Chief complaint… “Severe chest pain for 2 hours”—first thought? Is this an acute coronary syndrome?
• FIRST THINGS FIRST: Any patient with a suspected acute coronary syndrome should chew 160-325 mg of ASA; one simple therapy is associated with a 35-day mortality reduction exceeding 20%)
• Now, think…what structures are located in the chest and how should I go about considering this specific patient with chest pain?
Evaluation of chest pain…
• Cardiac—Acute coronary syndromes, aortic dissection, pericarditis, myocarditis
• Pulmonary—pulmonary embolism, pleuritis, pneumothorax
• GI—esophageal spasms, GERD, gall bladder
Evaluation of chest pain…
• Musculoskeletal—costochondritis, muscle strain, rib fracture
• Neurologic—herpes zoster (“band-like” burning pain may precede vesicular eruption)
• Psychological—panic disorder, depression
So, use the PQRST + AAA• Start with the P’s…Pinpoint the pain, what is the
precise location? “show me…”• LEVINE (pronounced “La Vine” sign…fist held over
sternum is pretty classic for angina or an MI• Swooping the hand from the back, under the axillary
region and to the front may indicate “shingles”• Moving the fingers up and down from the bottom of
the sternum to the top may indicate heartburn/GERD• Severe tearing chest pain radiating to the back – think
aortic dissection (and think it FAST) • Positional and pleuritic pain with pericarditis
What precipitated the pain?
• Exertion? • What were you doing when the chest pain
started? • How long did it take before the chest pain
started? Raking leaves? Shoveling snow? Cardiac pain usually has a “lag time” to start
• Did the pain start as soon as you picked up the shovel or the rake?
FYI: Snow-shovel-related medical mishaps1990-2006
• 195,000+ snow shovel-related injuries treated in emergency rooms in U.S. between 1990-2006
• 53.9% from acute musculoskeletal exertion• 20% slip and fall• 15% hit by a shovel• 6.7% cardiovascular related• 4.4% other• 63% sustained by 18-54 year-olds• Watson O.S, et al. Amer. J. Emer. Med, 2011
Back to the P’s• What palliates the pain?• Stopping the activity? How long did it take before
the chest pain stopped when you ceased the activity? (cardiac pain—lag time to stop)
• Did you put a little white pill under your tongue? If so, how many and how long did it take for the pain to stop?
• Did you take an antacid?• Does it hurt when you palpate the area? Consider
musculoskeletal pain (Cardiac pain is not reproduced with palpation)
Quality or Quantity
• What is the Quality of the pain? • Burning? Zoster? GERD? AMI• Squeezing? Angina• Crushing? Vice-like? Acute MI• Tearing? Aortic dissection• Pleuritic w/ dyspnea? pneumothorax
R is for Radiate/Referred
• Where does it Radiate? Is it Referred pain?• Front, back, side, down arm, up to the jaw,
between the scapula, elbow, jaw only?
The dermatome chart
Dermatomes
• Areas of skin that send their sensory information into specific spinal cord segments
• Visceral structures share these sensory afferents with skin areas
• T1-T4—dermatomes shared with the myocardium, pericardium, aorta, pulmonary artery, esophagus, and mediastinum
• Maximal intensity of the visceral pain is in the retrosternal area/precordial area, up the neck, down the inner arm
Dermatomes• C3,4, (the phrenic nerves) the center of the
diaphragm and shoulder pain• The patient with substernal chest pain, left
shoulder pain and intractable nausea—right coronary artery, “inferior MI”?
• What’s below the center of the diaphragm? The first part of the duodenum (the “organ of nausea”…
• The older patient with fever, tachypnea, shoulder pain and confusion—lobar pneumonia
• A fair, fat, fertile, forty-ish female with flatulence and right shoulder pain? Gall bladder? AMI
Severity
• What is the severity of the pain…• On a scale from 1-10, with 1 being the least
and 10 being “outta control”—where do you rank pain on this scale?
• The classic MI—9 or 10 or greater
Does severity tell you anything special about outcomes after an acute MI?
• No…in fact, severe chest pain does not herald worse outcomes.
