Drugs For Angina, Myocardial Infraction and

Cerebrovascular Accident

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 Table of Contents:

Introduction………………………………………………………………………………….….……………………..3

Angina…………………………………………………………………………………………….….……………………3

- Pathophysiology……………………………………………………………………….……………….………….4

- Medications…………………………………………………………………………….……………….……………5

Myocardial Infraction………………………………………………………………..…………….……………..5

- Pathophysiology…………………………………………………………………..……………….………………6

- Medications…………………………………………………………………………..…………….…………………7

Cerebrovascular Accident…………………………………………………………………….………………….7

- Pathophysiology…………………………………………………………….………………………………………8

- Medications……………………………………………………………………………………………………………8

Conclusion………………………………………………………………………………………………………………..9

References……………………………………………………………………………………………………………….10

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Introduction:

Cerebrovascular disease is a collection of disorders affecting the blood vessels and

blood supply to the brain. These include angina, myocardial infraction, and a

cerebrovascular accident. The vascular system in the brain is a complex network

of arteries and veins. Arteries carry oxygenated blood from the heart to your

organs and tissues. Veins carry blood back to the heart.Cerebrovascular conditions

have a variety of causes. You can have them from birth or develop them over time.

In general, cerebrovascular disease is caused by genetic changes during

pregnancy, inherited conditions, poor lifestyle choices, physical trauma, and

individual characteristics beyond your control, such as age, race, and gender.

Angina:

Angina is chest pain or discomfort caused by a lack of oxygen-rich blood to the

heart muscle. You may feel pressure or squeezing in your chest. The discomfort

can also be felt in your shoulders, arms, neck, jaw, abdomen, or back. Angina pain

may also feel like indigestion. Furthermore, some people do not feel pain but do

experience other symptoms such as shortness of breath or fatigue. If these

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symptoms are caused by a lack of oxygen to the heart muscle, they are referred to

as "anginal equivalent."

- Pathophysiology:

Angina results from an imbalance between myocardial oxygen supply and

demand. It is critical to understand the factors that influence each of these

measurements. The coronary arteries are lined with endothelial cells, which

regulate vascular tone and prevent intravascular thrombosis. Any disruption to

these two functions can result in coronary heart disease. Multiple mechanisms

can cause injury or impairment to the endothelial lining. Stress, hypertension,

hypercholesterolemia, viruses, bacteria, and immune complexes are some

examples of these mechanisms. Endothelial injury activates an immune response,

which eventually results in fibrous tissue formation. Smooth muscle remodelling

and fibrous caps can result in coronary artery stenosis or acute coronary

syndrome.

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- Medications:

Nitrates or beta blockers are typically used as the first line of treatment for angina,

with calcium channel blockers added as needed. The number and type of

medications used are frequently determined by the frequency with which angina

occurs in a given week. However, people who have one or fewer angina episodes

per week may be advised to take sublingual (under the tongue) nitroglycerin

when an angina attack occurs and immediately before engaging in angina-causing

activities. Alternatively, these individuals may be prescribed medications to be

taken daily. People who experience two or more angina episodes per week are

typically advised to take longer-acting antianginal medications. This could include

a long-acting nitrate or a beta blocker.

Myocardial Infraction:

A heart attack (myocardial infarction) occurs when one or more areas of the heart

muscle do not receive adequate oxygen. This occurs when the blood supply to the

heart muscle is obstructed.The blockage is caused by the accumulation of plaque

in the arteries (atherosclerosis). Plaque consists of deposits, cholesterol, and other

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substances. When a plaque breaks or ruptures, a blood clot forms quickly. The

blood clot is the root cause of the heart attack.If the blood and oxygen supply is

cut off, the heart's muscle cells begin to suffer damage and die. Irreversible

damage occurs within 30 minutes of blockage. As a result of the lack of oxygen,

the heart muscle no longer functions properly.

- Pathophysiology:

An acute occlusion of one or more large epicardial coronary arteries lasting more

than 20 to 40 minutes can result in an acute myocardial infarction. The occlusion

is usually thrombotic, caused by the rupture of a plaque in the coronary arteries.

