Download Post MI Management

Post MI Management
Case DRPs
1. MM is at risk of experiencing signs and symptoms of
recurrent Myocardial Infarction due to having a recent ST
elevation MI and requires appropriate drug therapy,
prevention methods, and regular monitoring of his conditions.
2. MM is at risk of experiencing recurrent MI secondary to his
non-optimal blood glucose level (HbA1c = 8.2 ) and requires
adjustments to his diabetic drug management and patient
education.
3. MM is continuing to experience signs and symptoms of
hyperlipidemia due to receiving inappropriate lipid lowering
therapy and requires adjustments to his drug regimen.
4. MM is at risk of experiencing further cardiovascular events
due to receiving Diltiazem and therefore requires
discontinuation of Diltiazem. (b/c of negative contractility,
could also cause heart conductions and heart block)
Potential DRPs:
5. MM is at risk of experiencing drug drug interaction between
metoprolol and diltiazem and therefore requires adjustments to his
drug regimen
6. MM is at risk of experiencing worsening signs and symptoms of his
hypertension due to a potential contraindication to sumatriptan (a
migraine therapy that is contraindicated in hypertensive and cardiac
patients, which MM received in the past for his migraines) and
therefore requires patient education on avoiding sumatriptan.
(sumatriptan may increase blood pressure, hence it is
contraindicated in patients with uncontrolled or severe
hypertension)
7. MM is at risk of GI bleeds secondary to receiving ASA with his
existing GERD and requires close monitoring
Symptoms
- Chest pain (75-85% of pts), DM sometimes 0 pain
- Chest pressure/squeezing
- Diaphoresis, N/V, SOB
- Tingling, numbness
Signs
- 12-lead ECG changes, T-waves alterations early, Q waves
late
- Cardiac markers elevated:
o CK-MB within 24h, correlation w. q-wave
presence
o Troponins, more sensitive and more
predictive of mortality
S&Sx related to the case:
- He awoke with a pressure/tightness in his chest that radiated to
his left arm
- Also felt epigastric burning
- Was diaphoretic with mild nausea
- Mild shortness of breath
His chest discomfort was described to be 8 on a scale of 1 to 10
Pale
Vitals – BP 165/95; HR 95 and regular; RR 23 and he was
afebrile (has no fever)
CardioV exam – revealed normal heart sounds
LUNG exam– bibasilar rales
A 12-lead ECG – 3-4 mm ST segment elevation in the
anterior leads (ST elevation MI)
LAB work revealed: normal electrolytes, BUN, creatinine,
CBC and coagulation profile;
Day 3 in the hospital:
underwent angioplasty & stent insertion of a 90% Left
Anterior Descending (Coronary Artery) lesion
also had a 50% lesion in the RCA and minimal disease in
the circumflex artery
Anxious
Recurrent chest pain
Day 4 in the hospital:
Echocardiogram: some minor wall motion abnormalities
and a reasonably well-preserved LV with an ejection fraction
of 50%
Lipid profile: LDL =3.7mmol/L, TG = 2.8mmol/L , TC/HDL
ration = 5.2
HbA1c: 8.2 %

BP: 100/60 with a resting heart rate of 60bpm
Urgency:
Not too urgent at the moment but needs medical attention to
prevent complications. MM is diagnosed with ST elevation MI in
the anterior leads
anterior wall infarcts are associated with the highest mortality
rates of post MI (22%). The highest risk is within the first 48
hours.
Most serious consequence of MI is heart failure & death.
Pathophysiology
Definition of MI
Myocardial Infarction (MI) is precipitated by a sudden interrupted of
blood supply to an area of myocardium due to complete or near
complete occlusions of a coronary artery, which leads to myocardial
necrosis.
- Coronary Artery Disease  atherosclerotic plaques
- Plaques can rupture/fissure  1st platelet aggregation (white
thrombus), 2nd coagulation system (red thrombus)
- Leads to (near -NSTEMI) complete STEMI occlusion of
coronary artery
- Necrosis of myocardium
2 mechanisms:
1) Endothelial erosion which exposes surface of subendothelial
connective tissue of the plaque, thrombus adheres to plaque
surface
2)
Unstable plaque with large lipid core and thin fibrous cap ruptures,
lipid core is highly thrombogenic.
After a MI, cell death is not immediate, but it can occur within 15
minutes or up to 6 hours.
Some cells are able to survive ischemia if there is enough collaterol
blood flow within in the infarcted area.
