Acute coronary syndrome and myocardial infarction

An update to this arcticle is pending.


  • Acute coronary syndrome results from an abrupt reduction or cessation of blood flow locally within a coronary artery. This is often caused by a sudden rupture of an atherosclerotic plaque and the subsequent thrombus formation, which results in an abrupt reduction, or complete cessation, of blood flow within the coronary artery.
    • Imbalance between the myocardial oxygen need and the availability of oxygen, and consequently myocardial ischaemia may also be caused, in the absence of an acute coronary stenosis (plaque rupture), by tachycardia and bradycardia, coronary spasm, hypotension, anaemia, respiratory insufficiency or other severe disease..
  • Classification of ACS
    • ACS without ST elevation
      • Non ST elevation myocardial infarction (NSTEMI)
      • Unstable angina (UA)
    • ST elevation myocardial infarction (STEMI)

Symptoms and clinical diagnosis

  • The diagnosis of ACS is based on the ischaemic symptoms, clinical findings and ECG changes. The diagnosis is confirmed if the concentration of cardiac biomarkers is increased. For non-ischaemic causes of chest pain, see table T1.
  • Acute myocardial ischaemia causes chest pain.
    • Starts abruptly, often severe, crushing, heavy or "band-like” in nature and not greatly affected by breathing or changing position
    • Pain suggestive of myocardial infarction is prolonged, persisting for over 20 minutes, and usually has constant intensity.
    • Widespread in the retrosternal area, possibly radiating to the arms (usually to the left arm), back, neck or the jaw
    • In some patients the pain may resemble the symptoms of acute abdomen (pain begins in the upper abdomen accompanied by nausea).
  • In particular, elderly patients (> 75 years of age) and patients with diabetes, chronic heart failure, renal failure or dementia may present with a feeling of nausea, weakness or heaviness as well as sweating without chest pain.
  • UA is suggested by angina pain that occurs for the first time and is then experienced with increasing frequency or that is a known symptom of previously diagnosed stable angina which is rapidly worsening (over days – in less than 2 weeks).
  • Particularly in inferior wall damage, severe vagotonia may induce bradycardia and hypotension which will manifest as dizziness or fainting.
  • Other clinical manifestations of myocardial ischaemia include acute pulmonary oedema, loss of consciousness and sudden death.

Table 1. Non-ischaemic causes of chest pain
Disease Differentiating signs and symptoms
Aortic dissection (Aortic aneurysm and dissection)
  1. Sudden intense chest pain
  2. Blood pressure may be low and pulses asymmetrical
  3. New-onset aortic valve regurgitation
  4. Dissection may obstruct the origins of coronary arteries with signs of impending infarction
  5. Broad mediastinum on chest x-ray
Acute pulmonary embolism (Pulmonary embolism)
  1. Dyspnoea and tachypnoea as the principal symptoms
  2. Chest pain in about half of patients
  3. Tachycardia, RBBB, low blood pressure in extensive pulmonary embolism; echocardiography shows right-sided dilatation and increased pulmonary pressure
  4. Chest x-ray is often normal
  5. PaO2 decreased or normal, PaCO2 decreased or normal
  6. D-dimer assay positive; negative result excludes pulmonary embolism with high probability
  1. Spontaneous pneumothorax,
  2. tension pneumothorax (Pneumothorax)
  1. Dyspnoea, chest pain
  2. Quiet breath signs on auscultation
  3. Chest x-ray will confirm diagnosis
Oesophageal tear, perforated ulcer (Peptic ulcer disease, Helicobacter pylori infection and chronic gastritis) Chest pain, upper abdominal pain
Pericarditis (Pericarditis), myocarditis (Myocarditis)
  1. Pain is usually retrosternal and is sharp or tearing in nature
  2. The pain is aggravated by inspiration, coughing and changing of position
  3. A friction rub may be heard
  4. ST–T changes with almost daily alternations
Pleuritis (Pleural effusions and thoracentesis)
  1. Signs and symptoms of respiratory tract infection
  2. Stabbing chest pain, aggravated by inspiration and coughing
Costochondral pain (Tietze's syndrome)
  1. Pain on palpation
  2. Chest wall movements and breathing may aggravate the pain
Oesophageal inflammation(Gastro-oesophageal reflux disease) or spasm, dyspepsia (Dyspepsia)
  1. Heartburn, chest pain, upper abdominal pain
  2. May be worse in recumbent position and on exertion (reflux)
  3. No ECG changes
  4. Relief from PPIs
Early herpes zoster (Herpes zoster)
  1. No ECG changes
  2. Rash appears within a few days
  3. Localised paraesthesia before the appearance of the rash
Hyperventilation syndrome (Hyperventilation)
  1. Strong feeling of lack of air
  2. Fast and deep breathing
  3. Cold limbs with tingling and numbness
  4. Dizziness, headache, dry mouth
  5. PaCO2 decreased, PaO2 increased or normal
Depression (Recognition and diagnostics of depression)
  1. Continuous feeling of heaviness in the chest, no correlation to exercise
  2. ECG normal