• Long believed by clinicians that a 9 or 10 on the scale resulted in worse outcomes
• Severity of chest pain was not significantly associated with AMI (acute myocardial infarction) or the composite outcome of death (Edwards)
Atypical chest pain• Forty percent of AMI patients older than 85 present
with chest pain vs. 77% of AMI patients younger than 65; Elderly patients more likely to present with dyspnea, diaphoresis, N & V, syncope
• Women—54% are at risk for misdiagnosis vs. 33% of men; less likely to present w/ typical chest pain, but more likely to present with tachycardia and hypotension; more likely to report pain in the arm, neck, back and jaw; HA; N & V; dyspnea, cough; chest pain at rest, with mental stress, or during sleep
Timing or Temporal sequence
• Temporal sequence; Timing• When did it start? • How long did it last? • How often do you experience this type of
pain?• What’s unique about the time of day and an
acute coronary syndrome?
6 a.m.• Blood pressure and heart rate begin to rise due to adrenalin
and cortisol—increasing the workload of the heart• BP is lowest at 4 a.m.• Sharpest rise of BP at 6:45 a.m.• Increasing heart rate and BP help you to become upright in
the a.m.• Increasing blood pressure also means that the vessels are
constricting—risk?? • If on a beta blocker…QD beta blockers (long-acting) should be
taken at night• Example: Toprol XL (metoprolol)
How about that first morning cigarette when you first get up?
• vasoconstriction
8 a.m.-10 a.m.• Risk for AMI • The liver produces coagulation factors at night and
releases early in a.m.• The adrenal gland releases cortisol and adrenalin in the
a.m. which increases blood sugar and contributes to platelet aggregation; BP also rises as does heart rate in response to adrenalin in a.m.
• Inflammatory mediators are the highest• Take daily aspirin as soon as you get up to inhibit
platelet “stickiness”; • ASA stays in the body longer when taken at 7 a.m.
Not only are you at highest risk for an acute coronary syndrome in the a.m.
• Increased risk of heart irregularities (arrhythmias)
• Increased risk of sudden cardiac death (usually due to a ventricular dysrhythmia)
• Increased risk of deaths associated with congestive heart failure
(August 2005 Journal of Biological Rhythms)
The sure-fired way to avoid cardiovascular complications in the morning?
• Don’t get up.
PQRST• Any additional symptoms? • Sweating? Nausea? Fatigue? Impending doom?• Dizziness? Light-headedness • Dyspnea (cardiac or respiratory)?? BNP test (B-
type or brain- natriuretic peptide is released in response to an elevated left ventricular end diastolic pressure which attempts to decrease SVR and increase natriuresis—under 100 pg/mL rules out left ventricular failure; greater than 500 pg/mL rules in CHF)—gray zone between 100 and 500 pg/mL; under 50 pg/mL has a 97% sensivity
How about a 38 yo. woman with chest pain?
• Quick questions to rule OUT a myocardial infarction in a young woman…what is her risk of having an MI at age 32?
• Diabetes• Birth control pills? Obesity? • Autoimmune disease? SLE, RA, vasculitis• Methamphetamine, cocaine• Cardiotoxic chemotherapy• Surgical menopause? • Family history
The 7 common primary heart diseases are:
• congenital heart disease• ischemic heart disease (coronary artery disease)• hypertensive heart disease• valvular heart disease – acquired or congenital• pulmonary heart disease (cor pulmonale)• primary disorders of the myocardium (cardiomyopathies,
myocarditis)• pericardial diseases (pericarditis, tamponade)
Find your lines and your spaces…• Suprasternal notch• Clavicle (1st rib is under
the clavicle)• 2nd rib is the first palpable
rib • 2nd ICS R and L—base of
heart• 4th ICS parasternal border• 5th ICS on L (apical area)• Epigastric area• BASE vs. APEX—heart is
upside down
WTF?
• Apex is at the bottom• Base is at the top• No rational explanation• Get over it, but remember it!!
Cardiovascular exam --inspection
• Skin color, nailbeds, capillary refill (4-6 seconds is normal), ankle edema
• 5th L ICS @ MCL for apical impulse• Left 4th parasternal border for the R
ventricular area—R 4th for tricuspid• 2nd R ICS—aortic area—heave, pulsation• 2nd L ICS—pulmonic area—heave pulsation• Suprasternal notch—pulsation?• Epigastric area—pulsation?
Palpation…• The base of the heart…any thrills? Cat purring…• A thrill with a murmur means that the murmur is at
least a grade 4 (4/6)• Think valvular disease—aortic and pulmonic stenosis
in 2nd ICS• The 5th L ICS at the MCL The apical area—mitral stenosis
Palpation –palpating hearts and pulses since 1550 B.C. (Egyptians)
• Identify the apical impulse—should be no bigger than 1-2 cm in size; gentle, brief contraction (only present in 50% of the population—turn patient on L side to feel)—if >4 cm (LR 4.7 for a dilated heart)
• Where is it? Outside the MCL (>10 cm from the MSL)—LR for cardiomegaly is 3.4, depressed ejection fraction is 10.1, ↑LVEDV is 8.0, and increased PCWP 5.8)
• Is there a pulsation in the epigastric area? Beating up against the pads of your fingers? Beating against fingertips?