Causes
Over 90% of heart attacks are caused by a blood clot in a coronary
artery. Doctors refer to this as coronary thrombosis or coronary
occlusion. The formation of blood clots is often associated with
atherosclerosis, the build up of plaque (a combination of cholesterol,
cellular waste and other materials) on artery walls. When plaque
ruptures, it can form a blood clot capable of blocking one of the
coronary arteries.
Serious atherosclerosis can also cause a heart attack by "blocking off"
the flow of blood through a coronary artery.
Admitted to the Coronary Care Unit:
Cardiac Markers (CK and Troponin) were elevated
Post MI 2004
-1-
Heart attacks can also be triggered by a severe contraction or spasm in
one of the coronary arteries. When this happens, the artery narrows and
blood flow to part of the heart muscle decreases or even stops. What
causes a spasm is unclear, but it can occur in normal-appearing blood
vessels as well as vessels partly blocked by atherosclerosis.
Differential Diagnosis
ACS – STEMI/NSTEMI/UA
Non-ACS cardiovascular condition (e.g. acute pericarditis)
Non-cardiac condition (e.g. esophageal spasm, GERD,
musculoskeletal discomfort, unknown cause)
Diagnosis
Cardiac Markers
Troponin levels = more specific and better prognostic value than
CK and its MB isoenzyme (as troponin is not detectable in blood
of healthy people)
Creatine Kinase (CK-MB) = Useful for EARLY dianosis since
troponin levels not detectable until 2-4 hours after onset of chest
pain (Trop I lasts 7 days, Trop T lasts 10-14 days)
Typical rise and gradual fall in Troponin (I or T) or a more rapid
rise/fall ob biochemical markets (CK-MB) of myocardial necrosis
with at least one of the following:
1) Ischemic Sx
2) Develop’t of pathologic Q waves on the ECF (ST-segment
elevation MI)
3) ECG changes indicative of ischemia (ST-segment elevation or
depression) or new left bundle branch block
4) Coronary artery intervention (e.g. coronary angioplasty). This
criterion refers to patients who undergo percutaneous transluminal
coronary angioplasty (PTCA) and experience an increase in
cardiac biomarker levels following procedure.
Pre-discharge Diagnostic Tests:
1) Cardiac CATH/Angiography = gold standard
2) Echocardiogram = to see LV function
3) Submaximal Exercise Test (Exercise Tolerance Test)
Ischemic Sx, ischemia ECF changes, BP, arrhthmias
4) LV Function (left ejective fraction) via ECF
> 50 % EF = 3% 1 yr mortality.
< 30% EF = 45% 1 yr mortality
40-50 needs medical attention
5) Detection of Myocardiac Ischemia
ST-depression (ischemia), angina, increased BP, ventricular
ectopy)
For UNSTABLE, Sx patient = CATH
LOW EF (<40%) = CATH or Stress Test, if LV EF is greater than
60%, is normal.
NORMAL EF = Stress Test
Abnormal Stress Test = CATH
Normal Stress Test = Secondary Prevention
Risk Factor
1.
2.
3.
4.
5.
Modifiable
dyslipidemia
hypertension
diabetes
unstable/stable angina
Lifestyle
(smoking, obesity, diet
sedentary lifestyle)
Risk Factors for poor outcome:
Previous MI
Recurrent chest pain
Arrhythmias
Weakened LV
Post MI 2004
1.
Non-modifiable
Age (male  45, females 
55 or post-menopausal)
2.
Family hx of premature
CHD
Hemodynamic instability
Risk factors for recurrent MI:
Age >75
Diabetes
Hx of HTN
Prior MI
Female
Low exercise capability (failure of the systolic blood pressure to
rise above the resting value during exercise)
Obesity
Stress (ie. Worsens hypertension)
Diet (ie. High fat diet)
Cigarette smoking
Hyperlipidemia
Atrial fibrillation / resting tachycardia
Size of infarcted area
Identifying Risk Status
Clinical Factors:
- Left Ventricular Function
- Recurrent or persistent angina or chest pain (after
thrombolysis)
- Symptomatic arrhythmias
- Hemodynamically Unstable
Post MI: the 1st 48 hrs are critical as this puts the patient
(post MI) automatically at risk of experiencing
cardiovascular events such as MI, stroke etc. There is
damage done already to the heart from previous MI so it’s
weak
Drugs Causing MI:
cocaine use – coronary vasospasm and thrombosis; direct effects
on heart rate and arterial pressure; myocardial toxicity
Sumatriptan 50 mg (Imitrex) for migraines => contraindicated in
cardiac patients or hypertension, increases bp. (MM took this 1
year ago for his migraine attack)
Treatment Necessary
-  mortality
- 7-12% in hospital mortality (highest during 1st 48hrs)
-  complications:
eg.