Diagnostic investigations

Principles of ECG diagnosis

  • A 12 lead ECG is the most important diagnostic procedure, and it should be recorded immediately at the first point of care. The following additional leads should also be recorded: V3R, V4R (right ventricle); V7–V9 (posterior wall).
    • Contiguous leads: lateral leads I, aVL, V6; inferior leads II, III, aVF; anterior leads V4–V6; posterior leads V7–V9
  • Serial ECG recordings (every 15–30 minutes) are indicated if the pain continues, particularly when ECG changes are not noted in the initial recordings or changes are evident in the repeated recordings.
  • In the initial phase, it is advisable to leave the chest leads in place or mark their position on the skin to ensure the comparability of the subsequent recordings.
  • A Q wave in an ECG will increase the likelihood of coronary heart disease (CHD). See table T2 for the criteria of a prior Q wave myocardial infarction (MI).
  • Differential diagnosis of ECG changes, see table T3.

Table 2. ECG changes associated with prior (Q wave) myocardial infarction
ECG changes associated with prior Q wave myocardial infarction - an adaptation of the recommendations by the joint ESC/ACCF/AHA/WHF task force
1 Any Q wave in leads V2–V3 ≥ 20 ms or QS complex in leads V2 and V3
2 Q wave ≥ 30ms and ≥ 1 mV deep or QS complex in leads I, II, aVL, aVF or V4–V6 in at least two leads of a contiguous lead grouping (which are I, aVL; V1–V6; II, III, aVF, and V7–V9)
3 R wave ≥ 40 ms in V1–V2 and R/S ratio ≥ 1 with a concordant positive T wave in the absence of a conduction defect
Adapted from: Eur Heart J 2012;33:2551-2567.

Table 3. Conditions to be considered in the differential diagnosis of an MI when interpreting ECG changes
ECG change To be considered in the differential diagnosis
ST elevation Early repolarisation
Hypertrophic cardiomyopathy
Brugada syndrome
Pulmonary embolism
Left ventricular hypertrophy
ST depression Sympathicotonia
Microvascular angina
Left ventricular hypertrophy
Post tachyarrhythmia
Mitral prolapsed
T wave changes Normal variant
Increased intracranial pressure
An electrolyte disturbance
Acute cor pulmonale (pulmonary embolism)
Takotsubo cardiomyopathy
Q wave Left ventricular hypertrophy (Lead V1)
Hypertrophic cardiomyopathy
Right ventricular pressure and volume overload
Duchenne muscular dystrophy
Abnormal position of the heart (Leads II, III and aVF)
Left anterior fascicular block (right sided chest leads)
Source: Porela, Ilva. Sepelvaltimotautikohtauksen diagnostiikka ja epidemiologia (Diagnosis and epidemiology of acute coronary syndrome, In Finnish). In: Airaksinen et al. (eds.) Kardiologia, Kustannus Oy Duodecim, 2016, p. 392.

ECG diagnosis: UA and non ST elevation myocardial infarction (NSTEMI)

  • New ST depression of > 0.5 mm in two contiguous leads, even transient, is suggestive of myocardial ischaemia in a patient with chest pain.
  • The deeper and more widespread the ST depressions are, the more extensive ischaemia and worse prognosis they suggest.
  • T wave inversion (> 1 mm) in two contiguous leads with R/S ratio > 1.
  • Deeply inverted T waves (> 2 mm)
  • A normal ECG recording does not exclude acute myocardial ischaemia.

ECG diagnosis: ST elevation myocardial infarction

  • A new ST elevation of ≥ 2.5 mm in men below 40 years of age, of ≥ 2 mm in men at least 40 years of age, and of ≥ 1.5 mm in women in at least two anatomically contiguous leads V2–V3, and/or ST elevation of ≥ 1 mm in at least two other anatomically contiguous leads, provided that there are no LBBB or LVH changes or other abnormalities of the ST segment in the ECG, or ventricular pacing
  • New bundle branch block (LBBB) with chest pain
  • ST elevation of > 0.5 mm in leads V7–V9 (posterior wall) and reciprocal ST depression of > 0.5 mm in leads V1, V2, V3, R/S ratio > 1 in leads V1–V2
  • In inferior infarction, leads V3R–V4R are recorded in order to determine infarction changes in the right ventricle.
  • Comparison with an earlier ECG is important.

Special remarks

  • If the patient is known to have LBBB, new ST elevation of > 1 mm parallel to the QRS complex or new ST depression of > 1 mm parallel to the QRS complex in leads V1, V2 or V3 may be suggestive of a new ischaemic event.
  • ST elevation in leads aVR and V1 together with ST depression in leads V4–V6 is suggestive of obstruction of the left main coronary artery branch or of severe CHD.
  • If the patient has a ventricular-paced rhythm, comparison with earlier ECG recordings may reveal a new ST elevation; see LBBB (Bundle branch blocks in an ECG).

