Transcript Myocardial Infarction and Acute coronary syndromes

Acute Coronary Syndrome (ACS)
Matt Hafermann, PharmD, BCPS
Cardiology Clinical Pharmacist University
of Washington Medical Center
OBJECTIVES
1.
2.
3.
4.
Introduction and background to ACS
Outline treatment strategies for ACS
Review medications used in acute coronary
syndromes
Discuss quality performance medications used
upon discharge from the hospital after a
myocardial infarction
Cardiovascular Disease
•
•
•
Number one killer of Americans:
• Estimated 785,000 cases of CVD annually in the
US
• Coronary heart disease responsible for 1 in 6
deaths in the US
• 470,000 recurrent attacks
• 195,000 silent MIs
~34% of Americans have metabolic syndrome
$297.7 billion- Associated cost of CVD and related
conditions
Circulation 2012:125
Progression and Terminology of ACS
Plaque Disruption/Fissure/Erosion
Thrombus Formation
UA
STEMI
STEMI
Progression
Source: American Heart Association
Case study MR
•
•
•
•
MR is a 76 YO male who comes to
the ER complaining of 10\10
chest pain. He started to have
chest pain 3 hours ago while
watching TV
He states that it feels like “an
elephant is on my chest”
PMH: Hypertension, diabetes,
former smoker 1ppd x 20 years
FH: Father died at age 80 of a
stroke
SH: retired, spends a lot of time
watching TV
•
•
•
Medications upon admission
•
Aspirin 325mg QD
•
Atorvastatin 20mg QPM
•
Lisinopril 5mg daily
•
Glyburide 5mg daily
•
Sildenafil 25mg prn ED
Allergies: PCN
Physical exam:
•
Vitals: BP 140\100 HR 100
RR 24 O2 sat 98% RA, weight
= 111 kg
•
Ashen, diaphoretic, anxious
•
Normal heart sounds
Case study MR
•
•
ECG: sinus tachycardia
with ST segment
depression in the
anterior leads
suggesting ischemia
CXR: No apparent
edema, normal heart
size
•
•
•
Labs: CK-MB elevated at
10 ng\mL, first Troponin
0.7ng\mL (+)
ROS: Patient’s current
chest pain is now 7\10
and he is in distress
Assessment: admit with
rule out MI (ROMI)
protocol : serial enzymes,
ECG
Risk factors of Heart Disease
•
•
•
•
•
•
•
•
•
Male
Smoking
Family history
Hypertension
Diabetes
Elevated lipids
Obesity
Lack of exercise
Chronic kidney
disease
Determining a Treatment Plan
History and
physical
Biochemical
markers
ECG
Determine
treatment
plan
STEMI vs Non-STEMI?
“tombstones”
Interpretation
•
•
•
•
ST segment elevation = acute injury
• >1mm in 2 consecutive leads
ST segment depression
• >1mm = ischemia
High risk unstable angina
Non-ST segment elevation MI
Locations: anterior, lateral, and inferior
Initial Recognition and Management
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•
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Quality of chest pain:
• 10/10 chest pain , crushing band-like
• 20% of patients have “prodromal”
Pain at rest, change in pattern
Physical exam
•
•
Ashen, diaphoretic
Presence of risk factors
Laboratory Findings
•
Troponin is the gold standard
• Troponin q6h x 3 values
• CK-MB helpful for reinfarction
• Monitor until levels have plateaued or you
get 2 negative values
• Troponin-I value of >0.4ng\mL is
suggestive of myocardial infarction
• Can be laboratory dependent
Cardiac Enzymes
Relationship Between Degree of Troponin
Elevation and Likelihood for Long-term Mortality
% mortality at
42 days
8
6
4
2
0
<0.4
<1.0
<2.0
Troponin levels
Antman EM, it al. N Engl J Med. 1996; 335: 1342-1349.
<5.0
<9.0
9.0
Case of MR- Treatment Options
•
•
The ER attending decides
to admit this patient and
wants to start to initiate
therapy in the ER.
What we know so far:
• + ECG for ST segment
depression in the
anterior leads
• + History and physical
findings
• + First troponin and CK
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•
•
What are the treatment
goals for MR?
Devise a
pharmacotherapeutic
strategy to be initiated in
ER?
