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Trisulo Wasyanto, MD, FIHA, FAPSC, FAsCC

Department of Cardiology and Vascular Medicine, Faculty of Medicine

University of Sebelas Maret / Dr.Moewardi Hospital, Surakarta


Myocardial infarction (MI), commonly known as a heart attack, is the irreversible necrosis of
heart muscle secondary to prolonged ischemia. MI is considered part of a spectrum referred to as
acute coronary syndrome (ACS). ACS refers to a spectrum of clinical presentations ranging from
those for ST-segment elevation myocardial infarction (STEMI) to presentations found in non
ST-segment elevation myocardial infarction (NSTEMI) or in unstable angina. MI is dened in
pathology as myocardial cell death due to prolonged ischemia. MI usually precipitated by acute
thrombosis induced by a ruptured or eroded atherosclerotic coronary plaque, with or without
concomitant vasoconstriction, causing a sudden and critical reduction in blood ow. In the
complex process of plaque disruption, inammation was revealed as a key pathophysiological
element. The leading symptom of ACS is typically chest pain. The working diagnoses of ACS
are based on symptom of chest pain, changes of the ECG and cardiac enzyme (biomarkers) or
sometimes imaging modalities. Patients with ST-segment elevation MI require immediate
coronary recanalization with PCI or thrombolysis. Patients without persistent ST-segment
elevation should receive baseline treatment including: aspirin, low-molecular-weight heparin,
clopidogrel, beta blockers and nitrates.
Key words: acute myocardial infarction, ACS, STEMI, NTEMI, unstable angina, heart attack.

Cardiovascular diseases are currently the leading cause of death in industrialized

countries and are expected to become so in emerging countries by 2020. Among these, coronary
artery disease (CAD) is the most prevalent manifestation and is associated with high mortality
and morbidity. Myocardial infarction (MI) can be recognized by clinical features, including
electrocardiographic (ECG) ndings, elevated values of biochemical markers (biomarkers) of
myocardial necrosis, and by imaging, or may be dened by pathology.
Myocardial infarction is considered part of a spectrum referred to as acute coronary
syndrome (ACS). ACS refers to a spectrum of clinical presentations ranging from those for ST-
segment elevation myocardial infarction (STEMI) to presentations found in nonST-segment
elevation myocardial infarction (NSTEMI) or in unstable angina. In terms of pathology, ACS is
almost always associated with rupture of an atherosclerotic plaque and partial or complete
thrombosis of the infarct-related artery (2, 4, 5, 7).
The first goal for healthcare professionals is to diagnose in a very rapid manner whether
the patient is having an STEMI or NSTEMI because therapy differs between the 2 types of
myocardial infarction. Particular considerations and differences involve the urgency of therapy
and degree of evidence regarding different pharmacological options. As a general rule, initial
therapy for acute myocardial infarction is directed toward restoration of perfusion as soon as
possible to salvage as much of the jeopardized myocardium as possible. This may be
accomplished through medical or mechanical means, such as PCI or CABG
In the past, a general consensus existed for the clinical syndrome designated as MI. In
studies of disease prevalence, the World Health Organization (WHO) dened MI from
symptoms, ECG abnormalities and cardiac enzymes. However, the development of ever more
sensitive and myocardial tissue-specic cardiac biomarkers and more sensitive imaging
techniques now allows for detection of very small amounts of myocardial injury or necrosis.
Additionally, the management of patients with MI has signicantly improved, resulting in
less myocardial injury and necrosis, in spite of a similar clinical presentation. Moreover, it
appears necessary to distinguish the various conditions which may cause MI, such as
spontaneous and procedure-related MI. Accordingly, physicians, other healthcare providers
and patients require an up-to-date denition of MI (4, 5, 7).

