CAD

Coronary Artery Disease /

Coronary Atherosclerotic Heart Disease

Yang HaiBo MD
Department of cardiology,
1st affiliated hospital of ZZU
types of CAD
asymptomatic ischemia
angina pectoris
myocardial infarction
ischemic cardiomyopathy
sudden cardiac death
 Stable angina pectoris

Angina Pectoris
(AP)
Unstable angina pectoris
(UAP)

ST segment Elevation Acute Coronary

Myocardial Myocardial Infarction Syndrome( ACS)
Infarction (STEMI)

(MI) Non-ST segment

Elevation Myocardial
Infarction (NSTEMI)
stable
AP
epidemiology of ischemic heart disease

*6,750,000 Americans with angina pectoris

*350,000 new cases occur each year

*prevalence of angina pectoris in elderly
men : 21.1% (65 ~ 69 yrs) to 27.3% (80 ~ 84 yrs)
women : 13.7% (65 ~ 69 yrs) and 24.7%(≥85 yrs).
Etiology of ischemic heart disease
*Atherosclerosis :the most common cause
*Coronary spasm
*Coronary thrombi
*Coronary emboli
*Ventricular hypertrophy
*Aortic stenosis
*Oxygen-carrying capacity ↓:carboxyhemoglobin 、
anemia
*…….
Pathophysiology of ischemic heart disease

Could relax correspond to the demand↑ of oxygen

oxygen supply / demand balance maintained

Fixed when the oxygen demand increased→

imbalance between myocardium oxygen supply/demand→
symptoms and signs of ischemia
Pathophysiology of ischemic heart disease

cardiac ischemic pain arise from sensory afferents

located in the coronary vessels and myocardium
sensitive to stretch and irritation by local noxious chemical stimuli
Pathophysiology of ischemic heart disease

provoking factors alleviating factors

mental stress ↑ preload ↓

physical stress constriction periferal artery relax
cold air ↑ myocardium contractivity ↓
lying down ↑ heart rate ↓
↑ BP ↓
↓ supply angina Angina relief supply ↑

↑ demand Oxygen demand=BPs×HR demand ↓

Symptom
angina pectoris
angina pectoris(AP)
Definition
a syndrome
due to transient myocardial ischemia,
characterized by chest discomfort,
radiate to the back, neck, jaw,teeth& epigastrium,
usually caused by exertion & emotion ,
last several minutes
and relieved by rest or nitrates,
mostly the etiology is CAD
◆ character
◆ location and duration
◆ provoking or exacerbating factors

◆ alleviating factors
 First Description of Angina
Those who are afflicted with it are seized while they are
walking (more especially if it be uphill, and soon after
eating), with a painful and most disagreeable
sensation in the breast, which seems as if it would
extinguish life, if it were to increase or to continue; but
the moment they stand still, all this uneasiness
vanishes.This elegant description by William Heberden
first published 225 years ago eloquently captures the
symptomatic characteristics of angina pectoris. It is a
common and important symptom affecting many patients
with coronary artery disease.
Heberden W. Classics of Cardiology. Dover Publications, 1941; I:221.
Angina is unpleasant sensation,
usually not pain
The unpleasant sensation is more typically
characterized as a pressure or tightness,
a heaviness 、 squeezing or burning
Most patients with true angina do not use
this term to describe their sensation.
The pressure is not perceived by the patient
as pain such that the interviewer who
specifically asks about pain may be misled
CHARACTERISTICS OF TYPICAL AND
ATYPICAL ANGINA PECTORIS
Typical
• Substernal ,Characterized by a heavy, squeezing or burning
feeling
• Precipitated by exertion or emotion
• Promptly relieved by rest or nitroglycerin
Atypical
• Located in the left chest, abdomen, back, or arm in the absence
of mid-chest pain
• Sharp or fleeting
• Repeated, very prolonged
• Unrelated to exercise
• Not relieved by rest or nitroglycerin
• Relieved by antacids
• Characterized by palpitations without chest pain.
 The usual distribution is referral to all or part of the sternal
region, the left side of the chest, and the neck and down the ulnar
side of the left forearm and hand. With severe ischemic pain, the
right chest and right arm are often involved as well, although
isolated involvement of these areas is rare. Other sites sometimes
involved, either alone or together with other sites, are the jaw,
epigastrium, and back.
Provoking &Exacerbating
Factors
Classic Precipitation: exercise &
emotional stress
Other Precipitants: high pressure meeting
stressful emotional incident
cold weather activity
heavy meals
lying down (at times )←venous return↑
Alleviating Factors
*Cessation of activity
*Sublingual nitroglycerin--nonspecific
*Getting out of the cold
*Completing the uphill walk
In Summary :cessation
that increase cardiacofoxygen
a factor
demand
 Signs during Angina
*Softening of the S1- result of ischemic left ventricular
dysfunction