What other baseline data
should be obtained
before you can begin?
Treatment Options
Thrombolytic
therapy
Urgent PCI
Medical
therapy
• Targeted H and P for thrombolytic therapy
• If no available cath lab
• STEMI only
• Available cath lab
• Diagnostic or PCI
• If not a thrombolytic candidate
• If no viable targets
Early Management: Relieve pain, save myocardium
Immediate assessment < 10min
Immediate treatment
Measure vital signs
Oxygen at 4 liters\min
Measure oxygen saturation
Aspirin 160-325mg (chew) *
Obtain IV access
Nitroglycerin SL or spray 0.4mg
Q5min x 3 doses->IV
Obtain 12-lead ECG (MD review)
Morphine IV 2-4 mg q5-15 min
Perform brief targeted history and PE
(focus on thrombolytic therapy)
*memory aid “MONA”
(Morphine,O2,
nitroglycerin, aspirin)
Obtain initial serum cardiac marker
levels
Request CXR (<30 min)
* May consider clopidogrel if
aspirin allergic
Case of MR
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The ER attending decides to admit this patient. In order to initiate medical
therapy, what labs baseline labs should be drawn?
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Basic chem 7, CBC, Serial cardiac enzymes, INR
Your labs results return
First troponin + at 0.7ng/mL and CK-MB 10ng\mL
135
106
13
3.5
22
0.84
109
WBC
7
HCT
40
Plts
200
INR
1.2
ACC/AHA 2007 guidelines supports administration of nitrates only if 24 hours have
elapsed after last dose of sildenafil and 48hrs for Tadalafil
Case of MR
After MONA the BEST early treatment for this
patient is
A.
IV Heparin bolus 4000 units then IV heparin
at 1000 units per hour to obtain aPTT 60-100
B.
Oxycodone 20mg x 1 then 5mg q6h prn pain
C.
Call to cardiology fellow to mobilize the cath
lab and consider clopidogrel loading
D.
A and C
Goal is to prevent myocardial damage and treat chest pain
and resolution of EKG changes to baseline.
Diagnostic Algorithm for Acute Coronary
Syndrome Management
&/or
ST-segment elevation MI
Therapeutic goal: rapidly break apart fibrin mesh
to quickly restore blood flow
Non-ST Elevation ACS*
+ Tn &/or
+ CK-MB
Non-ST Elevation MI
Therapeutic goal: prevent progression to
complete occlusion of coronary artery
and resultant MI or death
Consider fibrinolytic therapy, if indicated
Consider GP IIb-IIIa inhibitor + aspirin +
heparin
Braunwald E, et al. 2002. http://www.acc.org/clinical/guidelines/unstable/unstable.pdf.
The role of the thrombus — mechanism of
action in ST-segment elevation ACS
Generally caused by a
completely occlusive
thrombus in a coronary artery
Results from stabilization of a
platelet aggregate at site of
plaque rupture by fibrin mesh
platelet
RBC
fibrin mesh
GP IIb-IIIa
The Role of the Platelet: Mechanism
of NSTE ACS
Generally caused by a
partially occlusive, platelet-rich
thrombus in a coronary artery
Results from cross-linking of
platelets by fibrinogen at
platelet receptors GP IIb-IIIa
at site of plaque rupture
Unobstructed
lumen
GP IIb-IIIa
platelet
thrombus
fibrinogen
Ruptured
plaque
Artery wall
Acute Coronary Syndromes Algorithm.
O'Connor R E et al. Circulation 2010;122:S787-S817
Copyright © American Heart Association
Treatment of Non-ST segment elevation MI
N-STEMI
Current Management of
Non-ST-segment Elevation ACS in the U.S.
