Transcript Myocardial_Infarction__2016

Myocardial Infarction
Acute Coronary Syndrome
Myocardial Infarction (MI) or Acute
Coronary Syndrome (ACS)
 MI is a result of reduced blood flow
through one of the coronary arteries.
This causes myocardial ischemia,
injury, and necrosis.
Acute Coronary Syndrome
 This term covers a range of thrombotic
coronary artery diseases, including
unstable angina, ST elevation
myocardial infarction (STEMI or Q wave
MI), and non ST elevation myocardial
infarction (NSTEMI or non-Q wave MI).
Patients with ACS have some degree of
coronary artery occlusion.
Acute Coronary Syndrome
Diagnosis
 Includes a complete history, physical
examination, electrocardiogram, and
serial cardiac enzymes.
Differentiating ACS from non-cardiac
chest pain is the primary challenge.
Symptoms
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SOB/Dyspnea
Chest pain
Nausea/vomiting
Orthopnea
Diaphoresis
Palpitations
Apprehension
Fatigue
Pain in jaw, neck, upper arm
Diaphoresis
Lightheadedness or dizziness
Syncope
Risk Factors
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High blood pressure
Elevated serum triglyceride levels, low density lipoprotein,
high cholesterol, and homocysteine levels and decreased
serum high-density lipoprotein levels
Cigarette smoking
Lack of physical activity
Obesity
Type 2 Diabetes
Older age >45 men, >55 women
Family history of chest pain, heart disease, or CVA
Stress
Use of amphetamines or cocaine
Excessive intake of saturated fats, carbohydrates, or salt
Causes
 ACS may develop slowly over time by the
building up of plaques in the coronary
arteries. These plaques, are made of fatty
deposits, causing the arteries to narrow
and make it more difficult for blood to flow
through them. This buildup of plaque is
known as atherosclerosis. Eventually, this
buildup means that your heart can’t pump
enough oxygen-rich blood to the rest of
your body, causing chest pain (angina) or a
MI.
Trigger Mechanism of Ischemia
 Passive collapse of a vessel near a stenotic
region
 Spasm, related to sympathetic tone
 Plaque rupture produces an ulcerated area
that attracts platelets
 Platelets attracted to plaque cause a
production of a powerful vasoconstrictor
(thromboxane A2)
 Protective mechanisms are prostacyclin and
nitric oxide are made by the endothelium
and are vasodilators and plaque inhibitors
Vasospasm
 Occurrences
-Occurs in large or small arteries
-Usually occurs near an artery damaged by plaque
 Factors that precipitate vasospasm
-Cold exposure
-Anxiety, fear
-Exercise, hyperventilation, cocaine abuse
 Factors that prevent vasospasm
-nitroglycerin, calcium channel blockers
-Endothelial factor
Law of Supply and Demand
 If myocardial oxygen demand increases, so
must oxygen supply
 To effectively increase oxygen supply,
coronary perfusion must also increase
 Tissue hypoxia the most potent stimulus,
causes coronary arteries to dilate and
increases coronary blood flow
 Normal coronary vessels can dilate and
increase blood flow five to six times above
resting levels. However, stenotic,diseased
vessels can’t dilate, so oxygen deficit may
result
Oxygen Balancing Act
 4 major determinants of myocardial oxygen
demand
-heart rate
-contractile force
-muscle mass
-ventricular wall tension
Cardiac workload and oxygen demand
increase if the heart rate speeds up or if
the force of contractions becomes stronger.
This can occur in HTN, ventricular dilation,
or heart muscle hypertrophy.
Oxygen Balancing Act
 When the myocardial cell is lacking in
oxygen, the cells begin to suffer
injury
 Normal circulation and oxygenation
need to be restored
 Remember ischemia and injury ARE
reversible. Infarct or cell death is
NOT!!