Cardiac biomarkers

  • Myocardial ischaemia causes tissue damage and myocardial cell death with the consequent release of measurable cardiac biomarkers into the circulation. Troponins (TnT and TnI) are the primary markers in use; creatine kinase isoenzyme MB mass (CK-MBm) is used in special cases.
  • When the high-sensitivity troponin assay is in use, concentrations exceeding the upper reference range threshold can be measured in almost all patients with myocardial infarction already 3 hours after the onset of symptoms. The reference range applied in the local organization must be taken into account.
  • The improved sensitivity of cardiac biomarkers has increased the number of myocardial infarction diagnoses and, respectively, reduced the number of UA diagnoses. The negative predictive value of sensitive troponin is excellent, and it excludes, in practice, the possibility of a myocardial infarction.
  • Increased troponin concentrations may be present in other conditions that are associated with myocardial damage without myocardial infarction. These include myocarditis, heart failure, cardiomyopathy, sequela of a tachyarrhythmic episode, severe anaemia and shock. The concentration may also increase in pulmonary embolism, sepsis, renal failure, cerebral infarction and subarachnoid haemorrhage.
  • An increase in the troponin concentration when it already was increased (renal failure, fresh myocardial infarction) may also be diagnostic in recurrent myocardial infarction (an increase of more than 20%). In such a case, CK-MBm measurement may also be used.
  • The plasma concentration of troponin increases on average about 6 hours after the onset of chest pain (interpatient variation 3–8 hours). The increased concentration reduces gradually, but increased concentrations may be detected after a period of 2 weeks.

Other investigations

  • A chest x-ray should be taken in the hospital to aid the haemodynamic assessment.
  • Echocardiography should be performed as soon as possible, in order to evaluate the myocardial function.

Initial management

  • The patient is placed at bed rest. Aspirin 250 mg to chew and swallow or 75–150 mg intravenously, unless the patient is allergic to aspirin. The initial dose should be followed by long-term treatment of aspirin 100 mg/day, unless contraindicated.
  • Short-acting nitrate spray to relieve chest pain, may be repeated twice with an interval of 5 minutes if necessary, provided that systolic blood pressure is over 100–110 mmHg.
    • Supplemental oxygen if the patient has dyspnoea or symptoms of cardiac failure, or if hypoxia is detected (SpO2 < 90 %) in continuous oxygen saturation monitoring. Oxygen saturation target is > 90%, in severe COPD 88–90%.
  • Continuous monitoring is started (ECG, blood pressure, SpO2) and an intravenous line is placed.
  • For persistent chest pain, an initial dose of morphine 4–8 mg followed by repeated intravenous bolus doses of 2–4 mg.
  • If reassurance is not sufficient to calm the patient, intravenous diazepam 2.5–5 mg may be given.
  • A nitrate infusion if chest pain continues (after 1–2 doses of nitrate spray), blood pressure is elevated or there are signs of heart failure. The patient must not be hypotensive (systolic BP should be > 100 mmHg) or hypovolaemic nor exhibit signs of right ventricular infarction.
  • Ondansetron 4 mg or droperidol (DHBP) 1.25 mg i.v. for nausea
  • If tachycardia, arrhythmias or hypertension occur, a beta blocker (metoprolol 2–5 mg i.v.) is commenced during the initial management period (be careful if the patient has hypotension or heart failure).

Evidence Summaries

Treatment of UA and NSTEMI

  • The risk of death and further cardiac events in patients with NSTEMI is greatest during the first few days after the acute event, and the risk will remain increased, at least, during the first month. The risk of short-term adverse outcomes must therefore be assessed (history, physical examination and ECG) without delay in all patients who are suspected to have cardiac chest pain. The more the high-risk criteria are fulfilled (table T5) the greater the likelihood of a cardiac event.
  • The treatment is started right after the diagnosis is confirmed, without waiting for the troponin results. The treatment aims at stabilizing the accelerated thrombotic process in the coronary artery and the hemodynamic status.
  • The treatment is carried out in a coronary care unit or another ward with facilities to continuously monitor the patient for the haemodynamic state and symptoms of ischaemia.

Table 5. Short-term risk stratification in UA and NSTEMI
Risk category Risk assessment criteria and urgency of angiography*
High risk Very high risk: angiography < 2 h
  • Haemodynamic instability or cardiogenic shock
  • Repeated or prolonged chest pain despite optimal medication
  • Significant arrhythmia (cardiac arrest, recurring ventricular tachycardia (VT), ventricular fibrillation (VF)
  • Acute heart failure, pulmonary oedema
  • Recurring ST depression or transient ST elevation or global ischaemia on ECG
  • Mechanical complication of myocardial infarction
High risk: angiography < 24 h
  • Elevated troponin concentration associated with an acute infarction
  • Dynamic ST–T changes on ECG
  • Mechanical complication of myocardial infarction
Medium risk: angiography within 3 days (72 hours)
  • Diabetes
  • Renal failure (eGFR < 60)
  • Decreased function of left venricle (LVEF < 40%)
  • Recurring pain or ischaemia soon after myocardial infarction
  • Earlier coronary balloon angioplasty
  • Earlier coronary bypass surgery
Low risk None of the above mentioned signs of danger
No repeating chest pain during observation
No changes suggesting ischaemia on ECG
  1. Modified from: Eskola et al. Epävakaa angina pectoris ja sydäninfarkti ilman ST-nousua (NSTEMI): vaaran arviointi ja ennuste. [Unstable angina pectoris and non-ST elevation myocardial infarction (NSTEMI): assessment of danger and prognosis] (In Finnish). Publication: Airaksinen et al. (ed.) Kardiologia. Duodecim Publishing Company Ltd., 2016, p. 404.
  2. *The timing of angiography indicated in the table is in accordance with the most recent European guideline. It is important to follow the guidelines locally agreed on.

