Coronary Artery Disease

This section has some of highest yield questions

Many physical findings
Many questions about what if first line treatment fails...what would you do next...very unique for
this section

Coronary artery disease (CAD)

Can be used interchangeably with atherosclerotic heart disease and ischemic
heart disease
All imply insufficient perfusion of coronary arteries starving off the myocardial
muscle from abnormal narrowing of vessels
insufficient O2 delivery to myocardial tissue
70% where we do surgery
prinzmetals (variant) angina
nonexertional chest pain, early in the morning
ST segment elevation
1/10 of 1% of all chest pain--extremely uncommon
MCC retrosternal, non-exertional, intermittent chest pain in middle age woman: GERD
Tip: Menstruating women virtually never have MIs
risk factors are most important with equivocal or uncertain histories
Tip: women>men eventually die of heart disease
Regular exercise--benefits a patients risk of coronary disease
Estrogen replacement at time of menopause-- but estrogen replacement did not help
CAD and there was actually an slight increase in mortality
Clear risk factors for CAD:
Diabetes-by far the worst one
Tobacco smoking
HTN- perhaps most common risk factor, >140/90; 130/80 in DM
20% population with high bp, 50% unaware theyre hypertensive
only 25% with htn sufficiently treated
Hyperlipidemia- as a single risk factor isnt so bad if you havent already had
coronary disease
High LDL is most dangerous in terms of risk for CAD...its not the total
cholesterol or low HDL, its LDL!! Running lowers LDL and raises HDL.
High HDL takes away one risk factor!
The danger of obesity is from its association with high LDL, DM, and
HTN. Obesity by itself is not that bad.
family h/o premature CAD first degree (father <55, mother <65)
Age >45 woman; >55 woman
Less clear risk factors for CAD
physical inactivity
excess EtOH
insufficient fruits & vegetables

emotional stress
CT scan calcium scores
PET scan
Takosubo
STsegement elevation in V2 to V4, troponin levels rise, coronary angiography is
normal including absensce of vasospasm. Echo shows Apical LV ballooning
Mechanism presumed to be massive catecholamine discharge
for a calm and quiet person--not sued to be upset and highly emotional
Unreliable (Unproven) Risk Factors for CAD--factors that if seen in a question should be
ignored
Homocysteine (dx test only for folate or B12 deficiency)--it goes up in both
Chlamydia infection
C-reactive protein
No clear benefit in therapeutic intervention on these factors
Tip: the most common wrong answer
If the risk factor question involves:
family history
mistaking CAD in elderly relatives as a risk for patient
Stopping smoking results in the most immediate benefit in CAD (risk goes down literally
goes down within 10 minutes of stopping)
If you stop smoking, your risk factor for lung cancer goes down to nearly to that of those
who never smoked within 7 years
What is the most likely diagnosis
Ischemic pain-- dull/sore; squeezing (pressure-like)--its a muscle!
Location of ischemic pain is substernal...not left sided (rarely) !!
Qualities that go against ischemic:
Sharp, knife-like or pointlike
Lasts a few seconds (vs 10-20 minutes)
Three features help tell whether or not the pain is ischemic in nature:
1. Changes w respiration (pleuritic)--worse when take breath (pleural, pneumo)
2. Changes with position of body (pericardial)
3. Changes with touch of chest wall (tenderness)
Each (pleuritic, positional, tender) excludes ischemia with 95% negative
predictive value (NPV)
<10% with chest pain in ED end up having an MI
50% have no cardiac disease at all
MCC of chest pain that isnt ischemic in nature is GI-related (reflux, ulcers, gallbladder)
Location of ischemic pain is substernal...not left sided!!