Tests and Diagnostics
 Electrocardiogram: Ischemia, Injury,
Infarction
 BMP, CBC, Cardiac Biomarkers
 Echocardiogram
 CXR
 Nuclear myoview
 CT angiogram
 Coronary artery calcium scoring
 Coronary angiogram (cardiac
Catheterization)
Acute Myocardial Infarction
Artery Specific Symptomology
Left Main Coronary Artery
 Extensive anterior wall infarct
 EKG Location - V1-V6
Complications
 Sudden cardiac death
 Dysrhythmias
 Ventricular rupture/aneurysm
 Ventricular septal defect
 Congestive heart failure
 Cardiogenic shock
Artery Specific Symtomology
Left Anterior Descending (LAD) Artery
Septal/Anterior wall infarct
(or combination of both)
EKG Location – V1, V2 (septal);
V3, V4 (anterior)
Complications
Dysrhythmias
Ventricular aneurysm
Congestive heart failure
Cardiogenic shock
Left Anterior Descending Artery
(LAD)
 LAD Supplies
-Anterolateral myocardium
-Apex
-Interventricular septum
-Typically supplies 45-55% of LV
-RBB
-Anterior fascicle of the LBB
Artery Specific Symptomology
 Right Coronary
Artery (RCA)
-Inferior/Posterior
wall infarct (or
both)
-RV
-ECG locationII,III,aVF
RCA Complications
 Dysrhythmias
 Papillary muscle rupture with mitral
regurgitation
 CHF
 Right ventricular failure
Right Coronary Artery
 RCA Supplies
-RA and RV
-Inferior and posterior walls of the LV
-SA node in 55% of people
-AV node in 90% of people
-Posterior fascicle of the LBB
Artery Specific Symptomology
Left Circumflex Artery
Lateral wall infarct
EKG Location–
High: I, aVL; Low: V5, V6
Complications
Dysrhythmias
Congestive heart failure
Circumflex Artery
 Supplies
-Lateral wall of LV
-Inferior and posterior wall of LV
(10% of population)
-Septal perforator of LBB
-SA (45% of population)
-AV node (10% of population)
STEMI
(ST Elevation MI)
 Occurs with myocardial injury
 Occurs when tissue is damaged, before it
becomes necrotic and has no electrical activity
 Defined as elevation in two or more leads
 Elevation is at least 1 mm per lead
Q Waves and MI
 Small Q waves (septal depol) are usual in
leads I, aVL, V5, and V6 (the lateral leads)
 Q criteria for MI
-duration >/= 0.04 sec or
-amplitude >/= ¼ of the R wave in the
same lead
 Present when damage involves the entire
thickness of the myocardial wall
NSTEMI
(Non ST Elevation MI)
 Smaller area of damaged heart
muscle from sub-total occlusion of
coronary artery
 No ST elevations on the 12 lead ecg
Mechanisms of ST Depression
 K+ is lost from the ischemic tissue
 Positive ion loss produces a current
vector toward the endocardium,
opposite of the mean QRS vector
 This appears as ST depression on the
ecg
Complications of an MI
Dysrhythmias
Ventricular or atrial rupture/aneurysm
Ventricular septal defect
Congestive heart failure/pulmonary edema
Cardiogenic shock
Sudden cardiac death
Pericarditis
Mural thrombi causing cerebral or pulmonary emboli
Papillary muscle rupture with acute mitral
regurgitation
 Psychological problems
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Electrical Conduction System
ST Segment Changes
Primary ST Segment Depression
Ischemic Heart Disease
12 Lead ECG’s
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Rate
Rhythm
Intervals
Axis
Hypertrophy
Ischemia/Infarct
ECG Changes In ACS
 Ischemia: T wave abnormality, flat or
down-sloping T wave
 Injury: ST segment elevation
 Infarction: Q wave
Normal 12 Lead ECG
I
aVR
V1
V4
II
aVL
V2
V5
III
aVF
V3
V6
Main Arteries and Areas They Perfuse
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Inferior……………………………………RCA, LCx
Inferior RV……………………………..Proximal RCA
Inferoposterior……………………….RCA, LCx
Isolated RV…………………………….LCx
Isolated Posterior………………….RCA, LCx
Anterior………………………………….LAD
Anteroseptal…………………………..LAD
