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79 Cards in this Set
- Front
- Back
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Ischemia
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Lack of Oxygen from inadequate perfusion
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Ischemic Heart Dz (IHD)
definition and presentation |
characterized by reduced blood supply to the heart muscle, usually due to coronary artery disease
May present as: * silent ischemia * chest pain (at rest or exertion) * MI |
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IHD
diagnosis and treatment options |
Diagnosis:
electrocardiogram, blood tests (cardiac markers), cardiac stress testing or a coronary angiogram treatment options: medication, percutaneous coronary intervention (angioplasty) or coronary artery bypass surgery (CABG) |
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IHD risk factors
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risk factors:
age, smoking, hypercholesterolaemia, DM, HTN, men and FH |
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Angina
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discomfort or pain in chest, arm, shoulder, back, or jaw
frequently worsened by physical exertion or emotional stress usually relieved by SL NTG pts usually have coronary artery dz (CAD) in at least one large epicardial artery |
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Acute Coronary Syndrome (ACS)
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Encompasses the following:
* unstable angina (UA) * Non ST-segment MI (NSTEMI) * ST-segment MI (STEMI) |
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Coronary Artery Dz (CAD)
Cerebrovascular Dz (CVD) Peripheral Vascular Dz (PVD) |
CAD: atherosclerosis of the coronary arteries (heart)
CVD: atherosclerosis of the cerebrovascular arteries (brain-stroke) PVD: atherosclerosis of the peripheral arteries (leg) |
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Heart Disease (HD)
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CHF (Chronic Heart Failure)
HTN CAD |
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Percutaneous coronary intervention (PCI)
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procedure to repoen a pratially or completely occluded coronary vessel
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Coronary artery bypass graft (CABG)
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surgical procedure that takes a vein from the leg and attached to the heart as a new coronary vessel to bypass a diseased vessel
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IHD
Normal physiology |
heart needs fixed amt of oxygen, so arterioles change their resistance and dilate as needed to allow more blood and oxygen in response to:
* ↑BP, ↑ mycocardial oxygen demand (MVO2), physical exertion |
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IHD
Normal physiology |
in atherosclerosis, plaque narrows the vessel causing arterioles to dilate at rest to prevent ischemia. So, with stress or exertion, result is ischemia and angina
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IHD
Pathophysiology |
Determinants of MVO2 (heart's Oxygen demand)
* HR - tachycardia → ↑ MVO2 * contractility → ↑ MVO2 * ↑ ventricular volume and pressure → → ↑ systolic wall force → ↑ MVO2 |
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IHD
Diagnostic procedures |
Exercise Tolerance Test
Stress Imaging (drugs "do the exercise" by increasing MVO2) * dobutamine * dipyrdamole and adenosine Cardiac Catheterization (Cath, angiography) * catheter guided to heart via femoral artery to release dye to image the extent of occlusion |
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IHD
Presentation |
1. Chronic Stable Angina
2. Prinzmetal's (Variant) angina (uncommon) 3. Silent ischemia |
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Chronic Stable Angina
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Sx caused by ↓O2 supply do to ↓ flow
stable if sx don't worsen over several weeks |
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Prinzmetal's (Variant) angina (uncommon)
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usually due to spsm w/o ↑ MVO2
severe atherosclerosis pts b/w ages 30 and 40 mainly sx at rest and awaken pt from sleep |
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Silent ischemia
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ischemia in absence of SX
75% of ischemic episode is pts with stable angina are undetected common in diabetic and post-mi pts |
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Chronic Stable Angina
pharmacologic management antiplatelets |
ASA → ↓ MI, CV events, and sudden death
** (in all pts w/ or w/o sx) clopidogrel (Plavix) > antithrombotic effect than ticlopidine (Ticlid) and fewer s/e ** Use plavix when ASA is absolutely contraindicated ASA + Plavix not in pts w/stable dz not undergoing PCI |
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Chronic Stable Angina
BBs - effects on MVO2 |
↓ MVO2 b/c inhibit catecholamines