Myocardial infarction, commonly known as a heart attack, is the irreversible necrosis of

heart muscle secondary to prolonged ischemia. This usually results from an imbalance in oxygen
supply and demand, which is most often caused by plaque rupture with thrombus formation in a
coronary vessel, resulting in an acute reduction of blood supply to a portion of the myocardium.
Myocardial infarction is considered part of a spectrum referred to as acute coronary syndrome
(ACS). The ACS continuum representing ongoing myocardial ischemia or injury consists of
unstable angina, nonST-segment elevation myocardial infarction (NSTEMI), and ST-segment
elevation myocardial infarction (STEMI). Patients with ischemic discomfort may or may not
have ST-segment or T-wave changes denoted on the electrocardiogram (ECG). ST elevations
seen on the ECG reflect active and ongoing transmural myocardial injury. Without immediate
reperfusion therapy, most persons with STEMI develop Q waves, reflecting a dead zone of
myocardium that has undergone irreversible damage and death. Those without ST elevations are
diagnosed either with unstable angina or NSTEMIdifferentiated by the presence of cardiac
enzymes. Both these conditions may or may not have changes on the surface ECG, including-
segment depression or T-wave morphological changes (4, 5).

ACS represents a life-threatening manifestation of atherosclerosis. It is usually

precipitated by acute thrombosis induced by a ruptured or eroded atherosclerotic coronary
plaque, with or without concomitant vasoconstriction, causing a sudden and critical reduction in
blood ow. In the complex process of plaque disruption, inammation was revealed as a key
pathophysiological element. In rare cases, ACS may have a non-atherosclerotic etiology such as
arteritis, trauma, dissection, thrombo-embolism, congenital anomalies, cocaine abuse, or
complications of cardiac catheterization.

MI is dened in pathology as myocardial cell death due to prolonged ischemia. After the
onset of myocardial ischemia, histological cell death is not immediate, but takes a nite period of
time to developas little as 20 min, or less in some animal models. It takes several hours before
myocardial necrosis can be identied by macroscopic or microscopic post-mortem examination.
Complete necrosis of myocardial cells at risk requires at least 2-4 h, or longer, depending on the
presence of collateral circulation to the ischemic zone, persistent or intermittent coronary arterial
occlusion, the sensitivity of the myocytes to ischemia, pre-conditioning, and individual demand
for oxygen and nutrients . The entire process leading to a healed infarction usually takes at least
5-6 weeks. Reperfusion may alter the macroscopic and microscopic appearance.
The spectrum of myocardial injury depends not only on the intensity of impaired
myocardial perfusion but also on the duration and the level of metabolic demand at the time of
the event. The damage in the myocardium is essentially the result of a tissue response that
includes apoptosis (cell death) and inflammatory changes. Therefore, the hearts of patients who
suddenly die from an acute coronary event may show little or no evidence of damage response to
the myocardium at autopsy. The typical myocardial infarction initially manifests as coagulation
necrosis that is ultimately followed by myocardial fibrosis. Contraction-band necrosis is also
seen in many patients with ischemia. This is followed by reperfusion, or it is accompanied by
massive adrenergic stimulation, often with concomitant myocytolysis (4, 5, 8, 9).
The key pathophysiological concepts such as vulnerable plaque, coronary thrombosis,
vulnerable patient, endothelial dysfunction, accelerated atherothrombosis, secondary
mechanisms of NSTE-ACS (Non ST ElevationAcute Coronary Syndrome) , and myocardial
injury have to be understood for the correct use of the available therapeutic strategies. The
lesions predicting ACS are usually angiographically mild, characterized by a thin-cap
fibroatheroma, by a large plaque burden, or by a small luminal area, or some combination of
these characteristics (4).


The leading symptom of ACS is typically chest pain. The term acute myocardial
infarction (MI) should be used when there is evidence of myocardial necrosis in a clinical setting
consistent with acute myocardial ischemia. The working diagnosis of NSTE-ACS is a rule-out
diagnosis based on the ECG, i.e. lack of persistent ST elevation. Biomarkers (troponins) further
distinguish NSTEMI and unstable angina. Imaging modalities are used to rule out or rule in
differential diagnoses. Traditionally, several clinical presentations have been distinguished (4, 5):
Prolonged ( >20 min) anginal pain at rest;
New onset (de novo) angina (Class II or III of the Classication of the CCS
Recent destabilization of previously stable angina with at least Canadian
Cardiovascular Society Class III angina characteristics (crescendo angina); or
Post-MI angina.

