Acute Coronary Syndrome: What You Need to know

Acute coronary syndrome (ACS) is an umbrella term used to describe any condition that causes a sudden decrease in blood supply to heart muscles.

The heart supplies oxygen and nutrients to all tissues in the body including itself.

Image showing coronary arteries surrounding heart muscles that are affected in acute coronary syndrome

The heart is wrapped in tiny blood vessels called coronary arteries that supply the heart with oxygen and nutrients it needs to function.

Interruption to blood flow through the coronary arteries will results in death of the tissues that it supplies.

Timely identification of patients with acute coronary syndrome will minimize cardiac cell death and preserve cardiac function.

Patient Presentation

Patients will commonly complain of feeling pressure in the chest that spreads out to the arms and jaw even when they are resting or with minimal activity. This is accompanied by excessive sweating, nausea and shortness of breath.

Patients often initially describe it as bad case of heartburn. Shortness of breath and radiating pain should lead you to a more worrisome diagnosis.

ACS has an in hospital mortality rate of up to 26%. It is very important to be able to identify patients with potential ACS. Treatment options are time sensitive.

Illustration showing orders for a patient presenting with acute coronary syndrome. Includes a a 12 lead ECG, aspirin and cardiac troponins.

If ACS is suspected, a 12 lead ECG and aspirin should be given within 10 mins.

Cardiac troponin levels should also be ordered.

The sooner we correct blockage the more muscle we save. The strength of contraction of heart muscle is the driving force of blood circulation.

Early intervention in ACS helps to preserve heart function.

Pathophysiology

Atherosclerotic Plaque

The most common cause of reduced blood flow to the heart is the rupture of plaque that has accumulated within blood vessels. This build up is referred to as atherosclerosis.

Illustration of an artery with blood flow restricted by the build up of plaque inside the walls of the vessel.

Atherosclerotic plaque is the build up of fatty tissue, cholesterol and other materials on the inner walls of arteries.

In addition to the build up itself reducing the diameter of the vessel and therefore blood flow, the plaque can break open and cause damage to the lining of vessel.

This stimulates an immune response at the site of injury. Macrophages, neutrophils and platelets rush to the site of injury forming a clot in an attempt to repair the rupture. This unfortunately further narrows the pathway for blood flow.

Pieces of plaque or pieces of the thrombus can also break off and be carried by the flow of blood. These fragments can cause blockage when they get to smaller vessels like coronary arteries. This is referred to as embolization.

Illustration showing how plaque build up in the arteries can lead to clot formation. Injury to the plaque stimulates an immune response that stimulates clot formation around the injured vessel, further restricting blood flow. Parts of the clot can embolize (break off) and clog off smaller vessels like coronary arteries.

Coronary Spasms

Less commonly, acute coronary syndrome can occur in the absence of atherosclerotic plaque formation via coronary vasospasm. This is a sudden narrowing of coronary arteries which restricts blood flow to the heart.

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Assessment

Cardiac Troponins

Cardiac troponins are proteins that regulate contraction of heart muscles.

Muscle contraction happens when actin and myosin (filaments that make up muscle fibers) connect and slide past each other.

In the presence of intracellular calcium, cardiac troponins will alter binding sites so that actin and myosin can interact. Binding initiates the filament slide which we see as cardiac contraction.

Illustration showing the role of cardiac troponin in heart muscle contraction. Troponin is bound to actin. Actin is a muscle fiber, that must slide past myosin (another muscle fiber) for contraction to occur.

Illustration showing the role of troponin and calcium in muscle contraction. When calcium binds to troponin. it changes the configuration so that actin and myosin can attach and slide past each other to cause muscle contraction.

As heart muscles die from prolonged lack of oxygen and nutrients, cardiac troponins are released from dying cells into blood.

ST Segment

The QRS wave on ECG is ventricular depolarization. During this time an electrical signal moves through the ventricles.

This triggers voltage gated sodium and calcium channels to open. The influx of positive ions stimulates muscle contraction.

The T wave on ECG is ventricular repolarization. The voltage gated channels close and potassium moves out. The heart muscles relax.

The ST segment on an ECG is the time between the end of ventricular depolarization and start of repolarization.

During this time the heart remains contracted, expeling blood into systemic circulation.

The ST segment is considered electrically neutral. It normally lies flat at baseline.

In ACS, the direction of displacement of the ST segment from neutrality is used to differentiate between the 2 broad categories of ACS and determine treatment.

NSTE-ACS & STEMI

NSTE-ACS and STEMI are the 2 broad categories of ACS.

Illustration showing the zones of the ECG where the ST segment would be observed in ST elevation versus ST depression when doagnosing acute coronary syndrome

When there is complete blockage of flow we will see ST elevation.

ACS with ST elevation is classified as a STEMI.

As long as blood flow to some healthy tissue can still be achieved we will see ST depression.

ACS with ST depression is classified as Non ST Segment Elevation-ACS. In NSTE-ACS blockage in incomplete.

NSTE-ACS can be further broken down into unstable angina (UA) and NSTEMI.

UA and NSTEMI are differentiated by the absence or presence of cardiac troponins.

Illustration showing how to differentiate between the 3 types of acute coronary syndrome in three simple steps

I. Unstable Angina

In UA there is partial occlusion of the coronary arteries. Since there is still blood flow with occlusion we see ST depression. The blockage is not sufficient to cause cell death (no myocardial infarction) so troponins levels will not increase.

Unstable angina (UA) will show ST depression and negative troponins.

II. NSTEMI

In non ST elevated myocardial infarction, there is partial occlusion sufficient to cause some call death. Because blood flow can still be directed to some healthy tissue we see ST depression. Because there is some cell death we see in a rise in cardiac troponins.

III. STEMI

In ST elevation myocardial infarction there is complete occlusion. Because there is no pathway for blood flow to healthier tissues we see ST elevation. No blood flow means cell death in inevitable, we see a significant rise in cardiac troponins.

Illustration comparing the ST segment and cardiac troponin levels in unstable angina, NSTEMI and STEMI.

4 Treatment Groups for ACS

In non STE-ACS (unstable angina and NSTEMI) the goal of treatment is to prevent complete occlusion as soon as possible.

In STEMI the goal of treatment is to restore perfusion as soon as possible.

This is achieved mechanically via a medical procedure known as percutaneous coronary intervention (PCI) where the affected artery is accessed and the blockage circumvented with a stent. This involves the use of antiplatelet medication and anticoagulation.

Perfusion can also be reestablished pharmaceutically with a combination of antiplatelet medications, anticoagulants or fibrinolytics.

The choice of therapy is dependent mainly on the category of ACS (UA, NSTEMI or STEMI) and patient stability.

Illustration of the treatment option in ACS. This includes ischemia directed therapy. percutaneous coronary intervention and fibrinolysis.

Each of these interventions will require their own unit.

As always you can dive right into the guidelines for the management of patients with acute coronary syndrome. Knowing the fundamentals presented here will give you a good framework to navigate those guidelines.

Check out our other cardiac units on Acute Heart Failure and Atrial Fibrillation.

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The information on this website is intended to be used solely for educational and informational purposes. While the content may be about specific medical and health care issues, it is not a substitute for or replacement of personalized medical advice and is not intended to be used as the sole basis for making individualized medical or health-related decisions.

Acute Coronary Syndrome: What You Need to Know

Patient Presentation