CORONARY

ATHEROSCLEROTIC
DISEASE
 Group 1

1. FINA CHALIMATUS SA’ADAH (I1J020002)

2. MILLATI HANIFAH (I1J020003)
3. NUR ALJANANTI (I1J020004)
4. ALIF SACHRUL MINSAID (I1J020006)
5. FUZNA DAHLIA MUDZAKIROH (I1J020010)
6. NURUL IZZAH ISLAMY (I1B020028)
 ISCHEMIA
Ischemia is disease caused by an imbalance between the
oxygen demand of the myocardium and its arterial blood
supply. In angina pectoris, ischemia resolves without
myocardial necrosis. In acute myocardial infarction,
myocardial necrosis is usually caused by blockage of the
coronary arteries atherosclerosis by thrombus.
Symptoms of Ischemia
Symptoms of ischemia depend on which organs are affected, such as :
• Heart, heart attack symptoms will arise.
• Brain, stroke symptoms will arise.
• In the lower leg, there will be symptoms of critical limb ischemia, which is
characterized by pain in the lower leg.
• Intestines, symptoms of mesenteric ischemia will occur.

Risk Factors for Ischemia

Some of the risk factors for ischemia include:
• Have certain diseases, such as diabetes, hypertension, hypotension, high
cholesterol, obesity, blood clotting disorders, sickle cell anemia, celiac disease and
heart failure.
• Has a smoking habit.
• Experiencing alcoholism.
• Abusing drugs.
• Rarely do physical activities such as exercise.
Ethylogy of Ischemia
Based on the cause, ischemia can be caused by 3 kinds of things, namely:

a. Reduced coronary blood flow (the cause in> 90% of cases) that occurs due to a
combination of atherosclerosis, vasospasm and coronary thrombosis. Conditions
that occasionally result in reduced coronary blood flow include arteritis, embolism,
cocaine-induced vasospasm and shock (leading to ischemic hypotension).

b. Increased myocardial demand (eg tachycardia, cardiac hypertrophy).

c. Hypoxia due to reduced oxygen transport (overall a less serious cause of ischemia
when compared to reduced blood flow given that in these circumstances nutrient
supply and metabolite excretion are not affected).  
Pathophysiology of Ischemia
Ischemic heart disease begins as a result of arteriosclerosis or hardening of the
arteries (arteries). The inner wall of the blood vessels (intima) in the body,
especially the arteries, is covered with a thin layer of cells, because it protects the
elastic tissue and muscle tissue. The next stage, blood clots quickly form on the
surface of the lining of the torn artery. The condition quickly results in total
narrowing and blockage of the arteries. If arteriosclerosis occurs in the arteries
of the heart muscle (coronary arteries), the heart muscles will be deprived of
oxygen, due to reduced blood going to the heart muscles. the result of reduced
oxygen levels encourages the myocardium to convert aerobic metabolism to
anaerobic metabolism. The end product of anaerobic metabolism (namely lactic
acid) will accumulate, thereby lowering the pH of the cell.
The heart muscles themselves need oxygen to function. This oxygen is supplied by the coronary
arteries. If one of these arteries is blocked due to arteriosclerosis, the part of the heart muscle
that is supplied with oxygen by the artery becomes damaged, and can even be permanently
damaged (infarction). If the blood contains excess cholesterol, it is possible that the cholesterol
will settle in the arteries that supply blood to the heart (coronary arteries). As a result, there is a
part of the heart muscle (myocardium) that dies and will then be replaced with scar tissue. This
scar tissue cannot contract like the heart muscle. The loss of pump power depends on how
much heart muscle is damaged. Sclerosis of the coronary arteries or heart blood vessels will
typically cause three important things, namely a heart attack, angina pectoris, and heart rhythm
disturbances.
 Diagnosis of Ischemia
The examination can be in the form of:
• Blood tests, to check blood cholesterol levels and blood clotting profiles.
Electrocardiography (EKG), to record the electrical activity of the heart,
• Echocardiography, to see the structure of the shape and motion of the heart.
Angiography, to see the severity of obstruction in blood vessels,
• Ischemia of the heart, including a CT scan to see the possibility of coronary heart disease, as well as
a pressure test (stress test) for example with an EKG, a treadmill while the patient is doing physical
activity.
 Treatment of Cardiac Ischemia
Cardiac ischemia is a condition of lack of heart blood supply due to obstruction
of flow to the arteries in the heart. Can be treated with Aspirin, Nitrates, beta
blockers (beta blockers), calcium antagonists, or ACE inhibitors,
Antihypertensives, such as ACE inhibitors, Cholesterol-lowering drugs,
Stenting, to support narrowed blood vessels to keep them open and bypass
surgery heart, to create other pathways or new blood vessels to meet the oxygen
supply from the heart muscle.
 Classification of Cardiac Ischemia