High-Risk
35%
70%
Diagnostic
catheterization
Diagnosis
PCI
15%
CABG
30%
20%
Low-Risk
Medical
management
Case of MR
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•
Pharmacotherapeutic plan before the cath lab:
• Antiplatelet therapy with:
• Aspirin
• Clopidogrel, prasugrel, or ticagrelor loading
Anticoagulant therapy:
• Unfractionated heparin or enoxaparin
• IIb \ IIIa inhibitor if deemed high risk. Timing
dependent on management strategy
Aspirin in Acute Coronary Syndromes
Primary
Prevention
2.5
*P<.0001
MI
2.2
Stable
Angina
15
*P=.0003
MI
12.9
UA/NSTEMI
15
*P=.012
Death or MI
15
12.9
*P=.008
Death or MI
11.9
Patients (%)
2
1.3*
1.5
10
10
10
6.2*
1
3.9*
5
5
5
3.3*
0.5
0
Placebo
ASA
N= 11034
11037
0
Placebo
ASA
155
178
0
Placebo
ASA
279
276
0
Placebo
ASA
118
121
MI, myocardial infarction; ASA, acetylsalicylic acid; RISC, Research on InStability in Coronary artery
disease; ISIS-2, Second International Study of Infarct Survival.
PHS. N Engl J Med. 1989;321:129-35.
Ridker PM, et al. AJC. 1991;114:835-839.
Cairns JA, et al. N Engl J Med. 1985;313:1369-1375.
Theroux P, et al. N Engl J Med. 1988;319:1105-1111.
Pathways to Platelet Aggregation
Antiplatelet therapy
Drug
Aspirin
Indication
STEMI
ACS
Dose
Adverse effects
162-325mg hospital day 1
Post PCI w\stent 162-325mg
daily otherwise 75-162mg
daily
Dypepsia, bleeding and
gastritis
Clopidogrel
(Plavix)
STEMI and
NSTEMI, PCI
with stent
added to
aspirin
Alternative to
aspirin in pts
with allergy
300-600mg loading dose,
then 75mg daily
Bleeding, diarrhea, rash,
TTP (rare)
Prasugrel
(Effient)
Patient
undergoing
PCI for ACS
60mg LD then 10mg Qday
Bleeding, diarrhea, rash,
TTP (rare)
Avoid in pts >75 yrs
UA, NSTEMI,
or STEMI
managed
medically or
with PCI
180mg loading dose followed
by 90mg twice daily
Ticagrelor
(Brilinta)
Caution in pts <60kg may use
5mg (less data)
Bleeding, dyspnea,
headache, fatigue, diarrhea
Monitoring
Clinical signs of
bleeding, baseline
CBC & every 6
months
Tips for Antiplatelet Therapy
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EVERYONE gets aspirin 81mg daily
 Older guidelines recommended higher doses
Clopidogrel
 Cheapest option
Prasugrel
 More expensive
 Not approved for medical management (only PCI)
 Dose reduction or avoid in patients >75 years or <60 kg
 Contraindicated in patients with previous stroke or TIA
Ticagrelor
 Newest agent
 Must use aspirin 81 mg daily (don’t use higher dose)
 Expensive
Antiplatelet agents
•
•
Bare metal stents
• Minimum of 1 month of clopidogrel. Ideal
treament is up to one year if patients are not
at a high risk of bleeding
Drug eluting stents
• Ideally up to at least 12 months of clopidogrel
in patients who are not at high risk of bleeding
Anticoagulants
Drug
Unfractionated
Heparin
Enoxaparin
Indication
STEMI, NSTE ACS, PCI
** For UA/ NSTEMI give for at least
48 hours if conservative
management chosen
Adverse Side Effects
Monitoring
Bleeding, HIT
aPTT until target or
change in dose. CBC ,
HIT if indicated
Bleeding, HIT
Avoid if severe
bleeding risk
CBC and Scr, HIT if
indicated. Avoid if
CrCl<15
Fondaparinux
STEMI, NSTEMI
(Not well studied in pts with PCI)
Bleeding
CBC and Scr
Bivalirudin
NSTE ACS, PCI
Bleeding
Direct thrombin
inhibition (DTI), CBC
and Scr
GP IIb \ IIIa inhibitors:
Abciximab
Tirofiban
Eptifibitide
With PCI:
Abciximab
Bleeding, Acute
profound
thrombocytopenia
Baseline Scr and
daily (for eptifibitide
and tirofiban)
Daily CBC (with
emphasis on Plt
count) 4hrs after
initiation
ACS: Epitifibitide
Tirofiban
For all above: Monitoring for clinical signs of bleeding
The Role of the Platelet: Mechanism
of NSTE ACS
Generally caused by a
partially occlusive, platelet-rich
thrombus in a coronary artery
Results from cross-linking of
platelets by fibrinogen at
platelet receptors GP IIb-IIIa
at site of plaque rupture
Unobstructed
lumen
GP IIb-IIIa
platelet
thrombus
fibrinogen
Ruptured
plaque
Artery wall
Platelet Adhesion, Activation,
and Aggregation
Vessel wall
White HD. Am J Cardiol. 1997; 80 (4A): 2B-10B.