The occlusion causes a lack of oxygen in the myocardium, resulting in

sarcolemmal disruption and myofibril relaxation. These changes are among the

first ultrastructural changes that occur during the MI process, followed by

mitochondrial changes. Prolonged ischemia eventually causes liquefactive

necrosis of myocardial tissue. The necrosis extends from the subendocardium to

the subepicardium. The subepicardium is thought to have increased collateral

circulation, delaying its death.

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- Medications:

• Aspirin, clopidogrel, heparin, or other anticlotting agents to prevent new

clots.

• Thrombolytic drugs to dissolve existing clots (clot-busting drugs such as

tPA).

• Oxygen to protect heart tissue.

• Nitroglycerin to widen coronary vessels.

Cerebrovascular Accident:

A stroke, or cerebrovascular accident, is an emergency medical condition

characterized by an acute compromise of the cerebral perfusion or vasculature.

The leading cause of ischemic stroke is hypertension whereas clotting disorders,

carotid dissection, and illicit drug abuse are common causes in the younger

populations. A quick diagnosis followed by prompt management needs to be set

in motion by the interprofessional team members to improve outcomes for those

with stroke.

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- Pathophysiology:

A stroke is caused by ischemia in a specific area of the brain. The Na+/K+ ATPase

pumps fail primarily due to low ATP production and failure of the aerobic

mechanism. Ischemia causes cell depolarization, resulting in calcium influx,

increased lactic acid, acidosis, and free radicals. Cell death increases glutamate

levels, resulting in a chemical cascade (excitotoxicity).

- Medications:

• Thrombolytic drugs, such as tPA, are commonly referred to as clot busters.

tPA, which stands for tissue plasminogen activator, can only be

administered to patients suffering from a blood clot-related stroke.

• Antiplatelet drugs help to keep platelets from sticking together, which

prevents blood clots from forming. Acetylsalicylic acid (ASA), also known as

aspirin, is the most commonly used antiplatelet drug.

• Anticoagulants are blood thinners that keep new blood clots from forming

and existing blood clots from growing larger. They work by interfering with

specific blood components required for clotting. They are typically

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 prescribed for people who have an irregular heartbeat (atrial fibrillation),

which can result in blood clots traveling from the heart to the brain.

Heparin and warfarin are anticoagulant medications.

Conclusion:

The term cerebrovascular is composed of two parts: 'cerebro' refers to the large

part of the brain, and 'vascular' refers to the arteries and veins. The term

cerebrovascular disease refers to a group of conditions that can result in a

cerebrovascular event, such as a stroke, mini-stroke, ischemic stroke, or transient

ischemic attack (TIA). These events have an impact on the blood vessels and the

supply of blood to the brain.Cerebrovascular disease can be difficult to detect

prior to an attack, but risk factors such as hypertension, smoking, obesity,

ischemic heart disease, and uncontrolled diabetes can also contribute to its

development.

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References:

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stroke rates, risk, and outcomes in the United States, 1988 to 2008. Am J

Med. 2014 Jul;127(7):608-15.

2. Lawes CM, Bennett DA, Feigin VL, Rodgers A. Blood pressure and stroke: an

overview of published reviews. Stroke. 2004 Apr;35(4):1024.

3. Kloner RA, Chaitman B. Angina and Its Management. J Cardiovasc

Pharmacol Ther. 2017 May;22(3):199-209.

4. hristie LG, Conti CR. Systematic approach to evaluation of angina-like chest

pain: pathophysiology and clinical testing with emphasis on objective

documentation of myocardial ischemia. Am Heart J. 1981 Nov;102(5):897-

912.

5. Reimer KA, Jennings RB, Tatum AH. Pathobiology of acute myocardial

ischemia: metabolic, functional and ultrastructural studies. Am J

Cardiol. 1983 Jul 20;52(2):72A-81A.

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 6. Yusuf S, Hawken S, Ounpuu S, Dans T, Avezum A, Lanas F, McQueen M,

Budaj A, Pais P, Varigos J, Lisheng L., INTERHEART Study Investigators. Effect

of potentially modifiable risk factors associated with myocardial infarction

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Sep 11-17;364(9438):937-52.

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