Cardiology - Part 2

Notes

Overview

Cardiology is one of the most commonly tested subjects in undergraduate medicine.

Cardiology is one of the most tested specialties in undergraduate examinations. This is because cardiac diseases are common and seen all the time in clinical practice.

There are many different conditions that affect the heart. Some of these are common whereas others are rare.

  • Common conditions: ischaemic heart disease, atrial fibrillation, hypertension
  • Rare conditions: long QT syndrome, restrictive cardiomyopathy, Brugada syndrome

Conditions that are common are more likely to be tested and the depth of knowledge required will be higher. Therefore, you should put your time into learning these common diseases well. Here are five really common conditions that are vital to know in depth:

In these notes, we cover the pertinent information required to help you understand each disease process. For more detailed information, check out our Cardiology section.

Approach to cardiology

We can approach learning cardiology by dividing diseases into their site of pathology.

Dividing and categorising diseases is useful to be able to conceptualise what you need to learn within the specialty. You can use this as a type of mental checklist to ensure you have covered the major diseases in each category when studying or revising for exams.

Cardiac diseases can be divided based on their site of pathology:

  • Pericardial disease
  • Vascular disease
  • Electrical disease
  • Valvular disease
  • Muscular disease

Categorisation of cardiac disease

Electrical diseases

The heart's electrical circuit is a highly specialised system that controls contraction.

Conduction system

The heart is a dual pump that sits at the centre of the cardiovascular system. It is composed of both contractile cells and autorhythmic cells (also known as pacemaker cells).

Approximately 1% of cardiac tissue is composed of pacemaker cells, which are organised into key structures and can undergo spontaneous depolarisation. Depolarisation refers to the electrical changes that occur within a muscle to allow it to contract. We can detect these electrical changes, which are associated with heart muscle contraction, using an ECG.

Organisation

The hearts pacemaker cells are organised into structures including the sinoatrial node (SAN), atrioventricular node (AVN), bundle of His, the right and left bundle branches and Purkinje fibres.

Structural organisation of the hearts pacemaker cells means there is coordinated electrical activity, which leads to a coordinated contraction of both atria and ventricles.

Conduction system

Autorhythmicity

Each structure has an intrinsic rate of autorhythmicity. This refers to the number of electrical signals, and thus contractions, that will occur each minute. The electrical activity starts with the SAN, which has the highest rate of autorhythmicity at 70-100 bpm. Depolarisation of the SAN spread throughout the atria and reaches the AVN. Electrical activity then travels through the bundle of His and bundle branches. Finally, it spreads at a slower pace through the ventricular muscle via the Purkinje fibres leading to coordinated ventricular contraction.

This is known as the hierarchy of spontaneous depolarisation. Failure of spontaneous depolarisation at the SAN causes initiation of activity lower down. Spontaneous depolarisation occurs because the membrane of pacemaker cells slowly drifts until the threshold potential is reached. This is in contrast to most nerve and skeletal muscle cells, in which membrane potential remains constant unless the cell is stimulated. Through repeated cycles of drifting and firing, these cells rhythmically initiate action potentials.

Spontaneous depolarisation

Pacemaker cell action potential (green line shows spontaneous depolarisation)

Electrical disease

Electrical disease of the heart can be broadly divided into both fast (‘tachy') and slow (‘brady’) rhythms.

The tachyarrhythmias (fast rhythms) can arise from the atria or the ventricles:

  • Supraventricular (above the ventricles): atrial fibrillation, atrial flutter, supraventricular tachycardia
  • Ventricles (within the ventricles): ventricular tachycardia, ventricular fibrillation

The bradyarrhythmias can arise due to dysfunction with the SAN or AVN

  • SAN dysfunction: sinus pause/arrest, sinus node exit block, sinus dysfunction
  • AVN dysfunction: 1st, 2nd or 3rd-degree heart block

Electrocardiogram (ECG)

ECG stands for electrocardiogram, which is a visual recording of the electrical activity of the heart.

The ECG is created by attaching a number of electrodes, or leads, to different areas of a patient’s skin. These electrodes can then detect the electrical activity from a variety of angles. This electrical activity is captured and a trace of it is drawn on a moving piece of paper that can be printed off and analysed. A standard 12-lead ECG utilises 10 leads to offer 12 different ‘views’ of the heart.

