Wednesday, 1 September 2021

 

Cardiomyopathy

Cardiomyopathy is a general term for diseases of the heart muscle, where the walls of the heart chambers have become stretched, thickened or stiff. This affects the heart's ability to pump blood around the body.

The abnormal heart muscle seen in cardiomyopathy is not caused by blocked arteries in the heart (coronary artery disease), high blood pressure (hypertension), disease of the heart valves (valvular disease) or congenital heart disease.

Most types of cardiomyopathy are inherited and are seen in children and younger people.

Dilated cardiomyopathy

In dilated cardiomyopathy the muscle walls of the heart become stretched and thin, so they cannot squeeze (contract) properly to pump blood around the body.

How serious is it?

If you have dilated cardiomyopathy, you're at greater risk of heart failure, where the heart fails to pump enough blood around the body at the right pressure.

Heart failure typically causes shortness of breath, extreme tiredness and ankle swelling. Learn more about the symptoms of heart failure.

There's also a risk of heart valve problems, an irregular heartbeat and blood clots. You'll need to have regular appointments with a GP so the condition can be monitored.

Who's affected?

Dilated cardiomyopathy can affect both children and adults. 

The following can all play a role in the condition:

  • inheriting a changed (mutated) gene that makes you more vulnerable to the condition
  • an underlying medical condition
  • uncontrolled high blood pressure
  • an unhealthy lifestyle, such as a lack of vitamins and minerals in your diet, drinking too much alcohol and using recreational drugs
  • a viral infection that causes inflammation of the heart muscle
  • a heart valve problem
  • a disease of the tissues or blood vessels – such as granulomatosis with polyangiitis (GPA)sarcoidosisamyloidosislupus, polyarteritis nodosa, vasculitis or muscular dystrophy
    • pregnancy – cardiomyopathy can sometimes develop as a complication of pregnancy

But for many people, the cause is unknown.

More information

Read the British Heart Foundation and Cardiomyopathy UK's booklet on living with dilated cardiomyopathy.

Hypertrophic cardiomyopathy

In hypertrophic cardiomyopathy, the heart muscle cells enlarge and the walls of the heart chambers thicken.

The heart chambers are reduced in size so they cannot hold much blood, and the walls cannot relax properly and may stiffen. Also, the flow of blood through the heart may be obstructed.

How serious is it?

In most cases, hypertrophic cardiomyopathy will not have an impact on daily life. Some people do not have any symptoms and do not need treatment.

But that does not mean the condition cannot be serious. Hypertrophic cardiomyopathy is the most common cause of sudden unexpected death in childhood and in young athletes.

The main heart chambers can become stiff, leading to back pressure on the smaller collecting chambers. This can sometimes worsen the symptoms of heart failure and lead to abnormal heart rhythms (atrial fibrillation).

Blood flow from the heart may be reduced or restricted (called obstructive hypertrophic cardiomyopathy).

Also, the mitral heart valve can become leaky, causing blood to leak backwards. Find out more about mitral regurgitation.

You'll also be at greater risk of developing a heart infection (endocarditis).

These heart changes can cause dizziness, chest pain, shortness of breath and temporary loss of consciousness.

If you have severe hypertrophic cardiomyopathy, you'll need to see your doctor regularly so your condition can be monitored.

Your doctor will advise about the level and amount of exercise you can do and recommend lifestyle changes you can make. 

Who's affected?

Hypertrophic cardiomyopathy is thought to affect 1 in 500 people in the UK. Most people inherit the disease from their parents.

More information

Read the British Heart Foundation and Cardiomyopathy UK's booklet on living with hypertrophic cardiomyopathy.

Restrictive cardiomyopathy

Restrictive cardiomyopathy is rare. It's most often diagnosed in children, although it can develop at any age. The walls of the main heart chambers become stiff and rigid and cannot relax properly after contracting. This means the heart cannot fill up properly with blood.

It results in reduced blood flow from the heart and can lead to symptoms of heart failure, such as breathlessness, tiredness and ankle swelling, as well as heart rhythm problems.

In many cases the cause is unknown, although sometimes the condition can be inherited.

More information

Find out more about restrictive cardiomyopathy from Cardiomyopathy UK.

Arrhythmogenic right ventricular cardiomyopathy

In arrhythmogenic right ventricular cardiomyopathy (ARVC), the proteins that usually hold the heart muscle cells together are abnormal. Muscle cells can die and the dead muscle tissue is replaced with fatty and fibrous scar tissue.

The walls of the main heart chambers become thin and stretched and cannot pump blood around the body properly.

People with ARVC usually have heart rhythm problems. Reduced blood flow from the heart can also lead to symptoms of heart failure.

ARVC is an inherited condition caused by a change (mutation) in one or more genes. It can affect teenagers or young adults and has been the reason for some sudden unexplained deaths in young athletes.

There's increasing evidence that prolonged, strenuous exercise makes the symptoms of ARVC worse. It's important that people with or at risk of ARVC discuss this in detail with their heart specialist (cardiologist).

