Medicine in a Minute

Chapter 1

Cardiology

Amar Vaswani, Teo Hooi Khee and Scott D. Dougherty

Basic principles

Bridge to clinical medicine

Anatomy

Coronary circulation

Conducting system of the heart

Cardiac muscle contraction and relaxation

Cardiac output

Heart rate

Blood pressure regulation

The jugular venous pressure (JVP)

Cardiovascular investigations

Cardiac pharmacology

Atherosclerosis

1.1 Stable angina

1.2 Acute coronary syndrome

1.3 Heart failure

1.4 Hypertension

1.5 Pericarditis

1.5.1Constrictive pericarditis

1.6 Rheumatic fever

1.7 Infective endocarditis

1.8 Arrhythmias

Approach to arrhythmias

1.8.1Bradycardias

1.8.2Tachycardias

Narrow complex tachycardia

Broad complex tachycardias

1.9 Cardiomyopathy

1.9.1Dilated cardiomyopathy

1.9.2Hypertrophic cardiomyopathy

1.9.3Restrictive cardiomyopathy

1.9.4Arrhythmogenic right ventricular cardiomyopathy

1.9.5Takotsubo cardiomyopathy

1.10 Myocarditis

1.11 Cardiac tumours

1.12 Valvular heart disease

1.12.1Mitral stenosis

1.12.2Mitral regurgitation

1.12.3Mitral valve prolapse

1.12.4Aortic stenosis

1.12.5Aortic regurgitation

1.12.6Right-sided valvular heart disease

1.13 Congenital heart disease

1.13.1Patent ductus arteriosus

1.13.2Coarctation of the aorta

1.13.3Atrial septal defect

1.13.4Patent foramen ovale

1.13.5Ventricular septal defect

1.13.6Tetralogy of Fallot

1.13.7Transposition of the great arteries

1.14 Miscellaneous cardiac conditions

1.14.1Digitalis toxicity

1.14.2Postural hypotension

1.14.3Cardiac syndrome X and Prinzmetal angina

Basic principles

The cardiovascular system, which consists of the heart and blood vessels, plays a vital role in the maintenance of homeostasis and transport of nutrients, waste compounds and respiratory gases. To achieve this, the heart and blood vessels must work in tandem with the respiratory and haematological systems to achieve adequate tissue and organ perfusion.

Contracting at an average rate of 75 beats per minute (bpm), the human heart is said to contract up to 3 billion times in an average 80-year lifespan.

Bridge to clinical medicine

Anatomy

The heart is covered by a fibroserous sac called the pericardium and is located in the thorax between the lungs, in an area known as the mediastinum

The heart is a four-chambered, muscular structure comprising two atria and two ventricles, which serve to pump deoxygenated (largely venous) blood to the lungs and transport oxygenated (largely arterial) blood to organs and tissues (see Fig. 1.1)

The right atrium receives venous drainage from two large systemic veins, the superior vena cava superiorly and the inferior vena cava inferiorly, as well as the coronary sinus (inferiorly) and the anterior cardiac vein anteriorly (draining the anterior heart)

The right atrial appendage or auricle is a pouch-like extension of the right atrium

Blood moves from the right atrium to the right ventricle through the tricuspid valve, which is made up of three leaflets (anterior, posterior and septal)

The tricuspid valve orifice is the largest in the heart and its leaflets are supported by chordae tendineae (‘heart strings‘), which link the ventricular aspect of the leaflets to the papillary muscles

The right ventricle is composed of the large inlet (sinus) and smaller outlet (conus); the inflow tract is typified by trabeculae carneae (irregular ridges), whereas the outlet tract has smooth walls

The infundibulum is a funnel-shaped muscular structure that forms the right ventricular outflow tract and supports the pulmonary valve, through which deoxygenated blood flows to the lungs via the pulmonary trunk

The true interatrial septum is limited to a shallow depression known as the fossa ovalis, which is a remnant of the now closed foramen ovale

The left atrium receives oxygenated blood from the four pulmonary veins

The left atrial appendage is a long, hooked and tubular structure that forms part of the left atrium and is important clinically because it is the major site of thrombus formation in atrial fibrillation

As blood moves from the left atrium to the left ventricle, it flows through the mitral valve, which has anterior and posterior mitral valve leaflets

Fig. 1.1 Gross anatomy of the heart.

