Coronary Heart

Disease

M Chadi Alraies M.D.

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The main reason to invest in prevention
is to promote health and extend life,
improve functioning and prevent
suffering.

 "The Role of Prevention in Health Reform", Russell,

Louise B., Ph.D., The New England Journal of Medicine,
July 29, 1993;329 (5):352-354.

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 General considerations
 number one killer in the
United States and
worldwide.
 Every minute, an
American dies of
coronary heart disease.
 Coronary heart disease
afflicts over 13 million
Americans.

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 The estimated cost for cardiovascular disease
in 1994 by the American Heart Association is
128 billion dollars.

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 An 82-year-old woman presents for her annual examination. She has
hypertension and is on chronic β-blocker therapy. She denies all
cardiac symptoms. She takes a daily 1-mile walk, and her exercise
tolerance has not changed during the past year.
 Physical examination shows a blood pressure of 138/86 mm Hg, a
regular pulse of 80/min, and a respiratory rate of 16/min. Her jugular
venous pressure is 10 cm H2O, her carotid upstrokes are normal,
and her lungs are clear. Cardiac examination reveals a normal S1, a
single S2, and a grade 3/6 early systolic murmur at the upper left
sternal border that radiates to her carotids. Abdominal examination
is benign, and there is 1+ peripheral edema. Laboratory data are
remarkable for a total cholesterol of 210 mg/dL (5.43 mmol/L), with
an LDL cholesterol of 110 mg/dL (2.84 mmol/L).
 Her echocardiogram from 2 years ago showed moderate calcific
aortic stenosis, with a maximum aortic velocity of 3.6 m/s (normal,
<1.5 m/s) a mean gradient of 30 mm Hg (normal, <5 mm Hg) and a
valve area of 1.2 cm2 (normal, >2 cm2) with normal left ventricular
systolic function. Echocardiography now shows a maximum aortic
jet velocity of 4.2 m/s, mean gradient of 44 mm Hg, and a valve area
of 1.0 cm2.

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 Which is the most appropriate next step?
 A Reassurance
 B Begin a cardiac rehabilitation program

 C Begin hydrochlorothiazide

 D Start statin therapy

 E Refer for aortic valve replacement

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 Risk factors
Abnormal lipids
Smoking
Hypertension
Diabetes mellitus
Abdominal obesity
Psychosocial factors
Consumption of too few fruits
and vegetables.
Too much alcohol
Lack of regular physical activity.

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What is the number one
preventable cause of
cardiovascular disease
worldwide?

SMOKING!
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1 year after quitting, the
risk of coronary heart
disease decreases by 50%

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Framingham score

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Women Men

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Define the metabolic
syndrome?

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 The metabolic syndrome
 Three or more of the following:
 Abdominal obesity
 Triglycerides 150 mg/dL

 HDL cholesterol < 40 mg/dL for men and < 50

mg/dL for women
 Fasting glucose 110 mg/dL

 Hypertension.

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 Obesity
 BMI = or > 30 kg/m2
 33% of the adult population in the 2003–2004
survey.
 Low-fat diets appear to be at least as effective
as other diets for weight loss

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 A 72-year-old woman is seen for a routine office evaluation to
establish care. Past medical history includes only hypertension,
hyperlipidemia, and a familial history of coronary artery
disease. She does not smoke. She is active and walks daily and
denies angina, dyspnea, fatigue, and edema.
 Physical examination reveals a blood pressure of 128/70 mm
Hg. There are no carotid bruits. There is a normal S1 and a
physiologically split S2. There is a grade 2/6 midsystolic
murmur that does not radiate and is best heard at the 2nd right
intercostal space. The rest of the physical examination is
unrevealing.
 Which of the following diagnostic tests is most appropriate at
this time?
 A No further testing at this time
 B Transthoracic echocardiography
 C Electron-beam CT
 D Treadmill stress echocardiogram
 E 24-hour ambulatory electrocardiographic monitoring
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Pathophysiology

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 Lipid metabolism in relation to
formation of atherosclerotic lesions

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Formation of a fatty streak in an artery

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Formation of atheroma

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 Plaque rupture
 Many atherosclerotic plaques remain stable or
progress only gradually.
 Rupture, often related to the inflammatory
process.
 The rupture causes…
 Turbulent flow
 Extrusion of lipids and fatty gruel

