This segment will review emergent/early treatment difficulties for patients with acute STEMI and refer to other sections for a more extensive explanation.

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The ECG may establish the diagnosis of STEMI in patients coming to the clinic with chest discomfort indicative of an acute coronary syndrome. Early biomarkers may be normal.

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Clinical presentation

Patients with typical MI may exhibit the following symptoms in the days or even weeks before the event (although typical STEMI may strike abruptly and unexpectedly):

• Fatigue
• Chest discomfort

Chest discomfort in acute MI is:

1. For 30-60 minutes, intense and unrelenting.
2. Substernal, and often radiates up the neck, shoulder, and jaw, as well as down the left arm.
3. Characterised by epigastric pain which is a symptom that occurs in certain people, along with a sense of indigestion or fullness and gas.

Vital signs in MI include:

1. The patient's heart rate being frequently increased (tachycardic) as a result of a high sympathoadrenal discharge.
2. The pulse being irregular due to ventricular ectopy, an accelerated idioventricular rhythm, ventricular tachycardia, atrial fibrillation or flutter, or other supraventricular arrhythmias; bradyarrhythmias may also be present.

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Patient history

The patient's history is crucial for identifying myocardial infarction (MI) and may sometimes give the sole information necessary for diagnosis during the earliest stages of patient presentation.

1. In patients with typical acute MI, symptoms of weariness, chest soreness, or malaise may be evident in the days leading up to the event; conversely, typical ST-elevation myocardial infarction (STEMI) may develop without warning.
2. Chest discomfort associated with acute MI is often severe and unrelenting for 30-60 minutes. It originates in the retrosternal region and often extends up the neck, shoulder, and jaws, as well as down the left arm. The chest discomfort is often characterised as a squeezing, aching, burning, or even stabbing feeling in the substernal region. In some people, the symptom is epigastric, accompanied by an indigestion-like sensation or a sense of fullness and gas.
3. In other situations, individuals are unaware of their chest pain, have an abnormally high pain threshold, or suffer from a disease that inhibits pain perception, resulting in a malfunctioning anginal alerting system (e.g. diabetes mellitus).
4. Additionally, some individuals may have changed mental state as a result of pharmaceutical side effects or decreased brain perfusion. Elderly people who have pre-existing altered mental states or dementia may have no memory of recent symptoms and may have no complaints at all.
5. During the first few hours of the day, most cases of MI occur. The morning increase in sympathetic tone, which results in increases in blood pressure, heart rate, coronary vascular tone, and myocardial contractility; the morning increase in blood viscosity, coagulability, and platelet aggregability; and the morning increase in serum cortisol and plasma catecholamines, which results in sympathetic overactivity and increased myocardial demand.
6. A short history should be obtained and a focused physical examination performed during the first quick assessment. Significant elements of the history, such as the nature of the pain and significant associated symptoms, as well as previous history of or risk factors for cardiovascular disease, are used to determine the likelihood that these symptoms represent acute coronary syndrome (ACS) and to forecast clinical outcomes.
7. Maintain a high index of suspicion for MI, particularly when examining women, diabetic patients, elderly adults, dementia patients, patients with a history of heart failure, cocaine users, patients with hypercholesterolemia, and patients with a positive family history of early coronary disease (see aetiology).
8. Any first-degree male relative aged 45 years or younger or any first-degree female relative aged 55 years or younger who have had a MI or had coronary revascularisation is considered a positive family history.

Additional myocardial infarction symptoms include the following:

• Anxiety, commonly described as a sense of impending doom
• Pain or discomfort in specific areas of the body, such as the arms, left shoulder, back, neck, jaw, or stomach
• Lightheadedness, with or without syncope
• Cough
• Nausea, with or without vomiting
• Profuse sweating
• Shortness of breath
• Wheezing
• Rapid or irregular heart rate

As an indicator of myocardial infarction, the patient may remember simply one episode of dyspepsia. In certain circumstances, individuals fail to detect chest pain, may be due to a stoic perspective, an abnormally high pain threshold, a nervous system condition that results in a malfunctioning anginal warning system (e.g., diabetes mellitus), or obtundation induced by medicine or reduced brain perfusion.