Peripheral arterial disease—a risk equivalent of CAD
• Have PAD? Most likely have CAD• Diffuse disease—males, diabetics, smokers,
hypertensive patients• Check all pulses--Dorsal pedalis? Posterior tibial? If
absent, try femoral and popliteal• In studies of large numbers of healthy individuals, the
dorsal pedalis pulse is not palpable 3-14% of the time and the posterior tibial is absent 0-10% of the time.
• Only 0-2% of healthy individuals are missing both pedal pulses).
• Listen for bruits over femoral arteries; bruits near umbilicus
Characteristics arguing for the presence of peripheral arterial disease
• Absence of both pedal pulses (LR 14.9)*• Presence of any limb bruit (LR 7.3)• Presence of wounds or sores on the feet (LR 7.0)• Absence of the femoral pulse (LR 6.1)• Presence of asymmetric coolness of the foot (LR 6.1)• Unhelpful findings—atrophic skin (LR 1.7), hairless lower
limbs (LR 1.7), prolonged capillary refill time (LR 1.9)• McGee S. Evidence-Based Physical Diagnosis. WB Saunders, Co. 2001
• *LR is the Likelihood Ratio
Peripheral arterial disease
• Intermittant claudication—muscular pain, aching, numbness w/ exercise; relieved by rest
• Ankle/brachial systolic BP—normal is 1-1.2; less than 0.9 = PAD; claudication 0.5-0.9; rest pain less than 0.4
• Risk of amputation is 15-40 x higher in the diabetic
• Tx with cilostazol (Pletal)—reduces time to claudication and improves exercise capacity (vasodilators don’t work)
• ACE inhibitors have recently shown to be helpful
Guys, if you’re not getting blood flow to the feet or the private parts… you are not getting enough blood
to the kidney
Acute mesenteric arterial occlusion
• Severe diffuse abdominal pain—frequently out of proportion to clinical findings
• Chronic occlusive disease involving the mesenteric circulation can manifest as abdominal angina—especially after “exercise”—a meal
• Weight loss, N & V, early satiety• DON’T forget this as a cause of acute abdominal
pain—especially in patients with CAD, PAD
Acute arterial peripheral occlusion—medical emergency—6 P’s
• Pulselessness• Pallor• Poikilothermia (temperature of the affected
extremity varies with ambient temperature• Pain• Paralysis• Paresthesia
Abdominal aortic aneurysm (AAA)—usually infrarenal
• Abdominal bruits for abdominal aortic aneurysm--
• Usually silent until complication develops; abdominal pulsation
• Ultrasound dx—screening for all men age 56-75 who have ever smoked
• risk of rupture increases exponentially with size; 3.0-4.4 cm diameter has a 2%/year risk; 4.5-5.9 cm diameter has a 10%/year risk; > 6 cm = 80% rupture within 2 years
Triple A--prognosis
• Rupture outside the hospital? 80-90% mortality; 50% die at scene; 50% who make it to the hospital die in the OR; 50% of those who survive the operation die of other co-morbid conditions prior to hospital discharge
• When to repair? Aneurysm expansion > 0,5 cm/year; thoracic aortic aneurysm > 6 cm (Marfan syndrome—other signs?); abdominal aortic aneurysms > 5.5 cm
Jugular vein distention…• The absolute best way to check the amount of
volume and pressure on the right side of the heart• Always check the R jugular vein in everyone but
especially elderly pts(direct route to heart; L veins cross the mediastinum where the
aorta may compress and falsely elevate).• If top of neck veins are elevated> 3 cm above sternal
angle check for other signs of heart failure• Hepatomegaly, peripheral edema, S3 gallop,
pulmonary crackles
Abdominal jugular reflex
• The pressure applied over the abdomen shifts blood into the thorax and right atrium
• If the right ventricle is unable to handle this increased load, the result is a sustained increase in JVP.
• Compression of the liver is unnecessary• Compression of the periumbilical area will suffice• Positive with a sustained increase in the JVP greater
than or equal to 4 cm.• LR ratio of 8 for detecting elevated left diastolic
pressures
Pitting edema…
• Subjective grading 1+-4+• 1+ slight pitting• 2+ deeper but no detectable distortion of
tissue• 3+ noticeably deep, extremity full and
edematous• 4+ very deep pit (your finger disappears)
dependent extremity is grossly distorted
Peripheral edema…what does it mean?
