CORONARY HEART DISEASE:

ANGINA PECTORIS

Anton V. Rodionov
Assistant Professor
Department of Internal Medicine #1
 Historical Perspective

“…. a disorder of the breast marked with strong and

peculiar symptoms, ….. the sense of strangling and
anxiety with which it is attended, ….. called angina
pectoris. Those afflicted are seized while 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, …. but the moment they stand still, all
this uneasiness vanishes.”
William Heberden, 1773
 Classification

Coronary
Heart
Disease

Acute Old Sudden

Angina
Myocardial Myocardial Cardiac
Pectoris
Infarction Infarction Death

Stable Unstable Q - MI Non Q - MI

 DEFINITIONS (1)

• Angina Pectoris - reversible ischaemia to

the myocardium, induced by increased work
load (causing characteristic chest pain) and
relieved by rest. The reversible ischaemia is
usually due to coronary artery disease.
• During ischemia an imbalance occurs
between myocardial oxygen supply and
demand.
 DEFINITIONS (2)

• Unstable angina – syndrome in which the patient’s risk

is intermediate between chronic stable angina and
myocardial infarction.
• A clinical diagnosis based on a history of chest pain:
– new onset (within 1 month)
– crescendo angina (accelerating symptoms of previous
stable angina: more severe, prolonged, or frequent)
– angina pectoris at rest as well as with minimal
exertion
• Exclusion of myocardial infarction by cardiac markers
level
 Epidemiology I
Death Rates for Total CVD, CHD, Stroke and Total
Deaths in Selected Countries (Revised 2005)
 Epidemiology II
Deaths From Cardiovascular Diseases
United States:2003*

Source: CDC/NCHS and NHLBI. *Preliminary

 Epidemiology III
Annual Number of Diagnosed Heart Attack
by Age and Sex (ARIC: 1987-2000)

500 000
New and Recurrent Attacks

410 000
400 000 372 000

300 000
250 000
Men
Women
200 000

88 000
100 000
34 000
10 000
0
29-44 45-64 65+
Ages
Source: Extrapolated from rates in the NHLBI’s ARIC surveillance study,
1987-2000. These data don’t include silent MIs.
 Etiology

• Atherosclerosis of the coronary artery is by far the

leading cause of CHD.
• Non-Atherosclerotic Coronary Artery Disease
– Congenital (anomalous origin of L or R coronary
arteries)
– Arteritis associated with auto-immune diseases
(SLE, Kawasaki’s)
– Coronary Ectasia
– Radiotherapy
– Syndrome X
– Prinzmetal’s Angina - spasm
 Risk factors I
Traditional risk factors for coronary heart disease

Lifestyles Biochemical or Personal

physiological characteristics (non-
characteristics modifiable)
(modifiable)
Diet high in Elevated blood Age
saturated fat, pressure Sex
cholesterol and Elevated plasma Personal history of
calories total cholesterol (LDL CHD or other
Tobacco smoking cholesterol) atherosclerotic
Excess (!) alcohol Low plasma HDL vascular disease
consumption cholesterol Family history of
Physical inactivity Elevated plasma CHD at early age (in
triglycerides men <55 years, in
Hyperglycaemia/diab women <65 years)
etes
 RISK FACTORS II
Novel risk factors (questionable importance)

• Homocysteine
• Elevated plasma lipoprotein(a)
• Postmenopausal state
• Leucocytosis
• C-reactive protein
• Protein С
• Antithrombin III
• Microalbuminuria
• Hyperuricemia
• Renin-angiotensin system activation
• Chlamydia pneumonia
• Genetic abnormalities
• Social and economic factors
• Stress and type of behavior
Atherosclerosis

Fibrous Plaque:
an advanced, complex,
occlusive lesion
characterized by a fibrous
cap of dense connective
tissue overlying a
collection of foamy
macrophages, necrotic
debris, T lymphocytes,
and smooth muscle cells.
Anatomy of the Atherosclerotic Plaque

Fibrous
Lumen cap
Lipid Shoulder
Core
Intima
Elastic Internal
Media laminæ
External

Source: www.lipidsonline.com
 Pathophysiology of angina

Rest Stress

O2 Supply = O2 Supply <

O2 Demand O2 Demand
Regulation of Coronary Blood Flow

• Coronary Anatomy
– Vessel diameter (larger vessel - easier
flow)
– Vessel resistance
• Directly related to length of lesion
– Collateral circulation
• Provides alternate routes for blood flow
What determines O2 supply?

How does vessel

resistance affect
blood flow?
(Coronary
Anatomy)
Normal vs. Ischemic Heart Disease

Normal Normal Exercise

Atherosclerotic Atherosclerotic Exercise

 Regulation of Coronary Blood Flow

• Metabolic Regulation (adenosine)

• Sympathetic Nervous System
– α1 mediated vasoconstriction
– β2 mediated vasodilatation
• Parasympathetic Nervous System
– Stimulation provides modest increase in coronary blood flow
• Vascular Endothelial Tone
– Endothelial Derived Relaxing Factor (EDRF)
• Characterized as nitric oxide
• Causes smooth muscle relaxation
• Coronary Reflexes
– Undetermined role
 CLASSIFICATION OF STABLE ANGINA

• Class I - strenuous or protracted exercise

• Class II - slight limitation with vigorous
physical activity such as walking up a hill
• Class III - marked limitation, with symptoms
during the activities of everyday living
• Class IV - inability to perform the activities of
daily living & angina at rest
Canadian Cardiovascular Society 1975
 Clinical Features

