Angina pectoris

Objectives
• Describe angina;
• Classify angina;
• Evaluate of management plan of angina;
Plan
• Definition
• Classification
• Risk factors and pathophysiology
• Clinical symptoms
• Diagnosis
• Treatment
• Angina pectoris refers to the pain caused by myocardial ischemia.
• Ischemiais usually caused by mismatched oxygen demand
(tachycardia, anemia, aortic stenosis, left ventricular hypertrophy of
other etiologies) and delivery in the setting of a hemodynamically
significant coronary stenosis due to atheroma, but it may have other
causes such as coronary artery spasm (Prinzmetal’s variant angina).
Angina is often classified according to its temporal pattern and its relation
to exertion because this loosely reflects prognosis.

• Stable angina is characterized by pain occurring after a relatively

constant level of exertion.
• Unstable angina is characterized by pain on minor exertion or at rest,
which is either new onset or a dramatic worsening of existing angina.
• Also, it can present as pain on ever-diminishing levels of exertion,
usually over a period of days.
Traditional clinical classification of
suspected anginal symptoms
• Typical angina
• Meets the following three characteristics: (i) Constricting discomfort
in the front of the chest or in the neck, jaw, shoulder, or arm; (ii)
Precipitated by physical exertion; (iii) Relieved by rest or nitrates
within 5 min.
• Atypical angina
• Meets two of these characteristics.
• Non-anginal chest pain
• Meets only one or none of these characteristics.
Clinical presentation
• Angina pectoris is characterized by a deep and diffusely distributed
central chest discomfort.
• Certain features of pain are of discriminative value.
• The pain is not sharp (some patients confuse “sharp” with “severe”).
• Pain lasts longer than a few seconds and rarely exceeds an hour
without varying in severity. Most episodes will last 1–5 minutes.
• The response to nitroglycerin, if any, will be almost immediate.
• Generally, responses taking more than 5 minutes are unlikely to be
related to the drug.
• Dyspnea, fatigue, nausea, and recurrent belching may also represent
underlying ischemia and can occur in the absence of the classical
central chest pain.
• The clue to underlying ischemic heart disease (IHD) lies in their
precipitation by exertion or emotional stress.
Physical examination
• Measure the pulse rate.
• Blood pressure measurement is
• Precordial examination should include palpation for left ventricular
• Examine for signs of heart failure by listening for fi ne, late-inspiratory
crackles at the lung bases and looking for dependent pitting edema
• 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.
Differential diagnosis
• The differential diagnosis of anginal chest pain is wide and includes
• Anxiety and hyperventilation
• Musculoskeletal chest wall pain
• Cervical or thoracic root pain
• Pneumothorax, pneumonia, or pulmonary embolus
• Esophageal problem (infl ammation/spasm)
• Other upper gastrointestinal (GI) problem (gastritis, peptic ulcer,pancreatitis,
cholecystitis)
• Pericarditis
• Aortic dissection
• Mitral valve prolapse
• Coronary emboli (LV mural thrombus, atrial myxoma)
Investigations
• Further risk stratify cation will add to the diagnostic certainty
achieved by history and examination.
• Measure complete blood count (CBC), chemistries, a full fasting lipid
profile (total, LDL and HDL cholesterol and triglyceride levels), and
blood glucose.
• Chest X-ray (CXR) is not mandatory but should be performed if there
is suspicion of heart failure, aortic dissection, a pulmonary condition
or an abnormality of the bony structures of the chest wall.
12 Lead ECG