 Exposure of tissue factor

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 Plaque rupture
 All result in a cascade of events culminating in
intravascular thrombosis.
 The outcome of these events is…
 Complete vessel occlusion.
 Partial vessel occlusion (causing the symptoms of unstable
angina or myocardial infarction)
 Restabilization often with more severe stenosis.
 Transient occlusion and/or embolization of platelet
and thrombin debris, which may result in elevation in
serum troponin, predispose to clinical events and
portend a worse prognosis.
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Plaque rupture

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 Screening and Diagnosis

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 A 22-year-old women who is 16 weeks pregnant is evaluated
for a 2-hour history of severe anterior chest pain radiating to her
mid back. She is a tall, thin woman with a pectus abnormality of
her chest and long, thin fingers. Her blood pressure is 140/80
mm Hg, her pulse is 94/min and regular, and her respiratory rate
is 24/min. Her chest wall is diffusely mildly tender to palpation.
Her lungs are clear to auscultation. Cardiac auscultation shows a
normal S1, a physiologically split S2, and a grade 2/6 diastolic
decrescendo murmur at the left sternal border. There is no
peripheral edema. Her electrocardiogram shows only
nonspecific ST-T changes. Oxygen saturation by pulse oximetry
on room air is 99%. Her D-dimer level is mildly elevated.
 Which is the most likely cause of her chest pain?
 A Pulmonary embolus
 B Acute myocardial infarction
 C Aortic dissection
 D Costochondritis
 E Pericarditis
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 Primary & Secondary
Prevention of Coronary
Heart Disease

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AHA/ACC Secondary
Prevention for Patients
With Coronary and
Other Vascular Disease
2006 Update

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 Coronary and Other Vascular
Disease
 Established coronary disease.
 Atherosclerotic vascular disease:
 Peripheral arterial disease,
 Atherosclerotic aortic disease, and

 Carotid artery disease.

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 SMOKING
 Goal: Complete cessation. No exposure to
environmental tobacco smoke.
 Ask about tobacco use status at every visit.
 Advise every tobacco user to quit.
 Assess the tobacco user’s willingness to quit.
 Assist by counseling and developing a plan for quitting.
 Arrange follow-up, referral to special programs, or
pharmacotherapy (including nicotine replacement and
bupropion).
 Urge avoidance of exposure to environmental tobacco
smoke at work and home.

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 A 55-year-old man is evaluated for cough, scant clear-to-
yellow sputum, and malaise of 3 days' duration. He has not
had fever, chills, wheezing, or pleuritic chest pain, or recent
contact with anyone who has been ill. He has a 40-pack-year
smoking history and has had similar symptoms three times in
the past 6 months, feeling well in the intervals between
episodes.
 On physical examination, temperature is 37.2 °C (99.0 °F),
and pulse rate, respiration rate, and blood pressure are normal.
The cardiopulmonary examination is normal, including clear
lungs on auscultation with no signs of consolidation.
 Which of the following is the most appropriate initial
smoking-cessation management step during this visit?

 A Recommend nicotine gum

 B Provide a clear, personalized message to the patient
 C Refer the patient to a behavioral-modification program
 D Prescribe bupropion
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 BLOOD PRESSURE CONTROL
 Goal: For patients with blood pressure
140/90 mm Hg (or 130/80 mm Hg for
individuals with chronic kidney disease or
diabetes.
 Initiate or maintain lifestyle modification—
weight control; increased physical activity;
alcohol moderation; sodium reduction; and
emphasis on increased consumption of fresh
fruits, vegetables, and low-fat dairy products.

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 BLOOD PRESSURE CONTROL
 Add blood pressure medication,
 Treating initially with ß-blockers and/or ACE
inhibitors.
 Addition of other drugs such as thiazides as
needed to achieve goal blood pressure .
 Use JNC 7

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 A 55-year-old man is evaluated for epigastric discomfort that
has been increasing in frequency despite the use of antacids.
The discomfort occurs with exercise, but at times he is able to
exercise without provocation of his symptoms. He has no
other medical conditions and takes only an 81-mg aspirin daily
and occasional chondroitin sulfate for joint aches.
 Physical examination, including vital signs and cardiac
examination, is normal. Electrocardiogram shows normal
sinus rhythm with normal waveforms. Lipid tests show total
cholesterol of 199 mg/dL (5.15 mmol/L), LDL cholesterol of
131 mg/dL (3.39 mmol/L), and HDL cholesterol of 35 mg/dL
(0.91 mmol/L).
 What is the most appropriate next step in the evaluation of this
patient?
 A Measurement of C-reactive protein
 B Measurement of coronary calcium by electron-beam CT
 C Measurement of serum homocysteine
 D Exercise electrocardiographic stress test
 E Exercise echocardiogram
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 LIPID
MANAGEMENT