Sinus rhythm

Standard 12-lead ECG

Depolarisation

The shape appearing on an ECG represents the average direction of the wave of depolarisation. Depolarisation moving towards a lead causes a predominantly upward (or positive) deflection. Depolarisation moving away from a lead causes a predominantly downward (or negative) deflection. The opposite is seen with repolarisation.

ECG deflections

Waveforms

The basic ECG strip is made up of a baseline with deflections caused by movement of electrical impulses either toward (positive deflection) or away (negative deflection) from electrodes. The deflections that make up a normal ECG are termed waves and are assigned arbitrary letters.

A normal ECG waveform is composed of:

  • P-waves: atrial depolarisation
  • QRS complexes (<120 ms): ventricular depolarisation. If first deflection is down it is a Q-wave, if the first deflection is up it is an R-wave.
  • T-waves: ventricular repolarisation.
  • U-waves: sometimes seen, origin disputed. May be pathological if follows abnormal T-wave

ECG waveform

The ECG may be deconstructed into additional key components:

  • PR-interval (120-200 ms): time taken for the electrical impulse to travel between the atria and ventricles.
  • ST-segment: should be isoelectric (i.e. on the baseline). Can be depressed or elevated (changes typical in ischaemia).
  • QT-interval*: varies with heart rate, long QT has many causes but may predispose to polymorphic ventricular tachycardia.

*NOTE: normal QT interval is 350-440 ms in men and 350-460 ms in women

ECG waveform 2

For more information on ECGs check out our accompanying notes and videos

Bradyarrhythmias

Describes several conditions where the heart beats at an unusually slow rate (< 60 bpm).

Bradyarrhythmias can be divided into those that affect the SAN or those affecting the AVN.

Sino-atrial disease

  • Sinus bradycardia
  • Sinus pause/arrest
  • Sinus node dysfunction
  • Sinus node exit block

For more information see our notes on Bradycardias.

Atrioventricular disease

  • 1st degree heart block
  • 2nd degree heart block
  • 3rd degree heart block

For more information see our notes on Conduction.

Clinical features

The clinical presentation of bradyarrhythmias may range from asymptomatic to shock.

Clinical features associated with bradyarrhythmias may be permanent or occur intermittently due to the paroxysmal nature of the arrhythmia. They can present with a wide range of symptoms and signs.

  • Fatigue, lethargy
  • Dizziness, pre-syncope
  • Syncope: transient loss of consciousness
  • Dyspnoea: may suggest pulmonary oedema
  • Chest pain: may suggest myocardial ischaemia
  • Shock: low BP (< 90 mmHg), pallor, sweating, cold
  • Impaired consciousness

The four cardinal features that suggest an unstable arrhythmia include syncope, myocardial ischaemia (chest pain), heart failure (breathlessness) and shock (BP < 90 mmHg).

Management

The same basic management principles should be applied to all bradyarrhythmias.

  • Urgent assessment (ABCDE)
  • Pharmacological therapies
  • Pacing

Assessment

Assessment of an unwell patient should be completed using the structure airway (A), breathing (B), circulation (C), disability (D) and exposure (E). This remains true for any patient with a bradyarrhythmia. The resuscitation council guidelines provide a clear structure on the acute management of bradyarrhythmias.

Bradycardia algorithm

Pharmacological therapy

Medications may be used in an attempt to increase the heart rate. Two common choices include atropine and isoprenaline.

  • Atropine (antimuscarinic): reversible antagonist of muscarinic acetylcholine receptors. Blocks the action of the vagus nerve on the SAN and AVN. This leads to increased SAN electrical activity and increased conduction through the AVN. Given as IV bolus, which can be repeated.
  • Isoprenaline (non-selective beta-adrenoreceptor agonist): positive inotropic and chronotropic effects on the heart via beta-receptors. Leads to an increase in heart rate and improved contractility. Given as IV infusion.

Medications usually act as a bridge to more definitive pacing or while the underlying cause of bradycardia is treated. If these medications fail, temporary or permanent pacing may be indication.

Pacing

Pacing (temporary or permanent) delivers electrical stimuli to the heart via pacing leads.

  • Temporary: use of transcutaneous, epicardial or intravenous pacing
  • Permanent: insertion of a permanent electronic device

Tachyarrhythmias

Describes several conditions where the heart beats at an unusually fast rate (> 100 bpm).

Tachyarrhythmias can be divided into those arising from the atria (supraventricular) and those arising from the ventricles.

