Ischemic Heart Disease Flashcards

1
Q

Epidemiology of CAD (7)

A

16 million Americans have heart disease
Coronary Artery Disease (CAD) is the number 1 killer in the US and worldwide
1 out of 5 deaths are from CAD
Every 60 seconds someone dies from CAD in the US.
600,000 will die each year in the US
Death from CAD has decreased every year since 1968
Survival is much worse in the elderly
Approx 50% die before the hospital, presumed from VT arrest

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2
Q

Risk Factors for CAD

A
Age > 65
Male Sex
Family History
Hypercholesterolemia
Smoker
Diabetes
Hypertension
Physical inactivity
Obesity
Poor diet
Alcohol, in excess
Metabolic Syndrome
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3
Q

Stable Angina

A

Stable angina is chest pain or discomfort that usually occurs with activity or stress. Angina is chest discomfort due to poor blood flow through the blood vessels in the heart.

Due to atherosclerotic heart disease
Vasospasm occurs at the site of a lesion
Can occur in normal vessels and in the setting of other heart disease

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4
Q

Symptoms of Stable Angina (5)

A

Usually occur during activity
Pts may want to be upright (lying down increases preload and myocardial work)
Tightness, squeezing, burning, pressing, choking, aching, bursting, “indigestion,” PRESSURE
Distribution of pain is pt dependent, BUT is usually in the same place in each pt unless there is some worsening occurring
Short duration (2-5 mins)
Nitroglycerin (NTG) usually resolves pain

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5
Q

3 Types of CAD

A

Stable Angina
NSTEMI
STEMI

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6
Q

Signs of Stable Angina (4)

A

HTN, hypotension in worsening disease
Cardiomyopathy (ischemic)
New Murmurs (MR from papillary muscle dysfunction)

Look for underlying diseases
DM
Thyroidtoxicosis
HTN
Myxedema
Cardiomyopathy
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7
Q

ECG for Stable Angina

A

ECG usually normal, may show chronic arrhythmias or old MIs, old BBB, LVH

Exercise ECG
Attempts to induce symptoms
Uses a treadmill to precipitate exercise
Uses the Bruce protocol to determine a + test or not
1 mm depression of the ST segment measured 80 milliseconds after the J point

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8
Q

Myocardial Stress Imaging for Stable Angina

A
Give you med like dobutamine 
There is myocardial stress imaging
Scintigraphy (Nuclear)
Echocardiography
MRI
PET
CT
Angiography
Ambulatory ECG
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9
Q

Prevention of Stable Angina (6)

A
Stop Smoking
Control HTN
Control DM
Control Dyslipidemia
Drug therapy
Diet
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10
Q

Treatment of Stable Angina

A

Sublingual nitroglycerin 0.4 mg q 3-5 mins
Onset in 1-2 mins
Nitrates
Vasodilate the arteries and veins
This reduces preload and afterload, reducing myocardial work

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11
Q

Treating the Underlying Cause for Stable Angina

A

Long acting nitrates (not good for acute angina)
Isosorbide
NO continuous use due to tolerance, so used 8 hours/day
Beta Blockers
Only med shown to prolong life
Inhibit myocardial O2 demand by dec HR and contractility
Calcium Channel blockers
No reduction of mortality (third line agent if can’t tolerate BB)
Ranolazine
New drug, decreases intracellular calcium by selective inhibition of sodium channels
Antiplatlet Therapy
Aspirin- if risk of benefit outweighs risk of bleeding
Plavix as an alt to ASA

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12
Q

Revascularization in Stable Angina

A
Failed medical therapy
LMA stenosis
3 vessel disease with LV dysfunction
Unstable Angina
Post MI with angina
? 2 vessel disease with LV dysfunction, >90% stenosis in any vessel, + stress test
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13
Q

Prognosis of Stable Angina

A

Mortality rates depend on the number of diseased vessels, severity of stenosis, LV function, complex arrhythmias
Nearly half of all deaths are sudden
Duke Treadmill Score, based on the Bruce protocol can stratify the risk of annual mortality.