Elderly people who have pre-existing altered mental state or dementia may have no memory of recent symptoms and may have no complaints at all.

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Evaluation

While one patient may be in good spirits and show no signs of a heart attack or stroke, another may be in excruciating pain, be suffering from major respiratory distress, or be in desperate need of life-saving mechanical ventilation.

Diaphoretic and pallid, patients with persistent symptoms tend to stay in bed and remain thus for the duration of their illness.

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Indicators of life's vitality

1. Pulse rate: 
   1. The heart rate of the patient is often elevated (tachycardia secondary to sympathoadrenal discharge). This may be due to ventricular or supraventricular arrhythmias that are causing the pulse to be out of syncs, such as atrial fibrillation/flutter, or ventricular ectopy.
   2. In rare circumstances, a low heart rate may also be observed. Sinus node dysfunction may be the cause of bradyarrhythmias. Additionally, an atrioventricular (AV) nodal block or infranodal block may be seen.
   3. Dissections of the abdominal aorta are often associated with chest discomfort spreading to the back and blood pressure differences of 15 mm Hg or more between both arms. Aortic regurgitation murmurs are also prevalent in patients with aortic dissection.
2. A rise in the heart rate: 
   1. Patients usually have high baseline blood pressure readings (hypertension because of peripheral arterial vasoconstriction resulting from an adrenergic response to pain, anxiety, and ventricular dysfunction). Acute myocardial infarction (AMI) may be precipitated by elevated blood pressure, however, this is not always the case.
   2. Additionally, hypotension may be present. Due to the massive infarct size or decreased global cardiac contractility, this is usually indicative of either right-ventricular MI or significant left-ventricular dysfunction.
3. Breathing rate: Anxiety or lung congestion may cause the respiratory rate to rise. Creatine Kinase (CK) levels in the blood are frequently elevated for 24 to 48 hours, and temperature fever is usually present during this time frame. In rare cases, a person's body temperature may rise beyond 102°F.
4. Veins in the neck: Distention of neck veins in individuals with acute inferior-wall MI with right ventricular involvement is a frequent symptom of right ventricular failure. Oedema and hepatomegaly are also common side effects of ventricular dysfunction in patients with congestive heart failure.
5. Heart: 
   1. There may be dyskinesis, perceptible S4 gallop, and a mild S1 sound when palpation is performed. As a result, the left ventricle's contractility has been reduced.
   2. Left bundle-branch block or prolonged pre-ejection interval with delayed valve closure may be the cause of paradoxical S2 splitting, despite lower stroke volume.
   3. Even when cardiac output is reduced, a new mitral regurgitation murmur (usually holosystolic towards the apex) implies papillary muscle failure or rupture, or mitral annular dilatation.
   4. There may be a ventricular septal rupture in certain patients with full-thickness MIs if a holosystolic murmur originating at the mid-sternal border and not the back radiates, sometimes with a palpable thrill. VSD murmurs become more pronounced and unpleasant when flow resistance and a larger pressure differential are present.
   5. To and fro rasping noises may be heard as the result of sliding contact between inflammation-roughened surfaces. Pulmonary hypertension, which is linked with widespread acute left ventricular myocardial infarction, may cause chest rales or wheezes. At the base of the lungs, pleural effusions may cause an egophony.
6. Abdomen: Tricuspid incompetence is common, and even in the absence of obvious hepatomegaly, hepatojugular reflux may occur. Pulsatile abdominal masses may indicate abdominal aortic aneurysms.
7. Extremities: Circulatory problems, such as peripheral cyanosis and oedema, as well as decreased pulse volume, may suggest vasoconstriction, a decreased cardiac output, or right ventricular dysfunction or failure. As previously indicated, pulse and neck-vein patterns may suggest further problems.