Supraventricular

  • Sinus tachycardia
  • Atrial flutter
  • Atrial fibrillation
  • Atrial tachycardia
  • Atrioventricular nodal reentrant tachycardia (AVNRT)
  • Atrioventricular reentrant tachycardia (AVRT)

For more information see our notes on Tachycardias.

Ventricular

  • Ventricular tachycardia
  • Polymorphic ventricular tachycardia
  • Ventricular fibrillation

For more information see our notes on Tachycardias.

Clinical features

The clinical presentation of tachyarrhythmias may range from asymptomatic to cardiac arrest.

Tachyarrhythmias are characterised by the development of chest pain and palpitations. Dangerous tachyarrhythmias may lead to reduced cardiac output and syncope (transient loss of consciousness) or even cardiac arrest. Symptoms may be persistent or transient if the abnormal rhythm is paroxysmal (i.e. occurring briefly). Clinical features may include:

  • Fatigue, lethargy
  • Dizziness, pre-syncope
  • Syncope: transient loss of consciousness
  • Dyspnoea: may suggest pulmonary oedema
  • Chest pain: may suggest myocardial ischaemia
  • Shock: low BP (< 90 mmHg), pallor, sweating, cold
  • Impaired consciousness

The four cardinal features that suggest an unstable arrhythmia include syncope, myocardial ischaemia (chest pain), heart failure (breathlessness) and shock (BP < 90 mmHg).

Management

The same basic management principles should be applied to all Tachyarrhythmias.

  • Urgent assessment (ABCDE)
  • Pharmacological therapies
  • Electrical therapies (e.g. cardioversion)

Assessment

Assessment of an unwell patient should be completed using the structure airway (A), breathing (B), circulation (C), disability (D) and exposure (E). This remains true for any patient with tachyarrhythmia. The resuscitation council guidelines provide a clear structure on the acute management of tachyarrhythmias.

Tachycardia algorithm

Pharmacological therapy

Medications may be used in an attempt to slow the heart rate or convert the abnormal rhythm back to normal sinus rhythm. These medications are collectively known as antiarrhythmics. The choice of agent depends on the underlying tachyarrhythmia, but some examples are listed below:

  • Beta-blockers (Antagonists of catecholamines at beta-adrenoceptors)
  • Calcium-channel blockers (Non-dihydropyridines CCBs block L-type calcium channels)
  • Adenosine (a purine nucleoside that acts on the SA node to reduce heart rate and the AV node to slow conduction)
  • Digoxin (inhibits a Na+/ K+ -ATPase pump on cardiomyocytes)
  • Flecainide (inhibition of fast sodium channels.)

For more information see our notes on Antiarrhythmics.

Electrical therapy

Electrical cardioversion is a treatment that aims to restore the heart back to normal activity using an electric shock. Electrical cardioversion may be planned or it may be needed in an emergency with a patient who has an unstable tachyarrhythmia. Electrical cardioversion is also used in patients who have gone into cardiac arrest and have a shockable rhythm (ventricular fibrillation, pulseless ventricular tachycardia).

Valvular disease

Disease of the heart valves causes two primary problems: obstruction or regurgitation.

There are four valves within the heart:

  • Aortic
  • Mitral
  • Pulmonary
  • Tricuspid

Heart valves

Disease of the heart valves may be due to narrowing (stenosis) or leakage (regurgitation).

  • Stenosis: narrowing inhibits flow across the valve that means the heart muscle has to work harder leading to increased pressure
  • Regurgitation: disruption of the valve structure causes leakage allowing blood to flow backwards and overload the heart chambers

Stenosis

Stenosis causes increased pressure gradients across the valve forcing the heart to compensate.

Over time, a narrowing of a heart valve leads to a reduction in the valve area. This usually occurs over many years. Consequently, the heart muscle has to work harder to pump blood through the stenotic valve leading to hypertrophy (increased size) which is a compensatory change. However, as the valve becomes more narrowed, these compensatory mechanisms can only continue for so long before the heart cannot cope and there is myocardial dysfunction. At this point, patients develop features of heart failure, arrhythmias and/or chest pain.

Stenotic valves

Regurgitation

Regurgitation causes an increase in blood flow across valves forcing the heart to compensate.

Damage to the valve structure causes blood to leak across the valve when it should be closed. This leads to an increased blood flow across the valve that overloads the ventricles (pulmonary/aortic regurgitation) or atria (tricuspid/mitral regurgitation). Over time, this forces the heart muscle to compensate for the increased volume of blood, which is typically seen as a combination of hypertrophy and dilatation. As the valve disease worsens, the heart can no longer cope leading to myocardial dysfunction and features of heart failure.

