Angina is chest pain or discomfort that occurs when the heart muscle does not get enough oxygen-rich blood. It has three main types: stable angina caused by physical exertion, unstable angina with lesser exertion or at rest, and variant angina caused by spasms in the arteries. Atherosclerosis is a disease where plaque builds up in the arteries, restricting blood flow. It is caused by damage to artery walls and risk factors like high cholesterol, high blood pressure, and smoking. Over time, plaque can rupture, causing blood clots that may lead to heart attack or stroke. Diagnosis involves symptoms, ECG, stress tests, and angiograms.

1. RVS Chaitanya Koppala
Pathophysiology Angina
&
atherosclerosis

2. Definition
Angina is the result of myocardial ischemia caused by an imbalance
between myocardial blood supply and oxygen demand.
It is a common presenting symptom (typically, chest pain) among
patients with coronary artery disease.
Type of chest pain: pressure or discomfort

3. ADAM.COM

4. Types of Angina
• Angina is classified broadly as stable or unstable, depending on its
pattern of occurrence and severity.
medmovie.com

5. Types of Angina (cont.)
Stable angina occurs when increased physical activity (e.g., hurrying
across a street or climbing a long stairs) which creates a greater demand for
oxygen-rich blood to reach heart tissue.
Unstable angina occurs with lesser degrees of exertion or while at rest.
Unstable angina that occurs at rest is the most serious form.
Formation of a blood clot at the site of a ruptured plaque in a coronary
artery.

6. Pathophysiology
Myocardial ischemia develops when coronary blood flow becomes inadequate to
meet myocardial oxygen demand.
This causes myocardial cells to switch from aerobic to anaerobic metabolism, with a
progressive impairment of metabolic, mechanical, and electrical functions.
Studies have shown that adenosine may be the main chemical mediator of anginal
pain.
During ischemia, ATP is degraded to adenosine, which, after diffusion to the
extracellular space, causes arteriolar dilation and anginal pain.

7. Clinical Presentation
Angina is a symptom of ischemic heart disease (IHD). Episodes of stable angina typically
are brought on by exertion or emotion and are relieved with rest.
An attack of stable angina lasts from 1 to 5 minutes and is described as
- squeezing,
- choking,
- smothering, or
- crushing pressure in the chest.
Angina pain may radiate to the shoulders, arms, back, neck, or jaw.
Patients with atherosclerosis also may experience sweating, shortness of breath (dyspnea).

8. Clinical Presentation (cont.)

9. Diagnosis
A diagnosis of stable angina is based primarily on symptoms, such as chest
pain.
A diagnosis of unstable angina is made when there is
- new onset angina that is severe and/or frequent;
- chronic stable angina who develop more frequent, severe, prolonged, or
more easily triggered episodes
- angina at rest.

10. Diagnostic Tests and Procedures
1- ECG (Electrocardiogram)
2- Stress ECG Testing
3- Coronary angiogram
4- Blood Tests

11. RVS Chaitanya Koppala
Pathophysiology
Atherosclerosis

12. Introduction
Atherosclerosis (also known as Arteriosclerotic Vascular Disease or ASVD)
Artery wall thickens (build-up of fatty materials such as cholesterol)
Affecting arterial blood vessels, a chronic inflammatory response in the walls
of arteries
Due to the accumulation of macrophage
Promoted by Low-density lipoproteins
Without adequate removal of fats and cholesterol from the macrophages

13. Hardening or furring of the arteries.
Formation of multiple plaques within the arteries.
Restrict blood flow.
These plaques can also burst, causing a blood clot.
Often considered a heart problem
Affect arteries anywhere in your body.
Atherosclerosis is a preventable and treatable condition.

14. TERMS
Arteriosclerosis is a general term describing any hardening (and loss of
elasticity) of medium or large arteries
Arteriolosclerosis is any hardening (and loss of elasticity) of arterioles (small
arteries);
Atherosclerosis is a hardening of an artery specifically due to an atheromatous
plaque.
Atherogenic is used for substances or processes that cause atherosclerosis.
Atherogenesis is the developmental process of atheromatous plaques

15. Causes
Atherosclerosis starts with damage or injury to the inner layer
of an artery. The damage may be caused by:
High blood pressure
High cholesterol
An irritant, such as nicotine
Certain diseases, such as diabetes

16. Pathophysiology
Atherosclerosis develops as a chronic inflammatory response of the
arterial wall to endothelial injury.
Lesion progression occurs through interactions of modified
lipoproteins, monocyte-derived macrophages, T-lymphocytes, and the
normal cellular constituent of the arterial wall.
The contemporary view of atherosclerosis is expressed by the response-
to-injury hypothesis.

17. Response-to-injury hypothesis
The following are the steps involved in the
hypothesis:
1. Chronic endothelial injury
2. Accumulation of lipoproteins
3. Monocyte adhesion to the endothelium
4. SMC proliferations and ECM
(extracellular matrix) production
5. Factor release
6. Platelet adhesion

19. Symptoms
Atherosclerosis develops gradually, typically begins in early adolescence,
and is usually found in most major arteries.
No atherosclerosis symptoms until an artery is so narrowed or clogged.
Sometimes a blood clot completely obstructs blood flow, or even breaks
apart and causes heart attack or stroke.

20. Atherosclerosis symptoms depend on which arteries are affected. For
example:
Atherosclerosis in heart arteries, have symptoms similar to those of a
heart attack, such as chest pain (angina).
Atherosclerosis in the arteries leading to brain, have symptoms such as
sudden numbness or weakness in your arms or legs, difficulty speaking or
slurred speech, or drooping muscles in your face.
Atherosclerosis in the arteries in arms and legs, produces decreased
blood flow is called peripheral artery occlusive disease (PAOD).have
symptoms such as leg pain when walking
Sometimes atherosclerosis causes erectile dysfunction in men.

21. Symptoms

22. Physiologic factors that increase risk
Various anatomic, physiological & behavioral risk factors for atherosclerosis are known. These
can be divided into various categories:, modifiable and non-modifiable.
1. Modifiable
Having diabetes or Impaired glucose tolerance (IGT)
Dyslipoproteinemia (unhealthy patterns of serum proteins carrying fats & cholesterol):
Tobacco smoking.
Having high blood pressure, on its own increasing risk by 60%
Elevated serum C-reactive protein concentrations

23. 2. Non modifiable:
• Advanced age
• Male sex
• Having close relatives who
have had some complication of
atherosclerosis (CVD/STROKE)
• Genetic abnormalities, e.g.
familial hypercholesterolemia
3. Lesser or uncertain:
• Being obese (in particular central
obesity,
• A sedentary lifestyle
• Postmenopausal estrogen deficiency
• High carbohydrate intake
• Elevated serum levels of triglycerides
• Elevated serum lipoprotein
concentrations
• Stress or symptoms of clinical depression
• Hyperthyroidism
• Elevated serum insulin levels
• Short sleep duration
Physiologic factors that increase risk