Acute Myocardial Infarction (AMI) also known as a heart attack is caused by the complete or partial occlusion of a coronary artery and requires prompt hospitalization and extensive care management. It is part of a spectrum of conditions that result from myocardial ischemia known as an acute coronary syndrome. Get more details on acute coronary syndrome here.

Acute MI includes both non-ST segment elevation myocardial infarction in short NSTEMI and ST-segment elevation myocardial infarction - STEMI.

Causes of acute myocardial infarction

Causes of Acute Myocardial Infarction are due to:

  • Reduced O2 supply to the heart.
  • Increased O2 demand by the heart.

Reduced O2 supply to the heart.

Severe pre-existing coronary artery disease (coronary atheroma),
Prinzmetal angina or drug-induced vasoconstriction,
Reduced O2 content (e.g. In Hypoxia or anemia).

Decreased coronary perfusion pressure (CPP=DAP-LVEDP) caused by hypotension or raised LV wall tension (hypertrophy or dilation).
Vasodilator drugs causing coronary steal,
Heart valve disease (particularly aortic stenosis).

Increased O2 demand by the heart.

Sustained tachycardia, arrhythmias (also reduce diastolic time),
Sympathetic stimulation (e.g. pain, agitation, or inadequate sedation),
Hyperdynamic states (e.g. pregnancy, hyperthyroidism, sepsis, inotropes including beta-agonists, calcium e.t.c.
Ventricular Hypertrophy.

The 3 acute coronary syndromes are:

ST-elevation myocardial infarction (STEMI)

ST-segment elevation myocardial infarction aka transmural MI is myocardial necrosis with electrocardiogram changes indicating ST-segment elevation not quickly reversed by nitroglycerin.

This is characterized by elevated troponin I or troponin T and Creatinine kinase. In practice, the ST elevation alone is sufficient to treat because the troponins take time to rise.

Non-ST elevation MI (NSTEMI)

Non–ST-segment elevation myocardial infarction also known as subendocardial MI is myocardial necrosis that is evidenced by elevation of cardiac markers in the blood specifically troponin I or troponin T and CK.

There is no acute ST-segment elevation. Electrocardiogram changes such as an ST-segment depression or T-wave inversion may be present.

 Unstable angina

Unstable angina is characterized by prolonged, severe angina, usually at rest, possibly with ECG changes.

NSTEMI and unstable angina are often grouped together as non-ST elevation ACS (NSTEACS)

Types of myocardial infarction

Based on the causative mechanism, myocardial infarction can be classified into five types:

Type 1: This is the commonest type. It occurs due to a primary coronary event such as atherosclerotic plaque rupture, fissuring, coronary dissection or erosion.  It is also referred to as a spontaneous myocardial infarction.

Type 2: This occurs due to an imbalance in myocardial oxygen supply and demands. This can be a case of ischemia because of an increased oxygen demand like in hypertension or due to decreased oxygen supply like in an embolism, coronary artery spasm, hypotension(reduced blood pressure), arrhythmia, anemia or tachycardia (increased heart rate). It usually happens during surgery or illness.

Type 3: This type is related to sudden cardiac death with ischaemic features on an electrocardiogram, angiography, or autopsy but before troponin could be checked.

Type 4a: This is a myocardial infarction that is associated with percutaneous coronary intervention whereby there are signs and symptoms of myocardial infarction with cTn values more than 5 × 99th percentile upper reference limit.

Type 4b: This type is associated with a documented stent thrombosis

Type 5: It is a myocardial Infarction associated with coronary artery bypass grafting (CABG) with features of myocardial infarction with cTn values >10 × 99th percentile upper reference limit.

Clinical Features of acute myocardial infarction

The patient with either STEMI or NSTEMI will present with similar symptoms:

Chest pain is usually the first symptom. It is deep, substernal or retrosternal/epigastric crushing severe pain. The pain radiates to the jaw, neck and down the inner part of the left arm and shoulders lasting at least 20 minutes to 7 hours.

It is accompanied by dyspnea, sweating, nausea, and vomiting, feeling of impending doom,

The pain is relieved little or only temporarily by rest or nitroglycerin.

Difficulty in ventilating (Dyspnea) and weakness may be the presenting complains in patients with left ventricular failure, pulmonary edema, shock, or with arrhythmia (Tachycardia or bradycardia, palpitations, ventricular arrhythmias),

some patients present with syncope,

Patients with a right ventricular infarction may present with an elevated right ventricular filling pressure, distended jugular veins clear lung fields, and hypotension.

Patients may have pallor, cool, and diaphoretic skin. Some may present with peripheral or central cyanosis.

In cases of hypotension, Pulse may be thready with variable low blood pressure, although many patients initially have some degree of hypertension during pain.

On auscultation, heart sounds are usually somewhat distant; a 4th heart sound is almost universally present in these patients. There may be a soft systolic blowing apical murmur that indicates a papillary muscle dysfunction.

Diagnostic Investigations

Chest x-ray to rule out other causes and check for heart failure.

Urea and electrolytes,

Liver function tests (LFT S),

Blood Glucose levels,

Magnesium, Calcium, Phosphate levels.

Arterial blood gas analysis,

Serial 12 lead Electrocardiogram shows ST-segment depression/elevation or T-wave elevation/inversion.