III.1. Physical examination

The physical examination is frequently normal. An important goal of the physical
examination is to exclude non-cardiac causes of chest pain and non-ischemic cardiac disorders
(e.g. pulmonary embolism, aortic dissection, pericarditis, valvular heart disease) or potentially
extra cardiac causes such as acute pulmonary diseases (e.g. pneumothorax, pneumonia, or pleural

III.2. Electrocardiogram
The resting 12-lead ECG is the rst-line diagnostic tool in the assessment of patients with
suspected ACS. It should be obtained within 10 min after rst medical contact. The characteristic
ECG abnormalities of NSTE-ACS are ST-segment depression or transient elevation and/or T-
wave changes. The nding of persistent (>20 min) ST-elevation suggests STEMI, which
mandates different treatment. If the initial ECG is normal or inconclusive, additional recordings
should be obtained if the patient develops symptoms and these should be compared with
recordings obtained in an asymptomatic state. Comparison with a previous ECG, if available, is
valuable, particularly in patients with co-existing cardiac disorders such as LV hypertrophy or
previous MI. ECG recordings should be repeated at least at 3-6 h and 24 h after rst presentation,
and immediately in the case of recurrence of chest pain or symptoms (4, 5, 6).

III.3. Biomarker
Cardiac troponins play a central role in establishing a diagnosis and stratifying risk, and
make it possible to distinguish between NSTEMI and unstable angina. Troponins are more
specic and sensitive than the traditional cardiac enzymes such as creatine kinase (CK), its iso
enzyme MB (CK-MB), and myoglobin. Elevation of cardiac troponins reects myocardial
cellular damage, which in NSTE-ACS may result from distal embolization of platelet-rich
thrombi from the site of a ruptured or eroded plaque. Accordingly, troponin may be seen as a
surrogate marker of active thrombus formation. In the setting of myocardial ischemia (chest pain,
ECG changes, or new wall motion abnormalities), troponin elevation indicates MI. In patients
with MI, an initial rise in troponins occurs within 4 h after symptom onset. Troponins may
remain elevated for up to 2 weeks due to proteolysis of the contractile apparatus. In NSTE-ACS,
minor troponin elevations usually resolve within 4872 h. There is no fundamental difference
between troponin T and troponin I (4, 5, 7).
In the clinical setting, a test with high ability to rule out (negative predictive value) and
correctly diagnose ACS (positive predictive value) is of paramount interest. Recently, high-
sensitivity or ultrasensitive assays have been introduced that have a 10- to 100-fold lower limit
of detection and full the requirements of analytical precision. Therefore, MI can now be
detected more frequently and earlier in patients presenting with chest pain. Other life-threatening
conditions presenting with chest pain, such as dissecting aortic aneurysm or pulmonary
embolism, may also result in elevated troponins and should always be considered as differential
diagnoses. Elevation of cardiac troponins also occurs in the setting of non-coronary-related
myocardial injury (Table 1) (4).

Table 1. Possible non-ACS causes of troponin elevation (bold: important differential diagnoses)