Anteroseptal-lateral……………….Proximal LAD
Anterolateral, inferolateral, or
posterolateral…………………………LCx
Indicative and Reciprocal Leads
Area of Infarct
Indicative leads
Reciprocal leads
Inferior
II, III, aVF
I, aVL
Septal
V1, V2
II, III, aVF
Anterior
V3, V4
II, III, aVF
Lateral
I, aVL, V5, V6
II, III, aVF
Posterior
V7, V8, V9
V1, V2
Lead Summary
I
Lateral
aVR
Circumflex
Artery
V1 Septal
V4 Anterior
LAD, RCA,
Posterior, LM
LAD, LM
II Inferior
aVL Lateral
V2 Septal
V5 Lateral
RCA
Circumflex
LAD, LM
Circumflex, LM
III Inferior
aVF inferior
V3 Anterior
V6 Lateral
RCA
RCA
LAD, LM
Circumflex, LM
Normal Sinus Rhythm
Primary ST Segment Depression
Ischemic Heart Disease
Inferior Wall MI
Anterioseptal Wall MI
Transmural Acute Anterior MI
Acute Anterior Wall Infarction
Old Inferior Wall Infarction
Acute Inferior Wall Infarction
Old Inferior Wall Infarction + Afib
+ PVC’s
Pharmacological
Management
MONA
 Morphine is used for pain relief
 Oxygen may reduce ischemic injury
 Nitrates are used to vasodilate
coronary arteries
 Aspirin dissolves fibrin in the clot and
prevents platelet aggregation
Morphine
 Usually given 2-4mg IV for continued
angina after use of nitrates
 Causes venodilation, decreases HR, BP,
workload of your heart, which decreases
the amount of oxygen that your heart
needs
 Decreases anxiety-Antiolytic
 CAUTION use of other analgesics such as
NSAIDS…can increase mortality, HF,
reinfarction
Oxygen
 Indications
-Respiratory distress
-Keep oxygen saturations >90%
-Prevent hypoxemia
Nitroglycerine
 Used for treating chest pain and
angina temporarily widening
narrowed blood vessels by
vasodilating the arteries. This
improves blood flow to and from your
heart. NTG is most valuable in
increasing oxygen supply if good
collateral circulation exists. It also
increases venous and arterial dilation.
Nitroglycerine (NTG)
 Indications
-Relief ongoing ischemic discomfort
-Control of Hypertension
-Management of pulmonary congestion
 Avoid if:
-BP <90mmHg
-Recent use of phosphodiestrase inhibitors
within 24-48 hours (ex. Viagra, Cialis,
Levitra)
-Suspect RV infarction
Aspirin
 Decreases platelet aggregation,
helping to keep blood flowing through
narrowed coronary arteries. One of the
first medications given in the setting of
suspected ACS. It should be chewed
so it is absorbed in the blood stream
more quickly.
Beta Blockers
 Beta Blockers
-Relax your heart muscle
- Slow your heart rate and decrease your
blood pressure
-Increase the blood flow through your heart,
decreasing chest pain and the potential for
damage to your heart during a heart attack.
-Decrease myocardial workload & myocardial
oxygen demand by decreasing HR and
contractility.
Beta Blockers
 Oral BB therapy within first 24 hrs
unless contraindicated
-No signs of heart failure or low output
state
-No increased risk of cardiogenic shock
Beta Blockers
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Carvedilol (Coreg)
non selective, + alpha blocking
Labetalol
non selective, + alpha blocking
Nadolol (Corgard)
non selective
Pindolol (Visken)
non selective
Propanolol (Inderal LA) non selective
Sotalol (Betapace)
non selective
Atenolol (Tenormin)
B1 selective
Metoprolol (Lopressor, Toprol XL) B1 selective
Nebivolol (Bystolic)
B1 selective
Acebutolol (Sectral)
B1 selective
Angiotensin-converting enzyme (ACE)
inhibitors and Angiotensin Receptor
Blockers (ARBs)
 Indications for ACE/ARB
- allow blood to flow from your heart more
easily
- Low Ejection Fraction
- Lower blood pressure and may prevent a
second heart attack
- Reduce mortality by about 20% when used
on a long-term basis in high risk post infarct
patients
- Early initiation in key in the potential benefit
of early ventricular remodeling.