*Paradoxical splitting of the S2-related to

asynergy and prolongation of left ventricular contraction results in
delayed closure of the aortic valve

*S3 & S4-result of ischemic left ventricular dysfunction

*Transient apical systolic murmurs-
attributed to reversible papillary muscle dysfunction secondary to
transient myocardial ischemia
Diagnostic Tests
X-ray
ECG
Echocardiography
Nuclear imaging techniques
Coronary angiography(CAG)
Diagnostic Tests:X-ray

Usually normal
……
Diagnostic Tests:ECG
Rest ECG
Captured during an episode
Exercise ECG
Ambulatory Holter monitoring
 Diagnostic Tests: Rest ECG
ECG at rest may commonly be normal in pts with AP.
In the Rochester, Minnesota, area, 59% of the 1154 individuals presenting with
chest pain were found to have normal resting ECGs (Mayo Clin Proc 1984; 59:247)

Useful to seek evidence of prior MI and persisting

ST↓, which portending an unfavourable prognosis
T-wave change, intraventricular conduction defects, and
atrial abnormalities may also be evident
 Diagnostic Tests :
ECG captured during an episode
Transient ischemic ST segment depression
T wave inversion
T wave pseudonormalization
ST segment elevation: Variant angina
Diagnostic Tests:Exercise ECG

TREADMILL STATIONARY BIKE

Diagnostic Tests:Exercise ECG
Cornerstone of diagnostic testing for SAP
It should be performed prior to moving toward more detailed, costly or
invasive procedures

There are at least four important potential objectives that may be

achieved by conducting this test:
Correlation of patient symptoms with the presence of ischemia
Definition of risk of future events
To provide the patient with an exercise prescription
To evaluate the efficacy of pharmacologic & revascularization therapy
Diagnostic Tests:Exercise ECG
Indications:
To determine the likelihood of coronary disease
To assess the likelihood of anatomic or functionally severe
disease that may be of prognostic importance
To determine functional capacity
To assess the effects of therapy
Diagnostic Tests:Exercise ECG
Clinical Contraindications:(to be continued)
Acute myocardial infarction
Unstable angina prior to a period of stabilization
Uncompensated severe CHF
Advanced AVB or life threatening arrhythmias
Acute myocarditis or pericarditis
Severe aortic stenosis
Severe resting hypertension& any medical condition that
precludes the patient from being able to walk safely on the
treadmill
Diagnostic Tests:Exercise ECG
Clinical contraindications:(continued)
Left bundle branch block
Left ventricular hypertrophy with strain
Ventricular preexcitation (WPW syndrome)
Permanent ventricular pacing on the ECG
(due to the uncertain diagnostic value of additional ST segment
changes in these settings, but do not preclude use of the ETT to
assess exercise performance or evaluate the risk of arrhythmia
when indicated)
Diagnostic Tests:Exercise ECG
Criteria:
Point : 60ms after J point