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14
Q

2 Types of Revascularization

A

Coronary artery bypass graft (CABG)

Percutaneous coronary intervention (PCI)

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15
Q

CABG

A

Very low mortality rate (1-3%) in healthy people
Mortality rate increases with worsening underlying disease
Can use the Left internal mammary artery (LIMA), Saphenous vein or radial artery
Venous grafts can occlude in 10-20% in first year, less as time goes on
Usually requires median sternotomy and cardiopulmonary bypass
Angina can reoccur in 25% of pts but often less severe

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16
Q

PCI

A

Can perform a balloon angioplasty or stenting
Two types of stents
Drug eluting (elute antiproliferative agents)
Bare metal
Risk are intimal dissection or rupture
Usually need anti-platelet therapy to prevent thrombosis, the length of time depends on the time of stent
6-9 months with BMS
12 months with DES

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17
Q

PCI Indications

A

Indications
Stable angina
More effective than medical management for relief of angina
? Utility in MI or unstable angina, may not reduce risk of further ischemia

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18
Q

Risk with PCI

A
Risk
Death < 0.5%
Emergency CABG < 1%
MI < 2%
Branch occlusion 5-10% (minor complications
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19
Q

Efficacy for PCI

A

Success in 95% of cases
More effective the medications up to 2 years post PCI
Restenosis in 20% in 6 months with bare metal stents
Angina in 10% in 6 months

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20
Q

PCI vs. CABG

A

PCI ok in 1 vessel disease
CABG better in severe multivessel disease
Mortality at 5 years is similar

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21
Q

PCI Benefit

A

Restenosis is a major limitation of the procedure

Risk at 6 months
Drug-eluting < 10 %
Bare metal 10-30%
No intervention 30-40%

PCI may not have any benefit over medical therapy in respect to mortality
Does improve symptomatology
Increased need to repeat procedures compared to CABG

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22
Q

Coronary Spasms

A

Coronaries can spasm (vasoconstriction) and cause similar effects of angina.
The blood vessels are without atherosclerosis

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23
Q

Causes of Coronary Spasms

A
Cocaine
Prinzmetal (variant) angina
Cold
Vasocontrictive medications
Ergot
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24
Q

Prinzmetal angina is caused by

A

vasoconstriction
Most commonly the RCA
“Syndrome X”
Can see ST elevation
Women under 50 yo
Usually in the early AM, often awakens pts
Seen with conduction defects and arrhythmias