ACE/ARB’s
 Give within the first 24 hours
-Anterior infarction
-Pulmonary congestion or ejection
fraction </= 40%
-Can cause hyperkalemia, renal
insufficiency, cough or angioedema
ACE/ARB’s
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Benazepril (Lotensin)
Captopril (Capoten)
Enalapril (Vasotec)
Fosinopril (Monopril)
Lisinopril (Prinivil,zestril)
Moexipril (Univasc)
Perindopril (Aceon)
Quinapril (Accupril)
Ramipril (Altace)
Tradolapril (Mavik)
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Candesartan (Atacand)
Irbesartan (Avapro)
Telminsartan (Micardis)
Valsartan (Diovan)
Losartan (Cozaar)
Olmesartan (Benicar)
Calcium Channel Blockers
 Contraindicated in STEMI, low EF: Negative
inotrope which decreases contractility
 Used for persistent symptoms of USA and
NSTEMI when Beta Blockers are
contraindicated
 Coronary vasodilator, smooth muscle
relaxant, negative inotrope, negative
chronotrope, negative dromotrope
 Used for chronic recurrent symptoms of
angina, treatment of HTN and arrhythmias
Different Classes of Calcium
Channel Blockers
 Dihydropyridine CCB’s
used to reduce SVR and
arterial pressure, but not
used to treat angina
Amlodipine (Norvasc)
Felodipine (Plendil)
Nicardipine (Cardene,
Madipine)
Nisoldipine (Sular)
Nifedipine (Procardia,
Adalat)
 Non-Dihydropyridine are
relatively selective for
myocardium, reducing
myocardial oxygen
demand & reverse
coronary vasospasm &
are often used to treat
angina
Verapamil (Calan)
 Benzothiazepine CCB
selective for vascular
calcium channels, reduce
arterial pressure
Diltazem (Cardizem)
Antiplatelet Therapy
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Platelet Aggregation Inhibitors
ASA
Plavix (clopidogrel)Now generic
Effient (prasugrel)
Brilinta (ticagrelor)
Ticlid (ticlopidine)
-Used to prevent platelet aggregation.
Heparin gtt may be prescribed to
prevent clotting or extension of clot.
Brilinta (Ticagrelor)/Antiplatelet
 MOA: Reduces platelet activation and
aggregation
 Proven superior to clopidogrel across
a broad range of ACS patients at
reducing thrombotic CV events,
including CV death
 Discontinue at least 5 days prior to
any surgery
Anticoagulants
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Unfractionated Heparin (UFH)
Enoxaparin (Lovenox)
Fondaparinux
Glycoprotein IIb/IIIa inhibitors
Unfractionated Heparin (UFH)
 Acute treatment of thromboembolic
disorders
 Administered intravenously
 Monitored by PTT
 Short biologic half life of
approximately 1 hour
Enoxaparin (Lovenox)
 MOA: binds to antithrombin III,
inhibits thrombin and Factor Xa (low
molecular weight heparin)
 Indications for USA, NSTEMI, STEMI
 1mg/kg SC Q12 hours
 Half-life 4.5-7 hours
 No monitoring
Fondaparinux (Arixtra)
 Similar to enoxaparin in reducing
ischemic events
 Substantially reduces major bleeding
 Can be used as treatment against HIT
 Given subcutaneously
 Long half life 17-21 hours
 No monitoring
Glycoprotein IIb/IIIa Inhibitors
 Inhibits platelet aggregation
 Helps prevent occlusion of the coronary arteries,
reducing the incidence of ischemic events
 Used in treating patients with USA
 Usually administered in combination with angioplasty
with or without PCI
 Given in combination with heparin or ASA to prevent
clotting before and during invasive heart procedures
 Examples
-Abciximab (ReoPro)
-Eptifibatide (Integrilin)
-Tirofiban (Aggrastat)
Fibrinolytics
 Drug that works to break up clots, “clot buster”
 Best outcome if administered within 12 hours or less
after the onset of the symptoms
 Examples
-Streptokinase (not used much anymore)
-Tissue plaminogen activator (tPA, Alteplase
-Urokinase
-Retaplase
-Tenecteplase
Hospital Care Anti-Thrombotic
Therapy
 Immediate ASA
 Clopidogrel, if ASA contraindicated
 ASA + clopidogrel for up to 1 month,
if medical therapy or PCI planned
 Heparin (IV unfractionated, LMW)
with antiplatelet agents above
 Enoxaparin preferred over UFH unless
CABG is planned within 24 hours or
with renal insufficiency
Stress Testing
 Types of Stress Tests
-Exercise
-Vasodilators: Dypyridamole, Lexiscan, Adenosine,
Dobutamine
-Dobutamine or exercise Stress Echocardiogram
 Measure of Induced Ishemia
-ECG changes with exercise or vasodilator
-Perfusion defects with radionuclide myocardial
perfusion imaging