Chronic or acute renal dysfunction

Severe congestive heart failure acute and chronic
Hypertensive crisis
Tachy- or bradyarrhythmias
Pulmonary embolism, severe pulmonary hypertension
Inammatory diseases, e.g. myocarditis
Acute neurological disease, including stroke, or subarachnoid haemorrhage
Aortic dissection, aortic valve disease or hypertrophic cardiomyopathy
Cardiac contusion, ablation, pacing, cardioversion, or endomyocardial biopsy
Apical ballooning syndrome (Tako-Tsubo cardiomyopathy)
Inltrative diseases, e.g. amyloidosis, haemochromatosis, sarcoidosis, sclerodermia
Drug toxicity, e.g. adriamycin, 5-uorouracil, herceptin, snake venoms
Burns, if affecting >30% of body surface area
Critically ill patients, especially with respiratory failure, or sepsis
Due to low sensitivity for MI, a single negative test on first contact with the patient is not
sufficient for ruling out ACS, as in many patients an increase in troponins can be detected only in
the subsequent hours. Therefore, repeated measurements after 69 h have been advocated. The
recently introduced high-sensitive troponin assays better identify patients at risk and provide
reliable and rapid prognosis prediction allowing a fast track rule-out protocol (3 h).
Biomarkers more specifically reflecting vascular inflammation processes or markers of
oxidative stress have the greatest potential by better reflecting the underlying mechanisms.
Among these, myeloperoxidase, growth differentiation factor 15, and lipoprotein associated
phospholipase A-2 present promising options. Early diagnosis of ACS may be improved by
measurements of fatty acid-binding protein or ischemia-modified-albumin as well as markers of
systemic stress (copeptin) (4, 5).

III.4. Imaging
III.4.1. Non-invasive imaging techniques
Echocardiography is the most important modality in the acute setting because it is
rapidly and widely available. LV systolic function is an important prognostic variable in patients
with CAD and can be easily and accurately assessed by echocardiography. In experienced hands,
transient segmental hypokinesia or akinesia may be detected during ischemia. Furthermore,
differential diagnoses such as aortic dissection, pulmonary embolism, aortic stenosis,
hypertrophic cardiomyopathy, or pericardial effusion may be identified.
Cardiac magnetic resonance (CMR) imaging can integrate assessment of function and
perfusion, and detection of scar tissue in one session, but this imaging technique is not yet widely
available. CMR imaging is useful to assess myocardial viability and to detect myocarditis.
Multidetector computed tomography (CT) is not currently used for the detection of
ischemia, but offers direct visualization of the coronary arteries. Therefore, this technique has the
potential to exclude the presence of CAD (4, 5).

III.4.2. Invasive imaging (coronary angiography)

Coronary angiography provides unique information on the presence and severity of CAD
and therefore remains the gold standard. Data from the Thrombolysis In Myocardial Infarction
(TIMI)-3B studies show that 3038% of patients with unstable coronary syndromes have single-
vessel disease and 4459% have multivessel disease (>50% diameter stenosis) (3, 4, 5).



All patients being transported for chest pain should be managed as the pain were
ischemic in origin, unless clear evidence to the contrary is established. Most deaths caused by
myocardial infarction occur early and are attributable to primary ventricular fibrillation (VF).
Therefore, initial objectives are immediate electrocardiographic monitoring; electric
cardioversion of VF. Approximately 65% of deaths caused by myocardial infarction occur in the
first hour. Treatment of ACS is aimed at the following:

Restoration of the balance between the oxygen supply and demand to prevent further
Pain relief
Prevention and treatment of complications

Treatment in the Emergency Department (ED) begins with focused cardiovascular

historytaking and physical examination, the establishment of intravenous (IV) access, the use of
12-lead ECG and continuous rhythm monitoring. All patients with suspected myocardial
infarction should be given chewable aspirin, 160-325 mg, unless they have a documented allergy
to aspirin.

Pulse oximetry should be performed, and appropriate supplemental oxygen should be

given (maintain oxygen saturation >90%) to prevent hypoxemia. High concentrations may be
counterproductive because of vasoconstriction and the lack of augmented myocardial oxygen
delivery in normoxemic patients.

Initial stabilization of patients with suspected myocardial infarction and ongoing acute
chest pain should include administration of sublingual nitroglycerin; if pain persists, 2
additional doses of nitroglycerin may be administered at 5-minute intervals. Patients should be
free of contraindications, such as hypotension (systolic blood pressure < 90 mm Hg),
bradycardia, tachycardia, or findings suggestive of right ventricle [RV] infarction.

