is STEMI or non-STEMI preferrable

AMI Pathophysiology● Myocardial ischemia; too little perfusion for O2 demand

usually due to coronary vessel stenosis 2 CAD

● coronary blood flow- NO Ischemic 's w/ rest until stenosis >95%; activity ischemia can occur at 60% stenosis

● CAD characterized by thickening/obstruction of Coronary arterial lumen by atherosclerotic plaque.

● Plaque composition varies; Fibrous plaques stable but can produce angina w/ exertion b/c stenosis

AMI Pathophysiology● Initiation of ACS by Endothelial damage & atherosclerotic

plaque disruption

● Fibrolipid plaques rupture from arterial lumen inflammation thrombus & platelet aggregation; acute obstructioncell death

● Thrombus formation is Integral factor in ACS & platelet rich thrombi > Resistance to throbolysis than fibrin/RBC rich thrombi

● Damage extent depends on collateral circulation, plaque character, amount vessel obstruction

ACS Vasospasm

● 10% of MI's w/ thrombus formation w/o significant CAD

● Induced by local mediators/vasoactive substances after occlusionin blood flow

● Vasomotor hyperactivity

● Sympathetic stimulation; Epi & Serotonin; platelet clot & neutrophil-mediated vasoconstriction

More myocardial damage...

● Calcium, Oxygen, & cell debris occlude distal vessel...● ● Neutrophils & inflammationperfusion

causing further inury & Ventricular dys-fxn... by ROS, proteolytic enzymes, and chemoattractants

● AKA Myocardial Stunning or reperfusion dysrhythmias.

Pre-hospital● Tx: NTG, ASA (oral), IV Morphine

● 12-lead EKG (99% specific) & + predictive value (93%); AMI pts- atraumatic CP... EMS time at scene 3 minutes

● Earlier detection ST segment elevation in AMI, hence more rapid reprofusion therapy, esp w/ long route times

ED Eval & Hx● Type of pain, on set, location, radiation, duration, what

makes better/worse, same Sx before???

● CAD Risk; male, age, smoking, HTN, DM, FmHx, lipids, menopause, cocaine use.

● 80/122,000 CAD have 1 of 4 (DM, smoking, HTN, lipids)

● Note; Risk factors are population phenomenon and have no ability to or likelyhood of condition of any 1 pt

● Risk Hx not as impt as HPI, ST/T wave changes or markers

Classical Hx● Angina- term means “tightening” ● Discomfort; squeezing, pressure, fullness, heaviness or

burning sensation

● Substernal/precordial location +/- radiation; jaw arm neck if down arm; ulnar aspect

● Location L chest but can be R

● Initiated by; heavy meal, exertion, cold, relieved w/ rest, lasting 5 to 20 minutes

● Assoc Sx; SOB, N/V, diaphoresis, weakness, fatigue, dizzy... can be considered anginal equivalent syndrome

Atypical Hx● atypical features of pain;pleuritic, positional, or reproduced by

palpation, burning, indigestion, sharp, or stabbing

● Large Study 435,000 pts dx AMI, 1/3 did NOT have CP at presentation

● More often in older pts >85yr old, or 40% Diabetics (no CP), or 60% female (No CP) at time of AMI

● c/o indigestion/anxiety/sleep disturbance/dizziness in women

● Nonwhite populations likely to have atypical Sx

Table 77-2 -- Symptoms of Acute Myocardial Infarction: Typical and AtypicalSymptom Bayer et al[*],[†] Tinker[‡] Uretsky et al[§] Pathy[||]TypicalChest pain 515 51 75 75AtypicalDyspnea 118 19 14 77Syncope 72 4 1 27Confusion 46 1 51Stroke 32 6 2Fatigue 36 2 4 10Nausea or emesis 28 1 10Sudden death 31Giddiness 18 3 22Diaphoresis 18 2Arterial embolus 3 19Palpitation 4 14Renal failure 11Pulmonary embolus 8Restlessness 4Abdominal pain 5 Arm pain only 1 Cough 1 SilentNo symptoms 17 1 Total 777[*] 87[¶] 102[**] 387[¶]