-Wall motion abnormalities with echocardiography
Resting and Stress Myocardial
Perfusion Imaging
Reperfusion
 Pharmacologic
Fibrinolysis
 Percutaneous coronary intervention
 Possible surgical measures
Cardiac Catheterization Laboratory
• In the cath lab the patient undergoes
angioplasty
▫ Balloon-tipped catheter threaded
through the femoral artery
▫ Threaded to the site of the blockage
and inflated to remove the clot restoring
normal blood flow
▫ Metal stents are often placed to keep
the arteries open
▫ IABPs, Impella ventricular assist
devices and temporary pacemakers are
also placed if necessary
Treatment of AMI in the Cardiac
Catheterization Laboratory
 Angioplasty and stent implantation
 Mechanical thrombus extraction
 Blood thinners
-ASA
-Thienopyridines (clopidogrel)
-GPIIb/IIIa inhibitors (abciximab)
-Low molecular weight heparin
Anatomy
Cardiac Catheterization
Left Coronary System
Right Coronary System
Cardiac Catheterization
Acute Myocardial Infarction
 Thrombus in the
Left Main Coronary
Artery
Plain old Balloon Angioplasty
(POBA)
 1977 POBA first trialed
 In the past, plain old ballon angioplasty or
POBA, had the potential to cause elastic
recoil effect
 Occurred in approximately 5-10% of
patients within the first few hours or even
minutes of surgery
 After the procedure the coronary artery
experienced rebound and subsequent
occlusion
 This often lead to complications including
MI
Balloon Angioplasty
Angioplasty Causes
 Neointimal hyperplasia is the immune
system’s reaction to the intrusion of
angioplasty
 Damage incurred on the endothelial barrier
at the site of balloon inflation, the
extracellular matrix can become exposed
 Leads to hyperproliferation of smooth
muscle cells
 A response prompted by growth factors and
proteoglycans
 These cells move into the intima, where
they cluster and form a lesion
Angioplasty Continued
 The lesions become thickened and
scarred
 The artery undergoes a subsequent
remodeling of its structure
 End result is redevelopment of
arterial blockage and obstructed
flow, in other words restenosis
Stents
 In 1994, J & J produced the PalmzSchatz Balloon expandable stent. The
first approved by the FDA. In the
past decade, over 25 companies have
used various materials and designs in
the construction of the bare metal
stents (BMS). Over time, stents have
achieved greater durability and
flexibility
PCI Procedural refinements: Stents
 Expandable metal mesh tubes that buttresses the
dilated segment, limit restenosis.
 Drug eluting stents: further reduce cellular
proliferation in response to the injury of dilatation
Drug Eluding Stents
Balloon Deployment of Stent
Bare Metal Stents
 Tubular, lattent structure assembled by a
range of metals.
 Should be spring like and flexible,
conforming to the shape of the arterial wall
 Primary goal of the stent is to hold the
inner wall in its newly compressed position,
retaining the enlarged diameter
 Stent diameter range from 2mm-4mm,
depending on the diameter of the vessel
Bare Metal Stents
 Stents eliminated the concern for plain old balloon
angioplasty’s elastic recoil effect
 Incidence of restenosis dropped to around 25% of
patients, in-stent restenosis, or ISR within 3-6 months
after surgery
 Again, this resulted from the body’s tendency toward
neointimal hyperplasia
 Working with BMS’s, Interventional Cardiologists used
various techniques to attempt to decrease the effects
of restenosis by the use of brachytherapy, dose of
radiation emitted from a catheter that inhibits cell
division at the occluded site or anti-platelet drugs
Bare Metal Stents and Restenosis
 Multiple strategies attempted to
prevent restenosis (1990-1999):
-thromboxane A2 receptor blockade
-ACE inhibitors (Cilazapril)
-Enoxaparin, low molecular weight heparin
-Tirofiban
-Abciximab
 Mostly Unsuccessful!!
Bare Metal Stents and Restenosis
 Intra-Coronary Radiation(1999-2002)
-Most useful for treatment of restenosis
-Less useful in prevention
Drug Eluting Stents (DES)
 First used in 2003
 The interest in these anti-platelet drugs,
coupled with the desire to eliminate ISR,
inspired the development of DES’s
 This therapy involves coating the outside of
a standard coronary stent with a thin
polymer containing medication that can
prevent scarring at the site of the
intervention.