Refractory or severe pain should be treated symptomatically with IV morphine. Doses of

morphine, 4-8 mg IV, may be repeated every 5-15 minutes with relative impunity until the pain
is relieved or toxicity is manifested by hypotension, vomiting, or depressed respiration. Should
toxicity occur, a morphine antagonist, such as naloxone, may reverse it. The patient's blood
pressure and pulse must be monitored; the systolic blood pressure must be maintained above 100
mm Hg and, optimally, below 140 mm Hg. Relative hypotension may be treated by elevating the
lower extremities or by giving fluids, except in patients with concomitant pulmonary congestion,
in whom treatment for cardiogenic shock may be required. Atropine, in doses similar to those
given in the prehospital phase, may increase blood pressure if hypotension reflects bradycardia
or excess vagal tone (4, 5, 8, 9).

IV.1.1. Treatment of patients with STEMI

If STEMI is present, the decision as to whether the patient will be treated with
thrombolysis or primary PCI should be made within 10 minutes. Treatment options include the
immediate start of IV thrombolysis in the ED or the immediate transfer of the patient to the
cardiac catheterization laboratory for primary percutaneous transluminal coronary angioplasty
(PTCA). The goal for patients with STEMI should be to achieve a door-to drug time of within 30
minutes and a door-to-balloon time of within 90 minutes. In patients with STEMI who are to be
treated with primary PCI, delays in administering the procedure are associated with higher
mortality in these patients (4, 5, 8, 9).

Delays in the administration of thrombolysis often occur because of the following factors:

Delay in obtaining an ECG

Lack of immediate availability of thrombolytic agents
Outdated protocols requiring cardiology consultation before thrombolytic treatment
IV.1.2. Treatment of patients with NSTEMI

If STEMI is not present, then the workup should proceed looking for unstable angina or
NSTEMI and for alternative diagnoses. Confirmation of the diagnosis of NSTEMI requires
waiting for the results of cardiac markers. The cardiac troponin I (cTnI) assays are less sensitive
for outcome prediction among patients with myocardial injury. If a clinical suspicion of
myocardial infarction remains despite negative cTnI results, those results should be
complemented by results from more sensitive laboratory assays. In the case of unstable angina,
diagnosis may await further diagnostic studies, such as coronary angiography or imaging studies,
to confirm the diagnosis and to distinguish it from non coronary causes of chest pain. Although
patients presenting with no ST-segment elevation are not candidates for immediate
thrombolytics, they should receive anti-ischemic therapy and may be candidates for PCI
urgently or during admission (4, 5).


Critical care units (CCUs) have reduced early mortality rates from acute myocardial
infarction by approximately 50% by providing immediate defibrillation and by facilitating the
implementation of beneficial interventions. These interventions include the administration of IV
medications and therapy designed to do the following:

Limit the extent of myocardial infarction

To salvage jeopardized ischemic myocardium
Recanalize infarct-related arteries.

Prophylaxis for stress ulcers with oral sucralfate, 1 g given twice a day, or an H2-
antagonist (famotidine, ranitidine, or cimetidine), given orally or intravenously at 6- to 12-hour
intervals, is appropriate for patients at high risk, including those with sepsis, hypotension or
shock, bleeding diathesis, or elevated intracranial pressure or who have a requirement for
prolonged mechanical intervention.
Physical activity should be limited (bed-chair regimen) throughout the patient's CCU
stay, with gradual and carefully monitored resumption of ambulatory activity in the late hospital
phase. Educational programs targeting smoking cessation, lipid lowering, and treatment of
hypertension, as indicated, in addition to phased rehabilitation programs, should be started early
during the hospital course for patients with uncomplicated myocardial infarction.