Atypical Sx● Atypical presentation pts w/ ACS delayed & poor

outcomes

● 2nd Nat Registry of MI study (NRMI-2): MI w/o CP significantly more likely to die in hospital (23% vs 9%)

● More likely to have stroke, hypotension, CHF requiring intervention

● Typical presentation; Less likely to receive ASA, ß-blocker, Heparin, thromboysis & 1 angioplasty

Missed Dx of ACS● 2 to 8% pts w/ AMI to ED are DC'd w/o proper ID diagnosis

● Pts signif younger, women, nonwhite, atypical complaints, less likely to have ECG evidence of acute ischemia

● 53% missed AMI & 62% pts w/ unstable angina had normal ECG

● 11% of MI pts; ED physician failed to detect ST elevation 1 to 2mm

● Docs w/ > risk; < ED experience, < documented Hx, admitted fewer pts, difficulty in ECG interpretation

Early complications of AMI

● Bradydysrythmia & AV Block; 25-30% pts w/ AMI have sinus brady

● AMI + AV Block = respond poorly to TX; poor prognosis

● Tachydysrythmias; Atrial (afib, sinustach) or Ventricular (VT, Vfib); 1 Vfib 4-5% of AMI w/ 60% in 1st 4

● Cardiogenic shock risk; large MI, Low EJF, DM, age, prior MI

● LV wall rupture 1/3 in 1st 24rest in 3-5 days; sudden death, PEA, repetitive vomiting, precipitous decline, nearly 100% fatal... percardialcentesis temporary measure till surgery

Early complications of AMI cont

● Infarct Pericarditis assoc w/ AMI = transmural & infarct zone near epicardium. ST changes may be obscured

● Infarc Pericarditis- new CP 1st week post MI. Pleuritic & worse supine. risk embolization b/c risk Ventricular Aneurysm

● Dressler's Syndrome- does not need to be transmural. Uncommmon 1week-months; Fever, malaise, pleuro-pericardial pain, +/- Rub

● Dresslers..ESR & WBC ECG; pericarditis & PR depression. ? bloody or serous Pericardial/pleural effusions... immune mediated, use NSAIDS

Early complications of AMI cont

● Stroke may complicate AMI. Ischemic, thromboembolic most common. Emboization from LV mural thrombus w/ LVEJ or atrial w/ Afib.

● Higher rate in AMI (0.9 to 0.1% at day 28 after MI) vs control (0.014%)

● Hemorrhagic stroke rate w/ fibrinolytics is < 1%, rate w/age

● Percutaneous intervention risk vs fibrinoytic (1.6% tpA vs 0.7 angioplasty), over all (1% fibrinolytic vs 0.1% angioplasty)

ECG abnormalities in ACS

ECG changes in ACS● Hyperacute T wave changes- earliest findingT wave

tall/peaked w/in min. of occlusion ● Progresses to ST elevation seen in a classic MI

● Differential dx tall T's; ischemia, high K, benign early repolarzation, LVH, LBBB, & pericarditis

● Morphologic varations of ST segment elevation seen from the J point at end of QRS to apex of T wave; convex, concave or scooped.

● Concave morphology is commonly seen w/ other ST segment elevation syndrolmes

ECG changes in ACS

● ST seg. Elevation measured in mm's: 1 block=1mm in ht

● ST elevation benign/pathologic is common

● Men 90% have ST elevation, in precordial leads; 1mm or ● more in men. 1Mm less in women

● ST segment is concave/more prominent the deeper the corresponding S wave

ECG changes in ACS

● Differentiating normal/pathologic ST elevation of AMI is a new EKG change

● ST depression represents subendocardial/nononfarction ischemia

● NSTMI, may elevate segment in a ST segment elevation AMI, reflect “mirror image” of ST elevation of a post. MI, or represent recipocal ST depression seen in INF wall MI. (seen best in aVL)

ECG changes in ACS

● T wave inversion are can be non-specific, can suggest myocardial ischemia.