• Chest Pain
– Character (not pain but unpleasant sensation:
“pressing”, “squeezing”, “strangling”, “constricting”,
“bursting”, “burning”)
– Site (typically – retrosternal)
– Radiation (typically – left side: shoulder, arm, neck,
jaw, ear, scapula)
– Inducing Factors
– Relieving Factors
– Duration
• Dyspnea
 Physical Signs

• Usually none
• Features of left ventricular failure
 Diagnosis
The diagnosis of CHD based on:
• Clinical history of angina
• History of previous miocardial infarction
• Evidence of atherosclerotic lesions in coronary
arteries
• Demonstration of stress-induced ischemia or
reduced myocardial perfusion
• Demonstration of impaired myocardial metabolism
• The last three positions could be revealed by
different diagnostic methods, which include
noninvasive or invasive modalities.
 Lab Tests

• Blood account (anemia)

• Biochemical tests (cholesterol and its
fractions, cardiac markers)
• Coagulation and platelets aggregation
 Noninvasive tests
• Resting Electrocardiogram
• Exercise electrocardiography (exercise stress-test; including
transesophageal electrical atrial pacing)
• Radionuclide studies
– exercise single photon emission computed tomography (SPECT)
– pharmacological stress SPECT (dobutamine, dipyridamole or
adenosine)
– radionuclide ventriculography
• Stress-echocardiography
– pharmacological stress ECHO (dobutamine, dipyridamole or adenosine)
– stress-echocardiography with transesophageal electrical atrial pacing
• Positron-emission tomography
• Multispiral CT - angiography (or Electron-beam tomography)
• MR - angiography
• Ambulatory (Holter) ECG monitoring
 ISCHEMIC CASCADE

Angina/Symptoms
test

ECG changes ECG

course & severity of ischemia

Systolic
dysfunction

Diastolic ECHO
dysfunction

Metabolic changes

Radionuclide
Abnormal perfusion
Exercise stress-test
ECG - ischaemia
Thallium Scan
Echocardiography
 Invasive tests

• Coronary angiography (with left ventriculography)

• Intravascular ultrasound
 Indications for CAG in patients with
Stable Angina

Diagnostic Before
revascularization
• In patients with • In patients with
indefinite diagnosis class III-IV angina
(possible CHD) resistant to the
treatment
• Recurrent angina
after MI, CABG,
PCI
Coronary Angiography
 THERAPY

• Risk Modification
• Medical therapy
• Balloon Angioplasty
• Surgery
• Cardiac Rehabilitation
 Risk Modification

• Stop smoking
• Adequate treatment of hypertension
• Good diabetic control
• Lipids, treat LDL & TGs
• Weight reduction
• Regular exercise
 Reduction of mortality

• Aspirin (Clopidogrel if ASA is contraindicated)

• Statins
∀ β -Blockers
• ACE-inhibitors (Perindopril and Ramipril)
• CABG in selected patients
 Acetyl Salicylic Acid

• ASA blocks COX and tromboxane A2

synthesis in platelets
• Should be given to ALL patients with CHD
(except for those with absolute
contraindications)
• Daily dose – 75-100 mg
• Decrease the total CV risk for 33%
 Statins

• Block 3-hydroxy-3-metylglutaril-coenzym А-
reductase (HMG-coA reductase) and reduce
cholesterol synthesis at the liver
• Should be given to patients with CHD if the
LDL cholesterol is higher than 130 mg/dl
• The daily dose should be adequate to
maintain the LDL level < 100 mg/dl
• Decrease the total CV risk for 20-40%
 Beta blockers
• Selective β1 and unselective
• Antagonizes beta adrenergic effects
• Reduces work load (↓HR & ↓contractility)
• Improves survival as well as treat symptoms
• Side effects:
– lethargy & tiredness, cold peripheries
– unselective β-blockers (UBAB) cause
brochospasm (avoid UBAB in asthma & COPD)
• Caution in heart failure*
• Carvedilol, Metoprolol, Bisoprolol and Nebivolol
improves survival in pts. with heart failure
Mechanism of Action of Beta Blockers
 ACE-inhibitors

• Main mechanism of action – inhibition of

angiotensin converting enzyme
• Prevent and reduce the myocardium
remodeling
• Should be given to those patients with CHD
having previous MI, any systolic dysfunction,
diabetes mellitus or arterial hypertension
 Calcium Antagonists

• Smooth muscle relaxant, reduces pre & after

load.
• Direct cardiac depressant as well
• 3 classes
– Dihydropyridine – nifedipine, amlodipine,
felodipine
– Benzithiazepines – Diltiazem
– Phenylalkylamines – Verapamil
 Nitrates

• Smooth muscle relaxant

• Pre-load, after-load reduction
• Dilate coronary arteries
• Side effects - hypotension, flushing,
headaches, increased heart rate
• No favorable effects on mortality
 Potassium Channel Opener

• Nicorandil
• Causes venous & arterial vasodilatation
• Similar effects to nitrates & calcium channel
blockers
• Main side effect - headaches & dizziness
 Unstable Angina

• Aspirin (& clopidogrel)

• Low Molecular Weight Heparin (or
unfractioned if LMW isn’t available)
• Beta blockers
• Oxygen
• Nitrate infusion
• Monitor ECG & BP
• ?? Glycoprotein IIb/IIIa antagonists
• ?? Calcium antagonists
Transluminal coronary balloon
angioplasty and stenting
Coronary artery bypass grafting
Mental stress 