Use of sedative, anxiolytic, and hypnotic drugs at night may be helpful. Also important
are optimal communication with compassionate physicians and nurses and the reassurance it

IV.2.1. Thrombolytic Therapy

Thrombolytic therapy has been shown to improve survival rates in ST-segment elevation
myocardial infarction but is not indicated in the treatment for nonST-segment elevation
myocardial infarction. Door-to-drug time should be no more than 30 minutes. Thrombolytic
therapy administered within the first 2 hours can occasionally abort myocardial infarction and
dramatically reduce the mortality rate. Thrombolysis is generally preferred to PCI in cases where
the time from symptom onset is less than 3 hours and if there would be a delay to PCI, greater
than 1-2 additional hours to door-to-balloon time (4, 5).

The first generation of fibrinolytic drugs (eg, streptokinase, urokinase, acetylated

plasminogen streptokinase activator complexes [APSACs], reteplase, and novel plasminogen
activator [n-PA]) indiscriminately induce activation of circulating plasminogen and clot-
associated plasminogen. First-generation drugs invariably elicit a systemic lytic state
characterized by depletion of circulating fibrinogen, plasminogen, and hemostatic proteins and
by marked elevation of concentrations of fibrinogen degradation products in plasma.

Second-generation drugs (eg, t-PA, single-chain urokinase plasminogen activator),

including agents such as tenecteplase, preferentially activate plasminogen in the fibrin domain,
rather than in the circulation, as with free plasminogen. Therefore, these drugs have clot
selectivity. Tenecteplase should be initiated as soon as possible after the onset of acute
myocardial infarction (AMI) symptoms. In AMI patients, tenecteplase administered as a single
bolus exhibits a biphasic disposition from the plasma.
In optimal regimens, these agents induce clot lysis without inducing a systemic lytic
state, they are less prone than nonselective agents to predispose the patient to hemorrhage
necessitating transfusion, and they are effective in inducing recanalization in 80-90% of infarct-
related arteries within 90 minutes. Therefore, t-PA recanalizes 75-80% of infarct-related arteries;
by contrast, IV streptokinase recanalizes approximately 50% of infarct-related arteries.

IV.2.2. Antithrombotic Therapy

At present, IV unfractionated heparin (UFH) is routinely administered, in addition to

orally administered aspirin. Alternatives include low-molecular-weight heparin (LMWH or
enoxaparin), other inhibitors of coagulation (eg, hirudin, fondaparinux, bivalirudin), and
antagonists of binding of fibrinogen to the platelet surface glycoprotein IIb/IIIa (GPIIb/IIIa)
receptor (eg, abciximab, eptifibatide, tirofiban, orbofiban). Thienopyridines (eg, ticlopidine,
clopidogrel) similarly inhibit platelet aggregation by binding to platelet adenosine diphosphate
receptors, which block activation of the IIb/IIIa pathway.

In the management of all patients with ACS or suspected ACS, anticoagulation therapy is
the standard of care. In patients with or suspected unstable angina (UA)/NSTEMI,
anticoagulation therapy should be added to antiplatelet therapy as soon as possible. In patients
who have been selected to undergo an early invasive strategy for UA/NSTEMI, proven effective
anticoagulant therapy includes UFH, enoxaparin, fondaparinux, and bivalirudin.

In UA/NSTEMI, the duration of anticoagulation in uncomplicated conservative therapy is

48 hours for UFH and the entire hospital stay is up to 8 days for LMWH or fondaparinux. In
patients for whom CABG is chosen for revascularization, continue UFH up to the time of
surgery, discontinue LMWH/fondaparinux 24 hours before surgery, and switch to UFH;
alternatively, discontinue bivalirudin 3 hours before surgery and switch to UFH. If PCI is
performed, anticoagulation therapy can be discontinued safely post successful revascularization.