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25
Treatment of Coronary Spasms
``` ST elevations, should get a coronary angiogram. Look for stenosis Repair stenosis if indicated Medications if indicated Nitrates and CCB may help with Prinzmetal varient angina Stop smoking and/or cocaine use ? Pure beta activity in cocaine use Hotly debated in the literature May want to use an alpha/beta medication ```
26
Unstable Angina
Chest pressure at rest or with minimal exertion lasting > 10mins, severe and of new onset, occurs with a crescendo pattern NSTEMI is UA with signs of myocardial infarction
27
2 Types of NSTEMI
Unstable cardiac ischemia | Unstable Angina
28
Definition of Myocardial Infarction
``` Elevated biomarkers (troponin) Symptoms of cardiac ischemia ECG findings of a new New Q waves Loss of myocardial tissue New wall motion abnormality ```
29
Causes of NSTEMI
Plaque rupture or erosion with superimposed nonocclusive thrombosis (most common) Dynamic obstruction Progressive mechanical obstruction Increased myocardial oxygenation demand and decreased blood supply
30
Symptoms of NSTEMI
Chest pain (pressure) is the most common symptom in the emergency department Levine Sign Fist clenched over center of chest May occur at rest or on exertion May radiate Very similar to symptoms of chronic angina Signs of heart failure are usually associated with higher rate of mortality
31
Lab tests for NSTEMI
``` Markers of myonecrosis Troponin I and T CK and CK-MB Myoglobin Elevation of troponin and CK-MB maybe the only sign of myocardial ischemia ```
32
ECG Finding with NSTEMI
ST segment maybe depressed or flat, T wave flattening or inversion present in 30-50%
33
Treatment of NSTEMI
``` Admit the patient Treat symptoms= MONA O2 Pain medications Anxiolytics ```
34
Anticoagulation and Antiplatlet Treatment for NSTEMI
Aspirin Class 1A data Clopidogrel (in ASA allergic pts) Class 1C data Low-molecular weight heparin (enoxaparin or Fondaparinux) Unfractionated heparin Glycoprotein IIa/IIIb antagonist (tirofiban, eptifibatide, abciximab)
35
Nitroglycerin Treatment for NSTEMI
Nitroglycerin Sublingal, buccal or transdermal If pain persists may start IV
36
BB and CCB Treatment of NSTEMI
Beta Blockers Class IB in ACS and IA in MI Calcium Channel Blockers No favorable outcomes Third line agents
37
Statins and ACE-I Treatment of NSTEMI
Statins PROVE-IT trial Starting a statin immediately regardless of LDL levels improved outcomes (used atorvastatin 80 mg) ACE-I Class 1B3 for ACS and 1A for MI
38
Revascularization of NSTEMI
``` Class 1 Early (within 48 hours) invasive strategy for any of the following high-risk indicators Recurrent angina/ischemia at rest or with low-level activity Elevated troponin ST-segment depression Recurrent Ischemia with evidence of CHF High-risk stress test result EF < 40% Hemodynamic instability Sustained VT PCI within 6 months Prior CABG ```
39
TIMI Risk Score (Thombosis in Myocardial Infarction)
``` Age > 65 3 or more cardiac risk factors Prior coronary stenosis > 50% ST segment deviation 2 anginal events in prior 24 hours ASA in past 7 days (given for some cardiac event) Elevated cardiac markers Get 1 point for each and with each one increases the risk of mortality at 14 days ```
40
NSTEMI Treatment Summary
``` ABCs Morphine ASA Plavix if ASA allergey Some data for Prasagruel NTG Anticoagulation LMWH vs Heparin Bivalrudin and Glycoprotein IIa/IIB inhbitors for PCI lab only BB ACE Statin Cardiology Consultation +/- Revascularization ```
41
STEMI
Most caused by an occlusive lesion in one of the coronaries at the site of an atherosclerotic lesion Some can be caused by vasospams, cocaine, emboli, hypotension, increased metabolic demand, vasculitis, aortic root and coronary dissection
42
3 Phases of a STEMI
Acute from onset to 7 days Healing 7 to 28 days Healed > 29 days
43
Symptoms of a STEMI
Worsening angina, chest pressure, discomfort, crushing pain Pain usually at rest and, commonly in the AM NTG has little effect Fever, diaphoresis, malaise, anxiety Syncope, pre-syncopal, dyspnea, orthopnea, cough, n/v 1/3 of STEMIs are painless Elderly, women, DM Sudden Death 50% don’t make it to the hospital
44
Signs of a STEMI
``` Bradycardia common with inferior MI Tachycardia Decreased CO Arrythmia HTN Hypotension Respiratory failure, may indicate CHF Fever ```
45
Killip Classification and STEMIs
Standard way of classifing HF in pts with AMI Class I = absence of rales and S3 Class II = Rales that do not clear with coughing over 1/3 or less OR presence of an S3 Class III = Rales that do not clear with coughing over more than 1/3 of the lung fields Class IV = Cardiogenic shock (rales, hypotension and/or hypoperfusion)
46
Cardiac/PV Exam in STEMI
``` May have no signs JVD may reflect R sided failure S3 (less common) and/or S4 MR murmur Pericardial rub (with transmural MI) Edema +/- Cyanosis ```
47
Lab Findings in STEMI
``` CK-MB Troponin I and T More sensitive than CK-MB Each test maybe + in 4-6 hours after onset of the MI Abnormal for 8-12 hours Trops may hang around for 5-7 days CK-MB normalize within 24 hours More helpful for looking for reinfarction ```
48
ECG Findings with STEMI
``` ECG changes evolve as time progress Peaked T waves (hyperacute) ST segment elevation Q wave development T wave inversion Can occur over hours or days A new LBBB in a pt with symptoms of an MI is considered a STEMI ```