Reflux hits the CN 9, 10 supplying bitter taste to the back of the tongue
MI can cause fever...all clots and blood collections can cause fevers! PE, MI, etc

Features that DONT help answer the diagnosis question

Nausea
Fever
SOB (dyspnea)
Sweating (diaphoresis)
Anxiety
Best initial test for all forms of chest pain is certainly an EKG
In office-based setting: expect normal EKG
BUT you dont do other testing until you know the EKG
Cardiac enzymes are NOT the answer in
office/ambulatory case
Chronic or stable chest pain
If the patient has acute chest pain then the answer is:
transfer to the ED
Enzymes are the answer when:
acute cases of chest pain
ED
Exercise tolerance testing (ETT) is the answer when:
etiology is unclear and
EKG is not diagnostic
ETT without nuclear isotopes:
1. Read EKG (look for ST depression---ischemia)
2. Exercise
exercise means able to get up to a heart rate >80% of maximum
220-age=maximum heart rate
Thallium (Nuclear) Stress Test
Normal myocardium picks up thallium like potassium via Na/K-ATPase
Myocardium alive and perfused
nuclear isotopes will be picked up
Abnormalities/Ischemia or Infarction
decreased thallium or nuclear uptake
Ischemic tissue upon rest will reperfuse and pick up the thallium
Dobutamine or Stress Echo
Normal myocardium moves on echo
Abnormalities detected by decreased wall motion
Dyskinesis, Akinesis, hypokinesis
TIP ischemia vs infarction on stress test
ischemia = reversible decreased perfusion
reversal of decrease in thallium uptake or wall motion
it returns to normal after a period of rest

infarction = irreversible
ischemia is reversible wall motion or thallium uptake between rest and exercise.
Infarction is irreversible or fixed.
Cant exercise? (cant get it up to the maximal HR, also readable EKG)
Use chemicals- Persantine (dipyridamole) or adenosine (these increase perfusion of
heart) with nuclear isotopes (eg thallium or sestamibi)
OR
Dobutamine in combination with echocardiography
Dobutamine simulates exercise--it increases myocardial oxygen
consumption
provokes ischemia
ischemia decreases wall motion on echocardiogram
**Dipyridamole may provoke bronchospasm. Avoid in asthmatics!
Dipyridamole is a PDEi that increases cyclic AMP, which
induces bronchospasm
Therefore, in asthmatics used dobutamine echo or
sestalium ?

Tip: Nuclear and Echo are equal in sens and spec (sensitivity = specificity)
Exercise Thallium = Exercise Echo
Dipyridamole Thallium = Dobutamine Echo

Chemical dipyridamole thallium (decreased uptake) vs dobutamine echo (decreased wall

motion)
=>70% obstruction in 3 vessels or 2 in DM get bypass CABG
Angiogram (do when abnormal stress test)
detects anatomic location of disease
determines surgery, angioplasty, or other methods of revascularization
1-2 vessels: angioplasty
3 vessels or Left Main: CABG
sometimes used if noninvasive tests are equivocal
Stenosis (narrowing) <50% of diameter is i nsignificant!!!
Surgery or angioplasty is done for at least 70% stenosis
Holter monitoring
continuous ambulatory EKG monitor
use only for rhythm disturbances-- palpitations or syncope
records rhythm
usually for 24-hour period
may be for 48 to 72 hours
detects rhythm disorders:
A-fib. A fluuter

Ectopy (premature beats)

V-tach
Holter monitor does NOT detect ischemia, valve probs, MI, etc
Retrosternal pain--ischemic pain; left-sided pain--NOT ischemic pain

Treatments
Single most tested concept on step 3 cardio is which medications lower mortality--know
this!!!
Chronic angina (NOT an acute coronary syndrome)
Aspirin --most important bc decrease mortality and delay progression of
disease
Beta-blockers --most important bc decrease mortality and delay progression of
disease
Note: NONspecific beta blockers (eg propanolol) are NOT used routinely
in cardiology!
Propanolol is used for things like panic attack, essential tremor,
migraine ppx, thyroid storm
Metoprolol is used in cardiology--its a B1 specific drug
Nitroglycerin--used for chest pain, but does nothing for mortality
Chronic Stable Angina
Oral
Transdermal patch
Acute Coronary Syndrome
Sublingual
Paste (on chest wall)
Intravenous--ICU
Clopidogrel
used in all forms of acute MI in combination w
ith aspirin (not used
alone unless intolerant of aspirin!)
note: this has changed from previous recommendations that
stated this was only for those intolerant of aspirin
aspirin intolerance substitute (eg allergy)
recent angioplasty with stenting-- decreases restenosis
bare metal stent 1:3 will restenosis, but if use aspirin and
clopidogrel it decreases the restenosis rate to 15-20%
coated stent with aspirin and clopidogrel decreased restenosis
rate to 5-10%
Adverse Effects
Rare Thrombotic Thrombocytopenic Purpura