↓ HR ( neg. chronotrope - ↓s conduction through AV node) ↓ contractility (neg. inotrop - ↓s force of contraction) ↓ BP |
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Chronic Stable Angina
BBs - effects on oxygen supply - dosing |
none
* start low, go slow * titrate to resting hr 50-60bpm * avoid abrupt w/d → MI; taper over 2 days |
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Chronic Stable Angina
BBs - selection |
* cardioselective dec's a/e
* ISA BBs (CAPP) - not as effective b/c don't ↓ HR much; little ↓ MVO2 * ISA BBs reserved for pts with low resting HR with exercise-induce angina * BBs preferred in young pts with HTN, post-MI, ↑ rest HR, fixed angina threshold, mile HF |
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Chronic Stable Angina
BBs - Indications |
* 1st line - post MI
* initial tx w/o MI * BBs > nitrates and CCBs in silent ischemia * effective as monotx or in combo with nitrates and CCBs * avoid in Pronzmetal's * improves Sx 80% of time * all BBs effective; not all approved |
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Chronic Stable Angina
Characteristics |
* pain located over sternum
- may radiate to l sternum or arm, jaw, back, r arm, or neck * pressure or heavy weight on chest, burning, tightness, deep, squeezing, aching, vise-like * lasts 30s to 30m * precipitating factors: exercise, cold, postprandial, stress, sex * pain relieved w/SL nitro or rest |
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Chronic Stable Angina
Nitrates - effects on MVO2 |
* peripheral vasodilation → ↓ blood return → ↓ LV volume, ↓ wall stress, and therefore, ↓ MVO2
* arterial vasodilation → ↓ PR, ↓SBP, and ↓O2 demand * nitrates can cause reflexive ↑ in sympathomimetic act'y → ↑ HR / contractility and ↑ O2 demand - overcome with use of BB |
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Chronic Stable Angina
Nitrates - effects on O2 supply |
Dilation of epicardial coronary arteries in areas w/ or w/o stenosis ↑s O2 supply
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Chronic Stable Angina
CCBs - effects on MVO2 |
decreases MVO2 by:
* primarily: by ↓ing VR and arterial BP by vasodilation of systemic arteries * by ↓ing contractility and O2 requirem - all CCBs have some (-) inotropic effect: ver > dilt > nif * ver and dil also ↓conductance through AV node → ↓ HR |
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Chronic Stable Angina
CCBs - effects on O2 supply |
↓ vascular resistance
↑ coronary blood flow coronary vasodilation at sites of stenosis prevents/relieves angina by dilation of epicardial coronary arteries |
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Chronic Stable Angina
CCBs - indications |
* initial tx when BBs are contraind
* combine w/BB when BBs alone don't work * LA dihydros and non-dihydros effective in stable angina * avoid Short-Acting dihydros |
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Chronic Stable Angina
ACEi ↑←→↓ |
↓ incidence of MI, CV death, and stroke in patients at ↑ risk for CV dz (HOPE)
controversy whether all ACEis effective low-risk pts with stable CAD and normal LV f(n) may not benefit like high-risk pt |
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Chronic Stable Angina
ACEi - indications |
all CAD pts (by angiograpy or post-mi) who also have DM or LV dis(n)
in pts with CAD or other vascular dz in all pts w/DM who have no CI to severe renal dz |
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Chronic Stable Angina
Lipid-lowering TX - indications |
pts w/CAD or suspected CAD or CHD risk equivalents and LDL > 100
target LDLs * high risk pts < 70 * lower risk pts < 100 |
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Chronic Stable Angina
Prinzmetal's (variant) angina - treatment |
BBs make it worse
* induce vasoconstriction Nitrates for acute attacks CCBs more effective than nitrates Nif, dilt, verap equally effective |
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Chronic Stable Angina
Silent ischemia - treatment |
first - modifiy risk factors for IHD
**smoking, HTN, hypercholesterolemia BBs preferred in post-MI BBs more effective than CCBs |
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Unstable Angina/Non-ST-Segment Elevation MI (UA/NSTEMI)
3 distinguishing features of UA |
(1) it occurs at rest (or with minimal exertion), usually lasting >10 min
(2) it is severe and of new onset (i.e., within the prior 4–6 weeks); and/or (3) it occurs with a crescendo pattern (i.e., distinctly more severe, prolonged, or frequent than previously) |
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Unstable Angina/Non-ST-Segment Elevation MI (UA/NSTEMI)
Pathophysiology - 2 essential events |
1. Disruption of atherosclerotic plaque
2. Formation of platelet-rich thrombus clinical manifestation depends on extent and duration of thrombotic occlusion |
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Unstable Angina/Non-ST-Segment Elevation MI (UA/NSTEMI)
Presentation |
UA may occur unpredictably at rest which may be a serious indicator of an impending heart attack.