Antithrombotic therapy

  • A P2Y12 receptor inhibitor (ticagrelor, clopidogrel, prasugrel) is started. The drug is chosen according to the local guidelines and to the clinical assessment of the patient.
    • The initial loading dose:
      • ticagrelor 180 mg (continued with 90 mg × 2)
      • clopidogrel 600 mg (continued with 75 mg/day)
      • prasugrel 60 mg (continued with 10 mg × 1)
    • The effect of clopidogrel has a slower onset, and in some patients (about 20 %) its anti-platelet effect may remain inadequate.
  • Low molecular weight heparin [Evidence Level: A]: enoxaparin 1 mg/kg twice daily s.c.; the dose should be reduced in patients over 75 years (–25%) and in renal failure (GFR < 30 ml/min, 50%).
  • Thrombolysis is of no benefit.
  • If the patient is being treated with an anticoagulant
    • Warfarin therapy with INR in the therapeutic range (2.0–3.0) is continued without interruption instead of heparin treatment. If INR is below the therapeutic range, anticoagulation with warfarin can be continued at discretion together with a reduced dose of heparin until the target INR level has been reached, or with heparin only. If INR is too high, warfarin is paused. The action of warfarin can be reversed by administering Vitamin K1 (phytomenadione) 1–3 mg intravenously, even though there is only limited evidence of its benefit. Treatment with warfarin may then be continued. INR is determined daily, if warfarin is continued.
    • If the patient uses a direct oral anticoagulant (dabigatran, rivaroxaban, apixaban, edoxaban), it is paused and heparin treatment is started 12–24 hours after the last dose of the drug, taking into account the half-life of the drug. Local guidelines should be followed and a cardiologist performing invasive prodecures consulted.
    • Start ASA and clopidogrel for a patient with anticoagulant therapy. Use of ticagrelor and prasugrel is avoided. If a coronary angiography can be performed within less than 24 hours, one may consider refraining from starting clopidogrel until the angiograpy.
  • Always remember to assess the risk of thrombosis (CHA2DS2-VASc) and bleeding (HAS-BLED) (see tables in(Indications for and implementation of anticoagulant therapy in atrial fibrillation)). Factors increasing the risk of bleeding include anaemia, thrombocytopenia, age > 75 years, renal failure, liver failure, female gender, weight < 65 kg, systolic BP >160 mmHg, a previous history of a bleeding tendency and medications affecting the platelet function.

Anti-ischaemic and other treatment

  • A nitrate infusion if the chest pain persists, blood pressure is elevated or there are signs of heart failure. The patient must not be hypotensive (systolic BP should be > 100–110 mmHg) or hypovolaemic nor exhibit signs of right ventricular infarction. Nitrate infusion is more effective than the drug administered orally.
    • The initial dose is 13–20 µg/min = 8–12 ml/hour when the concentration is 100 µg/ml. If necessary, the dose may be increased every few minutes up to 120 ml/h whilst closely monitoring blood pressure.
  • A beta blocker (metoprolol) intravenously as 2.5–5 mg bolus doses if blood pressure is elevated or tachycardia or arrhythmias occur (be careful if the patient has hypotension < 120 mmHq or heart failure). A beta blocker already in use is continued, provided that there is no hypotension or cardiac failure.
  • Starting an oral beta blocker is considered within the first 24 hours, after haemodynamic stabilization, if the patient has heart failure or left ventricular dysfunction and if there are no contraindications for the drug.
  • An ACE inhibitor is started within the first 24 hours of treatment in patients with heart failure, systolic left ventricular dysfunction, anterior wall infarction or diabetes. Low blood pressure (systolic BP < 100 mmHg) should be avoided; exercise caution if the patient has renal failure.
  • Early introduction of a statin, i.e. during the first day of treatment with a large therapeutic dose is recommended.
  • NSAIDs should be stopped and should not be used for pain relief.
  • Stomach-protective medication should be considered when an anticoagulant and/or ASA and/or a P2Y12 receptor inhibitor is in use. The risk of GI bleeding is also increased by earlier GI bleeding, continuous glucocorticoid or NSAID medication, age > 65 years, dyspepsia, reflux disease and excessive use of alcohol.