Criteria : >0.1mV ST depression

 ST
ST

Slowly upsloping Downsloping

specific
STSegment
Depression
ST

Horizontal
Diagnostic Tests:Echocardiography
Left ventricular (LV) evaluation is
probably the single most important
*overall systolic function
*regional wall motion
*ventricular mass
*geometry
Diagnostic Tests:Exercise ECT
Nuclear imaging techniques

transverse

sagittal

coronal

TL201 SPECT stress & delayed images

 Exercise perfusion imaging incorporates all the components
of the exercise ECG with images of myocardial blood flow by
using either thallium-201 or a technetium-99m (99m Tc)-based
perfusion tracer. The radionuclide is injected intravenously at
peak exercise or at a symptom-limited endpoint, patient is
encouraged to exercise for another 30 to 45 seconds to ensure
that initial myocardial uptake of the tracer reflects the
perfusion pattern at peak stress.
Acquisition of the stress images is performed several
minutes later when the patient is at rest. A separate image
acquisition is obtained at rest to compare the stress images
with images of resting perfusion. Reversible perfusion defects
between stress and rest indicate exercise-induced ischemia,
whereas irreversible defects usually represent regions of
myocardial fibrosis
Diagnostic Tests: CAG
coronary angiography : gold criteria
Differential Diagnosis
Causes of chest discomfort and pain
Cardiac Noncardiac
Angina Esophagitis, esophageal spasm, or reflex
Acute myocardial Peptic ulcer
infarction
Aortic dissection Gall bladder disease
Pericarditis Musculoskeletal including
osteochondritis
cervical disc, thoracic outlet syndrome
Myocarditis Hyperventilation
Anxiety
Psychogenic
Mitral valve Pneumonia
prolapse Pulmonary embolus
Pneumothorax
Pulmonary hypertension
The key
to determining
whether the discomfort is cardiac is
to review its:
◆ character
◆ location and duration
◆ provoking or exacerbating factors, and
◆ alleviating factors
Diagnosis
Angina Grades
Canadian Cardiovascular Society grading scale
Class I experience angina only with strenuous or
protracted physical activity
Class II experience only slight limitation with vigorous
physical activity such as walking up a hill briskly
Class III have marked limitation, with symptoms during the

activities of everyday living

Class IV have the inability to perform the activities of daily

living because of symptoms as well as angina that

may occur at rest
Although this classification has some virtue it also has limitations, as recently
highlighted; hence, it does not address changes in the pattern or frequency of
angina or take into account the warm-up effect or the self-imposed alteration in
activities of daily living that may subtly modify symptomatic status
angina pectoris
stable ischemia syndrome
stable AP: symptom charactors fixed 1~3m
silent ischemia
syndrome X
unstable AP
initial onset AP : history<1m or…
accelerated AP :worsen in 3 m
angina decubitus
Prinzmetal variant angina
post infarction AP : in 1 m post AMI
Treatment of Stable Angina Pectoris
Principle of Management
relief of symptom
reduction of risk to future untoward
events known to develop, i.e., UAP, MI &
Death
retarding or halting the progression of
underlying atherosclerosis
Medical Therapy--aspirin
enteric-coated aspirin, 75 to 325 mg per day
produces a sustained functional defect in the platelet associated
with prolongation of the bleeding time

arachidonic acid
cyclo-oxygenase← inhibition (aspirin)

thromboxane A2(TXA2)
(the key modulator of irreversible platelet aggregation)
Medical Therapy:Nitrates

Reduce preload
Reduce afterload
Dilate epicardial coronary
Nitric oxide (NO)

Frishman WH: Pharmacology of

the nitrates in angina pectoris. Am
J Cardiol 56:8I, 1985.
Medical Therapy :Nitrates
Nitrate dosing*

