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CASEA man aged 43 years came with complaints of chest pain. Chest feels heavy burden

Ampek like overwritten. Pain is felt when the patient is doing the activity. pain lasted 20-30

minutes. Pain improved after the patient relax and stop its activity and after administration of

balm on the front chest and back. Pain accompanied by nausea but no vomiting, no dizziness,

no cough, no shortness of breath.

HRMS: Since 2 days ago the patient had no pain. But in the morning before entering the

hospital, the same pain came back along with shortness of breath. Pain is felt when the patient

perform the activity. The pain lasts longer, 1 hour. Pain does not improve after the patient

rested and giving balm. Patients feel anxious and uncomfortable, so that by the families of

patients taken to hospitals Wirosaban.

When Anamnesis: The patient complains of pain that is felt diminished, there was no

shortness of breath, no nausea, no vomiting, no dizziness, no cough. Intake, eating and drinking

well. CHAPTER normal, soft brown konsisitensi. Normal bladder, tends to many, patients do not

feel Anyang-anyangan. The same complaint history there in 2008, but not routine treatment,

no diabetes, and history of stroke. Mother patients also suffer from the same diseaseFrom the physical examination obtained vital sign temperature 36.5 oC, tension 140/80

mmHg, pulse 92 x / min regular, respiration 24 x / min, a second vesicular lung, heart sounds

regular SI-S2, no noise audible systolic. From the investigation found ECG ST elevation: V1 - V5,

LVH, pathological Q.

QUESTION1. Unfamiliar term?

2. Why the patients chests feel pain when he got activity?

3. After taking some rest and given some balm why does a patient pains feel better?

4. In the patient medical record, a doctor does not find chest pains with difficulties tobreathe, how can a patient gets chest pains with difficulties to breathe with longer

duration and does not recover after some rest before patient gets into the hospital?

5. Is there any relationship between diabetes and stroke record with the patients recent

disease?

6. Does family medical record contributes to patients recent disease?

7. What is the possible different diagnose in this patients case?

8. How can a doctor decide diagnose in the patients case?

9. What is the best treatment and management for the patient?

10.What is the possible complication that might exist if the patient does not get adequate

treatment?11.What is the patient prognosis?

12.What is the best way to prevent patient from recurring or even worst condition?

ANSWER1. Chest pain : is discomfort or pain that you feel anywhere along the front of your body

between your neck and upper abdomen.

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Diabetes : is a group of metabolic diseases characterized by hipergliemia caused by

defects of insulin secretion, impaired insulin or both

2. When someone do some activity, their heart need much oxygen to contract the muscle.

Oxygen is brought by blood that flow through artery coronary. If there are some plaque

that obstruct the artery, so blood supply to the miocardium decrease, indirectly oxygencant reach the target (muscle). This condition is named ischemia. But, myocardium

must be contract to supply many blood to all of the body (perifer), in the condition

without oxygen (anaerobic), the metabolism of myocardium through glycolisis

mechanism. There are many glucose that use in glycolisis, and the end product is lactat

acid. Not only lactat acid, but many product that can make pain is released, like

histamine or proteolitik enzym that didnt bring fastly by cononary blood flow that flush

slowly. The high concentration from this product can stimulate nerve of pain in

myocardium that bring impulse through sensory afferent nerve into central nervous

system.

3. The presence of physical activity lead to chest pain in patients. We know that in doing

physical activity, body requires energy. Energy derived from the metabolism of oxygen.

So, while on the move, the body requires more oxygen to meet the needs of the

network. If tissue hypoxia there was a shortage of oxygen supply network which if

sustained will lead to cell death.

Possibly, the initial pain attacks, the patient experienced only ischemia in heart muscle.

At rest, the body does not require too much energy, so it can reduce oxygen demand.

Thus, the work of the heart to pump blood throughout the body also decreases. If the

cardiac work is minimized, ischemia in heart muscles due to lack of oxygen supply will

be eased.

While giving balm, serves to provide relaxation. Feeling relaxed will participate reducestress, which will also play a role in dilating blood vessels. Dilation of blood vessels, will

facilitate the flow of blood. Thus, tissue oxygen deprivation will again receive oxygen in

sufficient quantities.