Thienopyridine- same class as clopidogrel and t iclopidine (causes neutopenia)

Aspirin is used with clopidogrel O
R prasugrel --both, when used with aspirin, provide a
mortality benefit

Prasugrel--lowers mortality
Antiplatelet medication for use in (along with aspirin):
angioplasty & stenting
all acute MI
intolerant of aspirin (so, can use as single agent)
NOTE: > 75 have an increased risk of hemorrhagic stroke!!
if pt is 75 or older use clopidogrel instead
ACE inhibitors or ARBs (angiotension receptor blockers)
used in all acute MIs
Low EF/systolic dysfunction (dilated CM) (best mortality benefit)
Regurgitant valvular disease--delays progression
Most common AE
ACEi only: 7% pts cough switch to ARBs (-sartans)
ACEi & ARBs: hyperkalemia switch to hydralazine & nitrates (afterload
reduction) (ACEi & ARBs increase K by inhibiting aldosterone)
do not answer add kayexalate (potassium-binding resin)--it is not
enough to say remove K from the body--you should eliminate the
cause and get an alternative replacement for the indication
give insulin and glucose to drive K into cells is not the right
answer unless you have an acute situation or EKG abnormalities
Statins (HMG-CoA reductase inhibitors)
When do they lower mortality the most? When you have C
AD w LDL
>100mg/dL HY!!
LDL >70: Treat when patient has CAD & DM together
remember: youre tested on National guidelines from n
onbiased federal
organizations-- not private organizations like ACC
Everyone will agree:
With CAD, goals of LDL at least <100 mg/dL
With CAD & DM, goals of LDL at least <70 mg/dL
CAD Equivalents
Use Statins to bring LDL down to <100 if:
Peripheral artery disease (PAD)
Carotid disease (NOT stroke)
Aortic disease (aortic ARTERY, not valve :)
Diabetes mellitus
MC AE of Statins?
Liver dysfunction!!
get LFT before initiating and during course of tx w statins
MC wrong answer to this question is Rhabdomyolysis (elevated
CPK)--this occurs in less than 1/10th of 1% of users (Liver dysfunction is
20-30x more frequent vs rhabdomyolysis)
do not need to follow CPK

Niacin, gemfibrozil, cholestyramine, and ezetimibe all have beneficial effects on

lipid profiles, but none of these are best initial therapy
they dont have clear mortality benefit statins provide
niacin and fibric acid derivative (gemfibrozil) have some mortality benefit,
but not as much as statins
statins have a benefit beyond lowering LDL, TGs and raising HDL...they
have an antioxidant effects on endothelial lining of coronary arteries
Niacin associated with:
glucose intolerance-- not diabetics?
elevated uric acid--dont use in gout
uncomfortable itchiness from histamine
Niacin is excellent to a
dd to statins if full lipid control is not achieved with statins
alone
Although statins, exercise, and cessation of tobacco use will all raise HDL level,
niacin will raise HDL somewhat more
Fibric Acid derivatives (gemofibrozil, fenofibrate)
lower TG levels > statins
benefit of lowering TG alone not proven as useful as straightforward
mortality benefit of statins
use caution combining fibrates with statins b/c:
Fibrates + Statins = Increased Myositis HY!!
Bile Acid Sequestrant (Cholestyramine)
significant interactions w
ith (fat soluble) m
edications i n gut
potentially blocking meds absoprtion (by the mxn by which they work)
cholestyramine associated with uncomfortable GI complaints/AEs
constipation & flatus
no benefit beyond statins
Ezetimibe
definitely lowers LDL but N
O clear benefit to patient!
LDL levels are an imperfect marker of benefit with cholestrol-lowering
therapies
Ezetimibe: No better than placebo
No change in MI, stroke, or death
well tolerated (no AE) and nearly useless!
Lipid lowering therapy--what is clear?
statins lower mortality the most
questions about AEs
MC AE of statins: LF abnormalities (inc LFTs), NOT
rhabdomyositis
Fibrates + Statins = increased myositis
this would be a which drug is dangerous to combine with
statins (or with the gold standard of treatment for this dz)