Formulation? Dose Frequency Onset/duration action

Sublingual tablet GTN 0.3~.6 mg As required 2 min/20~30 min
Sublingual tablet ISDN 2.5~10 mg As required 5~10 min/1?~2h
Oral spray GTN 0.4-mg metered dose As required 2 min/20~30 min
Oral GTN SR 2.6 mg 2.6.5.2 Three times a day 2~5 min/3~5h
Buccal tablet GTN 1, 2, 3, and 5 mg Two or three times a day 2~5 h/3~5 h
Oral ISDN 10~30mg Two or three times a day 15 min/4~6h
Oral ISDN SR 80~120 mg Daily 60 min/10~12 h
Oral IS-5-MN 20 mg Twice a day 30 min/5~7h
Oral IS-5-MN SR 60~240 mg Daily 60 min/10~14 h
GTN ointment 2% 0.5~2” Twice a day 15 min/8 h
Transdermal GTN patch 0.2~.8 mg/h* Daily 30 min/12~24h

* Adapted from Abrams J. Therapy of angina pectoris with long acting nitrates: Which agent and when. Can J Cardiol 1996; 12C:9C-16C.
GTN indicates nitroglycerin; ISDN, isosorbide Dinitrate; IS-5-MN, isosorbide-5-mononitrate; and SR, sustained release.
* A nitrate-free interval of at least 8 h per 24-h period should be provided to avoid tolerance.
Medical Therapy :Nitrates
Principle side effects
headache flushing lightheadness
Occasionally side effects
nitrates syncope
Because: a rapid decline in systolic blood pressure in the
upright position, associated with arterial dilatation and venous
pooling.
Medical Therapy :ß-blocker
Mechanism
 ß-blocker
Medical Therapy: Pharmacology
classes of ß-receptors :ß -1 and ß -2

Cardioslectivity:
nonselective: affect the heart, peripheral vasculature, bronchial
tree, and modulation of hepatic and skeletal muscle
glyconeogenesis
ß -1 selective: (metoprolol and atenolol) tends to circumvent the
undesirable consequences (constriction of the bronchial tree and
arterial smooth muscle ) of nonselective b-blockade
Selective b-1 blocker effects, however, are only relatively selective,
and at increased doses these agents produce ß -2 blockade
Medical Therapy :ß-blocker
Name (proprietary) Property Frequency Daily dose, mg
Propranolol (Inderal) Nonselective Twice a day 80-320
(Inderal LA) Daily 60-320
Nadolol (Corgard) Nonselective Daily 80-240
Timolol (Blocadren) Nonselective Twice a day 15-45
Metoprolol (Lopresor) B1 selective Twice a day 100-400
(Lopresor SR) Daily 100-400
Atenolol (Tenormin) B1 selective Daily 50-200
Acebutolol (Sectral) B1 selective partial ISA Twice a day 200-600
Pindolol (Visken) Nonselective ISA Twice a day 15-45
Three times a day (>30 mg total)
Sotalol (Sotacor)* Nonselective with type 3 Twice a day 160-480
antiarrhythmic effect
* Sotalol is not approved for angina pectoris use. ISA indicates intrinsic sympathomimetic activity.
Medical Therapy :ß-blocker
Untoward effects of nonselective ß-blockade
Coronary vasoconstriction : Prinzmetal variant angina×
Peripheral circulatory vasoconstriction : Raynaud’s disease×
Bronchial constriction: Asthma, COPD ×
↓Response to hypoglycemia
Impaired hepatic gluconeogenesis
Impaired general awareness
↓Triglycerides/↓high-density lipoprotein cholesterol
Medical Therapy :Calcium-blocker
When symptoms persist or side effects limit
treatment with ß-blockers and/or nitrates, the
use of calcium antagonists may provide
significant additional relief.
It has been suggested that a special niche for
calcium antagonists resides with Prinzmetal’s
variant angina patients .
Medical Therapy :Calcium-blocker
Classification of calcium-blocker