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 LDL
“The lower the better”

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 HDL
“The higher the better”

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 LIPID MANAGEMENT
1. Start dietary therapy.
2. Reduce intake of saturated fats (to <7% of total
calories),
3. Cholesterol (to <200 mg/d).
4. LDL-C <100 mg/dL
5. non-HDL-C should be <130 mg/dL    
6. Adding plant stanol/sterols (2 g/d) and viscous fiber
(>10 g/d) will further lower LDL-C.    
7. Encourage increased consumption of omega-3 fatty
acids in the form of fish or in capsule form (1 g/d)
for risk reduction.

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 LIPID MANAGEMENT
 Assess fasting lipid profile in all patients, and
within 24 hours of hospitalization for those
with an acute cardiovascular or coronary
event.

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 LIPID MANAGEMENT
 For hospitalized patients, initiate lipid-lowering medication as
recommended below before discharge according to the
following schedule:    
 LDL-C should be <100 mg/dL and…
 Further reduction of LDL-C to <70 mg/dL is reasonable.
 If baseline LDL-C is 100 mg/dL, initiate LDL-lowering drug therapy.
 If on-treatment LDL-C is 100 mg/dL, intensify LDL-lowering drug
therapy (may require LDL-lowering drug combination.
 If baseline LDL-C is 70 to 100 mg/dL, it is reasonable to treat to LDL-
C <70 mg/dL.
 If triglycerides are 200 to 499 mg/dL, non-HDL-C should be <130
mg/dL. And…
 Further reduction of non-HDL-C to <100 mg/dL is reasonable.

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 LIPID MANAGEMENT
 Therapeutic options to reduce non-HDL:
 More intense LDL-C–lowering therapy
 Niacin or   

 Fibrate therapy

 If triglycerides are 500 mg/dL, therapeutic

options to prevent pancreatitis are fibrate or
niacin before LDL-lowering therapy.

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 (HMG-CoA) reductase inhibitors (statins)

 Aggressive LDL lowering is associated with

greater benefits.
 The Heart Protection Study (HPS), simvastatin 40
mg a day reduces vascular events by more than 20%.
 The PROVE-IT trial showed that vascular events
were reduced with more aggressive lipid lowering
(atorvastatin 80 mg/d compared to pravastatin 40
mg/d following an acute coronary syndrome),
providing more evidence of "lower is better"
 The TNT (Treating to New Targets)

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 (HMG-CoA) reductase inhibitors (statins)

 Although true regression of plaque is

uncommon even with intensive lipid therapy
(as in the REVERSAL and ASTEROID trials),
progression can be prevented at least in the
short run in many patients.

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 HDL
 Has been shown to be Cardioprotective in the
Framingham Heart Study, and in retrospective
analyses of intervention trials such as the
Coronary Primary Prevention Trial and the
Multiple Risk Factor Intervention Trial 5-7

 The data were consistent with a 2% to 3%

decrease in CHD risk for each 1 mg/dL
increase in HDL, after adjustment to control for
other risk factors.

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 Treatment of low HDL
 Niacin in high dosages (2–3 g/d or more)
 Gemfibrozil (600 mg twice daily)

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 A 32-year-old woman is brought to the hospital with chest pain at rest after
a party. She has had similar pain previously, primarily in the morning and
rarely with exertion. The pain usually subsides spontaneously and
occasionally is associated with diaphoresis but rarely dyspnea. She almost
lost consciousness at work during the most recent episode. She smokes a
half pack of cigarettes a week and has occasionally inhaled cocaine. She is
otherwise healthy and takes no medications. She has no family history of
coronary artery disease.
 Her blood pressure is 128/70 mm Hg and pulse rate is 72/min. There is no
neck vein distention or carotid bruits. The lungs are clear and cardiac
examination reveals a normal S1 and S2 and a faint mid-systolic click but
no murmur. Examination of the abdomen and extremities is normal.
Electrocardiogram shows a 1-mV inferior ST-segment elevation; a
subsequent electrocardiogram is normal. Serum troponin concentration is
1.5 times the upper limit of normal. Therapy with heparin, aspirin,
metoprolol, and nitroglycerin is begun. The next morning, coronary
angiography shows normal angiographic appearance of the arteries and
normal left ventricular wall motion. The patient is prescribed a daily
aspirin and encouraged to stop using cocaine.