Mechanism of Action: GP IIb-IIIa Inhibitors
Vessel wall
White HD. Am J Cardiol. 1997; 80(4A):2B-10B.
Glycoprotein II b/ IIIa inhibitors
Abciximab
• PCI: 0.25mg\kg IV bolus, then 0.125mcg\kg\min x 12 hrs
• Cheapest option
• Only for PCI patients
Eptifibitide
• ACS: 180mcg\kg IV then 2mcg\kg\min
• PCI: 180mcg\kg x 2 (10 min after first bolus) then a drip of 2mcg/kg/min
• Adjust for renal dysfunction
Tirofiban
• ACS: 0.4mcg\kg\min x 30min, then 0.1mcg\kg\min infusion
• Adjust for renal dysfunction
Summary For UA/NSTEMI Treatment
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Antiplatelet
 Aspirin always
 P2Y12 inhibitor or Glycoprotein (GP) IIb/IIIa inhibitor
Heparin always
 Unfractionated or LMWH
 Bivalirudin can be used in place of heparin and
glycoprotein IIb/IIIa inhibitor
PCI vs medical management
 Determined by risk factors
 TIMI score, past medical history
Statin therapy
Pharmacologic treatment of ST
segment elevation MI
(STEMI)
Case:SS
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

Mr. SS is a 47 year old
male who presents to a
small hospital with 2hrs
of chest pain. The
hospital is without a
cath lab. His chest pain
is 10\10 in the ED
PMH: s\p kidney
transplant 2 yrs. ago,
HTN, hyperlipidemia
ECG shows ST segment
elevation in the
anterior leads.



Meds upon admission:
tacrolimus 2mg bid,
Cellcept 1000 mg bid,
prednisone 5mg daily,
amlodipine 5mg daily,
pravastatin 5mg daily
Vitals: BP 140/90, RR
16 HR 100, O2 sat 95%
Normal Labs: Na 130, K
4, Plts 300K, HCT 40,
INR 1.0
STEMI Class I Recommendations
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Get a 12-lead ECG at the site of first medical contact
Reperfusion therapy should be administered to all eligible
patients with STEMI with symptom onset within prior 12 hours
PCI recommended method of reperfusion when performed in
timely fashion
FMC-to-device time system goal of 90 minutes or less
Immediate transfer to PCI-capable hospital for PCI with a goal of
120 minutes or less
In the absence of contraindications, fibrinolytic therapy should
be given if anticipated FMC-to-device time >120 minutes
When fibrinolytic therapy is indicated or chosen, it should be
given within 30 minutes of hospital arrival
Circulation. 2013;127:529-555
STEMI Class I Recommendations


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
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Primary PCI should be performed within 12 hours of ischemic
symptoms
Aspirin 162-325mg before primary PCI
Continue aspirin 81mg indefinitely
Load with P2Y12 inhibitor before PCI
 Give for 1 year
UFH or bivalirudin for PCI
 GP IIB/IIIa inhibitor if using UFH (IIb)
Fibrinolytic therapy should be given to patients who cannot get
PCI within 120 minutes
 Aspirin and clopidogrel should be given with fibrinolytics
 UFH for for at least 48 hours after fibrinolytics
Circulation. 2013;127:529-555
STEMI - PCI
Load with aspirin 162-325mg
 Load with P2Y12 inhibitor
 IV GP IIb/IIIa receptor antagonist with UFH
 Bivalirudin in selected patients
 LMWH can be considered

STEMI – Fibrinolytics Indications
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Chest pain suggesting MI
ST-segment elevation > 1mm in 2 or more contiguous ECG
leads, or new LBB
PCI within 120 minutes not possible
Time to therapy < 12 hours (up to 24 hours considered)
Age < 75 yrs.
• Age > 75 yrs is NOT a contraindication to thrombolytic
therapy but carries a higher risk of Intra-cranial
hemorrhage.
