Infarto agudo de miocardio

What is acute myocardial infarction?

Myocardial infarction (MI) is one of the most severe presentations of coronary heart disease (CHD).¹

An acute myocardial infarction is caused by necrosis of myocardial tissue due to ischaemia, usually due to blockage of a coronary artery by a thrombus. Most myocardial infarctions are anterior or inferior but may affect the posterior wall of the left ventricle to cause a posterior myocardial infarction. Nearly half of potentially salvageable myocardium is lost within one hour of the coronary artery being occluded, and two thirds are lost within three hours.²

Myocardial infarction is now considered part of a spectrum referred to as acute coronary syndrome (ACS). This refers to a spectrum of acute myocardial ischaemia that also includes unstable angina and non-ST-segment elevation myocardial infarction (NSTEMI).³

The new criteria for diagnosing myocardial infarction are detection of rise and/or fall of cardiac biomarkers (preferably troponin) with at least one value above the 99th percentile of the upper reference limit, together with evidence of myocardial ischaemia with at least one of the following:⁴

• Symptoms of ischaemia.

• ECG changes indicative of new ischaemia (new ST-T changes or new left bundle branch block (LBBB).

• Development of pathological Q-wave changes in the ECG.

• Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality.

• Identification of an intracoronary thrombus by angiography or autopsy.

The British Heart Foundation (BHF) estimates that in the UK:

• CHD is one of the leading causes of death (responsible for around 68,000 deaths each year) and the most common cause of premature death.

• Around 2.3 million people are living with CHD (about 1.5 million men and 830,000 women).

• Around 100,000 hospital admissions each year are due to MIs.

• Around 1.4 million people have survived an MI (about one million men and 380,000 women).

Factores de riesgo

• Non-modifiable risk factors for atherosclerosis include increasing age, being male, family history of premature CHD, premature menopause.

• Modifiable risk factors for atherosclerosis include smoking, diabetes mellitus (and impaired glucose tolerance), metabolic syndrome, hypertension, hyperlipidaemia, obesity and physical inactivity.⁶

• Certain ethnic groups have higher risk of CHD. In the UK, the highest recorded rates of coronary artery disease mortality are in people born in India, Pakistan and Bangladesh.⁷ South Asians are thought to have a 40-60% higher risk of CHD-related mortality compared to other populations.

• Chest pain (central chest pain may not be the main symptom):

  • Three quarters of patients present with characteristic central or epigastric chest pain radiating to the arms, shoulders, neck, or jaw.

  • The pain is described as substernal pressure, squeezing, aching, burning, or even sharp pain.

  • Radiation to the left arm or neck is common.

  • Chest pain may be associated with sweating, nausea, vomiting, dyspnoea, fatigue and/or palpitations.

• Shortness of breath: may be the patient's anginal equivalent or a symptom of heart failure.

• Atypical presentations are common and tend to be seen in women, older men, people with diabetes and people from ethnic minorities. Atypical symptoms include abdominal discomfort or jaw pain; elderly patients may present with altered mental state.

Signos

Cardiovascular examination findings can vary enormously:

• Low-grade fever, pale and cool, clammy skin.

• Hypotension or hypertension can be observed depending on the extent of the myocardial infarction.

• Dyskinetic cardiac impulse (in anterior wall myocardial infarction) can be palpated occasionally.

• Third and fourth heart sound, systolic murmur if mitral regurgitation or ventricular septal defect develops, pericardial rub.

• There may be signs of congestive heart failure, including pulmonary rales, peripheral oedema, elevated jugular venous pressure.

• Consider the history of the pain, any cardiovascular risk factors, history of CHD and any previous treatment, and previous investigations for chest pain.

• Symptoms that may indicate ACS include:

  • Pain in the chest and/or other areas (eg, the arms, back or jaw) lasting for longer than 15 minutes.

  • Dolor en el pecho con náuseas y vómitos, sudoración intensa y/o dificultad para respirar, o inestabilidad hemodinámica.

  • Dolor torácico de nueva aparición, o deterioro abrupto de la angina estable, con dolor recurrente que ocurre frecuentemente con poco o ningún esfuerzo y que a menudo dura más de 15 minutos.

• La respuesta al trinitrato de glicerilo (GTN) no debe utilizarse para hacer un diagnóstico y los síntomas no deben evaluarse de manera diferente en hombres y mujeres o entre diferentes grupos étnicos.

• A los pacientes con angina preexistente se les debe aconsejar que cuando ocurra un ataque de angina, deben:⁹

  • Dejen lo que están haciendo y descansen.

  • Use el spray o las tabletas de GTN según las indicaciones.

  • Tome una segunda dosis de GTN después de cinco minutos si el dolor no ha disminuido.

  • Tome una tercera dosis de GTN después de cinco minutos más si el dolor aún no ha disminuido.

  • Call 999/112/911 for an ambulance if the pain has not eased after another five minutes (ie 15 minutes after onset of pain), or earlier if the pain is intensifying or the person is unwell.