Examples of Drug Eluting Stents
 Two FDA approved compounds:
Paclitaxel
anti-proliferative agent
extracted from bark of Pacific Yew
blocks cell mitosis
Sirolimus
immunosuppressive agent
isolated from soil on Easter Island
blocks cell progression by inhibiting DNA
synthesis
Current Drug Eluting Stents
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Cypher- Sirolimus(2003)
Taxus- Paclitaxel(2004)
Endeavor –Zotarilimus(2008)
Xience V /Promus – Everolimus(2008)
Drug Eluting Stents
Future Use
More complex coronary disease traditionally
correlated with higher restenosis rates
Lower restenosis rates with DES may improve
outcome in more difficult patient groups
Complex multivessel coronary disease
Left main disease
Disease in small vessels
Long areas of stenosis
Extreme vein-graft disease
Coronary disease in diabetics
Chronic total occlusions
Vascular disease outside the heart
ABSORB TRIAL
Conventional stents are permanent
ABSORB BVS is unique
It gradually disappears over time
Your artery does not need a
permanent stent to remain open
 With ABSORB, your artery becomes
free to move over time and meet the
needs of your heart
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Processes needed to heal the
plaque
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Resolution of inflammation
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Thrombus reorganisation
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Smooth muscle cell proliferation
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Re-endothelialisation
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Smooth muscle cell matrix
synthesis
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Return of vasomotor regulation
Drug eluting stents
can inhibit all
these processes
+ Foreign body reaction due to polymers giant cell inflammation
Endothelialization
 BMS take about 30 days to reendothelialize
 DES can take up to one year or more to
reendothelialize
 DES has a polymer coating and a drug,
either sirolimus or paclitaxel, mixed into
the polymer. This drug is delivered to the
area of the opened artery over a period of a
year or more
 An antiplatelet agent, Plavix or Effient, will
be needed to decrease the tendency of
their blood platelets to clot
Cost of Dual Antiplatelet Therapy
after DES
 $800- Bare metal stents
 $2400- Drug eluting stents + cost of
dual antiplatelet therapy+ risk of
bleeding
Impella Ventricular Assist Device
 Bridges to aid in perfusion until a
surgical procedure can be performed
 Assist device for either cardiogenic
shock or porphylaxis
 http://www.abiomed.com/products/impella.cfm
Impella Ventricular Assist Device
• Provides up to 2.5 liters per minute
ventricular unloading
• Placed percutaneously via femoral artery
• Threaded to and placed across aortic valve
• Small catheter-mounted “impeller” motor
blows blood across valve and into aorta
•Effectively increases cardiac output and end
organ perfusion
• Decreases workload of the heart
Impella Ventricular Assist Device
Intra Aortic Balloon Pump
“Counterpulsation Therapy”
• 30-40cc balloon inserted to below aortic
arch
▫ Rhythmic inflation/deflation in time with
cardiac cycle
▫ Inflation during cardiac diastole –
pushes blood back to aortic root to fill
aortic arteries
▫ Deflation during cardiac systole –
creates vacuum effect, helping to pull
blood from the ventricle, decreasing
cardiac workload and O2 consumption
•
Intra Aortic Balloon Pump
Coronary Artery Bypass Grafting
 Failed PCI
 Persistent or recurrent ischemia not a
candidate for PCI or fibrinolytic therapy or
significant area myocardium at risk
 Cardiogenic shock within 36 hours of STEMI
Severe multivessel or Left main disease
 Life-threatening ventricular arrhythmias in
presence of >/= 50% left main and or
tripple vessel disease
Coronary Artery Bypass Grafting
CABG
 1967:
 Kolessov: LIMA
LAD on a beating
heart
 Favaloro: SVG on still
heart
 Procedural refinements:
 arterial rather than
vein grafts
 avoid the
cardiopulmonary
bypass machine
 smaller thoracotomy
incision rather than
sternotomy
Discharge/Post Discharge
Medications
 ASA if not contraindicated
 Clopidogrel, when ASA
contraindicated
 ASA + Clopidogrel for up to 1 year
 Beta Blocker if not contraindicated
 Lipid Agents + diet, if LDL >130mg
 ACE inhibitor: CHF, EF <40%, DM, or
HTN
 Nitrates
Ranexa (Ranolazine)
 Indicated for chronic angina
 MOA: Unknown, reduces sodium
induced calcium overload in myocytes
 Dosing 500mg-1000mg BID; max
2000mg/day
QUESTIONS!!