For STEMI, initial ECG is usually diagnostic, showing ST-segment elevation ≥ 1 mm in 2 or more contiguous leads subtending the damaged area

Serial Serum cardiac markers / Cardiac enzymes particularly Troponin I and T (12 hours post-onset of chest pain) kinase (CK) – MB and isoforms, Myoglobin and other non-specific markers.

serial measurements of cardiac markers to help distinguish between unstable angina, ST-segment elevation myocardial infarction, and non-ST segment elevation myocardial infarction.

Immediate coronary angiography (unless fibrinolytics are given) for patients with STEMI.

Coronary angiography most often combines diagnosis with percutaneous coronary intervention. When possible, emergency coronary angiography and PCI are done as soon as possible after the onset of acute myocardial infarction.

Imaging – Echocardiogram (Ischemic section of the myocardium may be dyskinetic),

Nuclear imaging.

Differential Diagnosis

  • Pericarditis,
  • Dissecting aortic aneurysm,
  • Pulmonary embolism,
  • Gastrointestinal diseases such as esophageal reflux, spasm, or rupture,
  • Biliary tract disease like a perforated peptic ulcer, pancreatitis.,
  • Bundle branch block (BBB) may be confused with ST-segment changes that accompany ischemia,

Acute Myocardial Infarction Treatment

Treatment of acute myocardial infarction is the use of antiplatelet drugs, anticoagulants, nitrates, beta-blockers, statins, and reperfusion therapy.

Management is divided into;

  • Immediate prehospital management,
  • Further Management,
  • Difficult Situation management.

Management aims to Support and maintain vital functions.

Give cardio-pulmonary resuscitation (CPR).

Administer 100% oxygen 2 litres per minute via nasal canula.

Secure airway and ensure breathing/ventilation (endotracheal intubation may be required)

Ensure intravenous access.

Record 12 lead electrocardiogram.

Drug therapy and timing of revascularization depend on the clinical picture and diagnosis on arival at the emergency department.

For STEMI, reperfusion strategy can include fibrinolytic therapy or immediate PCI.

For patients with NSTEMI, angiography may be done within 24 to 48 h of admission if the patient is clinically stable. If the patient is unstable (eg, ongoing symptoms, hypotension or sustained arrhythmias), then angiography must be done immediately.

Restore oxygen supply to the myocardium by:

  • Giving aspirin 325mg to chew or via nasogastric tube STAT plus glycerin trinitrate sublingual 0.5mg every 5–10 minutes to a maximum of 5 tablets to reduce further damage to the heart.
  • Administer IV cutaneously (hypovolemia) minimum volume aiming at maximum intravascular volume expansion.
  • If severe anemia, give blood (with diuretic cover if required). Aim for Hemoglobin concentration. Of 7-9g/dl
  • If the blood pressure is restored but the cardiac output is poor, consider the use of iodilators such as Dobutamine.
  • Stop any vasopressor drugs if suspected as the precipitant.

Reduced oxygen demand by the myocardium

  • Treat any tachyarrhythmias. If still tachycardic, reduce heart rate using beta-blockers like Metoprolol or Esmolol.
  • If pain is the cause, give cardiostable analgesics such as Diamorphine, Fentanyl, Morphine.
    • 10mg (morphine must be diluted with normal saline or water for injection) OR pethidine 50–100mg IV/IM
  • If inadequate sedation is a suspected precipitant, consider careful titration of sedation.
  • If hypertensive, treat any cause and consider GTN infusion to reduce overload (50mg/50ml IV starting at 3ml/hr – titrating to effect.
  • GTN may be delivered sublingually to buy time.

These patients should receive;

  • Antiplatelet drugs: Aspirin, clopidogrel, or both.
  • Anticoagulants: A heparin (unfractionated or low molecular weight heparin) or bivalirudin for patients with a history of heparin-induced thrombocytopenia
  • Glycoprotein IIb/IIIa inhibitor for some high-risk patients like the ones with recurrent ischemia, dynamic ECG changes, or hemodynamic instability
  • Antianginal therapy usually nitroglycerin sublingually then IV drip. Nitroglycerin is preferable to morphine
  • Beta-blocker, Angiotensin-Converting Enzyme inhibitors enzyme inhibitor, and Statin is the standard therapy for all patients with unstable angina.

Advanced acute myocardial infarction treatment

All patients should be given antiplatelet drugsanticoagulants, and if chest pain is present, antianginal drugs.

  • Once stabilized on other therapy, wean off GTN.
  • Increased dose status may reduce long and short term mortality.
  • Consider adding calcium channel antagonists for continuing angina.
  • Start low molecular weight heparin or clopidogrel unless contraindicated. Stop when stabilized or pain-free for 24 hrs.
  • Consider unfractionated heparin instead/and or early angiography if the patient has recently undergone surgery
  • Check serial electrocardiogram and cardiac enzymes for 3 days.
  • Consider inserting an arterial line, central venous catheter in order to measure cardiac output.
  • Consider BiPAP/CPAP if ventilation is inadequate.
  • Defibrillation if ventricular fibrillation present.

Recanalization therapy (thrombolysis or primary angioplasty). For STEMI patients, emergency PCI is the preferred treatment of ST-segment elevation myocardial infarction.

Reperfusion using fibrinolytics is most effective if given in the first few minutes to hours after the onset.

Unstable NSTEMI patients should proceed directly to the cardiac catheterization laboratory to identify coronary lesions requiring PCI or CABG.