Importantly, if regurgitation occurs acutely (myocardial infarction, endocarditis), the heart does not have time to undergo compensatory changes. Instead, there is acute myocardial dysfunction with features of acute heart failure (i.e. haemodynamic compromise).

Regurgitant murmurs

Echocardiography

Valvular disease may be suspected clinically by the presence of a murmur. This refers to the characteristic sound of blood flow across the stenotic or leaky valve. However, a formal diagnosis requires visualisation of the valve structure and the flow of blood across the valve using an ultrasound scan of the heart known as an echocardiogram (ECHO).

An ECHO can give us lots of useful information such as:

  • Valve affected
  • Stenosis, regurgitation or both
  • Valve area
  • Pressure gradient across the valve
  • Compensatory changes (dilatation/hypertrophy)
  • Myocardial dysfunction (e.g. impaired ventricular function)

Stenotic valve disease

Stenosis can affect any of the four heart valves.

Stenotic lesions of the left-sided valves are far more common and usually related to calcification or previous rheumatic heart disease. The four stenotic lesions are:

  • Aortic stenosis
  • Mitral stenosis
  • Pulmonary stenosis
  • Tricuspid stenosis

Aortic stenosis

Aortic stenosis is a common valvular pathology affecting 2-7% over the age of 65. It is characterised by an ejection systolic 'woosh' that is often one of the easiest murmurs to identify as a medical student - as such it often comes up in OSCEs!

Aetiology: calcific (most common), bicuspid (congenital), rheumatic heart disease (common in the developing world)

Symptoms: syncope, angina, dyspnea (SAD)

Murmur: ejection systolic, described as crescendo-decrescendo. Radiates to the carotids.

Best heard: on expiration in the aortic area.

Additional signs:

  • Sustained apex
  • Slow rising pulse
  • Narrow pulse pressure
  • Heart sounds:
    • Soft S2 (sign of severe disease)
    • Fourth heart sound (S4): feature of abnormal filling (i.e. diastolic dysfunction)
    • Reversed splitting of S2 (splitting is heard during expiration and disappears during inspiration)

NOTE: S2 splitting refers to the desynchronised closure of the aortic and pulmonary valves on inspiration (more blood passes through the pulmonary artery leading to delayed pulmonary valve closure).

For more detail check out our notes on Aortic stenosis.

Mitral stenosis

Mitral stenosis (MS) is characterised by valvular obstruction to flow from the left atrium to the left ventricle. This leads to a murmur typically described as a low-pitched mid-diastolic rumble.

Aetiology: rheumatic heart disease (most common), congenital MS, mitral annular calcification, radiation-associated MS, carcinoid syndrome

Symptoms: dyspnea, chest pain, haemoptysis

Murmur: mid-diastolic

Best heard: at the apex with breath held in expiration, with the patient lying on their left side. It is best heard with the bell of the stethoscope.

Additional signs:

  • Mitral facies (rosy cheeks)
  • Pulmonary hypertension:
    • Right ventricular heave
    • Prominent a-wave
  • Right heart failure:
    • Raised JVP
    • Peripheral oedema
    • Hepatomegaly

For more detail see our notes on Mitral stenosis.

Pulmonary stenosis

Pulmonary stenosis is often seen as a component of congenital syndromes but may also be acquired later in life. Similar to aortic stenosis it results in an ejection systolic murmur.

Congenital associations: Noonan syndrome, tetralogy of Fallot, congenital rubella syndrome

Acquired causes: carcinoid syndrome, rheumatic fever

Symptoms: syncope, fatigue

Murmur: ejection systolic, described as crescendo-decrescendo. Often associated with a thrill.

Best heard: on inspiration at the pulmonary area.

Additional signs:

  • Pulmonary hypertension
    • Right ventricular heave
    • Prominent a waves
  • Fourth heart sound (S4): feature of abnormal filling (i.e. diastolic dysfunction)

Tricuspid stenosis

Tricuspid stenosis (TS) is characterised by valvular obstruction to flow from the right atrium to the right ventricle. TS is relatively rare and when it occurs it is normally associated with other valvular pathologies.