49
Imagining in STEMI
CXR may show pulmonary edema ECHO may show new WMA, new valve disorders (MR from pap dysfunction), VSD MRI Nuclear Scans
50
Hemodynamic Monitoring in STEMIs
``` Same as you would with any other critically ill patients Central lines Arterial lines Telemetry +/- Pulmonary artery monitors ```
51
Anticoagulation in STEMI
All patients should receive 162 to 325 mg of Aspirin at once Chewing increases absorption rate Reduces mortality by 27% (14.2% to10.4%) ASA allergies should receive clopidogrel a 300 mg loading dose then 75 mg daily Clopidogrel and ASA has shown benefit CLARITY Trial Clopidogrel with thrombotic therapy improved coronary patency on cath 3.5 days after thrombolysis, no increase in bleeding
52
Anticoagulation in STEMI--> COMMIT/CCS-2 trial
Clopidogrel reduced death, MI and CVA, with no increase in bleeding ASA and clopidogrel for min 14 days out to 1 year post STEMI “Double dosing” of clopidogrel may decrease restenosis post stent (600 mg x 1 then 150 mg daily)
53
Reperfusion Therapy in STEMI
Reperfuse within 12 hours of onset of symptoms PCI Therapy Superior to thrombolysis (with tpa) Need expertise, and lots of processes in place “Door to balloon” time is <90 mins Glycoprotein IIa/IIIb antagonist (specifically abciximab) or bivalrudin with stenting is generally standard of care HORIZONS trial Bivalrudin vs heparin and abciximab resulted in similar rates of thrombotic events but 40% less bleeding
54
So what if I cant get a PCI in < 90 mins?
No benefit of fibrinolytics and glycoprotein IIa/IIIB antagonists Either fibrinolytic and rescue PCI ASAP for reperfusion failure or PCI alone
55
Thrombolytic therapy-- Reperfusion in STEMI
``` Reduces mortality (by 50%) if given within 3 hours Major bleeding can occur (0.5-5%) Contraindications previous hemorrhagic CVA, CVA in past year, intracranial neoplasm, recent head trauma, active bleeding, HTN, recent major surgery ```
56
Types of fibrinolytics-- Reperfusion in STEMI
Alteplase (tpa) Reteplase Tenectplase Streptokinase (less commonly used in the US) Post Fibrinolytic Therapy ASA and heparin (at least 48 hours post), then lovenox (EXTRACT /OASIS-6 trials)/fondaparinux (OASIS-5 trial) x 8 days
57
Assessment of Effect for Reperfusion in STEMI
``` Improved Pain Resolution of ST changes At least 50% by 90 mins 10-20% of vessels with re-occlude and re-infarction Recurrence of pain and ST changes ```
58
Treatment Summary for STEMI's
``` ASA Plavix if going to cath lab Anticoagulation Heparin vs LMWH Fibrinolytic vs PCI Bivalrudin and glycoprotein IIa/IIB inhibitors for PCI lab BB ACE Statin Morphine and NTG for analagesia No NTG in R sided MI (drops preload as it increased venous capacity by vasodilation) ```
59
CCB and Anti- thrombotic therapy for STEMI's
CCB Not indicated, no trials support its use Long term anti-thrombotic therapy ASA daily WARIS-II trial warafarin post MI showed decreased mortality, MI, and CVA (not done in the US) CURE trial clopidogrel 75 mg/d for 3-12 months for NSTEMI and 1 year for STEMI reduced mortality, MI and CVA
60
Aldosterone Antagonist Treatment for STEMI's
RALES trial shows spironolactone reduces mortality in pts with advance HF EPHESUS trial showed 15% reduction in mortality with eplerenone with either HF or infarction
61
ARB Treatment for STEMI's
VALIANT trial showed valsartan is equivilant to captopril in reducing mortality Used in pts with ACE-I intolerance
62
ACE-I and Nitrate Treatment for STEMI's
Nitrates No improvement in outcomes (ISIS-4 and GISSI-3 trials) ACE-I (SAVE, AIRE, SMILE, TRACE, GISSI-III and ISIS-4 trials) show short and long term improvement in survival Esp good in pts with EF of < 40% Start early in pts wit no contraindications
63
Beta Blocker Treatment for STEMI's
Short term benefit started in first 24 hours (with no contraindications) No difference of IV over PO (COMMIT/CCS-2 trial) Prevents reinfarction, increased risk of shock in pts with HF (so no BB in HF) CAPRICORN trial showed carvedilol after acute phase showed benefit
64
Analgesia Treatment for STEMI's
NTG (SL, buccal, TD, IV) Opiods (Morphine) NSAIDS (other than ASA) can increase mortality
65
Post MI Angiography in STEMI
If reinfarciton noted, need rescue PCI Stress testing Poor stress testing should get a PCI
66
Complications of STEMI
``` Postinfarction ischemia Arrhythmias Myocardial Dysfunction RV infarction Mechanical Defects Myocardial Rupture LV Aneurysm Pericarditis (Dressler Syndrome) Mural Thrombus ```
67
Postinfarction Management
After 24 hours, treatment is based on prevention of reinfarction Risk stratification (TIMI) ACE if EF < 40% Stress testing
68
Secondary Prevention for STEMI
Hyperlipidemia treatment (Statin started before discharge) Smoking Cessation BP control Cardiac Rehab Exercise Beta Blockers Carvedilol 25mg IBD ASA Plavix x 1 year (? Praugrel, increased bleeding) ? Warfarin x 3 months (not compared to ASA and plavix) Antiarrhythmics ? ICD placement (postinfarct LV dysfunction, HF) DINAMIT trial showed no benefit in the 40 days post infarct
69
Demand Ischemia
Hypoperfusion to the myocardial tissue in the setting of increased physiologic requirements (oxygen) can result in a troponin leak Can see it in septic shock NOT an atherosclerotic lesion Need to restore perfusion