• Fluid retention—heart failure• Unilateral pitting—consider occlusion of major
vein• Edema without pitting—arterial disease and
occlusion• Edema as a side effect of drugs that retain
water or that are potent vasodilators—NSAIDS and Ca+ channel blockers
Now it’s time to listen--Notes on the stethoscope
• Ear plugs that fit—block out extraneous noise• Length of tubing no longer than 12”, but 8” is
ideal• Any stethoscope of a pastel color is worthless• Do not listen over clothes• The bell—LOW-pitched sounds; the diaphragm—
HIGH-pitched sounds• Quiet room—no TV; no visitors; no wives,
husbands, lovers, children; no construction
Heart valves
Position the patient…• Sitting up and leaning forward—brings base
of heart closer to chest wall Murmurs of the aortic and pulmonic
valves heard best in this position—high-pitched systolic sounds (aortic stenosis)—use the diaphragm of the stethoscope
• Left lateral recumbent—best position to hear low-pitched filling sounds during diastole (mitral stenosis)(use the bell of the stethoscope—don’t MUSH it on the skin, hold it lightly!!)
But if you only have a minute…
• …and the patient is NOT a cardiac patient—you can just listen to the apical or mitral area
If you had two minutes and you know the following…
• #1 diseased valve of the heart? MITRAL• #2 diseased valve of the heart? AORTIC
• SO WHERE WOULD YOU LISTEN FOR EACH OF THE ABOVE?
• L 5th ICS for mitral (apical)• 2nd R ICS for aortic (base)
Heart sounds—S1, S2
• S1 is the closure of the mitral and tricuspid valves—the END of diastole or filling of the heart (aortic and pulmonic valves open signaling the beginning of systole)
• S2 is the closure of the aortic and pulmonic valves—the END of systole or ejecting the blood (mitral and tricuspid valves open signaling the beginning of diastole)
• Opening and closing valves are silent unless diseased
Listening to heart sounds…
So…when you hear an extra heart sound…
• First decide if it’s in systole or diastole?• Extra heart sounds can be murmurs…• 50% of all murmurs are systolic…therefore, 50% of all murmurs are diastolic. DUH…Is the murmur after the LUB? Systolic?Is the murmur after the DUB? Diastolic
The third heard sound
• S3—a diastolic sound• Gallop…lub dub dub, lub dub dub• This can be a normal sound under the age of
35• however, consider the patient’s history
before using this age as a arbitrary number to dismiss a third heart sound
Characterizing a murmur…
• Timing—systole or diastole• Duration—early, mid, late, continuous in relation to
S1 and S2• Pitch—low, medium, high• Intensity—1 through 6 (4-6 usually assoc. with thrill)• Quality—descriptive (harsh, blowing, soft)• Location—where best heard• Radiation--where does it go
Functional or innocent murmurs…
• Functional or “innocent” murmurs..40-60% of all kids at some time; best heard with bell, grade I or II, no radiation, low to medium pitch, blowing, brief, 2nd L ICS parasternal border, lying down (may disappear when sitting or standing)
Characteristics of the 4 most common heart murmurs—AS, AR, MS, MR
• In general, stenotic valves lead to a state of pressure overload (aortic stenosis, mitral stenosis)—stenotic valves develop slowly over time
• In general, regurgitant valves lead to a state of volume overload; can develop acutely (AMI) or chronically
• Stenotic valves are heart when the valve is normally OPEN—aortic valve is open during systole (ejection) therefore aortic stenosis is a systolic murmur; the mitral valve is open during diastole (filling), hence, mitral stenosis is a diastolic murmur
Listening to heart sounds…
Characteristics of the 4 most common heart murmurs
• Regurgitant valves, also known as incompetent valves, result in a reversal of blood flow—in other words, the murmur is heard when the valve should be CLOSED
• Aortic regurgitation—the aortic valve is closed during the filling of the heart (diastole), hence, aortic regurgitation is heard during diastole
• Mitral regurgitation—the mitral valve is closed TIGHT during systole (ejection), therefore, mitral regurgitation is heard during systole
4 common heart murmurs and the cardiac cycle
S1 __________S2_______________S1____• systole diastole• AS, MR MS, AR
A few more notes…
• Acute aortic or mitral regurgitation can occur with infective endocarditis (any recent dental work?)
