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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