Crushing chest pain that can radiate.. similar to typical angina but worse pain not relieved by NTG may evolve to STEMI if not treated |
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Unstable Angina/Non-ST-Segment Elevation MI (UA/NSTEMI)
Diagnosis - Cardiac enzymes - ECG changes - Goals of TX |
Chest pain > 5m not relieved by NTG
UA - no cardiac enzymes, transient ECG changes if present at all NSTEMI - Yes Cardiac Enzymes, ECG changes always present Goals - complete restore of blood flow - prevent MI, arrhythmias, and ischemia |
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Unstable Angina/Non-ST-Segment Elevation MI (UA/NSTEMI)
classes of meds used |
Anti-ischemic tx
- BBs, Nitrates, CCBs, ACEis Antiplatelet tx - ASA, thienopyridines (eg clopidogrel), Clycoprotein IIb/IIIa inhibitors (GPIs) Anticoagulant tx - unfractionated heparin (UFH), LMWH, Lipid lowering tx |
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Unstable Angina/Non-ST-Segment Elevation MI (UA/NSTEMI)
Pharm management - indications MONA, BBs |
MONA - morphine, oxygen, nitrates,
aspirin BBs - prefer BBs w/no ISA - B1 sel in pts w/COPD, asthma |
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Unstable Angina/Non-ST-Segment Elevation MI (UA/NSTEMI)
Pharm management - indications CCBs, ACEis |
CCBs - no mortality benefit
- use in pts with CIs to BBs - non-dihydros if no LV disf(n) - avoid short acting CCBs ACEi - not for immediate treatment - good for pts w/DM, HF, high - risk CAD, HTN not controlled by CCBs and nitrates - ↓mortality in pts w/vascular dz and no HF (HOPE trial) |
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Types of cardiovascular diseases
↑←→↓ |
* Aneurysm
* Angina * Atherosclerosis * Cerebrovascular Accident (Stroke) * Cerebrovascular disease * Congestive Heart Failure * Coronary Artery Disease * Myocardial infarction |
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Vascular disease
Definition |
a form of cardiovascular disease primarily affecting the blood vessels.
Some conditions, such as myocardial ischemia, can be considered both vascular diseases and heart diseases. |
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Unstable Angina/Non-ST-Segment Elevation MI (UA/NSTEMI)
Pharm management - indications Nitrates |
all pts get NTG as SL or Spray followed by IV as initial relief for ischemia
long acting nitrates used as secondary prevention when CCBs and BBs aren't tolerated or don't relieve chest pain well |
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Unstable Angina/Non-ST-Segment Elevation MI (UA/NSTEMI)
Pharm management - indications ASA |
chew and swallow at first sign of chest pain
daily dose for life |
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Unstable Angina/Non-ST-Segment Elevation MI (UA/NSTEMI)
Pharm management - indications thienoppyridines |
clopidogrel = Plavix
Ticlopidine = Ticlid (severe toxicities) - alternative to ASA-intolerant pts - inhibition of platelet activation is irreversible and takes 3-5 days to reach full effect - clopidogrel is preferred - MOA differs from ASA - effx additive - use w/ASA in pts * w/stent for 6-12m * w/o PCI planned for up to 9m |
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Unstable Angina/Non-ST-Segment Elevation MI (UA/NSTEMI)
Pharm management - indications GPIs |
abciximab (ReoPro)
eptifibatide (Integrilin) tirofiban (Aggrastat) adjunctive TX in pts undergoing PCI in addition to heparin, ASA and clopidogrel should be given to pts w/a planned PCI GPI given during intervention procedure eptifbatide or tirofiban sholld be given in cobo w/ASA and LMWH/UFH to pts w/ACS who won't get PCI |
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Unstable Angina/Non-ST-Segment Elevation MI (UA/NSTEMI)
Pharm management - indications UFH, LMWH |
Heparin or LMWH should be given to all pts in combo w/ASA and clopidogrel
Heparin preferred over LMWH 24h b/4 CABG LMWH - enoxaparin (Lovenox), dalteparin (Fragmin) - enoxaparin may be superior to hehparin in pts w/UA/STEMI |
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Acute MI (STEMI)
Pathophysiology |
85% of MIs - athersclerotic plaque rupture leads to thrombus formation
aggregated platelets after plaque rupture aid thrombus formation leading to occlusive thrombus complete occlusion leads to abrupt and persistent ischemia; untreated = death |