● T waves inversion of ACS are narrow,symmetrically inverted

● Inversions best viewed by comparison to recent EKG

ECG changes in ACS

● T wave inversion are can be non-specific, can suggest myocardial ischemia.

● T waves inversion of ACS are narrow,symmetrically inverted

● Inversions best viewed by comparison to recent EKG

ECG changes in ACS

● Ischemic ST depression is horizontal/downsloping● Subendocardial ischemic ST depression is difffuse

● D/dx: ischemia/infarction, repolarization abn. LVH/RVH, BBB, pacer, dig FX,K, ↓K, PE, ICH, myocarditis, rate-related ST depression, post cardioversion, pneumo

ECG changes in ACS

● T wave inversion are can be non-specific, can suggest myocardial ischemia.

● T waves inversion of ACS are narrow,symmetrically inverted

● Inversions best viewed by comparison to recent EKG

ST elevation

ST segment depression

Inverted T wave

Inverted T waves● Can be inverted Norm in AVR, V1 & sometimes V2

● ACS narrow & symmetrically inverted

● Wellen's Synd; deep symmetric T wave inversion, biphasic T in Anterior precordial leads... No Q's... indicated LAD lesion

● D/dx; WPW, ACS, BBB,

Q wave

Q waves● 1/3 the amplitude of the QRS complex pathologic

● May disappear w/ time

Anterior AMI

Anterior AMI● V1-V4

● Septal involvement V1 & V2

● Reciprocal ST segment depression in III & AVF

● ANT wall supplied by LAD

● May involve lateral wall too b/c 1st diagonal branch from LAD is likely to be involved when ST elevation extends to I & AVL

Lateral AMI

Lateral AMI● Freq seen w/ ANT AMI, INF infarct or INF/POST infarcts

● Lat wall served by LAD, RCA, and L circumflex arteries.

● LAT involvement leads; I, AVL, V5, & V6 (high lat infarcts); occlusion L circumflex

● Reciprocal ST segment depression III, AVF, V1

INF AMI

Inferior AMI● Changes in II, III, AVF

● INF Wall heart & AV node; both RCA involved in 90%

● 10% L circumflex artery

● Reciprocal changes in AVL, I

Posterior AMI● 15% to 20% of all AMI's

● Seen w/ INF or INF-LAT infarcts

● Lesion in RCA; it's POST branch, or L Circ

● Reciprical changes in V1 to V3

● Additional leads V8 or V9 increases sensitivity

Cardiac Markers- Troponins I & T● best markers for myocardial cell injury; genetically

distinct from Trop in skeletal Musclek

● Majority bound to muscle fiber, cytolsol amounts smaller released 1st after cell injurty, hence biphasic raise in Trop level

● Begin to raise ~ 3 Release for 5-7 days, elevation > 7 days● Serial measure highly sensitive, TnT 50% 3-4h, 75% 6h &

100% at 12h

● Linear correlation b/t Trop elevation & Infarct. TnT can be elevated in Renal Failure pts or sketetal muscle dz, TnI not found in Rneal Failure > cardiac specific

Cardiac Markers- Creatinine Phosphokinase● Large quantity in cardiac & Skeletal Muscle w/in 3-8w/

peak 20-24 after injury; normalize 3 to 4 days

● ED presentation 37% sensitive 87% specific for Dx AMI; 1250% spensitive

● CK-MB subtype specific for Myocardial cells...w/in 3only 25% to 50% sensitive > 3more sensitive 40-100% esp 12-16

● Also elevated; rhabdo, Musc Dystrophy, Trauma, myosistis, extreme exercise

● Do Not rely on a single measurement

Cardiac Markers- Myoglobin● Found in muscle rapidly released in circulation after cell

injury

● Raise 1-2peaks 5-7 returns to base line 24

● Myocardial Myo not distinguishable from Skeletal Mus levels

● Elevated in renal failure b/c reduced clearance & trauma, exercise, signif systemic illness