4. From the results of anamnesis found chest pain is felt like a heavy burden and pain

overwritten arise while the patient is active. Pain is felt less than 30 minutes and

improved after the break and smeared balm. From these data, possibly before being

taken to hospital patients experienced angina pectoralis, which is chest pain caused by

myocardial ischemia. Lack of oxygen causes a change from aerobic to anaerobic

metabolism which would interfere with the function of metabolic, mechanical, andelectrical. Pain caused by chemical and mechanical stimulation of sensory afferents end

in the coronary vessel wall and myocardium which then would be perceived in the

cerebral cortex. n this case, the pain experienced at the beginning of complaints

probably due to blockages in coronary arteries is still less so after a quick break back

patients can move again, but the longer the greater the blockage so that the heart tissue

that should get more oxygen deficiency. The possibility of the original form of stable

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further examination.)

Possible pain got worse because

1. Plaque Rupture

Atreosklerosis plaque rupture is considered the most important causes of unstableangina pectoris, which occurred suddenly subtotal or total occlusion of coronary vessels

that previously had minimal narrowing. Atherosclerotic plaque consists of a nucleus that

contains lots of fat and protective fibrotic tissue (fibrotic cap). An unstable plaque

consists of a nucleus which contains fat and infiltration of macrophage cells. Usually the

rupture occurs at the edge of the plaque adjacent to normal intima or in the shoulder of

fat deposits. Sometimes cracks occur at the weakest wall plaque because of the

protease enzyme produced by macrophages and the enzymatic weaken the wall plaque

(fibrous cap).

The occurrence of rupture causes activation, adhesion and platelet aggregation and

activation causes the formation of thrombus. When thrombus closing blood vessels

100% will occur infarction with ST segment elevation, whereas if thrombi are not clog

100%, and only cause severe stenosis will occur unstable angina.

2. Thrombosis and Platelet Aggregation

Platelet aggregation and thrombus formation is one of the bases of unstable angina. The

occurrence of thrombosis after plaque disrupted due to interactions that occur between

the fat, smooth muscle cells, macrophages, and collagen. The core of fat is the most

important ingredient in the formation of platelet-rich thrombus, whereas smooth

muscle cells and foam cells (foam cells) present in plaque associated with expression of

tissue factor in unstable plaque. Once associated with blood, tissue factor interacts with

factor VIIa to initiate the cascade of enzymatic reactions that result in the formation ofthrombin and fibrin.

As a reaction to the disruption of endothelial physiology, there pletelet aggregation and

release the contents of granulation pletelet sparking a broader aggregation,

vasoconstriction and thrombus formation. Systemic and inflammatory factors

contribute to the changes incurred hemostase and coagulation and thrombosis play a

role in starting the intermittent, in unstable angina.

3. Vasospasm

The occurrence of vasoconstriction also has an important role in unstable angina. It is

estimated that the endothelial dysfunction and vasoactive substances produced byplatelets plays a role in changes in vascular tone and meenyebabkan spasm. Such

localized spasm in angina printzmetal can also cause unstable angina. Spasm often

occurs in an unstable plaque, and have a role in the formation of thrombus.

4. Plaque erosion without rupture

The occurrence of constriction can also be caused by the proliferation and migration of

smooth muscle in response to endothelial damage; a change in shape and lesions due to

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the increase in smooth muscle cells can lead to narrowing of the vessels with complaints

quickly and ischemia.

5. Diabetes mellitus (DM) has been known to be an important risk factor for coronary

heart disease. It is estimated that nearly 200 million people worldwide have diabetes,

either type 1 or type 2, but most suffer from type 2 diabetes. The number is expected torise to 2-fold in 2005.

Diabetes mellitus is a group of metabolic diseases characterized by hipergliemia

caused by defects of insulin secretion, impaired insulin or both. DM is a chronic disorder

and is associated with damage to various organs such as eyes, kidneys, nerves, heart

and blood vessels.

