Affect the the Cardiovascular

Pharmacology Pharmacology Drugs Drugs that that Affect Affect the the Cardiovascular Cardiovascular System System Topics Topics •• •• •• •• Electrophysiology Electrophysiology Vaughn-Williams Vaughn-Williams classification classification Antihypertensives Antihypertensives Hemostatic Hemostatic agents agents Cardiac Cardiac Function Function •• Dependent Dependent upon upon –– Adequate Adequate amounts amounts of of ATP ATP ++ –– Adequate Adequate amounts amounts of of Ca Ca++ –– Coordinated Coordinated electrical electrical stimulus stimulus Adequate Adequate Amounts Amounts of of ATP ATP •• Needed Needed to: to: –– Maintain Maintain electrochemical electrochemical gradients gradients –– Propagate Propagate action action potentials potentials –– Power Power muscle muscle contraction contraction Adequate Adequate Amounts Amounts of of Calcium Calcium •• Calcium Calcium isis ‘glue’ ‘glue’ that that links links electrical electrical and and mechanical mechanical events. events. Coordinated Coordinated Electrical Electrical Stimulation Stimulation •• •• Heart Heart capable capable of of automaticity automaticity Two Two types types of of myocardial myocardial tissue tissue –– Contractile Contractile –– Conductive Conductive •• Impulses Impulses travel travel through through ‘action ‘action potential potential superhighway’. superhighway’. A.P. A.P. SuperHighway SuperHighway •• •• •• •• Sinoatrial Sinoatrial node node Atrioventricular Atrioventricular node node Bundle Bundle of of His His Bundle Bundle Branches Branches –– Fascicles Fascicles •• Purkinje Purkinje Network Network Electrophysiology Electrophysiology •• Two Two types types of of action action potentials potentials –– Fast Fast potentials potentials •• Found Foundin incontractile contractiletissue tissue –– Slow Slow potentials potentials •• Found Foundin inSA, SA,AV AVnode nodetissues tissues Fast Fast Potential Potential Phase 1 +20 Phase 2 0 -20 Phase 3 -40 -60 Phase 4 -80 RMP -80 to 90 mV controlled by Na+ channels = “fast channels” Fast Fast Potential Potential •• •• •• ++ influx “fast sodium channels” Phase 0: Na Phase 0: Na influx “fast sodium channels” ++ efflux Phase 1: K Phase 1: K efflux ++ efflux Phase 2: (Plateau) K Phase 2: (Plateau) K efflux –– AND AND Ca Ca ++++ influx influx •• •• ++ efflux Phase 3: K Phase 3: K efflux Phase Phase 4: 4: Resting Resting Membrane Membrane Potential Potential Cardiac Cardiac Conduction Conduction Cycle Cycle Slow Slow Potential Potential dependent upon Ca++ channels = “slow channels” 0 -20 -40 -60 -80 Phase 4 Phase 3 Slow Slow Potential Potential •• Self-depolarizing Self-depolarizing –– Responsible Responsible for for automaticity automaticity •• Phase Phase 44 depolarization depolarization –– ‘slow ‘slow sodium-calcium sodium-calcium channels’ channels’ –– ‘leaky’ ‘leaky’ to to sodium sodium •• Phase Phase 33 repolarization repolarization –– K K++ efflux efflux Cardiac Cardiac Pacemaker Pacemaker Dominance Dominance •• Intrinsic Intrinsic firing firing rates: rates: –– SA SA == 60 60 –– 100 100 –– AV AV == 45 45 –– 60 60 –– Purkinje Purkinje == 15 15 -- 45 45 Cardiac Cardiac Pacemakers Pacemakers •• SA SA isis primary primary –– Faster Faster depolarization depolarization rate rate ++ •• Faster FasterCa Ca++‘leak’ ‘leak’ •• Others Others are are ‘backups’ ‘backups’ –– Graduated Graduated depolarization depolarization rate rate ++ •• Graduated GraduatedCa Ca++leak leakrate rate Potential Potential Terms Terms RRP relative refractory period ERP effective refractory period APD action potential duration Dysrhythmia Dysrhythmia Generation Generation •• Abnormal Abnormal genesis genesis –– Imbalance Imbalance of of ANS ANS stimuli stimuli –– Pathologic Pathologic phase phase 44 depolarization depolarization •• Ectopic Ectopicfoci foci Dysrhythmia Dysrhythmia Generation Generation •• Abnormal Abnormal conduction conduction •• Analogies: Analogies: –– One Oneway wayvalve valve –– Buggies Buggiesstuck stuckin in muddy muddyroads roads Reentrant Reentrant Circuits Circuits Warning! Warning! •• All All antidysrhythmics antidysrhythmics have have arrythmogenic arrythmogenic properties properties •• In In other other words, words, they they all all can can CAUSE CAUSE dysrhythmias dysrhythmias too! too! AHA AHA Recommendation Recommendation Classifications Classifications •• Describes Describes weight weight of of supporting supporting evidence evidence NOT NOT mechanism mechanism •• Class Class II •• Class Class IIa IIa •• Class Class IIb IIb •• Indeterminant Indeterminant •• Class Class III III •• View View AHA AHA definitions definitions Vaughn -Williams Vaughn-Williams Classification Classification •• Class Class 11 –– Ia Ia –– Ib Ib –– Ic Ic •• •• •• •• Class Class IIII Class Class III III Class Class IV IV Misc Misc •• Description Description of of mechanism mechanism NOT NOT evidence evidence Class Class I:I: Sodium Sodium Channel Channel Blockers Blockers •• •• ++ movement in phases 0 and 4 Decrease Na Decrease Na movement in phases 0 and 4 Decreases Decreases rate rate of of propagation propagation (conduction) (conduction) via via tissue tissue with with fast fast potential potential (Purkinje) (Purkinje) –– Ignores Ignores those those with with slow slow potential potential (SA/AV) (SA/AV) •• Indications: Indications: ventricular ventricular dysrhythmias dysrhythmias Class Class Ia Ia Agents Agents •• Slow Slow conduction conduction through through ventricles ventricles •• Decrease Decrease repolarization repolarization rate rate –– Widen WidenQRS QRSand andQT QT intervals intervals •• May Maypromote promoteTorsades Torsades des desPointes! Pointes! •• PDQ: PDQ: –– procainamide procainamide ® (Pronestyl (Pronestyl®)) –– disopyramide disopyramide ®®) (Norpace (Norpace ) –– qunidine qunidine ® –– (Quinidex (Quinidex®)) Class Class Ib Ib Agents Agents •• Slow Slow conduction conduction through through ventricles ventricles •• Increase Increase rate rate of of repolarization repolarization •• Reduce Reduce automaticity automaticity –– Effective Effectivefor forectopic ectopic foci foci •• May May have have other other uses uses •• LTMD: LTMD: ®®) –– lidocaine (Xylocaine lidocaine (Xylocaine ) ® –– tocainide tocainide(Tonocard (Tonocard®)) ® –– mexiletine mexiletine(Mexitil (Mexitil®)) ® –– phenytoin phenytoin(Dilantin (Dilantin®)) Class Class Ic Ic Agents Agents •• Slow Slow conduction conduction through through ventricles, ventricles, atria atria & & conduction conduction system system •• Decrease Decrease repolarization repolarization rate rate •• Decrease Decrease contractility contractility •• Rare Rare last last chance chance drug drug •• flecainide flecainide (Tambocor (Tambocor®®)) •• propafenone propafenone ®®) (Rythmol (Rythmol ) Class Class II: II: Beta Beta Blockers Blockers ++ •• Beta receptors in heart attached to Ca Beta11 receptors in heart attached to Ca++ channels channels ++ influx –– Gradual Gradual Ca Ca++ influx responsible responsible for for automaticity automaticity ++ •• Beta blockade decreases Ca Beta11 blockade decreases Ca++ influx influx ++ channel –– Effects Effects similar similar to to Class Class IV IV (Ca (Ca++ channel blockers) blockers) •• Limited Limited ## approved approved for for tachycardias tachycardias Class Class II: II: Beta Beta Blockers Blockers •• •• •• ®®) propranolol (Inderal propranolol (Inderal ) ®®) acebutolol (Sectral acebutolol (Sectral ) ®®) esmolol (Brevibloc esmolol (Brevibloc ) Class Class III: III: Potassium Potassium Channel Channel Blockers Blockers •• •• •• •• ++ efflux during repolarization Decreases K Decreases K efflux during repolarization Prolongs Prolongs repolarization repolarization Extends Extends effective effective refractory refractory period period ®®) Prototype: bretyllium tosylate (Bretylol Prototype: bretyllium