● Sensitivity 21-100% Serial testing 2-4after intial improves diagnostic power... doubling 1-2still nonspecific

● Excellent negative predictive value for AMI not ACS

Mngt Goals ACS● Inc Mycardial Oxygen supply w/ O2

● Dec Oxygen Demand/F contractions via B-Blocker

● Inc Metabolic substrate to mycardium; NTG, MSO4, Fibrinolytic, Angioplasty

● Dec inflamm or tox injury... anti-inflammatory Rx

● Prevent reocclusion of Coronary A w/ Antiplatelet & Anticoagulants

Time to Tx w/ Outcomes...● 1970s wave phenomenon ischemic cell death... myocardial

necrosiss went subendocardium epicardium. Release of occlusion earlier smaller infarct & > transmural progression

● Beneficial reperfusion; shorter time of AMI & Tx; early patency--> > Myocardial salvage.

● GUSTO; Preserved LV fxn, & improved at 24 days related to angiographic patency in 1st 90 minutes. Fibrinolytic Th w/ AMI signif > benefit w/ Tx in 1st 1-2

● Myocardial Infarction Triage & Intervention (MITI) trial; mortality rate AMI w/ Tx w/in 70 min 1.3% vs 8.7% later Tx

Time to Tx w/ Outcomes...● Pts tx in 1st hour have 40 -50% dec mortality. Tx 2-12 after

AMI have modest yet beneficial

● Pt-bystander delays in seeking Tx via EMS 2-6.5● AMI pts delay > 4b/f seeking care. Signif delay due

to self Tx ~ 1/3 of pts w/ AMI & sudden Death!!!

● Prehospital Delay- calling PCP 1st Only ½ of AMI pts call EMS Many drive themselves, or live far distance from Hospital

● In hospital AVG time to fibrinolysis 45 to 90 minutes AHA recommends tx w/in 30-60 minutes of ED arrival, or PTCA < 90 minutes

Time is short, move swiftly & decide... ● 4 D's: ● Door (events prior to ED arrival)

● Data (obtain ECG, Lab)

● Decision (AMI dx & decide Th)

● Drug (Fibrinolytic or passing Angioplasty Cath)

● Triage ID AMI, Have Rx ready, Immediate Cardio consult

Groovy Drugs-NTG● Preload & sml fx on afterload, venous compliance, hence

reduction myocardial oxygen demand

● Vasodilation Coronary Arteries... pos collateral blood flow. Meta-analysis small trials show 35% mortality w/ IV NTG

● Pts w/ SBP >90 should receive SL NTG 0.4mg on presentation. If no relief of Sx w/ 3 NTG SL then IV NTG

● CAUTION; Hypotension, INF MI, RV MI, Bradycardia● Initial infusion 10mics/min titrate SX free; 10% reduction

Normotensive and 20-30% reduction in HTN

I Feel Good- Morphine :)● Use in Unstable Angina NOT eval in Large randomized Trials!

● Opioid Analgesic w/ weak sympathetic blocker, anxiolytic fx, systemic Histamine realease... all can benefit ACS

● Use if continued Sx w/ NTG & anti-ischemia Therapy

● Relieve Pain & Anxiety Oxygen demand & myocardial work, Some Vasodilatory FX w/ preload reduction

● 2 to 5 mg IV dose Q 5-30 min prn● Caution: Hypotension (mngt IVF bolus), allergic RXN

The Big Dog Rx; B-Blocker● Relieves Catecholeamine-induced Tachycardia, contractility

& myocardial Oxygen demand!

