Coronary Artery Disease is also known as Ischemic Heart Disease
Stages of Development of Coronary Artery Disease
Arterial Injury - Atherosclerosis
Myocardial Ischemia – Angina Pectoris
Myocardial Necrosis – Myocardial Infarction
CORONARY ATHEROSCLEROSIS
Coronary Atherosclerosis is an abnormal accumulation of lipid or fatty substances and fibrous tissue in the vessel wall.
These substances create blockages or narrow the vessel in a way that reduces blood flow to the myocardium.
Atherosclerosis is a progressive and potentially life-threatening process
ATHEROSCLEROSIS | ARTERIOSCLEROSIS |
- Narrowing of Artery - Lipid or Fat Deposits (Plaques) - Tunica Intima | - Hardening of Artery, Thicken - Calcium And Protein Deposits - Tunica Media |
PATHOPHYSIOLOGY
Atherosclerosis begins as fatty streaks, lipids that are deposited in the intima of the arterial wall
T lymphocytes and monocytes (that become macrophages) infiltrate the area to ingest the lipids and then die; this causes smooth muscle cells within the vessel to proliferate and form a fibrous cap over the dead fatty core.
These deposits, called Atheromas or plaques, protrude into the lumen of the vessel, narrowing it and obstructing blood flow
If the fibrous cap of the plaque is thick and the lipid pool remains relatively stable, it can resist the stress from blood flow and vessel movement.
If the cap is thin, the lipid core may grow, causing it to rupture and hemorrhage into the plaque, allowing a thrombus to develop.
The thrombus may obstruct blood flow, leading to sudden cardiac death or an acute myocardial infarction (MI), which is the death of heart tissue.
Angles of the coronary arteries. The many angles and curves of the coronary arteries contribute to the vessels' susceptibility to atheromatous plaques.
RISK FACTORS
Non-modifiable
Family history of CAD (first-degree relative with cardiovascular disease at 55 years of age or younger for men and at 65 years of age or younger for women)
Increasing age (more than 45 years for men; more than 55 years for women)
Gender (men develop CAD at an earlier age than women)
Race – black (higher incidence in African Americans)
Modifiable Risk Factors
Hyperlipidemia
Cigarette smoking, tobacco use
Hypertension
Diabetes mellitus
Metabolic syndrome
Obesity
Physical inactivity
CLINICAL MANIFESTATIONS
Symptoms and Complications according to:
Location and degree of narrowing of the arterial lumen
Thrombus formation
Obstruction of blood flow to the myocardium
Clinical Manifestations are -
May be asymptomatic( in those older, women, have diabetes , a history of heart failure)
Acute onset of chest pain
Typical symptoms: Dyspnea, Tachycardia, Palpitations, Diaphoresis
PREVENTION OF CORONARY ARTERY DISEASE
Four modifiable risk factors— Cholesterol Abnormalities, Tobacco Use, Hypertension, and Diabetes Mellitus have been cited as major risk factors for CAD and its complications. So the CAD is prevented by the controlling these factors.
CONTROLLING CHOLESTEROL ABNORMALITIES
The desired goal is to maintain low LDL values and high HDL values.
The desired level of LDL depends on the patient -
Less than 160 mg/dL for patients with one or no risk factors
Less than 130 mg/dL for patients with two or more risk factors
Less than 100 mg/dL for patients with CAD or a CAD risk equivalent
A fasting lipid profile should
LDL cholesterol less than 100 mg/dL (less than 70 mg/dL for very high-risk patients)
Total cholesterol less than 200 mg/dL
HDL cholesterol greater than 60 mg/dL
Triglyceride less than 150 mg/dL
Serum cholesterol and LDL levels can be controlled by –
Dietary Modification –- Balance intake of Total calories and expenditure to maintain desirable weight
Total fat - 25%–35% of total calories
Saturated fat - <7% of total calories
Polyunsaturated fat- Up to 10% of total calories
Monounsaturated fat - Up to 20% of total calories
Carbohydrate- 50%–60% of total calories
Protein Approximately - 15% of total calories
Dietary fiber - 20–30 g/day
Cholesterol - < 200 mg/day
Physical Activity - The goal is a total of 30 minutes of moderate exercise (such as walking) daily. Physical activity and weight reduction increases HDL levels and reduces triglyceride levels, decreasing the incidence of coronary events and reducing overall mortality risk.
Medication Therapy - If diet & Physical Activity alone cannot normalize serum cholesterol levels, medications can have a synergistic effect with the prescribed diet and control cholesterol levels.
PROMOTING CESSATION OF TOBACCO USE
Effects of smoking
The inhalation of smoke increases the blood carbon monoxide level, causing hemoglobin to combine with CO than with O2. A decreased amount of available oxygen may decrease the heart's ability to pump.
The nicotinic acid in tobacco triggers the release of catecholamine's, which raise the heart rate and BP.
Nicotinic acid can also cause the coronary arteries Vasoconstriction.
Use of tobacco increases platelet adhesion, leading to a increase the probability of thrombus formation
To Stop Smoking –
Reduce the risk of CAD up to 30-50% within the 1st year, and
The risk continues to decline as long as they refrain from smoking.
MANAGING HYPERTENSION
Hypertension – BP repeatedly exceed 140/90 mm Hg.
Long-standing elevated BP may result in increased stiffness of the vessel walls, leading to vessel injury and a resulting inflammatory response within the intima.
Hypertension can also increase the work of the left ventricle, which must pump harder to eject blood into the arteries. Over time, the increased workload causes the heart to enlarge and thicken (ie, hypertrophy), a condition that may eventually lead to cardiac failure.
CONTROLLING DIABETES MELLITUS
For 65% to 75% of patients with diabetes, cardiovascular disease is listed as the cause of death.
Hyperglycemia fosters dyslipidemia, increased platelet aggregation, and altered red blood cell function, which can lead to thrombus formation
TREATMENT
PTCA - Percutaneous Transluminal Coronary Angioplasty
Objectives of PTCA
Revascularize myocardium
To prevent angina
Increase survival rate
CABG - Coronary Arterial Bypass And Graft Surgery
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