tosylate (Bretylol ) –– Initial Initial norepi norepi discharge discharge may may cause cause temporary temporary hypertension/tachycardia hypertension/tachycardia –– Subsequent Subsequent norepi norepi depletion depletion may may cause cause hypotension hypotension Class Class IV: IV: Calcium Calcium Channel Channel Blockers Blockers •• Similar Similareffect effectas asßß blockers blockers •• Decrease DecreaseSA/AV SA/AV automaticity automaticity •• Decrease DecreaseAV AVconductivity conductivity •• Useful Usefulin inbreaking breaking reentrant reentrantcircuit circuit •• Prime Primeside sideeffect: effect: hypotension hypotension& & bradycardia bradycardia •• •• ®®) verapamil (Calan verapamil (Calan ) ®®) diltiazem (Cardizem diltiazem (Cardizem ) •• Note: Note: nifedipine nifedipine doesn’t doesn’t work work on on heart heart Misc. Misc. Agents Agents ®®) •• adenosine (Adenocard adenosine (Adenocard ) ++ influx –– Decreases Decreases Ca Ca++ influx & & increases increases K K++ efflux efflux via via 22ndnd messenger messenger pathway pathway •• Hyperpolarization Hyperpolarizationof ofmembrane membrane •• Decreased Decreasedconduction conductionvelocity velocityvia viaslow slowpotentials potentials •• No Noeffect effecton onfast fastpotentials potentials •• Profound Profound side side effects effects possible possible (but (but shortshortlived) lived) Misc. Misc. Agents Agents •• •• Cardiac Cardiac Glycocides Glycocides ®®) digoxin (Lanoxin digoxin (Lanoxin ) –– Inhibits Inhibits NaKATP NaKATP pump pump ++ –– Increases intracellular Ca Increases intracellular Ca++ ++-Ca++ •• via Na via Na -Ca++exchange exchangepump pump –– Increases Increases contractility contractility –– Decreases Decreases AV AV conduction conduction velocity velocity Pharmacology Pharmacology Antihypertensives Antihypertensives Antihypertensive Antihypertensive Classes Classes •• •• •• •• •• diuretics diuretics beta beta blockers blockers angiotensin-converting angiotensin-converting enzyme enzyme (ACE) (ACE) inhibitors inhibitors calcium calcium channel channel blockers blockers vasodilators vasodilators Blood Blood Pressure Pressure == CO CO X X PVR PVR •• •• Cardiac Cardiac Output Output == SV SV xx HR HR PVR PVR == Afterload Afterload BP = CO x PVR cardiac factors heart rate contractility 1. Beta Blockers 2. CCB’s 3. C.A. Adrenergics circulating volume salt ACEi’s aldosterone Diuretics Key: CCB = calcium channel blockers CA Adrenergics = central-acting adrenergics ACEi’s = angiotensin-converting enzyme inhibitors BP = CO x PVR Hormones 1. vasodilators 2. ACEI’s 3. CCB’s Peripheral Sympathetic Receptors alpha 1. alpha blockers beta 2. beta blockers Central Nervous System Local Acting 1. CA Adrenergics 1. Peripheral-Acting Adrenergics Alpha Alpha11 Blockers Blockers Stimulate Stimulate alpha alpha11 receptors receptors -> -> hypertension hypertension Block Block alpha alpha11 receptors receptors -> -> hypotension hypotension •• •• •• doxazosin doxazosin (Cardura (Cardura®®)) ®®) prazosin (Minipress prazosin (Minipress ) terazosin terazosin (Hytrin (Hytrin®®)) Central Central Acting Acting Adrenergics Adrenergics •• Stimulate Stimulate alpha alpha22 receptors receptors –– inhibit inhibitalpha alpha11stimulation stimulation •• hypotension hypotension •• •• clonidine clonidine (Catapress (Catapress®®)) ®®) methyldopa (Aldomet methyldopa (Aldomet ) Peripheral Peripheral Acting Acting Adrenergics Adrenergics •• •• •• •• •• ®®) reserpine (Serpalan reserpine (Serpalan ) inhibits inhibits the the release release of of NE NE diminishes diminishes NE NE stores stores leads leads to to hypotension hypotension Prominent Prominent side side effect effect of of depression depression –– also also diminishes diminishes seratonin seratonin Adrenergic Adrenergic Side Side Effects Effects •• Common Common –– dry dry mouth, mouth, drowsiness, drowsiness, sedation sedation & & constipation constipation –– orthostatic orthostatic hypotension hypotension •• Less Less common common –– headache, headache, sleep sleep disturbances, disturbances, nausea, nausea, rash rash & & palpitations palpitations RAAS ACE ACE Inhibitors Inhibitors Angiotensin I . ACE Angiotensin II 1. potent vasoconstrictor - increases BP 2. stimulates Aldosterone - Na+ & H2O reabsorbtion Renin -Angiotensin Renin-Angiotensin Aldosterone Aldosterone System System •• •• •• •• Angiotensin Angiotensin IIII == vasoconstrictor vasoconstrictor Constricts Constricts blood blood vessels vessels & & increases increases BP BP Increases Increases SVR SVR or or afterload afterload ACE-I ACE-I blocks blocks these these effects effects decreasing decreasing SVR SVR & & afterload afterload ACE ACE Inhibitors Inhibitors •• Aldosterone Aldosterone secreted secreted from from adrenal adrenal glands glands cause cause sodium sodium & & water water reabsorption reabsorption •• Increase Increase blood blood volume volume •• Increase Increase preload preload •• ACE-I ACE-I blocks blocks this this and and decreases decreases preload preload Angiotensin Angiotensin Converting Converting Enzyme Enzyme Inhibitors Inhibitors •• •• •• •• •• •• •• ®®) captopril (Capoten captopril (Capoten ) ®®) enalapril (Vasotec enalapril (Vasotec ) ®® & Zestril®®) lisinopril (Prinivil lisinopril (Prinivil & Zestril ) ®®) quinapril (Accupril quinapril (Accupril ) ®®) ramipril (Altace ramipril (Altace ) ®®) benazepril (Lotensin benazepril (Lotensin ) ®®) fosinopril (Monopril fosinopril (Monopril ) Calcium Calcium Channel Channel Blockers Blockers •• Used Used for: for: •• Angina Angina •• Tachycardias Tachycardias •• Hypertension Hypertension CCB CCB Site Site of of Action Action diltiazem & verapamil nifedipine (and other dihydropyridines) CCB CCB Action Action •• diltiazem diltiazem & & verapamil verapamil •• •• decrease decreaseautomaticity automaticity& &conduction conductionin inSA SA& &AV AVnodes nodes decrease decreasemyocardial myocardialcontractility contractility •• •• decreased decreasedsmooth smoothmuscle muscletone tone decreased decreasedPVR PVR •• nifedipine nifedipine •• •• decreased decreasedsmooth smoothmuscle muscletone tone decreased decreasedPVR PVR Side Side Effects Effects of of CCBs CCBs •• Cardiovascular Cardiovascular •• hypotension, hypotension, palpitations palpitations & & tachycardia tachycardia •• Gastrointestinal Gastrointestinal •• constipation constipation & & nausea nausea •• Other Other •• rash, rash, flushing flushing & & peripheral peripheral edema edema Calcium Calcium Channel Channel Blockers Blockers ®®) •• diltiazem (Cardizem diltiazem (Cardizem ) ®®, Isoptin®®) •• verapamil (Calan verapamil (Calan , Isoptin ) ®®, Adalat®®) •• nifedipine (Procardia nifedipine (Procardia , Adalat ) Diuretic Diuretic Site Site of of Action Action . Distal tubule proximal tubule Collecting duct loop of Henle Mechanism Mechanism ++ •• Water follows Na Water follows Na ++ is reabsorbed into the blood •• 20-25% of all Na 20-25% of all Na is reabsorbed into the blood stream stream in in the the loop loop of of Henle Henle •• 5-10% 5-10% in in distal distal tubule tubule & & 3% 3% in in collecting collecting ducts ducts •• IfIf itit can can not not be be absorbed absorbed itit isis excreted excreted with with the the urine urine •• ⇓⇓ Blood Blood volume volume == ⇓⇓ preload preload !! Side Side Effects Effects of of Diuretics Diuretics •• •• •• •• •• •• ++ & K++ ] electrolyte losses [ Na electrolyte losses [Na & K ] fluid fluid losses losses [dehydration] [dehydration] myalgia myalgia N/V/D N/V/D dizziness dizziness hyperglycemia hyperglycemia Diuretics Diuretics •• Thiazides: Thiazides: ® •• chlorothiazide chlorothiazide(Diuril (Diuril®))& &hydrochlorothiazide hydrochlorothiazide ® ® (HCTZ (HCTZ®,,HydroDIURIL HydroDIURIL®)) •• Loop Loop Diuretics Diuretics ® ® •• furosemide furosemide(Lasix (Lasix®),),bumetanide bumetanide(Bumex (Bumex®)) •• Potassium Potassium Sparing Sparing Diuretics Diuretics ® •• spironolactone spironolactone(Aldactone (Aldactone®)) Mechanism Mechanism of of Vasodilators Vasodilators •• •• Directly Directly relaxes relaxes arteriole arteriole smooth smooth muscle muscle Decrease Decrease SVR SVR == decrease decrease afterload afterload Side Side Effects Effects of of Vasodilators Vasodilators ®®) •• hydralazine (Apresoline hydralazine (Apresoline ) –– Reflex Reflex tachycardia tachycardia ®®) •• sodium nitroprusside (Nipride sodium nitroprusside (Nipride ) –– Cyanide Cyanide toxicity toxicity in in renal renal failure failure –– CNS CNS toxicity toxicity == agitation, agitation, hallucinations, hallucinations, etc. etc. Vasodilators Vasodilators •• •• •• •• ®®] diazoxide [Hyperstat diazoxide [Hyperstat ] ®®] hydralazine [Apresoline hydralazine [Apresoline ] ®®] minoxidil [Loniten minoxidil [Loniten ] ®®] sodium Nitroprusside [Nipride sodium Nitroprusside [Nipride ] Pharmacology Pharmacology Drugs Drugs Affecting Affecting Hemostasis Hemostasis Hemostasis Hemostasis •• Reproduce Reproduce figure figure 11-9, 11-9, page page 359 359 Sherwood Sherwood Platelet Platelet Adhesion Adhesion Coagulation Coagulation Cascade Cascade •• Reproduce Reproduce following following components components of of cascade: cascade: –– Prothrombin Prothrombin -> -> thrombin thrombin •• Fibrinogen Fibrinogen-> ->fibrin fibrin –– Plasminogen Plasminogen -> -> plasmin plasmin Platelet Platelet Inhibitors Inhibitors •• •• •• •• Inhibit Inhibit the the aggregation aggregation of of platelets platelets Indicated Indicated in in progressing progressing MI, MI, TIA/CVA TIA/CVA Side Side Effects: Effects: uncontrolled uncontrolled bleeding bleeding No No effect effect on on existing existing thrombi thrombi Aspirin Aspirin –– Inhibits Inhibits COX COX •• Arachidonic Arachidonicacid acid(COX) (COX)-> ->TXA2 TXA2(⇓ (⇓aggregation) aggregation) GP GP IIB/IIIA IIB/IIIA Inhibitors Inhibitors GP IIb/IIIa Receptor Fibrinogen GP IIb/IIIa Inhibitors GP GP IIB/IIIA IIB/IIIA Inhibitors Inhibitors •• •• •• ®®) abciximab (ReoPro abciximab (ReoPro ) ®®) eptifibitide (Integrilin eptifibitide (Integrilin ) ®®) tirofiban (Aggrastat tirofiban (Aggrastat ) Anticoagulants Anticoagulants •• Interrupt Interrupt clotting clotting cascade cascade at at various various points points –– No No effect effect on on platelets platelets •• •• ®®) Heparin & LMW Heparin (Lovenox Heparin & LMW Heparin (Lovenox ) ®®) warfarin (Coumadin warfarin (Coumadin ) Heparin Heparin •• Endogenous Endogenous –– Released Releasedfrom frommast mastcells/basophils cells/basophils •• •• Binds Binds with with antithrombin antithrombin III III Antithrombin Antithrombin III III binds binds with with and and inactivates inactivates excess excess thrombin thrombin to to regionalize regionalize clotting clotting activity. activity. –– Most Mostthrombin thrombin(80-95%) (80-95%)captured capturedin infibrin fibrinmesh. mesh. •• Antithrombin-heparin Antithrombin-heparin complex complex 1000X 1000X as as effective effective as as antithrombin antithrombin III III alone alone Heparin Heparin •• •• Measured Measured in in Units, Units, not not milligrams milligrams Indications: Indications: –– MI, MI, PE, PE, DVT, DVT, ischemic ischemic CVA CVA •• Antidote Antidote for for heparin heparin OD: OD: protamine. protamine. –– MOA: MOA: heparin heparin isis strongly strongly negatively negatively charged. charged. Protamine Protamine isis strongly strongly positively positively charged. charged. ® warfarin ( Coumadin warfarin (Coumadin®)) •• Factors Factors II, II, VII, VII, IX IX and and X X all all vitamin vitamin K K dependent dependent enzymes enzymes •• Warfarin Warfarin competes competes with with vitamin vitamin K K in in the the synthesis synthesis of of these these enzymes. enzymes. •• Depletes Depletes the the reserves reserves of of clotting clotting