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Diagnosis

ACC/AHA and ESC guidelines recommend that cardiac biomarkers should be measured upon presentation in patients with suspected MI, and the only biomarker recommended for the diagnosis of acute MI at this time is cardiac troponin due to its superior sensitivity and accuracy.

Myocardial necrosis results in the production of troponin, a contractile protein that is ordinarily absent from the bloodstream. The following are some of the laboratory tests that may be performed to diagnose MI:

• Comprehensive metabolic panel
• Lipid profile
• Electrocardiography
• Complete blood cell count

An early examination and triage of individuals suspected of having an acute coronary syndrome (ACS), such as a coronary artery disease (CAD), relies heavily on the ECG. Approximately 80% of the time, it serves as a confirmation of the diagnosis.

Imaging the heart: Coronary angiography may be utilised to clearly detect or rule out coronary artery disease in patients with a high probability or proven acute MI.

Assessing the situation and making a decision: Initial examination to establish a working diagnosis is critical since this will define care due to the fact that each component of the ACS spectrum has different management processes and durations.

Patients with symptoms indicative of acute myocardial infarction (MI) should have a thorough physical examination and a detailed medical history taken. An expert physician should evaluate a 12-lead electrocardiogram (ECG) and provide intravenous (IV) access within 10 minutes after arrival.

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Initial management

To be on the safe side, all patients with chest discomfort should be treated as though it is ischaemia unless otherwise proven. It is preferable to use advanced cardiac life support (ACLS)-trained unit to transfer patients who are haemodynamically unstable or have trouble breathing.

The following objectives guide the initial care of individuals with acute MI:

1. Preventing additional ischaemia by restoring the balance between oxygen supply and demand
2. Pain alleviation
3. Prevention and treatment of problems

Oxygen: Pulse oximetry monitoring of oxygen saturation is required for all patients. If a patient is hypoxic (oxygen saturation 90% or PaO2 60 mm Hg or has heart failure, supplemental oxygen through a mask or nasal cannula should only be used in cases of extreme hypoxia.

Aspirin: Patients with ACS should be given non-enteric-coated chewable aspirin in the range of 162 to 325 mg unless there is obvious evidence of an aspirin allergy. Aspirin should still be given to patients with aspirin intolerance at the time of presentation. Faster therapeutic levels may be achieved with chewable aspirin since it enhances quick bloodstream absorption. Reduction in the discomfort associated with heart disease.

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Nitrates

When it comes to relieving chest discomfort caused by ischaemia, nitrates are the most often utilised drugs. However, their usage is not connected with a lower risk of death from cardiovascular disease.

1. The use of nitrates should be avoided in individuals with severe hypotension or bradycardia, or if there is a strong suspicion that the right ventricular infarction occurred.
2. Nitrates are powerful vasodilators that primarily operate on the venous system. Vascular preload (the amount of blood returning to the heart through the venous system) is reduced as a consequence of systemic venodilation; this reduces cardiac workload, oxygen demand, and ischaemia discomfort.
3. Nitrates are often administered sublingually at a dosage of 0.4 mg, with the patient's chest discomfort and haemodynamic reaction being closely monitored.
4. Additional nitrates may be given if the first dosage is handled adequately. Hypotension and headache are the most prevalent adverse effects of nitrates. A starting dose of 5 to 10 mcg/min of IV nitrates is commonly used, and the dosage is progressively raised until the discomfort subsides.
5. In order to avoid life-threatening hypotension caused by the simultaneous use of phosphodiesterase (PDE) inhibitors (e.g. sildenafil), physicians should pay close attention to the patient's past medical history.

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Analgesia

1. It's best to use IV morphine to address the pain that's refractory or severe.
2. To treat pain or avoid tolerance-inducing effects including hypotension, vomiting, or reduced respiration, an IV bolus dosage of 2 to 4 mg morphine may be administered as an initial dose.
3. In order to keep the patient safe, the patient's systolic blood pressure must remain above 100 mm Hg and below 140 mmHg, respectively.
4. Non-steroidal anti-inflammatory medications (NSAIDs) and other analgesic treatments should be avoided whenever feasible since they have been linked to cardiovascular events.