DM is classified into type 1 diabetes, type 2 diabetes, gestational diabetes and

other types. Vascular complications due to diabetes were divided into macrovascular

complications such as coronary heart disease, peripheral vascular disease and stroke,

and microvascular complications such as retinopathy, nephropathy and neuropathy.

The mechanism is thought to occur in DM so that the process occurs aterogenesis:

- Abnormalities in the distribution of particles and lipoprotein apoprotein.

- Glkosilasi and advanced glycation proteins in plasma and arterial walls.

- Glycoxidation and oxidation

- Procoagulant state

- Insulin resistance and hyperinsulinemia

- Proloferasi smooth muscle cells and the formation of the "from cell" due to hormonal

stimulation, growth factor, and cytokine.

If DM can be controlled by both course the incidence of complications is much

smaller. In fact 50% of patients with DM had been diagnosed diabetic complications atthe time the first time.

Actually at this moment not only ensured that the DM that worsen the

prognosis, but also proved that the conditions associated with increased pre

diabetespun process of atherosclerosis by 2.4-fold increased risk for cardiovascular

events in 15 years. Risk of failure jantungpun increases with blood sugar levels in those

who are not in the diagnosis of DM.

Peripheral vascular disease is also a common complication that accompany

diabetes. In contrast with those without diabetes, peripheral vascular disease in patients

with DM more virulent because of its involvement in the more distal vessels and is

usually accompanied by neuropathy so as if asymptomatic so it will come too late andmore who have to undergo amputation.

Hypertension is more of 1.5 to 3 times found in people with diabetes compared

to those without DM. Each increase of 5 mmHg systolic or diastolic blood pressure

increases the risk of cardiovascular disease by 20-30% in patients with DM.

Incidence of cardiovascular disease because diabetes is also associated with the passage

of time, the longer the greater the DM diidap cardiovascular events.

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Currently, DM is considered a CHD risk equivalent. Those suffering from diabetes

even without a history of acute myocardial infarction have the same number of

cardiovascular events with those without DM but had experienced myocardial

infarction. Patients with DM have a risk of cardiovascular events in 10 years by 20%.

Those who suffer from diabetes also have high mortality rates when experiencing

cardiovascular events, they are dying more and more that get complications.Hence, for those who suffer from DM laksananya governance must be more

aggressive, such as blood pressure control targets on them must be less than 130/80

mm Hg. Controlling cholesterol in patients with low and Dmpun must lebi aggressive LDL

target of less than 100mg/dl. Treatment is given if cholesterol levels above 130 mmHg,

but can also be given if LDLnya cholesterol levels less than 130 mg / dl.

6. Diabetes mellitus is an endocrine metabolic disease that can be genetically inherited.

The risk of diabetes in children is greater if the parents have diabetes mellitus with a

ratio of 1:10. And in this scenario the data obtained from the anamnesis that the

mothers of patients suffering from diabetes mellitus, which is a risk factor for diabetes

mellitus in these patients. And the emergence of patient complaints due to his diabetes,

and exacerbated by strokenya history.

7. Differential Diagnosis

1. Acute Coronary Syndrome

Apts (Unstable angina pectoris)

- Pain chest at rest or mild activity, relieved by nitrates.

- The ECG: T segment depression, T wave innervation, no wave Q.

- Cardiac enzymes did not increase.

# NSTEMI (Non ST Elevation Myocardial Infarction)

- Chest pain is more severe and longer.- Not relieved by nitrates, need to be opium.

- Results EKG: ST segment depression, T wave inversion

- Cardiac enzymes increased at least 2 times the upper limit of normal value.

# STEMI (ST Elevation Myocardial Infarction)

- More severe and long (> 30 minutes), not relieved by nitrates, need to be opium.

- Hyperacute T

- T segment elevation

- Q waves

- T wave inversion

- Increased minimum of 2 times the upper limit of normal value.

2. Acute myocardial infarction

Anamnesis

- Chest pain left

- Felt like the press, sliced or in cekik and was spreading to the jaw, left hand, back and

right chest to his right hand.

- Chest pain is usually menentap> 20 minutes.