• Ischemic Heart Disease Without Infarction The need for oxygen that exceeds the oxygen
supply capacity of the affected blood vessels causes local myocardial ischemia. Transient
ischemia will cause reversible changes at the cellular and tissue level, and suppress myocardial
function. The manifestation of myocardial ischemia is chest pain but not as severe as
infarction.
• Ischemic Heart Disease With Ischemic Infarction that lasts more than 30-45 minutes will cause
irreversible cell damage and muscle necrosis or death. In addition, thrombus formation from
plaque rupture followed by thrombus formation by platelets can also cause myocardial
infarction. The part of the myocardium that experiences infarction or necrosis will
permanently stop contracting. The infarcted tissue is surrounded by an ischemic area that can
potentially be viable if prompt and prompt ischemia treatment is carried out.
 Ischemia Prevention

In some conditions and areas, ischemia is difficult to prevent.

One of the suggestions that you can do is to maintain the
health and smooth circulation of blood vessels. Maintain a
healthy lifestyle through adequate exercise activities which
will greatly help maintain blood circulation, intake of foods
rich in fiber and antioxidants, and adequate and quality rest
time.
ISCHEMIA
PATHWAYS
 MIOCARD
INFARK
Acute myocardial infarction (AMI) is defined as
myocardial cell necrosis caused by obstruction of
blood flow due to the presence of plaque in the
coronary arteries or the presence of other obstructive
mechanisms (such as spasm of the plaque-free
coronary arteries). Plaque is part of atherosclerosis.
 Miocard Infark
Causes
1. Causing Factors
• Decreased supply of 02 to the myocardium
* Vascular factors → Atherosclerosis, spasm, arteritis
* Circulatory factors> Hypotension, aortic stenosis, insufficiency
* Blood factors> Anemia, hypoxemia
• Cardiac Outflow ↑
* Excessive activity, emotions, hyperthyroidism * Myocardial O2 needs ↑ on> myocardial damage,
myocardial hypertrophy, hypertension.

2. Prediposition Factors
• What cannot be changed: age> 40 years old, ♂ ↑ & ♀ ↑ after menopause, black race ↑
• Modifiable: major> hypertension, obesity, diabetes, smoking
* Minor> psychological stress, physical inactivity.
 Miocard Infark Symptoms
1. Symptoms: A history of typical chest pain
Typical symptoms:
• Front chest pain (under the sternum) with / without spreading, sometimes in the form of chin, neck / toothache-like
pain, the patient cannot show pain with one finger but with the hand.
• Quality of pain such as pressure, heaviness / burning sensation.
• Duration. 15 to 30
• Sometimes accompanied by nausea, cold sweat, palpitations / tightness
• Pain does not go away with rest / sublingual nitroglycerin
2. Symptoms: There is a change in the EKG
Typical Symptoms:
a. Pathological Q waves (significant infarction) / Q
b. ST elevation
c. Gel T increases / decreases
3. Symptoms: Increase in heart muscle enzymes
Typical Symptoms:
a. CKMB is a specific enzyme as a marker of heart muscle damage, this enzyme increases 6 - 10 hours after chest pain &
returns to normal in 48 - 72 hours.
b. Px. Aspartate Amino Transferase (AST) ps. On day 3 chest pain / LDH (increased lactate dehydrogenase after day 4 &
normal on day 10.
 The Pathophysiology
The main pathophysiology of acute myocardial infarction (acute myocardial infarction)
is death of myocardial cells due to a prolonged ischemic process. Myocardial cell death
does not occur immediately after ischemia, but several minutes after the onset of
ischemia. This condition is also influenced by other factors, namely persistence or
absence of coronary artery occlusion and also collateralization of the bleeding system
in the heart itself. 90% of myocardial infarction is caused by atherosclerosis, rupture of
atherosclerotic plaques and thrombus formation. Atherosclerotic plaque rupture and
erosion in the coronary arteries in the form of thin-cap fibroateroma (TCFA) is thought
to be a lesion that increases the risk of coronary artery occlusion.
 The Pathophysiology
Cont..