factors. factors. •• Delayed Delayed onset onset (~12 (~12 hours) hours) due due to to existing existing factors factors Thrombolytics Thrombolytics •• Directly Directly break break up up clots clots –– Promote Promotenatural natural thrombolysis thrombolysis •• Enhance Enhance activation activation of of plasminogen plasminogen •• ‘Time ‘Time isis Muscle’ Muscle’ •• streptokinase streptokinase (Streptase (Streptase®®)) •• alteplase alteplase (tPA (tPA®®,, ®®) Activase Activase ) ®®) •• anistreplase (Eminase anistreplase (Eminase ) ®®) •• reteplase (Retevase reteplase (Retevase ) ®®) •• tenecteplase (TNKase tenecteplase (TNKase ) Occlusion Occlusion Mechanism Mechanism tPA tPA Mechanism Mechanism Cholesterol Cholesterol Metabolism Metabolism •• Cholesterol Cholesterol important important component component in in membranes membranes and and as as hormone hormone precursor precursor •• Synthesized Synthesized in in liver liver –– Hydroxymethylglutaryl Hydroxymethylglutaryl coenzyme coenzyme A A reductase reductase –– (HMG (HMG CoA CoA reductase) reductase) dependant dependant •• •• Stored Stored in in tissues tissues for for latter latter use use Insoluble Insoluble in in plasma plasma (a (a type type of of lipid) lipid) –– Must Must have have transport transport mechanism mechanism Lipoproteins Lipoproteins •• Lipids Lipids are are surrounded surrounded by by protein protein coat coatto to‘hide’ ‘hide’ hydrophobic hydrophobic fatty fatty core. core. •• Lipoproteins Lipoproteins described described by by density density –– VLDL, VLDL,LDL, LDL,IDL, IDL,HDL, HDL,VHDL VHDL •• LDL LDL contain contain most most cholesterol cholesterol in in body body –– Transport Transportcholesterol cholesterolfrom fromliver liverto totissues tissuesfor foruse use (“Bad”) (“Bad”) •• HDL HDL move move cholesterol cholesterol back back to to liver liver –– “Good” “Good”b/c b/cremove removecholesterol cholesterolfrom fromcirculation circulation Why Why We We Fear Fear Cholesterol Cholesterol •• •• Risk Risk of of CAD CAD linked linked to to LDL LDL levels levels LDLs LDLs are are deposited deposited under under endothelial endothelial surface surface and and oxidized oxidized where where they: they: –– Attracts Attractsmonocytes monocytes-> ->macrophages macrophages –– Macrophages Macrophagesengulf engulfoxidized oxidizedLDL LDL •• Vacuolation Vacuolationinto into‘foam ‘foamcells’ cells’ –– Foam Foamcells cellsprotrude protrudeagainst againstintimal intimallining lining •• Eventually Eventuallyaatough toughcap capisisformed formed –– Vascular Vasculardiameter diameter& &blood bloodflow flowdecreased decreased Why Why We We Fear Fear Cholesterol Cholesterol •• •• •• •• •• •• •• Plaque Plaque cap cap can can rupture rupture Collagen Collagen exposed exposed Clotting Clotting cascade cascade activated activated Platelet Platelet adhesion adhesion Thrombus Thrombus formation formation Embolus Embolus formation formation possible possible Occlusion Occlusion causes causes ischemia ischemia Lipid Lipid Deposition Deposition Thrombus Thrombus Formation Formation Platelet Platelet Adhesion Adhesion Embolus Embolus Formation Formation Occlusion Occlusion Causes Causes Infarction Infarction Antihyperlipidemic Antihyperlipidemic Agents Agents ®®) •• Goal: Decrease LDL • lovastatin (Mevacor Goal: Decrease LDL • lovastatin (Mevacor ) ®®) –– Inhibition •• pravastatin (Pravachol Inhibitionof ofLDL LDL pravastatin (Pravachol ) synthesis synthesis ®®) •• simvastatin (Zocor simvastatin (Zocor ) –– Increase LDL Increase LDL ®®) • atorvastatin (Lipitor • atorvastatin (Lipitor ) receptors in liver receptors in liver •• Target: Target: << 200 200 mg/dl mg/dl •• Statins Statins are are HMG HMG CoA CoA reductase reductase inhibitors inhibitors Thank Thank You! You! •• To To Temple Temple College College EMS EMS Professions Professions for for permission permission to to use use their their materials materials