Cholestyramine (bile acid sequest) cause significant interactions

with dat soluble medications in the gut, GI gut
discomfort/AEs--constipation, flatus, abdominal cramping etc
Niacin causes increase in uric acid, glucose intolerance, histamine
release itchy redness/pruritis
Besides the benefit of statins in CD with LDL levels >100 mg/dL, the only
truly clear aspect of other therapies is their AEs
Check AST (drugS) & ALT (viraL) with statins-- get baseline LFT & check
Calcium Channel Blockers
Dihydropryridine CCBs: Do not lower mortality in CAD
Nifedipine, Nitrendipine, Nicardipine, Nimodipine
lower BP (only place where they lower mortality is hypertension,
not cocaine--though are used when have cocaine induced pain)
negative inotropes, relax smooth muscle
should decrease myocardial O2 consumption, but really dont
increased heart rate in the aggregate will increase
myocardial O2 consumption
used in people who cant tolerate BB
May increase mortality with CAD because of raising heart rate (cause
vasodilation and reflex tachycardia), only lower HR in arrhythmia, not
lower HR in sinus rhythm
Bottom line: do N
OT routinely use CCBs in CAD...None of the CCBs
have been shown to lower mortality in CAD
Verapamil and diltiazem, which do n
ot increase heart rate, are used in
those who cannot tolerate BB bc of severe asthma (70-80% asthmatics/
reactive airway disease can tolerate B1-specific BBs--metoprolol)
Use them when you have Afib, AFlutter, SVT--to slow HR in atrial
arrhythmia
Use CCBs V
erapamil and D
iltiazem in CAD o
nly with:
severe asthma p
recluding the use of BB
Prinzmetal variant angina
Cocaine-induced c hest pain
AEs of CCBs
Edema (dilate the precapillary sphincter you increase the
hydrostatic pressure and the starlings forces inside the capillaries
and you are increasing the extravasation of fluid--increased
hydrostatic pressure will increase the flow of fluids into the
peripheral tissues as an AE)
Constipation ( remember bowel is a big tube of smooth
muscle--CCBs block smooth muscle constipation)
Heart block (rare-- in toxic doses)
Revascularization
Only way you will know if a person needs revascularization is angiography

Angioplasty or PCI...OR...CABG/bypass surgery

Symptoms alone cannot tell the number of vessels involved

CABG
Lowers mortality only with:
3 vessels with >70% stenosis in each
Left main occlusion
2 vessels with diabetes
persistent symptoms despite maximal medical therapy
all in combo with LV dysfunction
Benefit greatest with LV dysfunction
Internal mammary artery grafts last 10 years
Saphenous vein grafts last 5 years
Percutaneous Coronary Intervention (PCI) (Angioplasty)
Which circumstances does PCI lower mortality the most?
Intervention best therapy in acute coronary syndromes
Particularly, those with ST Elevation ACS
MC Wrong answer is in 1-2 vessel coronary disease
The main indication for using angioplasty is to acutely reverse a clot or
plaque rupture that happened within the hour. And although we use it to
decrease symptoms stable angina in 1-2 vessel disease, but it hasnt
been shown to lower mortality in chronic stable angina--may not be
normal, but have compensated--and no mortality benefit over meds
Maximal medical therapy with aspirin, BB, ACEi/ARBs, and statins has
proven benefit thats >
PCI in stable CAD
PCI decreases dependence on medication
PCI decreases frequency of angina episodes
Moreover, PCI best in ACS particularly with ST segment elevation. PCI
doesnt provide clear mortality benefit for stable patients

Congestive Heart Failure

MC reason in the US to be admitted to the hospital
All forms of CHF or cardiomyopathy are result in with shortness of breath
(dyspnea)--essential feature of CHF
All forms result in decreased forward flow of blood- whether its systolic or diastolic
dysfunction you cannot tell difference in patients symptoms because whether you can
contract but cant relax or you can relax but cant contract the symptoms for the patient
are the same-- which is a sense of breathlessness of insufficient oxygen delivery
particularly as you exercise
Dysfunction of heart as a pump of blood
Insufficient oxygen delivery and fluid in the lungs
if the fluid builds up in the lungs, it does not matter if it is from systolic or diastolic
dysfunction bc blood does not move forward and feed the tissues
The only way to differentiate is by ECHO, you cannot tell by symptoms/presentation

