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Angina Pectoris

Angina Pectoris
 Angina Pectoris is varying forms of chest discomfort caused
by reversible myocardial ischemia due to insufficient
myocardial oxygen that produces disturbance in myocardial
function without causing myocardial necrosis.
 Angina is a clinical syndrome characterized by pain

(discomfort or heaviness) in the chest, jaw, shoulder, back, or


arm, which is aggravated by exertion or stress and relieved by
nitroglycerin.
 Angina usually occurs in patients with coronary artery disease.

It can also occur in individuals with valvular heart disease,


hypertrophic cardiomyopathy, and uncontrolled hypertension.
Types of Angina
 Stable or Classic angina
◦ Most common form
◦ Effort induced pain from physical activity or emotional stress
◦ Relieved by rest, nitroglycerin or both
◦ Due to fixed obstruction in a coronary artery
 Unstable angina
◦ Increased symptom frequency, severity or duration (>20 mins), and
symptoms at rest
◦ Due to significant coronary artery disease
 Prinzmetal’s or Variant or Vasospastic angina
◦ Pain at rest and in the early morning hours, but is not exertion or emotional
induced
◦ Not relieved by rest
◦ Due to coronary artery spasm

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Signs & Symptoms (Clinical Presentation)

New York Heart Associates, nyheart.net © Reed Group


Medical Disability Advisor,
mdguidelines.com
 A sensation of pressure or burning over sternum or
near it which often radiates to left jaw, shoulder and
arm for 30 seconds to 30 minutes
 Abnormal heart sounds
Precipitating factors/Etiology
 Physical exertion
 High emotion, such as anger or excitement
 Exposure to very hot or cold temperature
 Cigarette smoking
 Heavy meal
 ↑ Cholesterol level
 Obesity
 Diabetes
Pathophysiology
 Angina pectoris is as a result of ischemia of the heart which is due to
antherosclerosis of the coronary arteries which restricts blood flow to the
myocardium.
 In most patients angina are precipitated by abrupt plaque change followed by

thrombosis.
 Stable plaques ---------unstable plaques----- atherothrombotic lesion --------by

rupture, superficial erosion, ulceration, platelet aggregation-thrombosis.


 Vasoconstriction compromises lumen size and increase local mechanical

forces that contribute to the triggering of ischemic event.


 Vasoconstriction is triggered by:

a. locally released platelets


b. impaired secretion of endothelin derived relaxation factor
c. release of inflammatory mediators
 Due to myocardium ischemia, the myocardial tissues are
deprived of oxygen and nutrients for the aerobic
metabolism.
 This causes myocardial cells to switch from aerobic to

anaerobic metabolism, with a progressive impairment of


metabolic, mechanical, and electrical functions.
 Anaerobic metabolism leads to accumulation of lactic acid.
 Due to increase of lactic acid, myocardial nerve fibers are

irritated and these transmit a pain message to the cardiac


nerves and upper thoracic posterior nerve roots.
 All these lead to cardiac pain.
Diagnosis
 A diagnosis of stable angina is based primarily on symptoms,
such as chest pain.
ECG (Electrocardiogram)
 It detects and records the electrical activity of the heart.
Certain electrical patterns that the ECG detects can suggest
whether CAD is likely. However, some people with angina
have a normal ECG.
 The ECG is usually normal between attacks. During an
attack there may be a transient ST segment depression.
 If the angina is provoked by exertion, an exercise stress
ECG should be performed.
Stress ECG Testing
 Typically, this test involves taking an electrocardiogram (ECG) before,
during, and after exercise on a treadmill or stationary bicycle. Patients
who are at risk for a coronary event with exercise are, instead, given a
drug to increase the heart rate.
Coronary angiogram
 Is obtained by injecting contrast material into the bloodstream and
taking X-rays of the coronary arteries. This enables the physician to
see blockages, malformations, and stenosis in the vessels.
Blood Tests
 Blood tests check the levels of certain fats, cholesterol, sugar, and
proteins in blood. Abnormal levels may indicate risk factors for CAD.
Some studies suggest that high levels of CRP (C-reactive protein) in
the blood may increase the risk for CAD and heart attack.
Radioisotope
 This involves the use of different nuclear imaging
techniques to evaluate heart muscles.
 Regions of ischemia appear as areas of diminished
activity.
Ultrafast computed tomography
 It enables detection of the amount of calcium in the
coronary arteries. High coronary calcium rate is
associated with obstructive coronary disease.
Goals of therapy
 To reduce or prevent angina symptoms
 To prevent CHD events such as MI, arrhythmia, and

