Coronary Heart

Disease

M Chadi Alraies M.D.

M Chadi Alraies 1
 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.

M Chadi Alraies 2
 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. M Chadi Alraies 3
 The estimated cost for cardiovascular
disease in 1994 by the American
Heart Association is 128 billion
dollars.

M Chadi Alraies 4
 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
M Chadistenosis,
Alraies with a 5
 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

M Chadi Alraies 6
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.
M Chadi Alraies 7
 What is the
number one
preventable cause
of cardiovascular
disease worldwide?
SMOKING!
M Chadi Alraies 8
 1 year after
quitting, the risk of
coronary heart
disease decreases
by 50%
M Chadi Alraies 9
Framingham
score

M Chadi Alraies 10
M Chadi Alraies 11
Women Men

M Chadi Alraies 12
Define the
metabolic
syndrome?

M Chadi Alraies 13
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.

M Chadi Alraies 14
 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

M Chadi Alraies 15
 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 M Chadi Alraies 16

Pathophysiology

M Chadi Alraies 17
Lipid metabolism in relation
to formation of
atherosclerotic lesions

M Chadi Alraies 18
Formation of a fatty streak in
an artery

M Chadi Alraies 19
Formation of atheroma

M Chadi Alraies 20
 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

M Chadi Alraies 21
 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. M Chadi Alraies 22
Plaque rupture

M Chadi Alraies 23
 Screening and Diagnosis

me me show s
as asu
ur res
es

c
ifi
od

ec

coronaries
sp
ele ctrical

Electro- blo Stress Coronary

cardiogram Test Angiography

ar t

Si t
he

es
es su

of
to
l s pp
pu ly
Narrow i
ng in
im

M Chadi Alraies 24
 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 embolusM Chadi Alraies 25
 Primary &
Secondary
Prevention of
Coronary Heart
Disease
M Chadi Alraies 26
 AHA/ACC
Secondary
Prevention for
Patients With
Coronary and
Other Vascular
Disease
2006 Update
M Chadi Alraies 27
M Chadi Alraies 28
 Coronary and Other
Vascular Disease
 Established coronary disease.
 Atherosclerotic vascular disease:
 Peripheral arterial disease,
 Atherosclerotic aortic disease, and

 Carotid artery disease.

M Chadi Alraies 29
 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 ofM Chadi
exposure
Alraies
to 30
 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
M Chadi Alraies message to the patient 31
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-
M Chadi Alraies 32
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

M Chadi Alraies 33
 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 M Chadi Alraies 34
 LIPID
MANAGEMENT

M Chadi Alraies 35
 LDL
“The lower the better”

M Chadi Alraies 36
 HDL
“The higher the better”

M Chadi Alraies 37
 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.
M Chadi Alraies 38
 LIPID MANAGEMENT
 Assess fasting lipid profile in all
patients, and within 24 hours of
hospitalization for those with an
acute cardiovascular or coronary
event.

M Chadi Alraies 39
 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. M Chadi Alraies 40
 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.
M Chadi Alraies 41
 (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"
M Chadi Alraies 42
 (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.

M Chadi Alraies 43
 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.
M Chadi Alraies 44
 Treatment of low HDL
 Niacin in high dosages (2–3 g/d or
more)
 Gemfibrozil (600 mg twice daily)

M Chadi Alraies 45
 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 Mtherapy

Chadi Alraies
should be prescribed at 46
discharge?
 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.
M Chadi Alraies 47
 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.

M Chadi Alraies 48
 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.
M Chadi Alraies 49
 DIABETES MANAGEMENT
 Goal: HbA1c <7%

M Chadi Alraies 50
 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.

M Chadi Alraies 51
 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.
M Chadi Alraies 52
 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.
M Chadi Alraies 53
 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 testingM Chadi Alraies 54
 RENIN-ANGIOTENSIN-
ALDOSTERONE SYSTEM
BLOCKERS

M Chadi Alraies 55
 ACE inhibitors
 Start and continue indefinitely in all
patients with…
 LV EF 40%.
 HTN,

 DM

 Chronic kidney disease.

M Chadi Alraies 56
 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.

M Chadi Alraies 57
 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?
3. Valsartan
4. Spironolactone M Chadi Alraies 58
 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.

M Chadi Alraies 59
 ß-BLOCKERS
 Myocardial infarction,
 Acute coronary syndrome,
 LV dysfunction
 Vascular disease
 Diabetes

M Chadi Alraies 60
 INFLUENZA VACCINATION
 Patients with cardiovascular disease
should have an influenza vaccination.

M Chadi Alraies 61
 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.

M Chadi Alraies 62
 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.

M Chadi Alraies 63
 Hormone replacement
therapy HRT
 In HERS trial, neither combined
estrogen–progesterone nor estrogen
alone therapy is protective (in fact
both cause harm).

M Chadi Alraies 64
 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.

M Chadi Alraies 65
 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
M Chadi Alraies 66
 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.

M Chadi Alraies 67
 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.
M Chadi Alraies 68
 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.

M Chadi Alraies 69
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.
M Chadi Alraies 70
 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.
M Chadi Alraies 71
 Myocardial Hibernation &
Stunning
 A related phenomenon, termed
"myocardial stunning," is the
occurrence of persistent contractile
dysfunction following prolonged or
repetitive episodes of myocardial
ischemia.

M Chadi Alraies 72