Invasive treatment, revascularization (PTCA and CABG)

  • Urgent invasive assessment and treatment without delay
    • If the patient is in cardiogenic shock, if he/she has chest pains despite treatment, or if the haemodynamic state is regarded as unstable (arrhythmias, hypotension, heart failure; see table T5).
  • Early invasive assessment and treatment 24–72 h
    • Individual risk assessment and timing of the invasive investigation according to its results (e.g. < 24 hours or < 72 hours)
    • Signs of increased risk (recurrent ST–T fluctuations, high release of cardiac biomarkers, heart failure, earlier PCI/CABG, diabetes, renal failure) have an influence on the more specific timing of the investigation.
  • In most cases only the occluded infarct-related artery is treated, and other possible stenoses are treated at a later date.
  • If the chest pain does not recur, the ECG changes during chest pain are minor and no release of cardiac biomarkers is detected, but the pretest probability of coronary heart disease is nonetheless increased (≥ 15%), an exercise stress test, a myocardial perfusion scintigraphy or a coronary angiography is carried out.
    • Counselling and advice concerning risk factors are provided.

Evidence Summaries

Treatment of STEMI

  • STEMI is, more often in men than in women, the first presentation of CHD without preceding angina pain. The patient may therefore not necessarily be able to interpret the symptoms as originating from the heart, which results in an unnecessary delay before the first medical contact is made.
  • It is of the utmost importance that primary care providers are able to recognise the symptoms since STEMI is associated with a high risk of life threatening arrhythmias, conduction defects and sudden death. Integrated care pathways incorporating local guidelines implemented in all health care facilities providing on-call services facilitate the easy identification and management of STEMI patients.
  • A diagnosis should be made as quickly as possible, and an ECG must be recorded as soon as the first medical contact is made. Serial ECGs should be recorded if no changes are noted but the symptoms are suggestive of an MI.

Initial management

  • See above .
  • If the ST elevation is corrected with nitrate, the underlying condition may consist of a coronary artery spasm either with or without an acute myocardial infarction. A cardiologist should be consulted; in suspected case of an infarction coronary angiography is performed within < 24 hours, and if ST elevation and chest pain recur, without delay.

Reperfusion: emergency percutaneous coronary intervention (PCI) / thrombolytic therapy?

  • Choosing the most suitable reperfusion treatment option requires a consultation with a cardiologist on call or with an emergency physician at a hospital.
  • The first-line choice for reperfusion treatment is a primary PCI (PPCI) if that can be performed within less than 120 minutes after making the diagnosis. Thrombolytic therapy is an alternative if PPCI is not available.
  • A PPCI is the first-line choice particularly if > 3 hours have passed since the onset of infarct pain, if there are contraindications for thrombolytic therapy (table T7) or if there is no treatment response to thrombolytic therapy within 60 minutes, or if the patient is hemodynamically unstable or a high-risk patient. Also uncertainty of the STEMI diagnosis (ventricular pacing, LBBB, difficulty in interpreting the ECG) speak for a PPCI.
  • Coronary angiograpy and a PPCI is recommended for patients
    • whose symptoms have continued for > 12 hours
    • whose ECG shows signs of ischaemia
    • who have recurrent chest pain and dynamic ECG changes, or signs of cardiac failure, of arrhythmias that threaten haemodynamics or of a cardiogenic shock.
  • The results achieved with thrombolytic therapy are best if it is started rapidly within 1–2 hours of symptom onset. If a PPCI is not available, it is recommended to consider thrombolytic therapy for patients whose symptoms have started less than 12 hours ago and there are no contraindications for thrombolytic therapy (table T7). The benefit of the treatment is markedly reduced when more than 6 hours have elapsed from the symptom onset and no benefit is to be expected when more than 12 hours have elapsed from the symptom onset.
  • Agents used in thrombolytic therapy and their doses are presented in table T6.

Table 7. Contraindications to thrombolytic therapy in STEMI
Absolute contraindications Relative contraindications
Ischaemic stroke or SAH treated in preceding 6 months TIA in preceding 6 months
Cerebral haemorrhage or stroke of unknown origin at any time previously Anticoagulant therapy
Central nervous system neoplasms or blood vessel anomalies, untreated aneurysm in a cerebral blood vessel Pregnancy or within 1 week post partum
Major trauma, head injury or major surgery within preceding 3 weeks or neurosurgical operation within preceding 1 month Systolic BP >180 mmHg or diastolic BP > 110 mmHg, refractory to treatment
Gastrointestinal bleeding within one month Infective endocarditis
Known bleeding disorder (coagulation disorder, anaemia, thrombocytopenia) Active peptic ulcer
Confirmed or suspected aortic dissection Prasugrel or ticagrelor therapy, especially in patients who have just received a loading dose
Recent intervention (liver biopsy, lumbar puncture) Prolonged or traumatic resuscitation

Table 6. Agents used in thrombolytic therapy
Drug Initial dose
  • Halving the tenecteplase dose is recommended in patients > 75 years old.
Single i.v. bolus dose according to weight
weight < 60 kg 30 mg
60–69 kg 35 mg
70–79 kg 40 mg
80–89 kg 45 mg
≥ 90 kg 50 mg
Reteplase 10 units × 2 i.v. bolus doses given 30 minutes apart
  • Patients who arrive to treatment with delay (12–48 h from the onset of symptoms) with no pain and even in a haemodynamically stable condition, who have undergone an STEMI may benefit from an invasive assessment and treatment. Haemodynamically stable patients with no pain who have had an infarction more than 48 hours ago do not benefit from a routine revascularization of the infarct vessel.