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STEMI vs NSTEMI
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STEMI
- totally occlusive thrombus - more extensive damage - affects whole thickness of heart wall - worse myocardial necrosis b/c ischemic for longer - lytic TX or reperfusion is mainstay |
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RV STEMI vs LV STEMI
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manage similarly EXCEPT in RV NTG, diuretics, and other preload reducing agents should be avoided
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STEMI
dignosis |
2 of following:
- chest pain > 30m - ECG ST-seg elevation - cardiac isoenzymes * TroponinT or I elevation * CK-MB elevations |
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STEMI
Medications/Techniques used in treatment |
- MONA
- Nitrates - Reperfusion TX - Fibrinolytic TX - Heparan, LMWH TX - BBs - GPIs - ACEis, ARBs, Aldosterone Inhibitors - Lipid lowering - CCBs - warfarin - treatment of ventricular fibrillation (VF) post-MI |
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STEMI
Indications: Nitrates |
use for first 24h in all pts w/MI who don't have hypottension, bradycardia, or tachycardia
insignificant reduction in mortality is used beyond 48h |
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STEMI
Indications: Fibrinolytic TX - ie use when: |
- presentation < 12 h of SX onset
- in pts > 75yo - presentation 12 to 24h if still chest pain Don't use when: - time to TX (ie presentation) is > 24h - ST depression |
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STEMI
Indications: Heparin TX |
- adjunct w/fibrinolytics for prevention of
recurrent coronary thrombosis - pts at high risk for systemic emboli: (anterior MI, afib, previous emboli, known LV thrombus) * Use IV UFH, LMWH, or dalteparin * hold UFH for 6h after thrombus broken up; start aPTT monitoring ** change to SC heparin, ASA, or warfarin alone after 48h - Use SC UFH or LMWH in al pts not treated w/a thrombolytic - consider SC UFH or LMWH for DVT prophylaxis |
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STEMI
Indications: LMWH |
Do NOT use in pts > 75 or pts < 75 with renal dysfunction
Use in pts at ↑ risk for systemic emboli |
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STEMI
GPIs |
role is evolving
more complete reperfusion at cost of more bleeding abciximab reduces incidence of combined death, MI, and recurrent ischemia in pts with STEMI |
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STEMI
Renin-angiotensin-aldosterone (RAA) system inhibition ACIi - limit the remodeling precess and slow progression to HF after MI |
use in all pts w/o CIs w/in first 24h
benefits much better in pts w/ventricular dysfunction (LVEF < 40% or HF Sx) Marked benefit in pts w/previous MI, HF, and anterior MI w/o thromolytic therapy Acute treatment should be continued indefinitely in pts w/hx of MI, HTN, DM |
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STEMI
RAA system - ARBs and Aldosterone Atgs |
Use ARB in pts who should get an ACE but are intolerant (see above)
ACEi ARB combo in pts w/persistent HF Use Aldosteron Atgs longterm in pts on ACEi w/LVEF <40% AND either sx of HF or DM Avoid aldosterone atgs w/Scr<2.5 or hyperkalemia (>5) |
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STEMI
Indications - CCBs |
verap or dilt only w/continuing ischemia when BBs CI'd or used at full dose
verap or dilt shold not be use in pts with systolic dysfunction, AV block, or bradycardia |
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thrombus vs emboli
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Thrombus
- blood clot that forms along the wall of the heart or a blood vessel - can slow blood flow, and may stop the flow of blood in the vessel Embolus - is a clot that forms in one area but dislodges and block another vessel in the body |
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STEMI
Treatment - warfarin use post-STEMI |
longterm anticoag w/warfarin controvercial
use in pts w/indications for anticoag: - LV thrombus, Afib, etc..? warfarin not studied in pts>75 for secondary prevention post-STEMI clopidogrel preferred over warfarin in pts who cannot tolerate ASA for secondary prevention unless clear indication for warfarin |