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- Trigger factor before the attack, such as heavy physical activity, emotional stress

- Sometimes complain shortness of breath

Physical examination

- Often seen pale

- Nadi usually regular

- Tachycardia- Tension rises

Patients with AMI can have a picture of the different ECG:

- Normal or non-specific ECG

- ST-T wave changes of ST depression or inverted T (inverted)

- EKG-specific, ie there are typical changes in the form of ST elevation, T wave changes,

and the emergence of pathological Q waves.

Check cardiac enzymes

- Increase in the enzyme creatine kinase (CK) and creatinine kinase myocardial band

(CKMB)

3.Angina pectoris is a discomfort in the chest as a result of an ischemic

without myocardial infarction. Clinical classification of angina are basically useless for

evaluate the mechanisms of ischemic. Although the pathogenesis of angina experienced

change from year to year, but in general can be distinguished 3 types of angina:

1. Classical effort angina (angina classical)

At necropsy usually obtained coronary atherosclerosis. In these circumstances,

coronary obstruction does not always lead to such ischemic time

break. However, when the blood flow needs exceed the amount that can be

pass through the obstruction, but the ischemic and angina symptoms. Angina

pectoris will arise in every activity that can increase the rate

heart, blood pressure and cardiac inotropic atatus so O2 will needsuch increases in physical activity, cold air and eat a lot.

2. Variant angina (Prinzmetal angina)

The form is rare and usually occur at rest, due to a decrease

O2 supply blood to the myocardium of a sudden. Recent research shows

obsruksi the dynamic result of coronary spasm in both arteries

pain and normal. Increased coronary obstruction that does not settle this

occurrence of angina during the break clearly accompanied by decreased blood flow

coronary artery.

3. Unstable angina (unstable angina / ATS)

Another term often used is preinfark angina, angina decubitus,Angina kresendo. Acute coronary insufficiency or mid coronary syndrome.

This shape is a group who can change a situation like

complaints increased progressively, formerly with unstable angina or angina

the first time. Angina may occur at rest or work. In

pathology is usually found in areas that have characteristics of myocardial ischemic

own.

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Clinical manifestations

1. Symptoms

Obtained discomfort in the chest that is not always a pain, but

can also be a feeling of fullness in the chest, depression, pain, choking or burning

sensation.

Pain can occur in the neck, throat, the area between the scapula bone,the jaw or arm. When angina occurs, patients can be crowded

breath or weakness that disappeared after the angina disappeared. Can also occur

palpitations, cold sweating, dizziness or nearly fainted.

2. Physical examination

While angina may not show abnormalities. On auscultation may

sound of galloping atrial or ventricular and systolic murmur at apex.

Heart rate may drop, settle or increased in time

angina attack.

3. ECG

ECG should be done at the time of angina attacks, when a normal resting ECG,

stress test should be done with a treadmill or bicycle ergometer.

The purpose of the stress test is:

e-USU Repository 2004 University of North Sumatra

3 - assess whether the chest pain comes from the heart or not.

- Assessing the severity of diseases such as when abnormalities occur in blood vessels

The main will give strong positive results.

Electrocardiography ATS patients may be depressed ST segment, segment depression

ST accompanied by T wave inversion, ST segment elevation, barriers to His bond branch

and without changes in ST segment and T wave ECG Changes in ATS

temporary and each can occur alone or

sersamaan. These changes arise during angina attacks and return tonormal picture or early after complaints of angina disappeared within 24 hours.

If the changes are settled after 24 hours or Q wave evolution occurs,

then referred to as IMA.

4. The enzyme LDH, CPK and CK-MB

At ATS enzyme LDH and CPK levels can be normal or increased but not

exceeds the value of 50% above normal. CK-MB is the most sensitive enzyme

for myocardial muscle necrosis, but false positives can occur. This

demonstrate the importance of enzyme levels in serial to

get rid of the IMA.