Other medication in association with reperfusion

  • Consult first with the cardiologist on call at the cardiology unit regarding the feasibility of primary PCI and the antithrombotic medication.
  • ASA 250 mg orally or 75–150 mg intravenously before both thrombolytic therapy and PPCI (see initial management )
  • An initial loading dose of an P2Y12 receptor inhibitor before PPCI: primarily ticagrelor 180 mg (continued with 90 mg twice daily); alternatively clopidogrel 600 mg (continued with 75 mg/day), prasugrel 60 mg (continued with 10 mg once daily). The effect of clopidogrel has a slower onset, and in some patients (about 20 %) its anti-platelet effect remains inadequate.
  • Before thrombolytic therapy, 300 mg of oral clopidogrel is given to patients under 75 years; maintenance dose 75 mg is given to patients over 75 years. If the patient has received a loading dose of prasugrel or ticagrelor, thrombolytic therapy must not be given.
  • Enoxaparin before PPCI: starting dose 30 mg intravenously or 0.5 mg/kg
  • Enoxaparin before thrombolytic therapy: 30 mg intravenously for patients under 75 years; not for patients over 75 years. 15 minutes after thrombolytic therapy: for patients under 75 years, a 1 mg/kg dose of enoxaparin s.c. twice daily (neither of the two first doses should exceed 100 mg), for patients over 75 years 0.75 mg/kg s.c. twice daily (maximum single dose 75 mg); the medication is continued, at maximum for 8 days, until discharge or revascularization.
  • If renal impairment is present (eGFR < 30 ml/min ), the enoxaparin dose should be halved and the anti-FXa concentration monitored.
  • Patients under anticoagulation therapy
    • Warfarin treatment within therapeutic range (INR 2.0–3.0) is continued. INR is controlled daily; heparin therapy is not started.
    • Direct anticoagulant therapy is paused. Local guidelines are followed and a cardiologist on call is consulted.
  • Patients with STEMI who decline reperfusion therapy, or in whom it is not possible due to comorbidities, are treated with ASA and/or clopidogrel (doses as prior to thrombolytic therapy) and with enoxaparin, or as considered suitable at the given situation.

Complications of thrombolytic therapy

  • Intracranial bleed is a rare (1–2%) but serious complication of thrombolytic therapy. The signs of intracranial haemorrhage include a reduced level of consciousness, confusion and neurological deficits.
    • If haemorrhage is suspected or the patient exhibits cerebral symptoms, a CT scan of the head must be carried out.
  • Intestinal and other bleeds (haematemesis, melaena) are more frequent (5–10%) than intracranial haemorrhage.
  • Bleeding complications associated with thrombolytic therapy usually appear within 24 hours.
  • Age > 75 years, female gender, systolic BP > 160 mmHg, lighter body weight and concurrent anticoagulant therapy are significant predictors of haemorrhage.

Assessment of revascularization

  • The most useful sign of successful thrombolysis is ST segment resolution > 50% in the lead with the highest elevation within 60–90 minutes of the start of thrombolytic therapy.
  • Disappearance of chest pain and reperfusion arrhythmias are suggestive findings but when appearing alone are not sufficient to confirm revascularization.
  • Thrombolysis fails in about one third of patients, and reocclusion develops during hospitalisation in about 20% of patients after initial successful thrombolysis. In a large share of patients a significant occlusion remains in the coronary artery after thrombolysis.
  • Patients who received thrombolytic therapy are transported to a hospital with the capacity to perform a PPCI, where a coronary angiograpy is carried out within 24 hours,

Evidence Summaries

Arrhythmias in the acute phase


  • The mechanisms of arrhythmias include myocardial ischaemia and damage, reperfusion changes, autonomic imbalances as well as electrolyte and acid-base disturbances.
  • Rapid reperfusion therapy (PPCI) should be pursued if any of the following is detected: ventricular fibrillation (VF), ventricular tachycardia (VT), abundant ventricular ectopic beats or disturbances in the AV conduction.

Ventricular fibrillation (VF)

  • Primary VF occurring within 24–48 hours of the onset of STEMI does not increase long-term risk of an arrhythmia or mortality.
  • VF is treated with immediate defibrillation. Recurrent VF is treated with defibrillation and with a beta blocker and/or amiodarone. Ischaemia starts recurrent VF; therefore, it should be rapidly evaluated by coronary angiography and revascularisation should be aimed at.
  • The risk of recurrence can be reduced by optimising the drug therapy for myocardial ischaemia and heart failure (adequate beta blockade, ACE inhibitors, nitrates). Similarly, electrolyte disturbances must be corrected as well as factors associated with fluid balance and oxygenation.