The mitral valve is so named because of its resemblance to a bishop’s mitre (ceremonial head-dress).

The majority of the blood flow from the left atrium to the left ventricle is passive, with only 30% of flow resulting from left atrial contraction

Like the right ventricle, the left ventricle consists of a trabeculated inlet and a smooth outlet

The left ventricle is thicker and larger than the right ventricle because it must generate enough force to push blood around the entire body

The left ventricle pumps oxygenated blood to the entire body, first through the aortic valve and then through the aorta

The aortic and pulmonary valves, which are similar in structure, are each composed of three cusps, and are also known as semilunar valves

Coronary circulation

The heart consumes more oxygen per tissue mass than any other organ in the body: myocardial blood supply occurs via the right and left coronary arteries, which arise as the first branches of the aorta at the right and left sinuses of Valsalva, respectively

The heart is drained mainly by the great, middle and small cardiac veins, and to a lesser extent by other cardiac veins into the coronary sinus, which empties into the right atrium

The right coronary artery (RCA) has three major branches (see Fig. 1.2):

The sinoatrial (SA) nodal branch, which supplies the sinoatrial node, the dominant pacemaker of the heart

The atrioventricular (AV) nodal branch, which supplies the atrioventricular node

The posterior descending artery

The left coronary artery (LCA), which supplies a large surface area of the heart, is subdivided into (see Fig. 1.2):

The left main stem

The left anterior descending (LAD) artery, also known as the ‘widowmaker’, because occlusion of this vessel can lead to rapid death

The left circumflex (LCX) artery

Fig. 1.2 The coronary circulation.

One might appreciate the beauty of individuality within each heart, perhaps anatomically reflected in the variation observed in arterial supply:

90% of the population have a right dominant heart, in which the posterior descending artery originates from the terminal branch of the RCA; whereas the LCX normally supplies the posterior descending artery in a left dominant heart

The SA nodal artery is supplied by the RCA in two-thirds of the population, and by the LCX in one-third

The AV node, on the other hand, is supplied by the RCA in 90% of the population and by the LCX in the remaining 10%.

Cardiac cycle

The cardiac cycle can be divided into two distinct phases: systole (contraction) and diastole (relaxation).

Coronary blood flow mainly occurs during diastole. When the heart is contracting, the intramuscular blood vessels are compressed and blood flow is at its lowest. During diastole, the myocardium relaxes, allowing blood flow to resume. Any increase in the heart rate reduces diastolic time more than systolic time, thus reducing coronary artery perfusion time. In patients with pre-existing disease (such as coronary artery disease or aortic stenosis), tachycardia may lead to reduced myocardial perfusion.

The cardiac cycle takes place over four major phases (see Fig. 1.3):

Fig. 1.3 The cardiac cycle.

Conducting system of the heart

The intrinsic pacemaker of the heart is usually the sinoatrial node (SA node) because it has the fastest rate of automaticity of all cardiac fibres (see Fig. 1.4)

However, other fibres also generate automatic rhythmical impulses (such as the AV node), albeit at slower rates, and these may act as the cardiac pacemaker if there is a problem with the SA node

The action potential from the SA node is propagated through the atrial myocytes, which have intercalated discs at a structural level, allowing for the action potential to move freely across both atria

The impulse then travels to the AV node, which lies in the interatrial septum

Conduction is delayed at the AV node for 0.1 seconds before continuing on towards the bundle of His; this time delay allows for ventricular filling to take place

Depolarisation then continues through the bundle of His (which subdivides into left and right bundle branches) and then through Purkinje fibres to the ventricular muscle, which provokes contraction

Fig. 1.4 The conduction system of the heart.