• Lower treatment rates with lytics (~60%) as compared
with PCI (90%)
• Associated with higher bleeding risk than with PCI
Prehospital fibrinolytic checklist.
O'Connor R E et al. Circulation 2010;122:S787-S817
Copyright © American Heart Association
Fibrinolytics and IIb \ IIIa inhibitors
Drug
Indication
Fibrinolytics:
TPA
Retaplase
Tenecteplase
STEMI
II b \ III a
inhibitors:
Abciximab
Eptifibitide
Tirofiban
With PCI:
Abciximab
High risk ACS:
Epitifibitide
Tirofiban
Adverse side effects
Bleeding, especially
intracranial
hemorrhage
Monitoring
Clinical signs of
bleeding
CBC with
platelets, INR,
Apt in
Bleeding, Thromoboconjunction
Cytopenia,
with heparin
ACS: STEMI
•
Thrombolytics
• TPA (>67kg)
• Loading dose 15mg IV
over 1-2min followed by
0.75mg\kg (50mg)over 30
min then 0.5mg\kg over
60min (35mg) (NTE
100mg)
• Reteplase 10mg IV q30
min x 2 doses
• Tenecteplase bolus with
30-50mg
•
Heparin
• With lytics: UFH 60units\kg
load then 12units\kg\hr
• Without lytics:
• LD 50-70 units\kg then
infusion till aPTT therapeutic
• Enoxaparin:
• NSTEMI with ACS: 1mg\kg
SQ q12h
• STEMI with PCI:
Additional
0.3mg\kg IV at time of PCI
*(Adjust for renal function)
Comparison of Fibrinolytic Agents
Agent
Fibrin
Specificity
TIMI-3 Blood
Flow Complete
Perfusion at 90
Minutes
Systemic
Bleeding
risk/ICH Risk
Streptokinase
(Streptase)
+
35%
+++/+
Infusion over 60
minutes
Alteplase
(rt-PA)
(Activase)
+++
50-60%
++/++
Bolus followed by
infusions over 90
minutes, weight
based dosing
$3,826 Pulmonary embolism,
acute ischemic stroke,
clearance of an
occluded arteriovenous
catheter
Reteplase
(rPA)
(Retavase)
++
50-60%
++/++
Two bolus doses,
30 minutes apart
$2,896
++++
50-60%
+/++
Single bolus dose,
weight-based
dosing
$2,918
Tenecteplase
(TNK-tPA)
(TNKase)
Administration
AWP
Other Approved Uses
$563
Pulmonary embolism,
DVT, clearance of an
occluded arteriovenous
catheter, intraplueral
administration for
clearance of pulmonary
effusion
DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey LM: Pharmacotherapy: A Pathophysiologic
Approach, 7th Edition: http://www.accesspharmacy.com
Treatment of Patients Who Present Late
RR = 26%
12
RR = 5%
RR = 14%
Placebo
t-PA
12
35-Day Mortality (%)
10.3
10
8.9
9.2
8.9
8.7
8
6
4
2
0
Treated at 6-12 h
P=0.02
RR, risk reduction.
Treated at 12-24 h
P=0.60
Treated at 6-24 h
P=0.07
Symptom Onset to Treatment (hours)
Wilcox R, et al. Presented at 14th Annual Congress of the European Society of Cardiology; September 1992;
Barcelona, Spain.
Other Early Medications
•
•
•
ACE or ARB (for patients with EF less than 40%)
Anxiolytics and Analgesics
• Morphine as the drug of choice
Vasodilators
• Nitroglycerin
• IV beta blockers in select groups of patients
Treatment options
Early
(first 24-48 hours)
MONA
(Aspirin at admission)
Mid to late
Beta blocker
ACE or ARB PO
ACE or ARB Continued
if LVEF is less than 40%
(in the absence of
hypotension)
Lytics and\or
Percutaneous
intervention (PCI)
Discharge medications
For secondary
prevention
Aspirin
Beta blocker
ACE\ ARB
Statin
ACE or ARB
Clopidogrel (RX
management Or PCI)
Early Beta-blocker
The COMMIT study
•
•
•
Earlier studies: beta blockers administered early
during AMI hospitalizations significantly reduce
post infarction angina and re-infarction.