• A resting electrocardiogram (ECG) may not confirm the diagnosis but

can point toward ischemic heart disease.
• The presence of Q waves suggests previous myocardial injury. The
presence of ST depression and, to a lesser extent, T-wave inversion
during pain is a marker of ischemia and patients with these signs
should be further investigated.
• If ST-segment deviation is observed at rest, an acute coronary
syndrome must be excluded.
Tests for inducible ischemia
• Tests such as exercise ECG, stress echocardiogram (ECHO), or
myocardial perfusion scanning are useful adjuncts to confirm the
diagnosis and aid management.
• Exercise stress testing is commonly used for the detection of
CAD in patients with chest pain or dyspnea on exertion who are
at intermediate risk of acute coronary syndrome.
• Exercise ECG testing does not present a diagnostic value in the
presence of LBBB, paced rhythm, and Wolff-Parkinson-White
syndrome, in which cases, the ECG changes cannot be evaluated.
• False -positive results are more frequent in patients with abnormal
resting ECG in the presence of left ventricular hypertrophy,
electrolyte imbalance, intraventricular conduction abnormalities, and
use of digitalis.
• Exercise ECG testing is also less sensitive and specific to women. The
ECG tracing is also an important indicator for the evolution of
coronary heart disease.
• Duke treadmill score = maximum exercise time in minutes – 5×ST
segment deviation in mm – 4×angina index (where 0 = no angina, 1 =
non-limiting angina, 2 = exercise limiting angina).
• A Duke treatment score ⩾5 indicates low risk for cardiovascular
events (predicted 4 year survival was 99%). This population does not
need further investigation with coronary angiography.
• A score <–10 indicates high risk for cardiovascular events (predicted 4
year survival was 79%). These patients require further investigation
with coronary angiography.
• A score between 4 and –10 indicates intermediate risk. Such patients
may require further investigation with myocardial perfusion scanning
or coronary angiography, or both, depending on the pretest
probability.
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.
Aspirin

• 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 gastroprotective agent
such as an H2 antagonist or proton pump inhibitor.
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. However, the underlying
risk of events must be taken into account when considering starting
the drug, because absolute risk reduction in young patients with low-
risk IHD may be very small, with possible harm of myositis, hepatic
failure, and reduced compliance with other medications.
Prinzmetal Angina

• Vasospastic angina, variant angina, or Prinzmetal angina is a known

clinical entity characterized by chest pain at rest with transient
ischemic electrocardiographic changes in the ST segment, with a
prompt response to nitrates. These symptoms are attributed to
coronary arteries spasm.
Etiology

• Diffuse or segmental spasm in the coronary arteries causes Printzmetal

angina. There is a decrease in blood supply to the myocardium
generating symptoms like chest pain. The coronary arteries may
develop spasm as a result of exposure to cold weather, exercise, or a
substance that promotes vasoconstriction as alpha-agonists
(pseudoephedrine and oxymetazoline).
Criteria diagnosis
• A chronic pattern of episodes of chest pain at rest that last 5 to 15 minutes,
from midnight to early morning.
• Pain decreases with the use of short-acting nitrates.
• Typically, these patients have ischemic ST-segment changes on an
electrocardiogram during an episode of chest discomfort, which returns to
baseline on symptom resolution.
• Typically, the chest pain is not triggered by exertion or alleviated with rest
as is typical angina.
• Often, the patient is younger with few or no classical cardiovascular risk
factors.
•
 Pharmacological Therapy
• Calcium antagonist plays an important role in the management of vasospastic
angina. It is a first-line treatment due to a vasodilation effect in the coronary
vasculature. Calcium antagonist is effective in alleviating symptoms in 90% of
patients. of myocardial infarct-free survival in vasospastic angina patients.
• The use of a long-acting calcium antagonist is recommended to be given at night as
the episodes of vasospasm are more frequent at midnight and early in the morning.
A high dose of long-acting calcium antagonists like diltiazem, amlodipine,
nifedipine, or verapamil are recommended, and titration
• Long -acting nitrates are also effective in preventing vasospastic events, but chronic
use is associated with tolerance. In patients on calcium antagonist without an
adequate response to treatment, long-acting nitrates can be added.
• Nicorandil, a nitrate, and K-channel activator also suppress vasospastic attacks.
• The use of beta-blockers, especially those with nonselective adrenoceptor blocking
effects, should be avoided because these drugs can aggravate the symptoms.
Differential Diagnosis
• Acute pericarditis
• Angina pectoris
• Anxiety disorders
• Aortic dissection
• Cocaine toxicity
• Esophageal spasms
• Gastroesophageal reflux disease
• Myocardial infarction
• Panic disorder
• Unstable angina
•
Complications

• Arrhythmia
• Sudden death
• Myocardial infarction
References
1. 2019 ESC Guidelines for the diagnosis and management of chronic
coronary syndromes: The Task Force for the diagnosis and
management of chronic coronary syndromes of the European
Society of Cardiology (ESC)
2. Ginghina C, Ungureanu C, Vladaia A, Popescu BA, Jurcut R.
The electrocardiographic profile of patients with angina
pectoris. J Med Life. 2009;2(1):80-91.
3. https://www.aafp.org/afp/2017/0901/p293.html
4. http://www.csecho.ca/wp-content/themes/twentyeleven-
csecho/cardiomath/?eqnHD=stress&eqnDisp=duketsc