● Beta-1-Receptors in Myocardium, SA-node AV conduction● Beta-2 located in vascular muscle & Lungs

● mortality pts w/ AMI &Meta-analysis 13% risk develop AMI

● IV metoprolol 5mg over 1-2 min x3. Alt are Atenolol (longest acting), Esmolol (shortest acting; use in COPD, CHF; pts < likely to tolerate B-blockers)

● CI; AV block, Hypotension, Bradycardia, Pulm Edema, +/-COPD/Asthma

ACE is the Place: ACE Inhibitors● Benefit CHF also may reduce M&M in AMI, best in 1st 24

● Reduction cardiovascular mortality, CHF develop, fewer recurrent AMI's

● benefit when used w/ other agents; ASA, fibrinolytics

● MOA, thought in plaque rupture related to < intracoronary shear force or neurohumoral factors

● Use in ED especially if long stay in ED● Caution; Hypotension, watch Renal Fxn

Think long & hard: Calcium Channel Blockers

● 1benefit is Sx relief.

● Significant Vasodilatory FX Hypotension worsen Coronary Ischemia

● Neg Inotropic FX perfusion

● AV block significant in pts treated w/ B-Blocker

● DO Not Use Unless for Rate Control in Supraventricular dysrhythmia in pt unable to tolerate B-blocker

GreAt mindS think Alike; Antiplatelet Therapy● In non-ACS pts, > reduction in progression to acute Infarction w/

aggressive antiplatelet Therapy● Pts in ACUTE phase of AMI, signif reduction Mortality 25-50%

● ASA give early. Irreversibly acetylates platelet cyclooxygenase

life of platelet (8-10 days) Stops production Thromboxane A2 & indriect antithrobotic agent too!

● ASA blocks endothelial cyclooxygenase & prostacyclin

● 2nd International Study of Infarct Survival shows 23% reduction Mortality AMI w/o Fibrinolytics and 43% with. 325Mg chewed & swallowed

Glycoprotein IIb-IIIa Receptor Blockers● Activated Platelet Membrane surface proteins that cross-

link platelets to form platelet plug

● 3 drugs abciximab, eptifbatide, and tirofiban, aka GPI's... monoclonal Ab's specific for glycoprotein Iib/IIIa provides proloonged inhibition platelet aggregation

● Numerous studies bottom line... use if plan PCA, bennefits 35% or greater mortality benefit. Studies to show benefit w/o PCA (even w/ fibrinolysis, ASA, heparin) NONE!!!

Along came Plavix; Antiplatelets cont...● Potent platelet inhibitor... > than ASA, ASA+ Plavix >

effectiveness than ASA alone in cardiovac death

● Inhibit transformation of glycoprotein Iib/IIIa receptor into high-afinity ligand-binding state, irreversibly inhibiting platelet aggregation

● Rapid onset, Max platelet inhibition after 3 to 5 days of 75mg earlier onset of platelet inhibition w/ loading dose 300-600mg

● Use often when PCA is not anticipated due to bleeding complications when mechanical interventions done... ask cardiologist

Antithrombins● Signif dec in progression to Acute/recurrent/extension of

infarction and death

● Unfractionated Heparins, Low Molecular Wt Heparin, and direct Thrombin Inhibitors (Hirudin and bivalirudin).

● Recurrent Anginal pain, AMI (STEMI & NSTEMI), + serum markers, & dynamic EKG changes

Heparins● Mixture of several mucopolysaccaride chains various lengths

& mol wts unfractionated – antithrombotic properties

● Std dose binds Antithrombin III then inactivates Thrombin (factor II) & active factor X... prevents fibrinogenfibrin, thus clot propagation

● Heparin by itself has no Anticoagulant property.

● Synergistic FX w/ ASA in mortality in ACS

● Initial dose 60U/kg & 16U/kg/hr maintenance

Low Molecular Wt Heparins● LMW heparins~ 1/3 Mol Wt of Unfractionated < size difference

● Inhibit coagulation similar to Heparin; 1/3 of molecules bind both antithrombin III & thrombin, remainder bind factor Xa, hence differences in activity

● High-ratio preps have advantage over heparin... Lovenox highest ratio & better bioavailability & longer half life

● Inhibtion eariler in coagulation cascade > the antithrobotic FX

● LMH esp Lovenox w/ Anti Xa/IIa ratio >short term benefit over Heparin. 1mg/Kg BID dose

Direct Thrombin Inhibitors; Hirudin & bivalirudin

● Antithrombin anticoagulants; signif advantage over heparin

● Derivitive of leech salivary gland, but sythesized & recominant

● Higher affinity to thrombin & inactivates already fibrin-bound thrombin (clot bound thrombin).