CHF due to ventricular remodeling
Stroke
Arrhythmias
A.Fib
- necessary to remove clot to allow for reperfusion
- prevent re-infarction
- Anterior wall MI most severe
Goals of Therapy: Restore coronary blood flow
- Prevent & minimize complications
- Prevent recurrent MI
- Prevent other cardiovascular diseases like stroke, angina
etc.
- Prevent mortality
Pharmacological Options for Acute MI
Immediate treatment for anyone suspected of MI (MONA):
Morphine, Oxygen, Nitroglycern, ASA
1. Morphine:
Efficacy:
effective pain & anxiety control
MOA
-2-
decrease the release of catecholamines
arterial dilation
reduce O2 demand
Dosing
- 2-5 mg iv q5-15 min prn for pain
- use until pain relief or hypotension occurs
Side Effects
- hypotension
- respiratory depression
- allergic reaction
Monitor
- blood pressure
- respiration
2. Oxygen:
treat hypoxia
always used in the initial hr of therapy
3. Nitroglycerin:
Efficacy:
effective in relieving myocardial ischemia
MOA:
coronary & peripheral vasodilation
Dosing:
iv NTG to manage ischemia for 1st 24-48 hrs
used beyond 48 hrs for complicated pt.
Side affects:
headaches
hypotension
dizziness
Monitor:
blood pressure
4. ASA
Efficacy
- significantly reduce mortality
- reduces recurrent CVD
MOA
- decrease platelet aggregation
Dosing
- Anyone suspected MI should chew & swallow 160-325 mg
of non ec ASA
Side Effects
- Bleeds
Treatment Once Confirmed STEMI:

Anti-ischemic

Anti-platelet

Reperfusion therapy: assess risk vs. benefit

Adjuctive therapy: anti-thrombotics, B-blockers, Aceinhibitors
Anti-ischemic: morphine, NTG(see above), B-Blockers
B-blockers:
iv: Metoprolol
po metop, atenolol, propranolol, timolol
Efficacy:
give within 12hr of onset can reduce reinfarction,
ischemia, ventricular arrhythmias
reduce death
control of tachyarrhythmias (A.Fib)
MOA:
decrease O2 demand by  HR, BP, contractility
Side Affects:
hypotension
fatigue
dyspnea
Interactions:
Post MI 2004
-
digoxin
CCB
Amiodorone
Anti-platelet: ASA (see above) , clopidogrel
Clopidogrel:
used if allergic to ASA
300 mg po load, then 75mg daily
Reperfusion therapy: Alteplase, Reteplase
Assessment of risk vs. benefit:
Absolute CI:
-had hemorrhagic stroke or stroke in 1 yr
-intracranial neoplasm
-internal bleed
-suspected aortic dissection
Relative CI:
- severe BP >180/110
-pericarditis
-pregnancy
-oral anticoagulants INR >2-3
-recent trauma
-internal bleeding in 2-4wks
-active PUD
-Hx of severe hyptxn
Who will benefit the most?
early treatment
large infacts
elderly
small or absent of Q waves
restoring TIMI 3 Flow
Efficacy:
-dissolves thrombus & reestablish blood flow
-reduce mortality up to 50%
-door to needle time<12hrs after symptoms start
Dosing:
Alteplase: 15 mg IV bolus followed by 90min infusion
Reteplase: IV over 35 min
Side Effects:
Stroke & intracranial hemorrhage
Allergic rxn
S/E higher with strep  not used anymore
Monitor:
want to see pain relief
resolution of ST elevation within 90 min
if therapy fails consider invasive procedure
Adjunctive therapy: Anti-thrombotics, Ace-inhibitors, Bblockers (see above)
Anti-thrombotics:
1. Heparin:
Efficacy:
beneficial effect when combined with t-PA or TNK for 48
hrs
reduce reinfarction & increase patency of infacted artery
MOA:
binds anti-thrombin III
Side Affects:
bleeding
TCP
Monitor:
aPTT
look for serious bleed
-3-
Comments:
- if patient at risk of systemic emboli (eg. Large anterior MI,
CHF, A.Fib, LV thrombus, previous embolic events) then full
anticoagulation (iv Hep with warfarin) for 2-3 months is
needed
2.