• Acute mitral regurgitation from an acute MI (papillary muscle dysfunction)
• No time for compensatory mechanisms to develop causing an acute elevation in pulmonary pressure and acute pulmonary edema
• Tricuspid endocarditis is almost exclusively caused by IV drug abuse
Notes on CHF (HF)
• 500,000 per year; 10% of patients over 70; diabetes is a high risk; categorized as:
• Hemodynamic state of CV system—(congestive vs. high output)
• Predominance of ventricle affected• Predominant form of myocardial dysfunction
(systolic, diastolic)• Time course (acute or chronic)
Causes of HF• Betrayed heart – let down by it’s friends –
(hypertension, coronary artery disease, COPD,, diabetes, thyroid, hemochromatosis)
• Befuddled heart – valvular heart disease• Broken heart – cardiomyopathy (infiltrative
(amyloid, sarcoid); cocaine; “foam” cardiomyopathy (due to the cobalt they used to add to beer to make it foam); thiamine deficiency; chemotherapy (Herceptin, adriamycin/doxorubicin); myocarditis (viruses, expecially Coxsackievirus)
Signs and symptoms of CHF• Palpitations, skin color (pale, cyanotic), weak
pulses, dyspnea (orthopnea), nocturia, PND, (2-3 hours after falling asleep), cough, wheezing
• “funny things happen in the middle of the night” • S3 gallop—early soft diastolic sound, best heard
over apex; use bell, lean patient forward; indicative of abnormal ventricular function in adults
• One-year mortality rate is higher for those with a displaced apical impulse (39% vs. 12%) or a 3rd heart sound (57% vs. 14%)
• The higher the BNP the poorer the prognosis
Treatment of heart failure• Heart failure— “prils” to decrease preload and
afterload• REMEMBER: Heart failure is a hyperreninemic state—
triggering the release of more angiotensin 2 and subsequently her best buddy “AL-dosterone”
• Angiotensin is a potent “REMODELER” of the heart muscle
• RX? Block “Angie” and “Al” with ACE inhibitors; block additional “AL” with spironolactone/Aldactone or eplerenone (Inspra)—improve mortality rates (K+)
• carvedilol (Coreg)—to reduce remodeling (altho’ new studies at the AHA showed that “PRILS” were better
Treatment of heart failure• Loop diuretics; may add thiazide diurectics if resistant
to loops • Sodium restriction• Fluid restriction• Monitor daily weights• Treat acute pulmonary edema with Lasix, morphine,
nitrates, and O2• Hydralazine and nitrates in combiniation with standard
therapy reduce mortality for African Americans and class III and IV CHF
• ICDs for ejection fractions < 35%; biventricluar pacing
Diabetes and heart failure • ARIC study following 15,792 adults recruited
between ages 45 – 64 , living in communities in NC, MN, MD, MS
• Found that diabetes had the strongest association and was responsible for the highest incidence of hospitalization
• A five percent reduction in the incidence of diabetes in adults over age 45 could reduce the number of heart failure cases by 30,000
• September 26, 2012 J Am College of Cardiology
Atrial fibrillation• 3 main treatment concerns—rate control, rhythm
control, prevention of embolic events• Ventricular response to AF controlled with Beta
blockers, calcium channel blockers, or dig• Amiodarone may be considered as an alternative
to beta blockers and calcium channel blockers in patients with low-EF. SIDE EFFECT profile! How about dronedarone (Multaq)
• Cardioversion• Anti-coagulants (discussed previously)
Highlights—atrial fibrillation• New thinking? Why bother with meds? • Ablation trumps meds for atrial fibrillation treatment• Usual conservative method—drugs first—effectively stops
AF in 30% of patients• Catheter ablation is better at 40%• Surgical ablation is better at 90%• Only 40% of patients who undergo catheter ablation are
AF-free after 12 months• Go straight to the surgical ablation
2011 November Annual Meeting of the American Heart Association
Acute coronary syndromes
• Unstable angina (UA), non-STEMI, STEMI• ST segment elevated MI—ruptured plaque in a
coronary artery results in complete occlusion of coronary artery with thrombus, leading to myocardial necrosis of the area supplied Necrosis may occur throughout the entire thickness of the myocardium = pathologic Q waves
• Non-ST segment elevated MI—chest pain, elevated troponin, no ST segment elevations; no pathologic Q waves; UA is related to non-STEMI
Other causes of AMI