In STEMI, parenteral anticoagulant therapy with UFH or bivalirudin is a Class I

indication in patients undergoing primary PCI. Data are scant with regard to heparin efficacy in
patients not receiving thrombolytic therapy in the setting of myocardial infarction; however,
considerable rationale exists for ancillary heparin therapy to inhibit the coagulation cascade.
LMWH is commonly used because of convenient dosing, reliable therapeutic levels, and
decreased incidence of heparin-induced-thrombocytopenia, especially if anticipated use is greater
than 2-3 days. Assuming that a patient does not have significant renal dysfunction (serum
creatinine level >2.5 mg/dL in men or >2 mg/dL in women), LMWH may be used with caution
as an alternative to UFH as an ancillary therapy to fibrinolytics, regardless of age (note that
different loading and maintenance doses are used in patients aged >75 y).

Aspirin should be administered immediately if not already taken by the patient at home
or administered by EMS before arrival. Use clopidogrel in case of aspirin allergy. Data from the
CLARITY trial (CLopidogrel as Adjunctive Reperfusion Therapy Thrombolysis in Myocardial
Infarction [TIMI] suggest that adding clopidogrel to this regimen is safe and effective. The
clopidogrel dose used was 300 mg. Further studies suggest that a higher dose of clopidogrel may
have added benefit. The Antiplatelet Therapy for Reduction of Myocardial Damage During
Angioplasty-Myocardial Infarction (ARMYDA-6 MI) multicenter study demonstrated that in
patients with STEMI, a loading dose of 600 mg clopidogrel prior to primary PCI was associated
with a smaller infarct size when compared with a 300-mg loading dose (1, 2, 4).

Clopidogrel use along with aspirin and anticoagulation therapy has a class I indication
for the entire spectrum of acute coronary syndromes. In patients receiving dual antiplatelet
therapy (aspirin and clopidogrel), the prophylactic use of proton pump inhibitors may reduce the
rate of upper gastrointestinal bleeding (1).

IV.2.3. Preventive Therapy in the acute hospital phase

Beta-adrenergic blockers are of benefit when given intravenously within 4 hours of the
onset of pain and continued on a long-term basis. Mortality, sudden death, and infarct size are
reduced in patients with Q-wave myocardial infarction when beta-blockers are given early.
Patients with unstable angina also benefit through a reduction in the incidence or severity of
myocardial infarction.

Chewing an aspirin shortly after onset of chest pain is a ready means to inhibit
thrombosis. In the hospital, small trials indicate benefits (decreased size of infarcts and
mortality) from insulin infusion, along with glucose and potassium, presumably through an anti-
apoptotic effect. Patients with insulin-dependent diabetes mellitus and peripheral vascular
disease may be treated with caution; the benefit of angioplasty is decreased in these patients.

ACE inhibitors are useful for long-term therapy and also appear to benefit patients who
have no evidence of hypotension if administration is begun within the first 24 hours after the
onset of myocardial infarction.

Treatment with both beta-adrenergic blockers and ACE inhibitors may improve the
balance between myocardial oxygen supply and demand, and it may limit infarct size.
Appropriate treatment of fluid status to optimize left ventricular filling pressures, maintain
oxygen saturation, and control heart rate by avoiding reflex sympathoadrenal stimulation is also

Calcium channel blockers have not been beneficial in acute myocardial infarction, and
they may exert deleterious adverse effects alone or when given with other medications.
Therefore, they should generally be avoided. Diltiazem may be useful for rate control in patients
with atrial fibrillation. Verapamil may be useful in patients with obstructive hypertrophy (8, 9).

Acute Myocardial Infarction are a major healthcare problem and represent a large number of
hospitalizations annually throughout in the world. In spite of modern treatment the rates of
mortality, reinfarction and readmission with an acute coronary syndrome at 6-months follow-up
remain still very high. After clinical examination, it is necessary to record an electrocardiogram
followed by continuous multi-lead ST-T segment monitoring, if possible blood samples should
be obtained to determine troponin T or I, and CK-MB.
(A) Patients with ST-segment elevation require immediate coronary recanalization with PCI or
(B) Patients without persistent ST-segment elevation should receive baseline treatment including:
aspirin, low-molecular-weight heparin, clopidogrel, beta blockers (if not contra-indicated)
and nitrates.

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