-
LMWH eg. enoxaparin
alternative to heparin in combo with TNK or alteplase
more convenient (sc bid)
less bleeding and TCP
POST MI Management
Non-pharmacological Options
1. Eat healthy diet (low fat, high fiber)
2. Regular physical activity (30-60 mins 4-7 times/wk) tailored
to risk category
3. Maintain ideal body weight
4. Alcohol in moderation
5. Smoking Cessation
Pharmacological Options
Ace-Inhibitors:
Efficacy:
used within 1st 24 hr of MI
reduce mortality, CHF, reinfarction
MOA:
interferes with LV remodeling which can eventually
cause CHF
interrupt the RAA system (LV remodeling dependent on
RAA system)
Side Affects:
hypotension
altered taste
cough
angioedema
Other Medications:
CCB- not used unless CI to b-blockers, dihyropyridines
may increase risk in Post MI patients
Lidocaine, Amiodarone may be used in patients
presenting with arrhythmias
Atropine, pacing may be used for patients with
bradycardia or heart block
Post MI Treatment:
Risk Stratification (for High Risk pts)
Do not D/C if:
- LV dysfxn (on ECG also EF ≤ 40%)
- Recurrent chest pain (ischemia on exertion)
- Arrhythmias
- Hemodynamically unstable
30 Day Mortality based on:
- Age (>71)
-  SBP
- HF/LV dysfxn (EF ≤ 40%)
- Infarct location (anterior wall most severe)
- previous MI
- ischemia on exercise test
 group patients into high/mod/low risk (20-50%/10%/2-5% 1
yr mortality)  consider PCI/CABG for high risk
Goals of Therapy
- Prevent re-infarction
- Slow/delay atherosclerosis
- Prevent stroke if necessary
- Prevent/Tx Angina Sx
-  mortality
Post MI 2004
Statins - HMG CoA Reductase Inhibitor
Efficacy
- most effective; 1st line tx
- good M&M data –CARE  fatal CHD, 4S  major CVE, CV
death, MIRACL benefits for in-hosp initiation at 8-16 weeks
Onset = max effect ~ 2 – 3 weeks after starting tx
Pharmacokinetics
- atorvastatin, lovastatin, simvastatin – CYP 3A4 metabolized
- pravastatin – least protein bound; metabolized by multiple
pathways, mainly sulfation
- ( DI)
Dosing
- QHS
- fluvastatin, lovastatin BID at  doses
Side Effects
- Hepatic ( LFT’s)
- Myalgia
- GI interolerance (cramps, nausea, heartburn)
Contraindications
- pregnancy, breastfeeding
- active liver disease
Drug Interactions
- digoxin, warfarin (protein binding)
- 3A4 drugs/grapefruit juice (Atorvastatin, Cerivastatin,
Lovastatin, Simvastatin)
- niacin/fibrates  myalgia
Monitor
- LFT’s (baseline and q2mos for 1 yr; then q6m)
- muscle function (CK at first site of pain)
- INR, digoxin levels (if warfarin/digoxin used)
ACE Inhibitor
Efficacy
- All patients with atherosclerosis (HOPE)
- Start within 12-24 hours post MI
- Interfere with post MI ventricular remodeling
Side Effects
- Cough, taste disturbance
- H/A, dizziness
- Hyperkalemia
- rash
Contraindications
- pregnancy
- Hx of angioedema
- Hyperkalemia
Dosing
- OD
- Captopril TID
B-Blocker
Efficacy
- Reduce MI risk, improve survival post MI
- Evidence for propranolol, metoprolol, timolol
- ISA activity oxprenolol, pindolol, acebutelol
Side Effects
-Fatigue, bradycardia, bronchoconstriction,
-4-
-Peripheral vascular disease
Contraindications
-bradycardia,
-AV block
-acute decompensated HF
-severe asthma/ COPD
-DM1 w/ hypoglycemia
Dosing
- Bid/tid
Cost
Statins – $$$
ACEi – $$-$$$
BB - $$
Nitrates - $-$$
CCB - $$$
Warfarin - $$
ASA - $ (plavix: $$$$)
Therapeutic Plan:
Nitrates
Efficacy
-d/c with SL nitrate
-2nd line for Angina (solely symptomatic relief)
Side Effects
- Hypotensiontachycardia
- Dizziness / H/a,
- tolerence w/o NTG free period
Contraindications
- Viagra, aortic stenosis
Dosing
- Ntg-free period req’d
CCB
Efficacy
-not recommended
-palliative for CP
-does not  risk of another CVE post-MI, DHPs may  risk of