Systolic Dysfunction:
Low EF and dilation of heart
Diastolic Dysfunction:
EF is preserved...heart cant relax and receive blood
Important bc treatments are considerably different
MCC of CHF is HTN leading to diastolic dysfunction. Pt with MI can develop CHF rapidly
but far more people with hypertension where you initially have a preservation of EF. But,
overtime, the heart dilates up resulting in systolic dysfunction and low EF. This is simply
much more common than people who have MIs.
Valvular heart disease of all types results in CHF
MI is a very common cause of dilated CM and decreased EF
overall mortality from MI is considerably decreased by
Thrombolytics and angioplasty decrease it by 25% RRR
Aspirin, clopidogrel 25%
BB 10, 20, 30%
ACEi 10-20%
Statins 10%
As MI deaths continue to go down, the number of patients living with CHF goes up
Infarction (tissue dies) always dilates automatically lesions start to separate valve
leaflets regurgitation CHF
Less common causes of CHF (SOB, edema, orthopnea)--not dx tests to confirm/
determine these etiologies (except for hemochromatosis). Endomyocardial biopsy is
most accurate test is rarely if ever one. Hypertension and ischemia are far more
common causes fo CHF...take this list and add it up and multiple it by 10...still not as
common. The management and treatment is the same for all of these except for
revascularization.
EtOH
Postviral (idiopathic) myocarditis
Radiation
Adriamycin (doxorubicin) use
Chagas disease and other infections (doesnt present with chest pain, presents
with dilated CM...in south america :)
Hemochromatosis (also causes restrictive cardiomyopathy)
High iron, low iron binding capacity, high ferritin, 282Y mutation
Thyroid disease (hyper or hypo cause myopathy)
Peripartum CM
Thiamine deficiency-wet beri beri (rare)
In addition to dyspnea on exertion look for:
orthopnea is the positionality of SOB--one of the m
ost unique features of CHF.
when you lie flat, blood pools in your lungs (worse when lying flat, relieved when
sitting up)
Peripheral edema
Rales on lung exam

JVD...constrictive pericarditis can do too

paroxysmal nocturnal dyspnea (PND) (Sudden worsening at night, during sleep)
S3 gallop rhythm--with the exception of young healthy athletes--rapid ventricular
filling
Be prepared to ID the sound on the step!!

S4 gallop--sound of atrial systole into a stiff noncompliant ventricle

sign of hypertrophic CM of hypertension
just treat hypertension (no need to add something else)
S3 gallop is when the mitral valve opens and there is very rapid of the ventricle
like a big splash, all the blood build up from atrium and lungs
S3 gets diuretics
What is the most likely dx of SOB
Sudden onset of SOB, clear lungs: Pulm Embolus
Sudden onset SOB, wheezing, increased expiratory phase:
asthma
Slower onset SOB, fever, sputum, unilateral rales/rhonchi:
pneumonia
Decreased breath sounds unilaterally, tracheal deviation: pneumothorax
Circumoral numbness, caffeine use, h/o anxiety:
panic attack
as you hyperventilate it increases the binding of free calcium to albumin,
which lowers the free calcium in the blood which promotes a premature
depolarization of the neural tissue- makes you numb arounf the mouth
Pallor, gradual over days to weeks: anemia
pulsus paradoxus, decreased heart sounds, JVD: tamponade
PP decreased in >10 mmHg on inhalation
Palpiatations, syncope:
Arrhythmia (of almost any kind--in the ventricle),
sound LOC, sudden regaining of consciousness
Dullness to percussion at base:
pleural effusion
indication for chest tube/draining if pleural effusion causes SOB
Long smoking history, barrel chest: COPD, emphysema
Recent anesthetic use, brown blood not improved with O2, clear lungs on
auscultation, cyanosis:
oxidized iron that cant pick up O2
--methemoglobinemia-- tx w methylene blue
Burning building or car, wood burning stove in winter, suicide attempt, red blood:
carbon monoxide poisoning--give 100% O2 and hyperbaric O2
All of these will lack: orthopnea/PND (no positionality), S3 gallop
Key to dx of all forms of CHF is the Echo
most important (TTE 1st)
there is no OTHER way to distinguish w/o echo (not by h/p/ other tests: CXR,
BNP)
Best initial test of EF
TTE
Most accurate test of EF
MUGA (multiple-gate acquistion scan) or nuclear ventriculography