 What additional medical therapy should be prescribed at discharge?

 A Angiotensin-converting enzyme inhibitor
 B β-blocker
 C Calcium-channel blocker
 D Clopidogrel
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 ACTIVITY
 Encourage 30 to 60 minutes of moderate-
intensity aerobic activity, such as brisk
walking all days of the week (5 days is
acceptable).
 Supplemented by an increase in daily lifestyle
activities (eg, walking breaks at work,
gardening, household work).
 Encourage resistance training 2 days per week.

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 WEIGHT MANAGEMENT
 Assess body mass index and/or waist
circumference on each visit and consistently.
 Encourage weight maintenance/reduction
through an appropriate balance of physical
activity, caloric intake.

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 WEIGHT MANAGEMENT
 Maintain/achieve…
 A BMI (18.5 - 24.9)
 Waist circumference: men <40 inches, women <35
inches.
 The initial goal of weight loss therapy should
be to reduce body weight by approximately
10% from baseline. With success, further
weight loss can be attempted if indicated
through further assessment.

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 DIABETES MANAGEMENT
 Goal: HbA1c <7%

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 ANTIPLATELET AGENTS/
ANTICOAGULANTS
 Start aspirin 75 to 162 mg/d unless
contraindicated.
 For patients undergoing CABG, aspirin should
be started within 48 hours after surgery.
 Doses higher than 162 mg/d can be continued
for up to 1 year.

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 ANTIPLATELET AGENTS/
ANTICOAGULANTS
 Start and continue clopidogrel 75 mg/d in
combination with aspirin for up to 12 months
in patients after:
 ACS, PCI with stent placement
 Patients who have undergone percutaneous
coronary intervention with stent placement
should initially receive higher-dose aspirin at
325 mg/d for 1 month for bare metal.

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 ANTIPLATELET AGENTS/
ANTICOAGULANTS
 Manage warfarin to international normalized
ratio=2.0 to 3.0 for paroxysmal or chronic
atrial fibrillation or flutter
 Use of warfarin in conjunction with aspirin
and/or clopidogrel is associated with increased
risk of bleeding and should be monitored
closely.

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 A 68-year-old man recently diagnosed with adenocarcinoma of the cecum
undergoes preoperative evaluation before surgical resection. His medical
history includes inoperable coronary artery disease, heart failure with a left
ventricular ejection fraction (LVEF) of 35%, hypertension, and
hyperlipidemia. Angina is stable, occurring approximately monthly, and he
has no orthopnea or paroxysmal nocturnal dyspnea. Medications include
lisinopril, carvedilol, furosemide, simvastatin, and daily aspirin. He plays
golf weekly, using a cart, walks 2 miles three to four times weekly, and
carries groceries up a flight of stairs to his apartment.
 On physical examination, the pulse rate is 64/min, and blood pressure is
120/64 mm Hg. Jugular venous pressure is 6 cm. On cardiopulmonary
examination, the lungs are clear to auscultation, and the heart is regular
without an S3. There is no peripheral edema. Laboratory studies, including
complete blood count, serum electrolyte levels, and renal function, are
normal. The electrocardiogram is unchanged, with a normal sinus rhythm
and evidence of an old inferior infarction.
 Which of the following is the most appropriate next step in the
preoperative evaluation of this patient?
 A Plasma B-type natriuretic peptide measurement
 B Echocardiography
 C Exercise stress testing
 D Nuclear imaging for LVEF
 E No further evaluation

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 RENIN-ANGIOTENSIN-
ALDOSTERONE SYSTEM
BLOCKERS

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 ACE inhibitors
 Start and continue indefinitely in all patients
with…
 LV EF 40%.
 HTN,

 DM

 Chronic kidney disease.

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 Angiotensin receptor blockers
 Intolerance of ACE inhibitors
 Heart failure
 Myocardial infarction with left ventricular
ejection fraction 40%.
 Consider use in combination with ACE
inhibitors in systolic-dysfunction heart failure.