Ventricular tachycardia (VT)

  • Repeated and prolonged episodes of VT are suggestive of a worsening heart disease and ischaemia, and when recurring they are an indication for a rapid coronary angiography/PPCI.
  • If VT periods recur frequently, either a beta blocker or amiodarone is administered intravenously. When VT is sustained or causes haemodynamic instability, it is treated with immediate cardioversion, which is repeated as required.

Other ventricular arrhythmias

  • Ventricular ectopic beats are common in patients with MI during the first few days of treatment. If they are asymptomatic and hemodynamically well-tolerated, no specific treatment is required.
  • Idioventricular rhythm is a consequence of reperfusion and requires no specific treatment. Similarly, salvos of non-sustained VT (< 30 seconds) without haemodynamic effects require no specific treatment. None of the above mentioned arrhythmias serve as reliable predictors of VF.

Atrial fibrillation (AF)

  • AF is common in the acute phase of an MI (10–20%). It increases in-hospital mortality and the risk of stroke, also in long-term follow-up.
  • It is more prevalent in older patients with MI and in patients with left ventricular dysfunction or failure.
  • Anticoagulant therapy is indicated unless the patient is already under anticoagulant treatment; long-term therapy according to CHA2DS2-VASc criteria (see table in(Indications for and implementation of anticoagulant therapy in atrial fibrillation)); need for antithrombotic medication should be considered.
  • An intravenous, later oral beta blocker may be used to provide ventricular rate control in AF. If the patient has cardiac failure or beta blockers are not suitable or not effective enough, intravenous amiodarone or digoxin may be used.

Sinus bradycardia and AV conduction disturbances

  • Sinus bradycardia is common in the first few hours of an MI, particularly in inferior infarction. Medication reducing heart rate is paused. Opioids may also predispose to sinus bradycardia. If sinus bradycardia causes haemodynamic compromise it should be treated with atropine 0.5 mg intravenously, followed by supplemental doses of 0.2–0.3 mg up to 2.0 mg.
  • First-degree AV block is often associated with inferior wall damage and is usually transient requiring no treatment.
  • More serious conduction disturbances, such as second- and third-degree AV block as well as LBBB, RBBB and left fascicular block indicate extensive myocardial damage and a rapid coronary angiography is required. In such cases, temporary, sometimes even permanent, pacing is required. In second-degree AV block, atropine may improve the conduction. Isoprenaline may provide temporary help. Transient AV block is most commonly associated with an inferior MI.

Antiarrhythmic medication

  • Antiarrhythmic and antibradycardia medications are presented in table T8.

Table 8. Intravenous doses of antiarrhythmic and antibradycardia medications
Drug Intravenous dose
  1. 150 mg over 10 minutes. Supplemental bolus doses of 150 mg may be given over 10–30 minutes for recurrent arrhythmias, but limited to 6–8 supplemental boluses in any 24 hour period.
  2. A maintenance infusion of 1 mg/min for 6 hours followed by 0.5 mg/minute may be necessary after the initial dose.
Metoprolol 2.5–5 mg at an interval of 2–5 minutes, up to 3 doses
Digoxin 0.25 mg every other hour, up to 1.0 mg, patient-specific assessment!
Atropine Rapid bolus dose of at least 0.5 mg, repeated up to a total dose of 1.5–2.0 mg (0.04 mg/kg)
Isoprenaline 0.05–0.1 µg/kg/min, up to 2 µg/kg/min. The dose should be adjusted to heart rate and rhythm.
Adapted from the source: Eur Heart J 2008;29:2909-2945

Right ventricular infarction

  • Right ventricular infarction is caused by the occlusion of the proximal right coronary artery.

Symptoms and diagnosis

  • Clinical symptoms are hypotension and high jugular venous pressure. However, a chest x-ray will fail to demonstrate venous congestion or pulmonary oedema.
  • ST elevation ≥ 1 mm in lead V4R is strongly suggestive of right ventricular infarction. Q-waves and/or ST elevation in V1–V3 are also suggestive of right ventricular damage.
  • AF may lead to haemodynamic collapse when the synchrony between the atria and ventricles is lost. AF must be promptly treated aiming to restore sinus rhythm. AV conduction disturbances are treated with atropine or dual chamber pacing.


  • Early reperfusion; see the treatment of STEMI
  • Hypotension is treated with adequate intravenous fluid loading, initially 500–1,000 ml, in order to maintain adequate preload. Dobutamine may be indicated.
  • It is desirable to avoid drugs that lower blood pressure, such as ACE inhibitors, angiotensin receptor blockers, nitrates, diuretics and opioids.