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Reperfusion 

To maximise myocardial salvage and limit mortality, prompt restoration of myocardial blood flow is crucial. As quickly as feasible, a choice must be taken whether to use fibrinolytic drugs or primary (direct) PCI to establish reperfusion.

Patients with STEMI who are admitted to a hospital without access to PCI are advised to take the following course of action:

1. Full-dose fibrinolytic treatment and transfer to a PCI centre are recommended for patients who come within two hours of the beginning of symptoms. A local PCI centre's ability to execute the main PCI in less than 90 minutes is assumed to be the case here.
2. If a patient's symptoms linger more than two to three hours, they should be sent to the main PCI centre for treatment. When a patient comes after two hours, PCI cannot be performed in less than 120 minutes. Fibrinolytic treatment may be acceptable in individuals who have had symptoms for up to 12 hours in this situation.
3. Pre-treatment with anticoagulant and antiplatelet medication is recommended for all patients undergoing primary PCI.

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Anticoagulation 

1. There are a variety of anticoagulant medications on the market, and the effectiveness of each relies on the clinical situation and the reperfusion procedure used.
2. Anticoagulants should be administered to patients undergoing fibrinolytic treatment for at least 48 hours or for the rest of their hospital stay up to 8 days if revascularisation is not possible.
3. Whichever kind of reperfusion therapy is used, anticoagulant medications are a critical part of the treatment plan (ie, whether it is primary PCI or fibrinolysis therapy).
4. UFH, bivalirudin, and low molecular weight heparin (enoxaparin, for example) are all alternatives for primary PCI. Because of the increased risk of catheter thrombosis, fondaparinux should not be administered in this situation.
5. If LMWH (enoxaparin) is utilised, UFH (enoxaparin) is the recommended alternative. The use of enoxaparin is related to a greater risk of a cerebral haemorrhage in individuals over 75 years of age and those with poor renal function. The anticoagulant drug bivalirudin may be given to people who have heparin-induced thrombocytopenia (HIT) or who have had HIT in the past.

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Antiplatelet agents

1. An empiric aspirin loading dosage (150.5 to 325 mg) should be administered as soon as feasible and prior to reperfusion in all patients with STEMI. All individuals who have had a STEMI should get a daily dosage of (75 to 81 mg) for the rest of their lives.
2. Depending on the technique of reperfusion, P2Y12 receptor inhibitors (e.g. clopidogrel, ticagrelor, prasugrel) are also used in dual antiplatelet treatment. A loading dose of these medicines is given prior to or at the moment of reperfusion, and an extended duration maintenance dosage is given subsequently.
3. Patients having primary PCI should receive a loading dosage of 600 milligrammes of clopidogrel, 180 milligrammes of ticagrelor or 60 milligrammes of prasugrel. For patients who have received a stent, either a BMS or a DES, a maintenance dosage of P2Y12 receptor inhibitors should be maintained for at least a year.
4. Clopidogrel should be taken every day at 75 mg; ticagrelor at 90 mg twice a day; and prasugrel at 10 mg daily. The use of P2Y12 receptor inhibitors in individuals who have received a BMS should be discontinued sooner rather than later if there is evidence of increased bleeding. When a patient has had a stroke or a TIA, prasugrel isn't advised for them.
5. After a loading dosage of clopidogrel 300 mg, patients on fibrinolytic treatment should be given 75 mg of the drug every day for at least 14 days, ideally for a period of a year or more.
6. Additionally, intravenous (IV) glycoprotein (GP) IIb/IIIa receptor antagonists may be employed in STEMI therapy as antiplatelet medicines. If the thrombus burden is substantial or the P2Y12 receptor antagonist loading is insufficient, an individual PCI may benefit from the addition of GP IIb/IIIa medicines as a supplement.

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Disclaimer- The views and opinions expressed in this article are those of the author's and do not necessarily reflect the official policy or position of M3 India.

The author is a practising super specialist from New Delhi.