Whether early beta blocker use reduces mortality
in AMI patients remains controversial.
COMMIT study: While beta blockers significantly
reduced the risk of arrhythmic death and reinfarction, they significantly increased the risk of
cardiogenic shock within the first 24 hrs of
hospitalization
COMMIT TRIAL
Early Intravenous then oral metoprolol in
45,852 patients with acute myocardial
infarction: Randomized Placebo-controlled
trial. COMMIT Collaborative group
Lancet 2005;366:1622-32
•
•
•
•
•
Randomized, placebo controlled STEMI
and NSTEMI (in China)
Initial IV metoprolol vs. Placebo
Primary outcome: composite of death,
reinfarction or cardiac arrest
Secondary outcome: death from any
cause
Conclusion
•
No difference in combined endpoint
•
Early beta blockade reduces death
from arrhythmias by 22% but is
counterbalanced by an increase in
cardiogenic shock by 29% (5% vs.
3.9%). The highest risk of shock
was within the first 24h
Case BF
•
•
•
•
•
•
BF presented 2 days ago with
10\10 chest pain
• + first troponin and ECG
with ST wave elevation in
the anterior leads
Hospital course: rushed to
cath lab and received 1 DES
stent to LAD
MOA: None
Allergies: NKA
Vital signs: BP 140\90 HR 70
RR 18
Labs: all WNL
•
•
•
•
•
Hospital course:
It is 2 days after his MI
What are some
complications after an MI?
What test should be done
after an MI to predict
prognosis?
Develop a long term
monitoring plan for BF
Complications following an MI
•
•
•
•
Arrhythmias – early first 48 hrs and late
Left ventricular failure
• Pulmonary edema, atrial fibrillation
Right Ventricular failure
• Edema
Cardiogenic Shock
• Inotropes
• Intra-aortic balloon pump (IABP)
• May need consult for artificial heart support
Prognosis
•
•
•
•
Left ventricular function (EF<40%)
• Echo, Cardiac cath
Recurrent ischemia
• Exercise treadmill (ETT)
• Stress ECHO
• (dobutamine, persantine, adenosine)
• Nuclear medicine study
Late Arrhythmias
Other Coexisting disease related to CAD
Circulation Nov 2008:228;
Case BF
•
•
•
•
•
•
•
BF presented 2 days ago with 10\10
chest pain
•
+ first troponin and ECG with ST
wave elevation in the anterior
leads
Hospital course: rushed to cath lab
and received 1 DES stent to LAD
MOA: None
Allergies: NKA
SH: smokes 1\2 ppd
Vital signs: BP 140\90 HR 70 RR 18
Labs: all WNL
•
Hospital course:
•
It is now 4 days after his DES
stent and he is ambulating
the halls and ready for
discharge
•
Devise a pharmacotherapy
and risk factor modification
treatment plan for this
patient for discharge.
•
What are his long term
goals?
Treatment Options: Secondary
Prevention
Early
(first 24-48 hours)
Mid to late
MONA
(Aspirin at
admission)
Beta blocker
ACE or ARB PO
if LVEF is less than
40%
ACE or ARB
Continued
(in the absence of
hypotension)
Lytics and\or
Percutaneous
intervention (PCI)
Discharge
medications
Aspirin
Beta blocker
ACE\ ARB
Statin
Clopidogrel (RX
management Or PCI)
Quality indicators for MI
•
•
•
•
•
Explain the quality or
“Core” measures of
MI and explain the
rational behind each
indicator at discharge
Smoking cessation
ACE\ARB
Beta blocker
Statin
Secondary
prevention of:
• Death
• Stroke
• Recurrent
infarctions
Mid-Late Medications
•
Beta blockers
• Arrhythmias – around 25% of MI mortality within the first
24 – 48 hours 1
• Metoprolol is the drug of choice in the US
• Beta-1 selective
• Oral to IV conversion 2.5:1
• Metabolism: Hepatic
• If Hemodynamically stable with no history or signs and
symptoms of heart failure:
• IV Metoprolol 5mg q5min x 3 doses, then start 50mg
po bid and titrate up to 100mg po as tolerated
• Prophylactic lidocaine – No!