8. Enforcement diagnosis:

Anamnesis:

Patients complaining of chest pain, chest pain feels like overwritten until heavy

burden, pain is felt when the patient activity and pain lasts for 20-30 minutes, the chest

pain can be caused by many factors could result because there is interference by the

lower respiratory tract and may also be due to disorders of the heart, therefore the

diagnosis can be established based on seriol ECG and enzyme tests. pain in because of

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coronary heart disease can be divided into 3 types: atreriosklerotik heart disease caused

by the aging process is characterized as the occurrence of reduced elasticity of intima

thickening, accumulation of calcium, especially in large arteries, angina pectoris chest

pain usually occurs during the 1-5 minutes and if more than 20 minutes possible miokar

patient had an attack of acute infarction.

CHAPTER normal, brown mushy consistency (the consistency of soft brownmungin in because of an increase in serum lipids.

Uncontrolled diabetes stroke and hypertension could be a risk factor for AMI.

Physical examination:

Vital sign indicates 36.5 oC normal, 140/80 mmHg indicates tension Hipertesi

stage 1, Nadi 92 x / min indicates a normal regular, respiration 24 x / min indicates a

normal, indicating normal vesicular lung Second, the vesicular sound due to air through

the ductus alveolar and alveoli, the sound heard throughout the lung field, his voice

soft, low, inspiration is longer than the expiratory 3: 1, heard most clearly in the

peripheral lung, inspiration> expiration, the heart signifies regular SI-S2 normal, no

audible noise normal systolic sounds.

Here the patient has hypertension, we have seen in the chronic high blood

pressure will cause the gap and damage the endothelial lining of blood vessels. With the

rupture of endothelial damage arising teradinya recurrent factors that promote

inflammation cycle, accumulation of white blood cells and platelets and clot formation,

called a thrombus, thrombus formed can become detached and cause embolism,

damage also would interfere with the release of endothelial nitric oxide which is a

vasodilator so that the blood vessels so vasoconstriction , this causes reduced blood

flow and ischemia occur that cause pain.

Investigations ECG:ST elevation: V1 - V5 indicates miocardium injury, injury to the possibility of

describing the degree of cellular damage is more than just ischemia, and ST segment

elevation is usually a sign of who can be counted on to find out about the occurrence of

myocardial infarction has occurred and if the ST segment is usually returned to baseline

within several hours.

LVH: Left ventricular hypertrophy, left ventricular enlargement occurs.

Q pathology: indicate there has been an irreversible myocardial cell death,

because it is irreversible wave of Q tends to settle along the patient's life. Q wave

formation occurs when a region in the myocardium dead, he had no electrical activity

and no longer able to deliver electricity. As a result, all the heart's electrical force will bedirected manjauhi infarct region. Therefore, the electrodes are located above the infarct

region will record a negative deflection in.

When viewed from the ECG investigation showed that the patients had acute

myocardial infarction because there is ST elevation and pathologic Q visible presence

indicates injury to the miocardim.

In the anamnesis there was at IMA crushed chest pain such as heavy objects,

radiating to the mandible or the left arm, accompanied by nausea, sweating, shortness

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of breath. But on some of those who suffer from diabetes mellitus and the elderly

usually do not show these symptoms.

9. TREATMENTS OF ACUTE MYOCARDIAL INFARCTION

The main goals of ED medical therapy are rapid intravenous thrombolysis and/or rapid

referral for PCI, optimizing oxygenation, decreasing cardiac workload, and controllingpain.

ANTITHROMBOTIC AGENTS

These agents prevent the formation of thrombus associated with myocardial infarction

and inhibit platelet function by blocking cyclooxygenase and subsequent aggregation.

Aspirin

Administer as soon as possible. Inhibits cyclooxygenase, which produces thromboxane

A2, a potent platelet activator. Early administration has been shown to reduce 35-d

mortality rate by 23% compared with placebo. An added mortality benefit exists when

used in combination with thrombolytics.

Heparin

Augments activity of antithrombin III and prevents conversion of fibrinogen to fibrin.

Does not actively lyse preformed clot, but it is able to inhibit further thrombogenesis

after thrombolysis. Heparin should be administered to patients undergoing PCI.

Prevents reaccumulation of clot after spontaneous fibrinolysis. Benefit as adjunctive

therapy for streptokinase not clear.