● DOES NOT need endogenous cofactors (antithrombin III)● Inhibits thrombin-induced platelet aggregation

● NOT assoc w/ HIT as Heparin is, however no signif benefit as adjuct therapy in ACS pts, use in Heparin-Thrombocytopenia

Fibrinolytic Therapy

● Reopening infarct related artery w/ fibrinolytic or PCI, gives the best opportunity for salvage ischemic myocardium; M&M

● C/I & other limitations... PCI Tx of choice w/ or w/o stenting

● Agents; tPA, Streptokinase; GUSTO-1; 15% reduction in death w/ t-PA up to 1 year

● Trials; r-PA vs accelerated t-PA; r-PA no adjustment for wt advantage GUSTO-III showed rPA = to tPA, EXCEPT pts >4

● TNK vs tPA; TNK longer t-1/2, 14X more fibrin specific, 80X resistant to plasminogen activator inhibitor than tPA

● ASSENT-2; no diff in 30 d M&M, except for pts >4 Sx b/f ED

EKG fibrinolytic Therapy eligibility

● ST elevation 1mm+ in 2 or more anatomically contiguous limb leads & 2mm+ in 2 or more contiguous precordial leads

● OR New or presumed new LBBB

● No benefit w/ ischemic CP who lack above EKG findings

● LBBB + AMI = poorer outcome due to likely proximal LAD occlusion, putting Signif portion LV in ischemic jeapordy

● DO NOT USE in ST-depression... Signif poorer outcomes!!!● Remember Age is NO longer excluder, but age > 75 ICH

When to initiate

● Gen accepted from time onset ST elevation AMI 12 Earlier use though better outcome. Esp 1st 6 AMI

● No signif benefit 12 to 24 after Sx onset

● If BP controlled or can be lowered... b/c risk ICH, initial SPB > 150 (15/1000 lives saved); SPB > 175mm Hg or > (11/1000)

● Persistently BP 200/120 Absolute C/I

● Heart failure, shock, Hypotension (60/1000 lives saved) NOT an absolute C/I per FTT Collaborative Group Meta-analysis

When TO & When NOT TO

● Active Diabetic Retinopathy... strong relative C/I risk blindness● DM pts w/ AMI 2X more likely to DIE

● CPR > 10 minutes long or extensive Chest Trauma from CPR Hemithorax/cardiac tamponade Not dx in fibrinolytic survivors

● Prior Stroke/TIA, major risk for ICH, relative C/I, prior Hemorrhagic stroke ABSOLUTE C/I

● Prior MI in setting AMI ISIS-2; 26% Mortality; even if prior fibrinolytics... Hx CABG combo lysis & Angioplasty may be needed!

When TO & When NOT TO

● Recent Surgery/Trauma/GI Bleed w/in 10 days is absolute C/I

● Women menses w/ AMI consider use; excessVag bleeding after Fibrinolytics CTRL w/ Vag packing compressible site of bleeding

● GI bleed in 10 days Absolute C/I

● HTN; SBP > 180 or DBP 110

● Significant liver Dysfunction

Primary Percutaneous Coronary Intervention

● Consider in pts w/ C/I to Fibrinolysis, Cardiogenic shock, unstable angina

● Many advantages over Fibrinolysis... > # pts applies to, lower risk ICH, signif higher initial reperfusion rate, faster hospital D/C

● Disadvantages; $$$, location specific, time to application

● Meta-analysis 10 major studies; 30 day mortality less in PTCA vs Fibrinolysis 4.4% vs 6.5% & signif reduction in total stroke or ICH