Acute Myocardial Infarction

aCute myoCardial inFarCtion

Patient Presentation

STEMI patients typically delay seeking medical attention for their symptoms for up to two hours. Patient delay times are often longer in women and the elderly. It has been suggested that the delay can be attributed to:

• Patient’s symptoms differ from stereotypical presentation (intense crushing chest pain) • About one-third of patients with AMI don’t experience typical chest pain1 • Belief that the symptoms are trivial and self-limiting • Attributing symptoms to an existing disease • Fear of ‘crying wolf’ • Reluctance to bother others unless ‘really sick’ • Denial of being at risk • Financial hardship • Poor access to health care

Characteristic Myocardial Infarction Symptoms

Patient symptoms associated with myocardial infarction can be present in prodromal (early symptoms indicating onset) or acute fashion. Prodromal symptoms include malaise, intermittent chest discomfort, and fatigue. Characteristic acute symptoms include:

• Intense unrelieved chest pain for 30 minutes or more • Retrosternal chest pain • Pain radiation into neck, jaw, shoulder and left arm • Chest and retrosternal pressure / squeezing / aching / burning or stabbing • Epigastric pain / discomfort • GORD / fullness sensation.

1 O’Gara, P.T., Kushner, F.G., Ascheim, D.D., Casey, D.E., Chung, M. K., de Lemos, J.A., Zhao, D.X. (2013). 2013 ACCF/AHA Guideline for the Management of ST-Elevation Myocardial Infarction. A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation. 2013; 127:e362-e425.

Clinical Signs Associated with Acute Myocardial Infarction

A thorough patient assessment can also yield additional clues suggestive of myocardial infarction. This is especially useful in the face of atypical symptoms, or when communication with the patient is unreliable. While the following clinical signs aren’t specific to myocardial infarction, they can indicate myocardial ischaemia, ventricular dysfunction, or inappropriate stimulation of the autonomic nervous system:

• Chest pain / discomfort / pressure / fullness • Arm / shoulder / neck / throat / jaw discomfort • Increased heart rate and tachyarrhythmias • Bradycardia • Irregular rhythms • Abnormal rhythms • Ectopic beats and palpitations • Exertional dyspnoea and decreased exercise tolerance • Cool clammy skin • Nausea • Hypotension / Hypertension • Venous congestion and JVD • Pulmonary oedema

Complications of Myocardial Infarction

Figure 3.3: Complications of Acute Myocardial Infarction

The likelihood and severity of MI complications can be quantified through various risk stratification tools. More information can be found by clicking the icon below. The findings of these tools provide the patient with a sense of what to expect in the future, and identify their risk of arrhythmic death.

Demographic factors that increase the prediction of mortality include:

• Older age • Larger MIs • Anterior MI • Hypotension • Cardiogenic shock • Heart failure • Tachycardias • Wide QRS complex • Pulmonary oedema • Presence of risk factors (hypertension, smoking, previous CVA)

Ischaemic Complications

Infarction extension is an increase in myocardial necrosis within the infarct zone of the original MI. This increase can extend the necrosis into adjacent viable tissue, or increase the thickness of the infarct making it transmural.

Multi-vessel coronary artery disease (CAD) is common in patients with STEMI. It is estimated that up to 40% of STEMI patients demonstrate significant plaque in the non-affected vessels during angiography. This phenomenon may help explain the reocclusion rate of the infarct related artery post fibrinolytic therapy. Up to 10% of patients experience reocclusion at discharge, with the rate rising to 30% at 12 months. Percutaneous coronary intervention (PCI) has significantly reduced this rate to about 3% after 90 days.1

Angina that occurs up to 30 days post STEMI is termed infarction angina. This variant of angina is most likely to affect patients post NSTEMI, and those re-vascularised with fibrinolytic therapy as opposed to PCI.

Arrhythmic Complications

Approximately 90% of STEMI patients develop a cardiac arrhythmia during or after the event. About a quarter of these patients will have the arrhythmia manifest within 24 hours of infarction.2 The risk of life-threatening arrhythmia is greatest in the first hour, and declines thereafter.

Arrhythmias are caused by autonomic dysfunction that enhances the automaticity of myocardial tissue and the conduction system. This is further compounded through the presence of hypoxia and electrolyte imbalance. As tissue damage occurs, myocardial refractoriness is altered increasing the risk or re-entry circuit formation.

1 Grasso., A.W. (2014). Complications of Acute Myocardial Infarction. Cleveland Clinic Centre for Continuing Education. Retrieved from http://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/cardiology/complications-of-acute-myocardial-infarction/ 2 Kondur, A.K. & Afonso, L.C. (2014). Complications of Myocardial Infarction. Medscape. Retrieved from http://emedicine. medscape.com/article/164924-overview#a2

Arrhythmias seen in MI include:

• Supraventricular (PSVT, sinus tachycardia, PAC, AF and Atrial Flutter) • Junctional • Bradycardias (ventricular and junctional) • AV blocks • Bundle branch and fascicular blocks • Ventricular (PVC, idioventricular, VT and VF) • Reperfusion arrhythmias

Mechanical Complications

The three major mechanical complications of MI are:

1. Ventricular free wall rupture 2. Ventricular septal rupture 3. Papillary muscle rupture with mitral valve regurgitation While left ventricular failure accounts for the majority of MI fatalities, ventricular free wall rupture is the most serious mechanical complication. It is usually associated with a large transmural (full-thickness) infarct, or an extension of a previous MI.1 It is a common cause of death and accounts for 15-30% of deaths associate with MI. This catastrophic presentation leads to bleeding into the pericardial sac and cardiac tamponade.

1 Kondur, A.K. & Afonso, L.C. (2014). Complications of Myocardial Infarction. Medscape. Retrieved from http://emedicine. medscape.com/article/164924-overview#a2

Goals of STEMI Management

The first critical step in STEMI management is prompt recognition. Delays in reperfusion therapy reduce the efficacy of treatment, and translates to significant morbidity and mortality. Early intervention limits the size of the infarction and salvages jeopardised ischaemic myocardium.

The goals of STEMI management can be broadly classified as:

1. Early management meeting acute needs 2. Maintenance management designed to improve long-term prognosis

Early Management

• Haemodynamic support (assessment and correction of abnormalities) • Pain relief • Reperfusion (PCI or fibrinolytic therapy) • Prevent acute re-thrombosis or stent occlusion (antithrombotic therapy) • Rate control and arrhythmia suppression (typically ß-Blocker)

Maintenance Management

• Reduce the risk of re-thrombosis (antiplatelet therapy) • Prevent / Reduce left ventricular remodelling / hypertrophy (antihypertensive medication) • Reduce cardiovascular disease (statin therapy) • Prevent embolisation from thrombus or AF (anticoagulation therapy)