More information

Find out more about ARVC from Cardiomyopathy UK.

Diagnosing cardiomyopathy

Some cases of cardiomyopathy can be diagnosed after various heart scans and tests, such as:

If you've been diagnosed with an inherited type of cardiomyopathy, you may be advised to have a genetic test to identify the faulty gene (mutation) that caused this.

Your relatives can then be tested for the same mutation and, if they have it, their condition can be monitored and managed early.

Treating cardiomyopathy 

There's usually no cure for cardiomyopathy, but the treatments can be effective at controlling symptoms and preventing complications. Some types of cardiomyopathy have specific treatments and early diagnosis is very important.

Not everyone with cardiomyopathy will need treatment. Some people only have a mild form of the condition they can control after making a few lifestyle changes.

Lifestyle changes

Whether the cause of cardiomyopathy is genetic or not, it should generally help to:

Medicines

Medicines may be needed to control blood pressure, correct an abnormal heart rhythm, remove excess fluid or prevent blood clots. 

Find out more about:

Hospital procedures

In some people with obstructive hypertrophic cardiomyopathy, the wall dividing the left and right side of the heart (septum) is thickened and bulges into the main heart chamber. They may need to have either:

  • an injection of alcohol into their heart – this is to reduce part of the muscle in the septum
  • a septal myectomy – heart surgery to remove part of the thickened septum (the mitral valve may be repaired at the same time, if necessary)

Those with heart rhythm problems may need to have arrhythmia ablation. This treatment carefully alters the diseased heart tissue that causes the heart rhythm problems.

Or they may have a device implanted, such as:

  • a pacemaker to regulate the heart rate
  • an implantable cardioverter defibrillator (ICD) to prevent a life-threatening abnormal heart rhythm

Find out more about having a pacemaker implanted.

Find out more about implantable cardioverter defibrillators from the British Heart Foundation.

As a last resort, a heart transplant may be necessary.

Broken heart syndrome

Some people who experience significant emotional or physical stress, such as bereavement or major surgery, go on to experience a temporary heart problem.

The heart muscle becomes suddenly weakened or "stunned", causing the left ventricle (one of the heart's main chambers) to change shape. It may be caused by a surge of hormones, particularly adrenaline, during a period of stress.

The main symptoms are chest pain and breathlessness, similar to those of a heart attack. Always call 999 if you or someone else experiences these.

The condition – known medically as Takotsubo cardiomyopathy, or acute stress cardiomyopathy – is more common in women. It's temporary and reversible. It's unusual for it to happen again.

Find out more about Takotsubo cardiomyopathy from Cardiomyopathy UK.


file:///C:/Users/ebya00/AppData/Local/Temp/MicrosoftEdgeDownloads/56f4ee85-805f-4351-9358-561f40ba8686/m111d-life-with-dilated-cardiomyopathy.pdf


https://www.nhs.uk/conditions/cardiomyopathy/



Tuesday, 31 August 2021

STEMI/NSTEMI linked to MI

 


Myocardial Ischaemia Background

Non-ST-elevation acute coronary syndrome (NSTEACS) encompasses two main entities:

  • Non-ST-elevation myocardial infarction (NSTEMI).
  • Unstable angina pectoris (UAP).

The differentiation between these two conditions is usually retrospective, based on the presence/absence of raised cardiac enzymes at 8-12 hours after the onset of chest pain.

Both produce the same spectrum of ECG changes and symptoms and are managed identically in the Emergency Department.

Patterns of Myocardial Ischaemia
Two main ECG patterns associated with NSTEACS:

While there are numerous conditions that may simulate myocardial ischaemia (e.g. left ventricular hypertrophydigoxin effect), dynamic ST segment and T wave changes (i.e. different from baseline ECG or changing over time) are strongly suggestive of myocardial ischaemia.

Other ECG patterns of ischaemia

Morphology of ST Depression
  • ST depression can be either upsloping, downsloping, or horizontal (see diagram below).
  • Horizontal or downsloping ST depression ≥ 0.5 mm at the J-point in ≥ 2 contiguous leads indicates myocardial ischaemia (according to the 2007 Task Force Criteria).
  • ST depression ≥ 1 mm is more specific and conveys a worse prognosis.
  • ST depression ≥ 2 mm in ≥ 3 leads is associated with a high probability of NSTEMI and predicts significant mortality (35% mortality at 30 days).
  • Upsloping ST depression is non-specific for myocardial ischaemia.
ST segment depression upsloping downsloping horizontal

Examples of ST segment morphology in myocardial ischaemia

ST segment morphology in myocardial ischaemia

Distribution of ST segment depression

ST depression due to myocardial ischaemia may be present in a variable number of leads and with variable morphology:

  • ST depression due to subendocardial ischaemia is usually widespread — typically present in leads I, II, V4-6 and a variable number of additional leads.
  • A pattern of widespread ST depression plus ST elevation in aVR > 1 mm is suggestive of left main coronary artery occlusion.
  • ST depression localised to a particular territory (esp. inferior or high lateral leads only) is more likely to represent reciprocal change due to STEMI. The corresponding ST elevation may be subtle and difficult to see, but should be sought.
  • This concept of ST depression failing to localise is further discussed on Dr Smiths blog.
LMCA 2
Widespread subendocardial ischaemia due to LMCA occlusion

T wave inversion

T wave inversion may be considered to be evidence of myocardial ischaemia if:

  • At least 1 mm deep
  • Present in ≥ 2 continuous leads that have dominant R waves (R/S ratio > 1)
  • Dynamic — not present on old ECG or changing over time

NB. T wave inversion is only significant if seen in leads with upright QRS complexes (dominant R waves). T wave inversion is a normal variant in leads III, aVR and V1.

Lateral-TWI 2
Widespread T wave inversion due to myocardial ischaemia (most prominent in the lateral leads)

Wellens Syndrome
  • Wellens syndrome is a pattern of inverted or biphasic T waves in V2-4 (in patients presenting with ischaemic chest pain) that is highly specific for critical stenosis of the left anterior descending artery.
  • Patients may be pain free by the time the ECG is taken and have normally or minimally elevated cardiac enzymes; however, they are at extremely high risk for extensive anterior wall MI within the next 2-3 weeks.

There are two patterns of T-wave abnormality in Wellens syndrome:

  • Type A – Biphasic, with initial positivity and terminal negativity (25% of cases)
    Type B – Deeply and symmetrically inverted (75% of cases)
Biphasic T Waves (Type A)
Wellens Pattern A Type 1 T wave 2
Wellens Pattern A Type 1 T wave

Deeply Inverted T Waves (Type B)
Wellens Pattern B Type 2 T wave
Wellens Pattern B Type 2 T wave 2

NB. There is confusion in the literature regarding the naming of the T wave patterns, with some authors using Type 1 (Type A) for biphasic T waves and Type 2 (Type B) for inverted. It may be better to just describe the T wave pattern!

Wellens wave evolution

T wave changes can evolve over time from Type A to Type B pattern (Smith et al).

Evolution of T-wave inversion [A-D] after coronary reperfusion in STEMI reperfusion and in Wellens syndrome (NSTEMI)
Evolution of T-wave inversion [A-D] after coronary reperfusion in STEMI reperfusion and in Wellens syndrome (NSTEMI). Modified from Smith et al. Evolution of T-wave inversion. The ECG in acute MI, 2002

Non-specific ST segment and T wave changes

The following changes may occur with myocardial ischaemia but are relatively non-specific:

  • ST depression < 0.5 mm
  • T wave inversion < 1 mm
  • T wave flattening
  • Upsloping ST depression

More Myocardial Ischaemia ECG Examples
Example 1
Ischaemia1 2

Subendocardial ischaemia:

  • The most striking abnormality is the widespread ST depression, seen in leads I, II and V5-6. This is consistent with widespread subendocardial ischaemia.
  • There is also some subtle ST elevation in V1-2 and aVR with small Q waves in V1-2, suggesting that the cause of the widespread ischaemia is a proximal LAD occlusion.

Example 2
inferior-ST-depression 2

Reciprocal change:

  • The most obvious abnormality is the horizontal ST depression in III and aVF.
  • This could be misinterpreted as “inferior ischaemia” — however, subendocardial ischaemia does not localise.
  • Regional ST depression should prompt you to scrutinise the ECG for signs of reciprocal ST elevation… In this case there is subtle ST elevation in aVL.
  • This is a high lateral STEMI!

Example 3
Biphasic-T-waves 2

Wellens Syndrome:

  • There are abnormal T waves in V1-4 — biphasic in V1-3 and inverted in V4.
  • This pattern is known as Type A Wellens Syndrome and is highly specific for a critical stenosis of the proximal LAD artery.

Example 4a
nstemi1

Dynamic ST depression in a patient with chest pain:

  • Widespread ST depression (leads I, II, V5-6) indicates subendocardial ischaemia.
  • Q wave in lead III with slightly elevated ST segment suggests the possibility of early inferior STEMI.
Example 4b
nstemi2

ECG of the same patient after treatment with oxygen, nitrates, heparin and anti-platelets:

  • The ST changes have now resolved.
  • Inferior ST segments and Q waves are stable — this patient had a history of prior inferior MI.
  • Troponin was raised, confirming that the initial ST depression was due to NSTEMI.

Example 5
NSTEMI_U_wave-inversion_only2

NSTEMI presenting with isolated U wave inversion:

  • There are inverted U waves, most prominent in leads V5-6.
  • This is an infrequently recognised but very specific sign of myocardial ischaemia — this patient had a 12-hour troponin of 4.0 ng/mL.

Want to find out the full story behind this ECG?.



References

Advanced Reading

Online

Textbooks


LITFL Further Reading