re-infarction
-only if intolerant to BB/ACEi/ARB/diuretic
Side Effects
- Hypotension, h/a
Contraindications
- BB, amio, NSAIDs, anticoag, increase bleed risk
Dosing
-od
Warfarin
Efficacy
-for CI to ASA, no evidence of incr efficacy ASA + warf
- ACC recommends use for LV thrombus/akinetic LV for at least
3 months (INR 2-3)
-also used for post-MI Afib
Side Effects
- hemorrhage
Contraindications
- Hemorrhage, amio, cipro, allopurinol,
- Additive bleed risk w/ ASA
Dosing
-od, monitor INR
ASA, Plavix
Efficacy
-in CAD lowers risk of MI 48%
-lowers risk of death 51%
Side Effects
- hemorrhage, especially GI
Contraindications
-nasal polyps
-active bleed
(use clopidogrel for CI and refractory cases or in combination
with ASA for up to 4 wks post stent procedure)
-additive with warf
Dosing
-81 / 325mg od
Post MI 2004
D/C Fenofibrate 160mg qpm
Usually reserved for patients with increased TG levels with minimal LDL
increase
Start MM on a Statin, use pravastatin 10-20 mg/day. Reassess after 6 weeks
to determine an increase in dose is needed. It is not the most potent statin but it
is not metabolized by CYP enzymes so no interaction with lansoprazole. Take
pravastatin at night to control lipid levels and discuss with MM about dietary
alternatives as well as moderate exercises.
-could also keep Fenofibrate and add statin.
Could stay on Diltiazem 240 mg OD
BBs and CCBs are equally effective in reducing blood pressure and contractility
to allow for less frequent anginal attacks. CCBs are contraindicated in patients
with recent MI with LVF or pulmonary edema. CCBs have been associated
with an increased risk of coronary events in post-MI patients.
-
-
-
-
Continue Ramipril 1.25mg or could increase Ramipril dose to 2.5mg but
need to make sure his potassium level is ok , and Metoprolol, ASA 81 mg.
Ramipril is efficacious in controlling BP, Post MI. Monitor closely with
ASA and Ramipril since ASA may lead to GI problems as well as
synergistic effect with ACEI (Ramipril)in lowering the BP. Metoprolol
can be continued since it is efficacious in keeping BP controlled up to 24
hrs and it has efficacy in post MI.
Continue Plavix for another month since CURE trial showed significant
effect in reducing the chance of further cardiovascular problems.
Although Plavix is expensive, it is efficacious and tolerable. Since MM
had a stent procedure on Day 3, Plavix can be continued for another month
while taking ASA 81 mg as well. ASA plus clopidogrel is commonly used
for 1 to 2 months after a PCI procedure since this will provide a rapid
onset of effect and could prevent stenosis. If MM develops intolerance to
ASA, he can stay on Plavix. MM may also apply for ODB coverage for
Plavix.
Monitor HbA1C in 3 to 6 months to see if the increased dose of metformin
(from 500mg increased to 1000mg bid) is working. If not, then need to
increase glyburide dose to 5 mg qid and monitor for hypoglycemia or side
effects as well as blood glucose level (HbA1c).
Monitor any signs of GI bleed
Patient education on Diet/Exercise and Stress management.
Therapeutic Plan Endpoints
Parameter
Degree of
Change
Prevent
Timeframe
GI effects
Renal dysfxn
Prevent
Normalize
Prevent or
normalize
Prevent
Prevent
Hyperkalemia
Hyperlipidemia
Myalgia
Prevent
Prevent
Prevent
LFTs
No increase
Duration of tx with BB
Ongoing
Duration of tx with
ACEI, BB
Duration of tx
Duration of tx with
ACEI, metformin
Duration of tx with ACEI
Ongoing
Duration of tx with
pravastatin
Duration of tx with
pravastatin
Myocardial Infarction and
other cardiovascular
complications
fatigue
HbA1C
Hypertension/Hypotension
Ongoing
+ all PT Endpoints
-5-