*Dihydropyridines
nifedipine
SR nifedipine
longer-acting: felodipine amlodipine

*Diltilzem
*Verapamil
Medical Therapy: Calcium-blocker
provoking factors alleviating factors

mental stress ↑ preload ↓

physical stress constriction periferal artery relax
cold air ↑ myocardium contractivity ↓
lying down ↑ heart rate ↓
↑ BP ↓
↓ supply angina angina relief supply ↑

↑ demand demand ↓
Medical Therapy :Calcium-blocker
Calcium channel blockers: dosing and properties

Blockers* Dose, mg/frequency Heart rate Atrioventricular Blood pressure

Nifedipine 30~120/three times a day ↑ → ↓↓
Nifedipine GITS 30~80/daily → → ↓↓
Diltiazem 30~90/three or four times a day ↓↓ ↓ ↓
Diltiazem SR 60~120/twice a day ↓↓ ↓ ↓
Verapamil 80~120/three or four times a day ↓ ↓↓ ↓
Verapamil SR 120~240/daily or twice a day ↓ ↓↓ ↓
Amlodipine 2.5~10/daily ↑ → ↓↓
Felodipine 5~20/daily ↑ → ↓↓
Nicardipine 10~20/three times a day ↑ → ↓↓
Isradipine 2.5~10 ↑ → ↓↓
Bepridil 200~400/daily ↓ →↓ ↓

* GITS indicates gastrointestinal system; SR, sustained release.

Risk Assessment & Reduction
Fundamental component of management

@dietary modification
@ideal body weight (obesity)
@reduces cholesterol and saturated fat
@cessation of smoking
@controlling elevated blood pressure and blood sugar
@regular physical activity into a patient’s daily
@HMG-Co A (hydroxy-methylglutaryl co-enzyme A ) reductase
big five risk factors
atherosclerosis
hypertension
smoking
diabetes
hypercholesterolemia
and family history
Risk Assessment & Reduction
HMG-Co A reductase inhibitor
HMG-Co A (hydroxy-methylglutaryl co-enzyme A )reductase
HMG-Co A reductase inhibitor (statin)

CH ↓25%
LDL↓35%

mortality ↓ ↓myocardial infarction ↓ ↓

Revascularization
Catheter intervention
PTCA
STENTING
…
CABG:coronary artery bypass graft
intracoronary

STENT
stent_webvsn.avi
Coronary artery
bypass graft
(CABG)
Approach to Patients with Chronic Stable Angina

1.Identify and treat precipitating factors, such as

anemia, uncontrolled hypertension, thyrotoxicosis,
tachyarrhythmias, uncontrolled congestive heart
failure, and concomitant valvular heart disease.
2.Initiate risk factor modification, physical
exercise, diet, and life style counseling. Initiate
therapy with an HMG-CoA reductase inhibitor, as
needed, to reduce LDL cholesterol below 100
mg/dl.
3.Initiate pharmacotherapy with aspirin and a beta
blocker. Strongly consider an ACE inhibitor as
first-line therapy in all patients with chronic CAD.
4.Use sublingual nitroglycerin for alleviation of
symptoms and prophylactically.
5.If episodes occur more than two or three times per
week, the next step is addition of a calcium antagonist
or a long-acting nitrate via eccentric dosing schedules
to prevent nitrate tolerance. The decision to add a
calcium antagonist or a long-acting nitrate is not based
entirely on the frequency and severity of symptoms.
The need to treat concomitant hypertension or the
presence of left ventricular dysfunction and symptoms
of heart failure may be an indication for the use of one
of these agents, even in patients in whom episodes of
symptomatic angina are infrequent.
6.If angina persists despite two antianginal agents (a beta
blocker with either a long-acting nitrate preparation or a
calcium antagonist), add the third antianginal agent.
7.Coronary angiography, with a view to considering coronary
revascularization, is indicated in patients with refractory
symptoms or ischemia despite optimal medical therapy; it
should also be carried out in patients with "high-risk"
noninvasive test results and in those with occupations or life
styles that require a more aggressive approach.