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STEMI
Treatment of ventricular fibrillation (VF) |
risk of VF highest first 4h post-MI
prophylactic antiarrhythmic use leads to increased mortality when used to prevent VF amiodarone ok if pts have VF post-MI |
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STEMI
treatment - BBs |
early tx
- all pts with acute MI w/in 12h of MI regardless if getting thrombolytic tx - IV or PO treatment should be started in all pts asap w/in 12-24h after sx onset Late Tx: - give to all pts w/o clear CI - begin w/in a few days and continue indefinately |
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STEMI
Revascularization - PCI procedures |
baloon angioplasty (PTCA)
Coronary stenting Ablative technologies (laser, atherectomy) |
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STEMI
Primary PCI |
-very effective
-suitable for >90% pts -goal of arrival to balloon time of < 90m -favored over fibrinolytic tx b/c * ↓ shrotterm mortality * ↓ reinfarctions * ↓ hemorrhagic strokes |
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STEMI
Drug eluting stents (DES) |
restenosis
- loss of >50% of diameter of in-stent lumen of initially successful placement - occurs w/in first 3-6months DES ↓ irestenosis Sirolimus and paclitaxel are two egs. |
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STEMI
anticoagulation during PCI |
mandatory
UFH is mainstay bivalirudin may be as effective by w/less bleeding |
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STEMI
PCIs and GPIs |
timing of PCI dictates which agent
- abciximab or eptifibatide if PCI <4h after presentation - tirofiban for pts treated medically for first 48h abciximab should not be used in pts w/o plans for PCI |
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STEMI
CABG |
indicated in pts w/multi vessel dz w/LV dysfunction or significant dz of a major coronary vessel
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IHD
risk factors - modifiable |
smoking
HTN Hyperlipidemia Hyperchomocysteinemia DM Metabolic syndrome Obesity Pysical inactivity Alcohol consumption |
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IHD
risk factors - nonmodifiable |
age: men >45, women >55 (early historectomy at any age)
Race: AA males and females ↑ risk FH: father or brother w/coronary event < 55yo, < 65 if mother or sister |
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IHD
primary prevention pharm TX |
ASA - pts > 50 w/at least one major RF
Lipid lowering - consider in all pts at risk for coronary event antioxidants and vit E - no consistent evidence to justify use in primary prevention |
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IHD
primary prevention - ACEi |
ACEi
- HOPE - ramipril - ↓risk of MI, stroke and death in pts at high risk for major CV events - EUROPA - perindopril - similar to above but also in pts w/no SX of HF or LV dysfunction - PEACE - low risk pts receiving BB, ASA, and lipid-lowering TX, do not benefit from adding trandolapril |
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Fibrinolytic drugs used in fibrinolytic or thrombolytic tx
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streptokinase (Streptase)
tissue plasminogen activator (Alteplase) reteplase (Retavase) tenecteplase (TNKase) MOA: converts plasminogen to plasmin which activates body's natural thrombolytic system to lyse the clot |
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LMWHs
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enoxaparin (Lovenox)
dalteparin (Fragmin) |
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Anticoagulants
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- Heparin
- LMWH - Thrombin inhibitors * DESIRUDIN () * LEPIRUDIN (Refludin) * ARGATROBAN (Argatroban) * BIVALIRUDIN (Angiomax) - Selective Factor Xa Inhibitor * FONDAPARINUX (Arixtra) - Warfarin |
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Antiplatelets
ANAGRELIDE HCl (Agrylin) DIPYRIDAMOLE (Persantine) |
Aggregation Inhibitors (Thienopyridines)
- MOA: blocks adenosine diphosphate - mediated platelet activation via blocking glycoprotein IIB/IIIa complex * CILOSTAZOL (Pletal) * CLOPIDOGREL (Plavix) * TICLOPIDINE (Ticlid) Glycoprotein IIb/IIIa Inhibitors * abciximab (ReoPro) * eptifibatide (Integrilin) * tirofiban (Aggrastat) |