heart failure
 To extend the patient’s life
Treatment
 Primary prevention: Modification of risk factors
(smoking, hypertension, hyperlipidemia, obesity,
sedentary lifestyle, hyperuricemia, stress, and drugs
like progestins, corticosteroids, cyclosporine).
 Secondary intervention reduces morbidity and

mortality.
 Unalterable risk factors include gender, age, family

history or genetic composition, environmental


influences, and DM.
Pharmacologic Therapy
 β-Blockers
 Decrease heart rate, contractility, and blood pressure.
 Reduce myocardial oxygen demand in patients with effort induced
angina.
 These agents improve symptoms in patients with chronic exertional
stable angina.
 Ideal for patients in whom physical activity is cause of attacks, patients
with coexisting hypertension, supraventricular arrhythmias,
postmyocardial infarction angina, and anxiety associated with anginal
episodes.
 First line drugs in chronic angina as these agents reduce episodes of
silent ischemia and early morning peak of ischemic activity and
improve mortality.
 Effective in chronic exertional angina as monotherapy and
in combination with nitrates and/or calcium channel
antagonists.
 Initial doses of β-blockers should be low and titrate

according to response.
 Adverse effects include hypotension, heart failure,

bradycardia, heart block, bronchospasm, altered glucose


metabolism, fatigue, malaise, and depression.
 Abrupt withdrawal in patients with angina has been

associated with increased severity and number of pain


episodes and MI.
 Calcium channel blockers
 Vasodilation of systemic arterioles and coronary arteries, leading

to a reduction of arterial pressure and coronary vascular resistance.


 Depression of myocardial contractility and the conduction velocity

of the sinoatrial (SA) and atrioventricular (AV) nodes.


 Reduction in myocardial oxygen demand.
 Improvement in coronary blood flow through areas of fixed

coronary obstruction.
 Ideal for patients with contraindications or intolerance to β-

blockers, coexisting conduction system disease, Prinzmetal


angina, peripheral vascular disease, severe ventricular
dysfunction, and hypertension.
Nitrates

Reduction of myocardial oxygen demand due to venodilation and arterial-
arteriolar dilation.
Relief of spasm.
Terminate an acute anginal attack and prevent effort or stress induced attacks.
Usually in combination with β-blockers or calcium channel antagonists.
Sublingual, buccal, or spray nitroglycerin products are preferred in anginal

attacks because of rapid absorption.


Sublingual nitroglycerin (0.3 - 0.4 mg) relieves pain within 3 minutes and causes

pain free in 5 - 15 minutes.


Pain persisting beyond 20 - 30 minutes after use of two to three nitroglycerin

tablets suggests Acute Coronary Syndrome (ACS), a emergency condition.


Adverse effects include postural hypotension with associated CNS symptoms,

headaches and flushing, and occasional nausea.


Nitrate Products
Treatment of Stable Exertional Angina
Pectoris
ABCDE approach for treatment of Stable
Angina
 Aspirin and Antianginals
 β-Blockers and Blood pressure control
 Cholesterol management and Cigarette cessation
 Dietary improvements and Diabetes control
 Education and Exercise
 Aspirin
 Antiplatelet agent
 It prevents platelet activation and thus thrombus

(blood clot) formation


Nonpharmacologic Therapy
 Revascularization
 Coronary Artery Bypass Grafting (CABG)
 Percutaneous Transluminal Coronary Angioplasty

(PTCA)
Thanks

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