Acute coronary syndrome triggered by other factors

  • An imbalance in the myocardium with regard to the need and availability of oxygen may be triggered by anaemia, a surgical procecured, a serious systemic disease, an infection or trauma.
  • When the acute condition improves, the myocardial ischaemia often improves or disappears.
  • The diagnosis and treatment of ischaemia are accomplished by following the aforementioned principles, taking into account the clinical starting points of each patient. Selection of antithrombotic medication is considered case-by-case.
  • The severity of the coronary artery disease is assessed by echocardiography, coronary angiography, CT scan or myocardial perfusion scan.

Inpatient treatment

Monitoring and care

  • Continuous cardiac monitoring is indicated during the first few treatment days, in an appropriate unit.
  • In an uncomplicated MI, a patient without chest pain is allowed to sit up straightaway, eat unassisted and use the commode at the bedside.
  • In a complicated MI (heart failure, arrhythmias) bed rest should continue longer (2–4 days), mobilisation when considered appropriate.
  • An ACE inhibitor [Evidence Level: A] should be introduced during the first treatment day. If an ACE inhibitor is not suitable, an angiotensin receptor blocker should be prescribed.
  • A beta blocker is started during the hospitalisation period when the patient is haemodynamically stable.
  • Nicotine replacement therapy [Evidence Level: A] is introduced for smokers.
  • Patient education and motivation for treatment is important. The patient should be given information about the disease, the associated drug therapy as well as the modification of risk factors.

Level of care

  • Treatment of an MI may justifiably be carried out within primary care if the treatment options are limited due to other diseases.

Follow-up management

  • The follow-up management of ACS consists of antithrombotic and anti-ischaemic drug therapy as well as of modification of risk factors with lifestyle changes and pharmacotherapy.
  • Aspirin long-term 100 mg daily. Clopidogrel 75 mg daily for patients with aspirin allergy.
  • A P2Y12 receptor inhibitor (ticagrelor, clopidogrel or prasugrel) is used in the treatment of ACS; both during the acute hospital phase and in the continued treatment (12 months) after the MI; 6 months if bleeding risk is increased. In special situations, when the risk of ischaemia is high without increased risk of bleeding, continuing the aspirin + P2Y12 receptor inhibitor (ticagrelor 60 mg twice daily) medication for more than 12–36 months may be considered.
  • If anticoagulation therapy (warfarin, dabigatran, rivaroxaban, apixaban, edoxaban) is necessary due to some other indication, after insertion of a coronary stent the patient is given triple therapy (ASA + clopidogrel + anticoagulant) for 1–6 months (individual assessment where antithrombotic and anti-ischaemic drug effect as well as bleeding risk are taken into account), then clopidogrel (or aspirin) + anticoagulant for a total of one year after the cardiac event. After one year, only anticoagulant is used.
  • Anticoagulant therapy is indicated for patients with a left ventricular thrombus, for 3–6 months. In association with recently appeared AF, the long-term need of anticoagulant therapy is assessed with CHA2DS2VASc criteria (Indications for and implementation of anticoagulant therapy in atrial fibrillation). It is recommended to consider a direct oral anticoagulant whereby the risk of an intracranial bleeding is smaller.
  • An ACE inhibitor should be prescribed for MI patients with heart failure (in the acute phase), EF < 40%, anterior infarction, hypertension or diabetes. The recommended maintenance doses should be used, or the highest tolerated dose. If an ACE inhibitor is not suitable, an angiotensin receptor blocker should be prescribed.
  • A statin should be prescribed for all patients with MI. Ezetimibe or fibrates may be used when statins are not suitable.
  • A beta blocker should be prescribed for those patients with MI who also have cardiac failure or EF ≤ 40%, unless contraindicated.
  • Calcium-channel blockers are mainly appropriate for the treatment of hypertension and/or chest pain if beta blockers are not suitable. There is no clear evidence of the benefit of calcium-channel blockers in terms of improved prognosis in CHD. See stable coronary heart disease: (Coronary heart disease).
  • A prescription for short-acting glyceryl trinitrate (GTN) should always be given to the patient on discharge after an MI.
  • Long-acting nitrates are reserved for patients with continuing chest pain.
  • Influenza immunization [Evidence Level: C] is indicated for all patients who have had an MI.
  • After the hospitalisation phase, the long-term management of patients who have sustained an MI will almost without exception be the responsibility of the general practitioner. Primary care health providers are in a key position to motivate the patient to adopt permanent lifestyle changes and to ensure that drug therapies to manage risk factors and improve prognosis are adhered to and that regular primary care follow-up visits are arranged.
  • Emphasis should be put on patient guidance (lifestyle changes, diet, exercise) both during the hospital stay and after that in the primary care. Progress of the changes should be actively monitored during follow-up visits. These factors are important in the rehabilitation of the patient back into normal life.
  • Rehabilitation measures are needed if the return to normal life is not actualized as planned.

Evidence Summaries


1. Levine GN, Bates ER, Bittl JA ym. 2016 ACC/AHA Guideline Focused Update on Duration of Dual Antiplatelet Therapy in Patients With Coronary Artery Disease: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Circulation 2016 [Epub ahead of print].  [PMID:27026020]

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