Aetiology: rheumatic heart disease, carcinoid syndrome, infective endocarditis

Symptoms: peripheral oedema, ascites, dyspnea, abdominal discomfort (secondary to hepatic congestion)

Murmur: mid-diastolic

Best heard: left sternal edge on inspiration

Additional signs:

  • Irregular pulse (AF)
  • Prominent a-wave (if in sinus rhythm)
  • Hepatomegaly
  • Peripheral oedema

Stenotic valve disease

Regurgitant valves

Regurgitation can affect any of the four heart valves.

Regurgitant lesions affecting the right-side of the heart are often ‘functional’. This means they occur due to structural cardiac changes (e.g. dilatation of the right ventricle) rather than intrinsic damage to the valve. The four regurgitant lesions are:

  • Aortic regurgitation
  • Mitral regurgitation
  • Pulmonary regurgitation
  • Tricuspid regurgitation

Aortic regurgitation

Aortic regurgitation (AR) results from an incompetent aortic valve causing regurgitant flow of blood in diastole. This leads to a murmur in early diastole. It is typically considered as either acute or chronic depending on its presentation.

Aetiology of acute AR: infective endocarditis, aortic dissection, acute rheumatic fever

Aetiology of chronic AR: rheumatic heart disease, bicuspid aortic valve, connective tissue disorders, arthritides

Symptoms: dyspnea, angina, palpitations

Murmur: early diastolic

Best heard: on expiration with the patient leaning forward, at the left sternal edge, fourth intercostal space.

Additional signs:

  • Displaced apex (chronic)
  • Soft S1
  • S2 may be soft
  • Signs of heart failure
  • The eponymous signs of AR (see link below)

For more detail see our notes on Aortic regurgitation.

Mitral regurgitation

Mitral regurgitation refers to incompetence of the valve that may occur due to abnormalities to the valve leaflets, subvalvular apparatus or left ventricle. It may be acute or chronic.

Aetiology: degenerative, infective endocarditis, rheumatic heart disease, congenital abnormalities, medications (e.g. ergotamine)

Symptoms of acute MR: rapid development of heart failure, flash pulmonary oedema

Symptoms of chronic MR: dyspnoea, orthopnoea

Murmur: pansystolic murmur

Best heard: over the apex. Depending on the direction of the regurgitant jet, may radiate to the axilla.

Additional signs:

  • Soft S1
  • Third heart sound (S3): due to rapid ventricular filling
  • Mid-systolic click (in valve prolapse due to tensing of chordae tendineae)

For more detail check out our notes on Mitral regurgitation.

Pulmonary regurgitation

Pulmonary regurgitation (PR) results from an incompetent pulmonary valve causing a regurgitant flow of blood in diastole. This leads to a murmur in early diastole. Mild PR is quite common and typically entirely asymptomatic. With more significant regurgitation, right ventricular dilatation, secondary tricuspid regurgitation (TR) and heart failure may result.

Aetiology: physiological, infective endocarditis, carcinoid syndrome, iatrogenic, pulmonary artery dilatation.

Symptoms: if right-sided heart failure develops, peripheral oedema, fatigue and arrhythmias may result.

Murmur: early diastolic

Best heard: on inspiration in the pulmonary area.

Additional signs:

  • Secondary TR
  • Peripheral oedema
  • Hepatic congestion

Tricuspid regurgitation

Tricuspid regurgitation refers to incompetence of the tricuspid valve. It may be primary (i.e. disease directly affects the valve and its apparatus) or secondary (i.e. caused by dilatation of the right ventricle). In adults most cases are secondary (also termed functional) in nature.

Aetiology of primary TR: rheumatic heart disease, carcinoid syndrome, infective endocarditis, Ebstein’s anomaly.

Aetiology of secondary TR: any cause of pulmonary hypertension and secondary dilation of the right ventricle.

Symptoms: fatigue, dyspnea, peripheral oedema, hepatomegaly

Murmur: pansystolic

Best heard: on inspiration at the lower left sternal edge, may be more lateral if right ventricle very enlarged.

Additional signs:

  • Prominent, pulsatile JVP
  • Large cv wave in JVP
  • S3/S4
  • Liver may be enlarged and pulsatile

Regurgitant valves

Valve disease management

The management of valvular diseases is complex.

There is no simple strategy for the management of valve disease. Determining the most appropriate treatment usually involves a ‘valve multidisciplinary team’ and needs to take into account the severity, aetiology, co-morbidities, and performance status of the patient.