However, apart from that, repeated events of the healing process and plaque rupture will also
cause coronary artery narrowing and plaque morphological changes that contribute to the
pathophysiology of myocardial infarction. After occlusion, there will be myocardial injury. In
normal aerobic conditions, the main energy source of the myocardium is fatty acids, which supply
60-90% of the synthesis of adenosine triphosphate (ATP). Sudden occlusion of the coronary
arteries will convert aerobic or mitochondrial metabolism to anaerobic metabolism. A decrease in
aerobic ATP, will stimulate glycolysis, increase myocardial glucose uptake, and breakdown of
glycogen. In addition, the decrease in ATP will inhibit Na K ATPase and cause cell edema. The
residual metabolism in the form of lactate causes a decrease in intracellular pH, a decrease in
contractility, and further increases the need for ATP to maintain Ca homeostasis. If this process
continues, the ischemic injury will become irreversible.
The Diagnosis
The diagnosis of acute myocardial infarction (acute myocardial infarction) must be made
quickly and precisely because it is a life-threatening condition. From the history, the suspicion
of acute myocardial infarction was made when the patient presented with left chest pain that did
not go away with rest. This suspicion is then confirmed by electrocardiography (EKG) and
cardiac enzyme tests.

History
History is very important in the diagnosis of acute myocardial infarction. Patients who
complain of the following should watch out for acute myocardial infarction:
• Chest pain, pain such as squeezing a heavy load and lasts more than 30 minutes which
is not relieved by rest. Pain can radiate to the left arm, but can spread to the left shoulder
or left jaw.
• Nausea or vomiting
• A cold sweat
• Hard to breathe
• Dizzy
• Sudden decrease in consciousness
• History of having risk factors for atherosclerosis
The Etiology
The etiology of acute myocardial infarction (acute myocardial infarction) is coronary artery occlusion which 90%
is caused by atherosclerotic processes. Atherosclerosis is a metabolic chronic vascular disease that is aggravated
by inflammation. Atherosclerosis forms plaque and when plaque ruptures it will cause aggregation of tombocytes
and the formation of thrombus which clogs the coronary arteries.

History
The epidemiology of acute myocardial infarction (acute myocardial infarction) in Indonesia is still not clearly
known. In the United States, the estimated mortality rate from cardiovascular disease is 222.9 per 100,000
population.

Management
Management of acute myocardial infarction (acute myocardial infarction) must be done as soon as possible,
because this condition is considered an emergency. An occupational diagnosis is needed urgently to initiate
initial management. Patients should immediately undergo examination and interpretation of ECG and
cardiac enzyme tests. Patients should be monitored and monitored because in the early stages of myocardial
infarction, cardiac arrest can occur most commonly due to ventricular fibrillation.
 Clinical Classification of
Acute Myocardial Infarction
Myocardial infarction is classified into STEMI and NSTEMI. ST-elevation myocardial infarction (STEMI) is a
patient with chest pain or other ischemic symptoms accompanied by ST segment elevation in two leads that
correspond to the ECG record. Meanwhile, NSTEMI is a patient with ischemic symptoms and increased
biomarkers of myocardial infarction markers but without ST segment elevation on the ECG. This classification is
used for the purpose of selecting therapy. Patients with STEMI should immediately receive reperfusion therapy
either mechanically with Percutaneous Coronary Intervention (PCI) in a catheterization laboratory or medical
reperfusion therapy with fibrinolytics. Mechanical intervention with PCI in NSTEMI patients is usually less
urgent and depends on the risk stratification score (Senter and Francis, 2009, Thygesen et al., 2012a). It is
important to note that the data from the Registry Observatoire sur la Prise en charge hospitaliere, l'Evolution a
un et les characteristics de patients pre´sentant un infArctus du myocarde avec ou sans onde Q (OPERA) in 2006
found that despite differences in treatment , however, the hospital outcome and clinical outcome in NSTEMI and
STEMI patients were the same.
Pathways of Infark