VASODILATORS

These agents oppose coronary artery spasm, which augments coronary blood flow and

reduces cardiac work by decreasing preload and afterload.

Nitroglycerin (Minitran, Nitrogard, Nitrol, Nitrolingual, Nitrostat, Nitro-Dur)

Causes relaxation of vascular smooth muscle by stimulating intracellular cyclicguanosine monophosphate production. Result is decrease in blood pressure.

BETA-ADRENERGIC AGENTS

These agents inhibit chronotropic, inotropic, and vasodilatory responses to beta-

adrenergic stimulation and reduce blood pressure, which decreases myocardial oxygen

demand.

Metoprolol (Lopressor)

Selective beta1-adrenergic receptor blocker that decreases automaticity of contractions.

During IV administration, carefully monitor blood pressure, heart rate, and ECG. Goal of

treatment is to reduce heart rate to 60-90 bpm.Esmolol (Brevibloc)

Excellent drug for use in patients at risk for complications from beta-blockade,

particularly those with reactive airway disease, mild-to-moderate LV dysfunction,

and/or peripheral vascular disease. Short half-life of 8 min allows for titration to desired

effect and quick discontinuation if needed.

THROMBOLYTIC AGENTS

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These agents prevent recurrent thrombus formation and rapid restoration of

hemodynamic disturbances.

Alteplase (Activase)

Fibrin-specific agent with a brief half-life of 5 min. Adjunctive therapy with IV heparin is

necessary to maintain patency of arteries recanalized by tPA, especially during the first

24-48 h. Heparin may be administered during tPA infusion.Streptokinase (Kabikinase, Streptase)

Nonfibrin specific agent with a half-life of 23 min. Need for adjunctive therapy with

heparin is controversial. Acts with plasminogen to convert plasminogen to plasmin.

Plasmin degrades fibrin clots as well as fibrinogen and other plasma proteins.

PLATELET AGGREGATION INHIBITORS

These agents inhibit platelet aggregation and reduce mortality.

Clopidogrel (Plavix)

Selectively inhibits adenosine diphosphate (ADP) binding to platelet receptor and

subsequent ADP-mediated activation of glycoprotein GPIIb/IIIa complex, thereby

inhibiting platelet aggregation.

Eptifibatide (Integrilin)

Antagonist of the platelet glycoprotein (GP) IIb/IIIa receptor, which reversibly prevents

von Willebrand factor, fibrinogen, and other adhesion ligands from binding to the GP

IIb/IIIa receptor. End effect is the inhibition of platelet aggregation. Effects persist over

duration of maintenance infusion and are reversed when infusion ends.

ANALGESICS

These agents reduce pain, which decreases sympathetic stress.

Morphine sulfate (Duramorph, Astramorph, MS Contin)

DOC for analgesia because of reliable and predictable effects, safety profile, and ease ofreversibility with naloxone. Various IV doses are used; commonly titrated until desired

effect obtained.

ACE INHIBITORS

These agents prevent conversion of angiotensin I to angiotensin II, a potent

vasoconstrictor, causing lowered aldosterone secretion.

Captopril

Has short half-life, which makes it important drug for initiation of ACE inhibitor therapy.

Can be started at low dose and titrated upward as needed and as patient tolerates.

10.COMPLICATION OF ACUTE MYOCARARDIAL INFARCTION

Arrhythmias / Heart block:

Briefly, the LAD supplies most of the conduction system below the A-V node (the His-

Purkinje system), while the RCA supplies most of the conduction system at and above

the A-V node (including the S-A node and the A-V nodes themselves).

Hypotension:

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Hypotension may occur in various settings following acute MI. It is important to

distinguish between the various causes of hypotension in the setting of acute MI

because they are treated quite differently.

MECHANICHAL COMPLICATIONS AFTER AMI

Some of the potentially correctable mechanical complications of MI are describedbelow, and their peak incidence is usually between 3 and 7 days following MI, when the

myocardial tissue is softest, and most vulnerable to rupture.