• Amiodarone for VT or VF
1) Lancet 1986:2:57-66
Lipid Lowering Agents
•
•
•
•
Based on the ATP 3 guidelines
Patients with CAD have LDL cholesterol goal < 100 mg/dL
•
LDL cholesterol < 70 mg/dL: optional goal
All ACS patients should receive a statin
Statins have anti-inflammatory & anti-thrombotic properties
•
lipid lowering therapy at discharge is a quality care
indicator
68
Heart Disease Prevention
•
•
•
•
Stop smoking
Control blood pressure
• Goal <140/90 mm Hg
• Goal <130/80 with chronic kidney
disease or diabetes
Weight management
Take prescribed medications at discharge
Heart Disease Prevention
•
•
Weight loss and exercise
• 30 minutes at least 3 to 4 times a week
• Ideal BMI 18.5 to 24.9 kg/m2 = (weight in
lbs/2.2)/ (Height in inches x 2.54/100)2
• Waist circumference < 40 inches in men and
< 35 inches in women
Control Diabetes
• HbA1c < 7%
Discontinuation prior to surgery
•
•
•
LMWH (enoxaparin) 24 hours prior to cardiac
surgery
IIb \ IIIa (tirofiban and eptifibatide) 4-8 hours off
prior to to cardiac surgery (No ACC\AHA
guidelines)
Clopidogrel: 5-7 days prior to cardiac surgery
Case of BF
•
You discharge BF. What are the long term monitoring
plan for BF?
• Seen in clinic 1 week after discharge
• Monitor: vital signs
• HR, BP, RR
• Monitor labs: chem 7, CBC with platelets, LFT’s,
serum lipids, CK
•
Hb -A1c
• Monitor for side effects of medications
Minute to win it…how long to treat?
Case of SO
•
•
SO is a 85 YO M who had a NSTEMI 1 day ago and received a
drug eluting stent 2 days ago.
PHM: HTN, Renal insufficiency Scr 2.7, TIA’s 1 year ago.
• Which agent is best to load with clopidogrel, prasugrel, or
ticagrelor? Why?
• How long should you treat with an either of these agents?
• He has repeat chest pain and now needs coronary bypass
surgery as the stents are now occluded. How long should
he be off clopidogrel?
Minute to win it…….case
•
•
•
A.
B.
C.
D.
BF comes back in 4 months with repeated chest pain showing
NSTEMI
He is taken to the cath lab where he has an occlusion of the
stent.
The best management for this patient is:
Low dose fibrinolytic therapy since he already has a stent
Increasing the daily dose of clopidogrel
Take the patient back to the cath lab for a intervention
Start the patient on Imdur 60mg daily as an outpatient
Case




MR is a 90 YO who
presents to the ER with
shortness of breath
and dyspnea and chest
pain
PHM: STEMI with PCI 4
yrs ago, HTN,
hyperlipidemia and
depression, CHF , Hx of
stroke 1 yr ago
Vitals: HR 78, RR 12, BP
140/95
PE: + JVD, 2+ pitting
edema in the LE





Labs: Na 120, K 4, Scr 2.7 BNP
elevated at 900
MOA:
Clopidogrel 75mg daily.,
aspirin 325 daily, Toprol XL
50mg daily, atorvastatin
80mg QPM, Celexa 10mg
daily, lisinopril 10mg Q12H,
furosemide 80mg daily,
spironolactone 25mg daily.
CXR: bilateral infiltrates
suggesting edema
ECHO: Last EF 2 months ago =
30%
Case


This patient is still having chest pain and will be going to the
cath lab.
The team wants you to suggest a loading dose of an
antiplatelet medication. Choose the BEST answer from below:
A. Load with clopidogrel 300mg in preparation for the cath lab
B. Load with Prasugrel 60mg po x 1 since current clopidogrel
dose is not working
C. Load with both clopidogrel 600mg and Prasugrel 60mg
D. None of the above.
Summary
•
•
•
Recognition of Myocardial infarction includes:
patients history, ECG and Cardiac enzymes
Medications used in the acute phase are focused
on PCI, thrombolytics and antiplatelet medications.
Medications upon discharge should include:
Aspirin, Statin, ACE or ARB, Beta-blocker and
PY12 inhibitor (clopidogrel, prasugrel, ticagrelor) \.
Questions?