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2. Coronary circulation
The left main and right coronary arteries arise from the left
and right coronary sinuses of
the aortic root, distal to the aortic valve (Fig. 18.3). Within
2.5cm of its origin, the left
main coronary artery divides into the left anterior
descending artery (LAD), which runs in the anterior
interventricular groove, and the left circumflex artery
(CX), which runs posteriorly in the atrioventricular
groove. The LAD gives branches to supply the anterior
part of the septum (septal perforators) and the anterior,
lateral and apical walls of the LV. The CX gives marginal
branches that supply the lateral, posterior and inferior
segments of the LV.

3. The right coronary artery (RCA) runs
in the right atrioventricular groove, giving branches that
sup- ply the RA, RV & inferoposterior aspects of the LV.
The posterior descending artery runs in the
posterior inter- ventricular groove and supplies the
inferior part of the interventricular septum
Notes
Blockage of the left main coronary artery
will cause immediate death.
The RCA supplies the sinoatrial (SA)
node in about 60% of individuals and
the AV node in about 90%. Proximal
occlusion of the RCA therefore often
results in sinus bradycardia
and may also cause AV nodal block.

4. Atherosclerosis
Chronic stable
angina
Acute coronary
syndrome
Unstable angina
NSTEMI STEMI

5. CORONARY HEART DISEASE: CLINICAL MANIFESTATIONS AND
PATHOLOGY
Clinical problem Pathology
Stable angina : Ischaemia due to fixed atheromatous
stenosis of one or more coronary arteries
Unstable angina : Ischaemia caused by dynamic
obstruction of a coronary artery due to plaque rupture or
erosion with superimposed thrombosis
Myocardial infarction : Myocardial necrosis caused by
acute occlusion of a coronary artery due to plaque rupture or
erosion with superimposed thrombosis

6. Angina pectoris
Angina pectoris refers to the PAIN caused by myocardial ischemia.
Ischemia is usually caused by mismatched oxygen demand
(tachycardia, anemia, aortic stenosis, left ventricular hypertrophy of
other etiologies) and delivery in the setting of a hemodynamicaly
significant coronary stenosis due to atheroma, but it may have other
causes such as coronary artery spasm (Prinzmetal’s variant angina).

7. STABLE ANGINA
(sudden diffuse chest pain beneath sternum- squeezing, heaviness
often radiated to left shoulder , arm, back ,neck and epigastrium
) might associated with nausea ,vomiting .sweating ,dizzness
lasting less than 15-20 minutes and aggravated by trigger factors
and is promptly relieved by rest,
Trigger factors: exertion or other forms of stress , Cold exposure.
Heavy meals ,Intense emotion ,Physical exertion
Causes : Coronary atherosclerosis; spasm .embolism
,dissection vasc;litis
Other causes : anemia .hyperthyrodism, aortic stenosis
.hypertrophic cardiomyopathy

11. INVESTIGATION IN STABLE ANGINA
#A full blood count,
#fasting blood glucose, lipids, thyroid function tests
#cardiac markers : NO change in stable angina
#Resting ECG
Is often normal, there is T-wave flattening or inversion in
some leads during attack
#Exercise ECG
An exercise tolerance test (ETT) is usually performed
using a standard treadmill or bicycle ergometer
protocol( Planar or down-sloping ST segment depression
of ≥ 1 mm is indicative of ischaemia) .exercise capacity
220-age = >85%.

12. Physical examination
• Measure the pulse rate. This may be slowed by inferior ischemia due to
atrioventricular (AV) node ischemia. A resting tachycardia, if present, usually
represents activation of the sympathetic nervous system but may be due to
an arrhythmia precipitated by ischemia.
• Blood pressure measurement is essential to look for evidence of hypertension
(predisposing to atheroma) or hypotension (may reflect cardiac dysfunction or
overmedication).
• Precordial examination should include palpation for left ventricular hypertrophy
(LVH), cardiac enlargement, or dyskinesis, and auscultation for added heart
sounds (heart failure or acute ischemia), aortic stenosis, or mitral
regurgitation (due to papillary muscle dysfunction).
• Examine for signs of heart failure by listening for fine, late-inspiratory crackles
at the lung bases and looking for dependent pitting edema (typically bilateral
ankle ± leg edema, but sacral edema may be the only manifestation if the
patient has been recumbent for some time).
• Look for evidence of peripheral vascular disease by palpating for aortic
aneurysm; feeling the carotid and limb pulses; listening for carotid, renal, or
femoral artery bruits; and assessing tissue integrity and capillary refill of the
legs and feet.
• Examine for signs of hypercholesterolemia: the eyes for xanthelasmata and
corneal arcus, and the skin and tendons (especially the Achilles) for
xanthomata.

16. Management
Lifestyle
Smoking cessation is of paramount importance. Encourage daily aerobic exercise within limits of exercise capacity. Look at
the patient’s occupational needs and advise adjustment if symptom level is not compatible. Advise a healthy diet,
collaborating with dieticians if required.
Antiplatlets
Provide aspirin in all cases unless there is active peptic ulcer disease, allergy (desensitizing may be required), or bleeding
diathesis. Those with past peptic ulcer disease may take a gastro protective agent such as an H2 antagonist or proton
pump inhibitor.in, addition other antiplatlets are used eg. Tecagrilor, prasigril alone or in combination with apirin.
Anti-anginals
• B-Blockers: First line (e.g., atenolol 25–100 mg qd or metoprolol 25–50 mg bid). Start on suspicion of ischemic heart
disease. Avoid only if contraindicated (asthma with confirmed B-agonist response
(mortality improved in patients with angina and concomitant COPD if they can tolerate bronchospasm), uncontrolled
severe LV dysfunction, bradycardia, coronary artery spasm).
• Calcium antagonists (e.g., amlodipine or diltiazem): If B-blocker contraindicated or concern for vasospasm, calcium
antagonists become the drug of choice.
• Nitrates (e.g., nitroglycerin): Used for control of breakthrough angina. Long-acting nitrates (e.g., isosorbide mononitrate
60–120 mg qd) are a
useful addition to B-blockers for prevention of attacks.
.Statins
Statins (HMG-CoA reductase inhibitors) reduce mortality by approximately one-third in all risk groups.