Acute mitral regurgitation:

Acute MR may occur abruptly from rupture of a left ventricular papillary muscle

resulting in a flail mitral leaflet, usually the posterior leaflet. This results in an abrupt

decrease in forward cardiac output, leading to congestive heart failure and often to

cardiogenic shock.

Ventricular septal rupture:

Acute ventricular septal rupture can occur usually several days following the acute

infarction, due to softening of the necrotic portion of the septum. This can occur in both

inferoposterior and in anterior myocardial infarction. A loud systolic ejection murmur

usually occurs and results in an acute left-to-right shunt with congestive heart failure

and usually cardiogenic shock.

Left ventricular free wall rupture:

Rupture of the left ventricular free wall is analogous to ventricular septal defect but

occurs in the free wall of the left ventricle, usually resulting in abrupt cardiogenic shock

OTHER COMPLICATIONS AFTER AMI

Left ventricular aneurysm formation:

Left ventricular apical aneurysm formation usually occurs following antero-apical

myocardial infarction, after LAD occlusion. This weakening of the apical wall results in anoutpouching or "dyskinesis" of the apex of the heart during systole.

Right ventricular infarction:

Right ventricular infarction occurs almost exclusively in the setting of right coronary

artery occlusion. Hallmarks include elevation of the jugular venous pressure in the

absence of pulmonary congestion. Hypotension often occurs in the absence of an

elevated pulmonary capillary wedge pressure. Elevation of the ST segments may be

present in the right precordial EKG leads.

Pericarditis:

Post infarction pericarditis usually begins several days after the infarct, due to an

inflammatory exudate in the pericardium. Pericarditis pain is distinguishable frominfarct pain because of its pleuritic nature, radiation to the left trapezius ridge, and the

associated low-grade fever and pericardial friction rub.

Cardiogenic shock

Cardiogenic shock results when there is a marked reduction in forward cardiac output

leading to hypotension, decreased organ perfusion, and at the same time elevated left

ventricular filling pressures leading to congestive heart failure. This can be due to either

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massive left ventricular infarction or can be the result of one of the mechanical

complications described above.

11.The prognostic evaluation of the patient with an acute myocardial infarction is one of

the most interesting unanswered problems. This is both because of its complexity and

its implications in terms of secondary prevention. Several clinical studies haveemphasized the reliability of the prognostic evaluation based on data collected during

the first 24 hours. We therefore evaluated the prognostic relevance of 26 variables

measured in the coronary care unit in 1914 patients admitted to our Unit as a result of

acute myocardial infarction during the past 10 years. Twenty-four patients were lost to

follow-up so that the evaluation refers to 1,890 patients, 1,506 of whom are males aged

between 22 and 99 years (mean 58.1) and 384 are females aged between 29 and 88

years (mean 67.1); thus there is a greater prevalence of males. The sex-related

difference in the age distribution is statistically significant. In-hospital mortality was

analyzed using univariate and multivariate statistical methods (chi-squared test,

multiple logistic regression analysis). The prognostic relevance of the considered

variables in relation to the survival was analysed using the logrank test and using Cox's

model. The variables associated with a greater risk of in-hospital death were found to

be: age, presence of diabetes, anterior location of the infarct, arterial hypotension at

admission, Killip class III and IV and the presence of ventricular tachyarrhithmias. In

contrast, smokers had a lower in-hospital death risk. As to mortality during the follow-

up, there was an association with age, female sex, pre-existent coronary disease,

presence of high heart rate on admission, low peripheral tissue perfusion, x-ray

documented pulmonary congestion, supraventricular tachiarrhythmias and

intraventricular block. In contrast, the presence of obesity was associated with a

reduced death risk during the follow-up. During the follow-up the most frequent cause

of death was re-infarction, followed by sudden death, death from non-cardiac causesand heart failure.

12.Preventif for acute myocardial infarction prevention are: stop smoking, get used to

living healthy, avoid fatty foods, weight loss.

Controlling blood pressure, Lowers blood cholesterol levels with diet or with

medication, Doing sport regularly.