• Demand ischemia• Coronary artery dissection• Coronary vasospasm (Prinzmetal’s angina*,
cocaine-induced)• In situ thrombus formation (with hypercoaguable
disorder – lupus, Factor V Leiden)• Coronary embolism• Coronary vasculitis (Kawasaki syndrome)• Carbon monoxide poisoning
Prinzmetal’s (variant) angina• 1959 cardiologist Myron Prinzmetal was the first
to identify a variant form of angina, chest pain caused by a sudden and severe spasm of a coronary artery that obstructs blood flow
• The spasm is reversible and can occur at any time, often unprovoked
• Smoking and hyperventilation are triggers• Slightly more common in women and patients
younger than those with coronary artery disease• Malfunction of the endothelial cells and the
nerves that stimulate the arterial smooth muscle
Clinical findings• The usual suspects with atherosclerosis—(PAD--
pulses, bruits)• S3 may be present; S4 (decreased compliance of
an ischemic myocardium)• Mitral regurgitation (systolic murmur)• Pulmonary edema• ECG in the STEMI—increase in amplitude of T
wave (first minutes after vessel occlusion); ST-segment elevation (minutes to hours); Q waves (hours to days); resolution of ST-segment elevation (hours to days
Chest pain and Electrocardiogram• Q waves in 2 or more leads: previous MI• ST depression > 1 mm: ischemia• ST elevation: AMI or pericarditis (pericarditis often has
involvement of all leads and associated PR depression)• Left bundle branch block suggests underlying heart
disease (ischemic, hypertensive) (new onset? AMI)• Right bundle branch block: may be indicative of right
heart strain: pulmonary embolism• T-wave inversions and nonspecific ST changes: seen in
healthy individuals and in many diseases (not useful)
Troponin• High sensitivity troponin levels at admission and 3
hours later in the ER can rule in or rule out AMI. If troponin levels do not rise above the 99th percentile in 3 hours, the chance of an acute MI is nearly zero.
• Conversely, if troponin levels increase by 200% in 3 hours, the likelihood that a patient has had a heart attack is 96%
• Elevated troponin levels cannot rule out unstable angina—however patients w/ unstable angina need aggressive treatment anyway
• (Keller)
Treatment• O2, ASA (chewed) 162-325 mg• Sublingual NTG (0.4 mg every 5 minutes x 3)• (unless hypotensive) and if NO ED drugs• IV nitrates for persistent pain • IV morphine or fentanyl to reduce pain and decrease
pain-induced sympathetic drive (also lowers cardiac workload)
• IV beta blocker to control heart rate (with adequate BP and heart rate) (more contraindications
• Thrombolytic therapy—streptokinase, alteplase, tenecteplase (single infusion) reteplace
Contraindications to thrombolytic therapy
• Previous intracranial hemorrhage• Significant closed head injury in past 3 months• Stroke within 1 year• Intracranial neoplasm• Aortic dissection• Active bleeding (excluding menses)
Percutaneous Coronary Intervention
• Patients with NSTEMI and benefit from glycoprotein Iib/IIIa inhibitors prior to PCI (abciximab/Reopro;
• PCI –percutaneous coronary intervention for acute MI (1977)—most frequently performed therapeutic procedure in medicine; 500,000 per year; within 90 minutse of presentation
• Drug eluting stent releasing everolimus or zatarolimus• Followed by dual anti-platelet therapy (pasugrel/Effient and
ticagrelor/Brilinta are more potent than clopidogrel/Plavix)• CABG for multi-vessel disease and greater complexity
Stefanni G, Holmes R. Drug-Eluting Coronary Artery Stents; N Engl J Med 2013;368 (3):254-66)
And finally, what can YOU do to prevent heart disease?
• Stop smoking• Exercise• Lose weight, especially around your belly• Lower your blood sugars• Sleep (sleep apnea also increases the risk)• EAT RIGHT• Say YES to drugs!
Bibliography• Dornelas EA, Sampson RA, Gray JF, Waters D, Thompson PD. A
randomized controlled trial of smoking cessation counseling after myocardial infarction. Prev Med.2000;30:261-268.
• Edwards M, et al. Relationship between pain severity and outcomes in patients presenting with potential ACS Ann Emerg Med 2011 Dec.; 58:501
• Keller T et al. Serial changes I highly sensitive troponin I assay and early diagnosis of MI. JAMA 2011 Dec 28;306: 2681)
• Levine G. Cardiology Secrets. Mosby. 2010• McGee S. Evidence-Based Physical Diagnosis. WB Saunders, Co.
2001• Young VB et al. Medicine Blueprints. Wolters Kluwer. 2010