There are three major components to managing valve disease:

  • Medical therapy: this involves treating any heart failure, managing arrhythmia,s and using anticoagulation as needed for atrial fibrillation (AF is commonly due to valvular disease)
  • Transcatheter techniques: this involves a number of different strategies to replace or repair an abnormal valve using minimally-invasive techniques to avoid open-heart surgery
  • Surgery: this involves replacement or repair of a valve by open-heart surgery. Valve replacements may be prosthetic or metallic. Metallic valves require life-long anticoagulation (e.g. warfarin)

Muscular disease

Cardiomyopathy refers to disease of the heart muscle.

The term cardiomyopathy can be very confusing in clinical practice. In very simple terms it means disease of the heart muscle. However, many conditions can affect the heart muscle. Consequently, the term cardiomyopathy is reserved for disease of heart muscle that cannot otherwise be explained by common cardiovascular diseases or congenital heart disease.

The cardiomyopathies are classified based on morphological and functional phenotypes. This means what they look like structurally (e.g. dilated, thickened) and how they behave physiologically (e.g. impaired contraction, abnormal filling).

  • Hypertrophic cardiomyopathy (HCM)
  • Dilated cardiomyopathy (DCM)
  • Restrictive cardiomyopathy (RCM)
  • Arrhythmogenic cardiomyopathy (ACM)
  • Unclassified cardiomyopathies

Each phenotype listed above is then further divided into familial and non-familial causes.

  • Familial (inherited): cardiomyopathy phenotype that develops due to a genetic variant (mutation)
  • Non-familial (acquired): cardiomyopathy phenotype that develops due to a clear acquired cause (e.g. sarcoidosis, amyloid)

These cardiomyopathy phenotypes may be limited to the heart or form part of a systemic disease process (e.g. sarcoidosis).

Hypertrophic cardiomyopathy

HCM is defined as increased ventricular wall thickness or mass not caused by pathologic loading conditions.

It is commonly due to an abnormal gene that encodes one of the sarcomere proteins needed for myocardial contraction. The inheritance is usually autosomal dominant. Hypertrophy (i.e. thickening) may occur in any of the left ventricular segments but commonly involves the interventricular septum and is usually asymmetrical. Hypertrophy can lead to myocardial dysfunction through a number of mechanisms including left ventricular outflow obstruction.

Presentation is highly variable and many patients may be asymptomatic. It classically causes an ejection systolic murmur due to the left ventricular outflow obstruction and may cause heaves (visible or palpable pulsation) or thrills (palpable murmur). In severe cases, patients may have features of heart failure and can even get dangerous arrhythmias and sudden cardiac death.

Dilated cardiomyopathy

DCM is characterised by ventricular chamber enlargement and impaired contraction.

In DCM, there is dilatation and impaired contraction of one or both ventricles that commonly manifests as heart failure with features of breathlessness, fatigue, and fluid overload. A huge number of conditions can cause DCM. This includes infections (e.g. parvovirus B19, coxsackievirus), drugs (e.g. Doxorubicin), pregnancy (e.g. Peripartum) and inherited causes (e.g. abnormal sarcomere genes) amongst many others.

Restrictive cardiomyopathy

RCM is an uncommon cardiomyopathy characterised by abnormal ventricular filling.

RCM is characterised by abnormal ventricular filling in the ventricles that are non-dilated and usually have no evidence of hypertrophy. RCM is commonly the result of infiltrative diseases where there is a deposition of a substance in the myocardium such as amyloid, iron or granulomas.

The clinical presentation is similar to heart failure with features of breathlessness, fatigue, peripheral oedema, paroxysmal nocturnal dyspnea, reduced exercise tolerance and/or palpitations. Syncope may develop if arrhythmias develop, especially if the underlying infiltrative disease affects the Sino-atrial or atrio-ventricular node.

Arrhythmogenic cardiomyopathy

ACM are a group of disorders characterised by frequent arrhythmias and ventricular dysfunction.

ACM is broadly defined as the clinical presentation of an arrhythmia alongside myocardial structural abnormalities. However, the condition really reflects a group of disorders that are characterised by frequent ventricular arrhythmias and dysfunction of one or both ventricles. Arrhythmogenic right ventricular cardiomyopathy (ARVC) is the most well characterised ACM caused by a genetic mutation. Other causes can include Chagas disease or sarcoidosis.

Patients usually have clinical features of heart failure and arrhythmias (e.g. palpitations, dizziness, syncope).

Cardiomyopathies

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