SOURCES http://www.brown.edu/Courses/Bio_281-cardio/cardio/handout4.htm

http://emedicine.medscape.com/article/759321-treatment http://emedicine.medscape.com/article/159383-overview http://repository.usu.ac.id/bitstream/123456789/3489/1/gizi-bahri8.pdf

http://piofamul.com/wp-content/uploads/2010/09/pharmaceutical-care-penyakit-jantung-koroner.pdf

http://www.fkumyecase.net/wiki/index.php?page=DIAGNOSIS+DAN+TERAPI+AKUT+MIOKARD+INFARK+DENGAN+ST+ELEVASI

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PLENARI DISCUSSION

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TUTORIAL 6:

Teuku Rezki Amriza 20080310129

Herlambang Surya Perkasa 20080310034

Hengki Exsar Aritama 20080310046

Nurul Azizatus Solehah 20080310050

Fergiawan Indra Prabowo 20080310074Alindina Anjani 20080310078

Asti Haryani 20080310080

Verani Dwitasari 20080310081

Anita Setia Murdani 20080310110

Shorea Sylviana Puteri 20080310112

Yolanda Pitra Kusumadewi 20080310113

Galih Oktriasari Khoirunisa 20080310114

Aisha Yuswini A 20080310142

Dina Eka Bhintami 20080310159

The pathogenesis of Ath. remains unexplained,

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but endothelial damage (and chlamydiainfection?, see above) could be the primaryevent and the reaction to it may eventuallylead to plaque formation (response to injury

hypothesis; C). Plaques usually develop atsites of high mechanical stress (vessel bifurcation);in this way also hypertension becomes arisk factor. Among the reactions are an increasedlipid uptake in the vessel wall as wellas adhesion of monocytes and thrombocytes

(C2,3), helped by HoCys. The monocytespenetrate into the intima and are transformed

into macrophages (C4). These liberate reactiveO2 radicals, especially the superoxide anionO2

(also helped by HoCys), which have ageneral damaging effect on endothelial cellsand inactivate endothelium-formed NO on itsway to the endothelium and the vascular musculature:NO + O2

ONOO(C5). Thisresults in the loss of NO action, namely inhibitionof platelet and monocyte adhesion tothe endothelium as well as antiproliferativeand vasodilating effects on the vascular musculature.

The latter favorspasms (B andC7). Even in the early stages of Ath., O2 radicals modify by oxidation of those LDLs that have entered

the endothelium (C7). Oxidized LDLsdamage the endothelium and there inducethe expression of adhesion molecules which

allow vessel musculature to proliferate. Oxidationalso results in altered binding of LDLs.They can no longer be recognized by ApoB 100

receptors (p. 246ff.), but rather by so-calledscavenger receptors that are contained in largeamounts within the macrophages. Consequently,these now phagocytize large amountsof LDLs and are transformed into sedentary

foam cells (C9). Lipoprotein(a) can be oxidized

and phagocytized in a similar fashion.Simultaneously, chemotactic factors of monocytesand thrombocytes trigger the migrationof smooth muscle cells from the media into the

intima (C6). Here they are stimulated toproliferate by PDGF and other growth-promotingfactors (from macrophages, thrombocytes,damaged endothelium, and the muscle cellsthemselves). They, too, are transformed intofoam cells by uptake of oxidized LDLs

(C10). They form an extracellular matrix(collagen, elastin, proteoglycans) that alsocontributes to atheroma formation.The consequences of plaque deposition

(B) are narrowing of the lumen that can lead

to ischemia. Coronary heart disease (p. 218ff.) as well as chronic occlusive arterialdisease of the limbs with painful ischemia onexercise (intermittent claudication) are examplesof this. Other consequences of plaque formationare stiffeningof the vessel wall (calcification),thrombus formation that obstructs theresidual lumen and can cause peripheral emboli

(e.g., cerebral infarction, stroke) as well asbleeding into the plaques (additional narrowingby the haematoma) and the vessel wall.Thus weakened, the wall may be stretched(aneurysm; see below) and even rupture, withdangerous bleedinginto the surrounding tissues,for example, from the aorta (see below)or cerebral vessels