Vea también el separado Dolor en el pecho y Dolor torácico de tipo cardíaco en atención primaria articles.

• Cardiovascular: stable angina, another form of ACS (unstable angina or NSTEMI), acute pericarditis, miocarditis, estenosis aórtica, disección aórtica, embolia pulmonar.

• Respiratory: neumonía, a tensión.

• Gastrointestinal: espasmo esofágico, enfermedad por reflujo gastroesofágico, acute gastritis, colecistitis, pancreatitis aguda.

• Musculoskeletal chest pain.

Consider non-atherosclerotic causes of myocardial infarction in younger patients or if there is no evidence of atherosclerosis: coronary emboli from sources such as an infected cardiac valve, coronary occlusion secondary to vasculitis, coronary artery spasm, cocaine use, congenital coronary anomalies, coronary trauma, increased oxygen requirement (eg, hipertiroidismo) or decreased oxygen delivery (eg, severe anaemia).

• If diagnosis is suspected, immediately arrange urgent hospital assessment and admission. Call 999/112/911 ambulance.

• ECG:

  • May be helpful in a pre-hospital setting if the diagnosis is uncertain or in a remote area in the assessment for pre-hospital thrombolysis but otherwise should not delay getting the patient to hospital.

  • Features may initially be normal but abnormalities include new ST-segment elevation; initially peaked T waves and then T-wave inversion; new Q waves; new conduction defects.

  • Do not exclude an ACS when people have a normal resting 12-lead ECG.

In hospital

• FBC to rule out anaemia; leukocytosis is common; monitor potassium levels (electrolyte disturbances may cause arrhythmias, especially potassium and magnesium); renal function - estimated glomerular filtration rate (eGFR) - should be measured prior to starting an angiotensin-converting enzyme (ACE) inhibitor. Lipid profile needs to be obtained at presentation because levels can change after 12-24 hours of an acute illness. Measure C-reactive protein (CRP) and other markers of inflammation.

• Cardiac enzymes:

  • See also separate Cardiac enzymes and markers for myocardial infarction article.

  • Measurement of a biomarker of cardiac cell injury, preferably high-sensitivity cardiac troponin, is recommended in all patients with suspected ACS. In patients with MI, levels of troponin rise rapidly (usually within 1 hour if using high-sensitivity assays) after symptom onset and remain elevated for a variable period of time (usually several days).³

• Serial ECGs and continuous ECG monitoring in a coronary care unit (CCU).

• CXR: to assess the patient's heart size and the presence or absence of heart failure and pulmonary oedema. This may also assist in differential diagnosis.

• Pulse oximetry and blood gases: monitor oxygen saturation.

• Offer 64‑slice (or above) CT coronary angiography if:⁸

  • Clinical assessment indicates typical or atypical angina; o

  • Clinical assessment indicates non-anginal chest pain but 12‑lead resting ECG has been done and indicates ST‑T changes or Q waves.

• If CT coronary angiography is non-diagnostic, offer non-invasive functional imaging - eg:⁸

  • Myocardial perfusion scintigraphy with single photon emission computed tomography (MPS with SPECT); o

  • Stress echocardiography; o

  • First-pass contrast-enhanced magnetic resonance (MR) perfusion; o

  • MR imaging for stress-induced wall motion abnormalities.

• Echocardiography can define the extent of the infarction and assess overall ventricular function and can identify complications, such as acute mitral regurgitation, left ventricular rupture or pericardial effusion.

See the separate Manejo del infarto agudo de miocardio, Evaluación del riesgo cardiovascular y Cardiac rehabilitation articles.

See the separate Complicaciones del infarto agudo de miocardio article.

• The British Heart Foundation reports that in the 1960s, more than 70% of heart attacks in the UK were fatal; today, at least 70% of people survive an MI.

• The overall prognosis depends on the extent of heart muscle damage. A greater degree of myocardial necrosis is associated with a worse prognosis and a higher risk of heart failure.

• Other factors that can adversely affect prognosis include:

  • Delayed reperfusion.

    • Site of the infarction (anterior MI has a less favourable prognosis than inferior MI).

• Choice of treatment (people who undergo revascularisation have better outcomes than those who do not).

  • Comorbidities, eg, hypertension, diabetes, chronic kidney disease, congestive heart failure, and frailty.

    • Complications, eg, heart failure, arrhythmias, bleeding, and depression.

  • Edad avanzada.

  • Sexo femenino.

  • Poor compliance with secondary prevention measures.

• A systematic review assessed the prevalence of 30-day readmission following acute MI:¹⁰

• The 30-day readmission rates ranged from 11–14%.

• Acute coronary syndrome, angina, acute ischemic heart disease, and heart failure were the main cardiovascular reasons for 30-day readmission. Non-specific chest pain was the main non-cardiovascular reason for 30-day readmission.

• The other risk factors for readmission included kidney disease, female sex, diabetes mellitus, and chronic obstructive pulmonary disease.

See the separate Prevention of cardiovascular disease article.