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 A 55-year-old man with coronary artery disease is evaluated 2
weeks after having had a myocardial infarction. On discharge, his
medications included aspirin, sustained-release metoprolol,
isosorbide mononitrate, lisinopril, and atorvastatin.
Echocardiogram at that time showed inferior and posterior wall
akinesis and a left ventricular ejection fraction of 40%. On
examination, his heart rate is 60/min and his blood pressure is
130/70 mm Hg. Jugular venous pressure is normal and the chest is
clear. Cardiac rhythm is regular, with normal S1 and S2 and no
murmurs or extra heart sounds. Laboratory results from yesterday
are potassium 5.7 meq/L (5.7 mmol/L), creatinine 1.0 mg/dL
(88.42 µmol/L), and LDL cholesterol 65 mg/dL (1.68 mmol/L).
Lisinopril therapy is stopped.
 Wich of the following medications should be started in this patient?
1. Valsartan
2. Spironolactone
3. Amlodipine
4. Eplerenone
5. Hydralazine

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 Aldosterone blockade
 Use in post–myocardial infarction patients,
without…
 Significant renal dysfunction or
 Hyperkalemia

 Already receiving therapeutic doses of an ACEI

and BB.
 Left ventricular ejection fraction 40%

 Diabetes or heart failure.

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 ß-BLOCKERS
 Myocardial infarction,
 Acute coronary syndrome,
 LV dysfunction
 Vascular disease
 Diabetes

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 INFLUENZA VACCINATION
 Patients with cardiovascular disease should
have an influenza vaccination.

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 Antioxidant
 (HOPE) trial found that vitamin E may even
be harmful by increasing the likelihood of
heart failure and other trials have suggested
that vitamin E may hinder the effectiveness of
statin therapy.

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Elevated plasma homocysteine levels
 Associated with an increased risk of vascular
events.
 Reduced with dietary supplements of folic acid
(1 mg/d) in combination with vitamin B6 and
vitamin B12.
 RCT showed they are of little or no value in
preventing vascular events.

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Hormone replacement therapy HRT
 In HERS trial, neither combined estrogen–
progesterone nor estrogen alone therapy is
protective (in fact both cause harm).

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 Fish oil
 Fish, rich in omega-3 fatty acids, may help
protect against vascular disease, and it is
recommended that it be eaten three times a
week by patients at risk.

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 A 35-year-old man is evaluated during a routine examination.
He does not smoke and has no family history of early coronary
artery disease.
 On examination, BMI is 35.2, and waist circumference is 114
cm (45 in). Blood pressure is 142/88 mm Hg. The remainder
of the physical examination is normal. Laboratory studies
indicate borderline hyperglycemia (fasting plasma glucose,
121 mg/dL [6.7 mmol/L]). Serum total cholesterol level is 246
mg/dL (6.36 mmol/L), high-density lipoprotein level is 31
mg/dL (0.8 mmol/L), and low-density lipoprotein level is 158
mg/dL (4.05 mmol/L).
 Which of the following recommendations is most appropriate
for this patient?
 A Electron-beam CT
 B Exercise treadmill test
 C Hydrochlorothiazide
 D Intensive lifestyle modification
 E Intake of red wine
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Pathophysiology of Chronic Ischemia
& Acute Coronary Syndromes

 Chronic ischemia, including stable angina, is

classically caused by supply and demand
mismatch.
 Precipitants include exercise, eating, cold
weather, and emotional stress.

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Pathophysiology of Chronic Ischemia
& Acute Coronary Syndromes
 ACS of unstable angina and MI caused by:
 Plaque disruption
 Platelet and thrombin-mediated coronary
thrombosis
 Coronary spasm

 Microvascular dysfunction.

 These episodes occur in the early morning or

shortly after arising.

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Pathophysiology of Chronic Ischemia
& Acute Coronary Syndromes
 Antithrombotic therapy is directed toward
inhibition of platelet activity (aspirin,
clopidogrel, IIb/IIIa receptor antagonists),
inhibition of coagulation (unfractionated or
low-molecular-weight heparin), and
fibrinolysis for ST-segment elevation
myocardial infarction.

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 Types & Pathophysiology of
myocardial ischemia presentation

 Symptomatic, causing angina pectoris.

 Completely silent.
 In patients with diagnosed CAD silent
ischemic episodes have the same prognostic
import as symptomatic ones.

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 Myocardial Hibernation &
Stunning
 Areas of myocardium that are persistently
underperfused.
 Still viable
 May develop sustained contractile dysfunction.
 May lead to LV failure.
 Reversible following coronary revascularization.
 Identified by
 Radionuclide testing, (PET), MRI,
 Inotropic stimulation with dobutamine.

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 Myocardial Hibernation &
Stunning
 A related phenomenon, termed "myocardial
stunning," is the occurrence of persistent
contractile dysfunction following prolonged or
repetitive episodes of myocardial ischemia.

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