The heart derives its autonomic nervous supply mostly from the parasympathetic vagus nerve (cardio-inhibitor) and the C1–T5 sympathetic ganglia (cardio-accelerator) via superficial and deep cardiac nervous plexuses. The autonomic nervous system plays an important role in controlling the rate of SA node impulse formation and conduction and the strength of muscle contraction. For instance, in the denervated heart (e.g. in heart transplant patients), the resting heart rate is higher (90–110bpm) and the heart rate response is reduced during exercise (chronotropic incompetence).

Cardiac pain is not found exclusively in the chest, but often radiates down the medial side of the left arm and up to the neck and jaw. This is because radiation occurs to areas that send sensory impulses to the same level of the spinal cord that receives cardiac sensation. The sensory fibres from the heart then travel up to T1–T4, and radiation occurs in the medial left arm via dermatomes T1–T4.

Cardiac muscle contraction and relaxation

Cardiac myocytes, which differ in cellular structure from skeletal and smooth muscle myocytes, contract at a cellular level by means of a phenomenon known as calcium-induced calcium release.

Depolarisation causes calcium ions to enter the myocyte via L-type voltage-gated calcium channels

This in turn activates calcium-sensitive calcium release channels (also known as ryanodine receptors) in the sarcoplasmic reticulum, which causes sufficient flooding of calcium ions to initiate contraction

Calcium ions bind to troponin C, exposing the actin-binding site

Myosin then binds to actin, and contraction occurs via actin–myosin interactions secondary to hydrolysis of adenosine triphosphate (ATP)

As relaxation of the myocyte occurs, calcium ions disengage from troponin C binding sites and are actively transported out of the cytosol via an ATP-dependent cellular pump

Cardiac output

Ensuring an adequate cardiac output is vital for organ perfusion. Regulation of CO occurs via modification of heart rate or stroke volume.

Cardiac output (CO) = heart rate (HR) × stroke volume (SV)

Stroke volume (SV) = end diastolic volume (EDV) – end systolic volume (ESV)

Definitions

Heart rate

The normal heart rate is between 60 and 100bpm

Stroke volume

Affected by preload, afterload and contractility

Preload

Refers to the degree of stretch applied to a resting muscle at the end of diastole; this increased resting muscle length augments the strength of the subsequent muscle contraction

The Frank–Starling law (see Fig. 1.5) illustrates how the initial length of the muscle fibre is proportional to the cardiac contraction

The greater the stretch of the ventricle during diastole, the greater the force of contraction, and therefore the greater the stroke volume

Afterload

Refers to the load exerted on a muscle after the onset of contraction (e.g. systolic pressure), which must be overcome before the muscle begins to shorten

Afterload represents the resistance to ventricular ejection because the afterload force opposes muscle contraction

Afterload is inversely proportional to stroke volume

Contractility refers to the force of myocardial contractility, measured by EF

Fig. 1.5 Frank–Starling curve.

Blood pressure regulation

Blood pressure refers to the pressure exerted by circulating blood against the vessel walls

BP = CO × SVR (systemic vascular resistance)

Blood pressure is sensed by baroreceptors (mechanoreceptor sensory neurons) at the carotid sinus and aortic arch, which detect changes (e.g. low BP) based on the degree of stretch. Afferent information is then transmitted to the brain, which leads to reflexive vasoconstriction, an increased heart rate and contractility, increasing SV, CO and BP in turn.

Another mechanism that modifies BP is the renin–angiotensin–aldosterone system (RAAS; see Fig. 1.6). When the arterial pressure falls, renin is released from the juxtaglomerular cells of the kidney. Renin converts angiotensinogen (released from the liver) into angiotensin I.

Fig. 1.6 The renin–angiotensin–aldosterone system (RAAS).

Angiotensin-converting enzyme (ACE) then converts angiotensin I into angiotensin II, which mediates its effects, primarily by vasoconstriction and increased water retention.

The jugular venous pressure (JVP)

The JVP is an indirect measure of central venous pressure and can be examined at the bedside.

It has a distinctive double waveform pulsation. Two waves are visible on examination (see Fig. 1.7):

A wave, signifying atrial contraction

V wave, reflecting atrial venous filling

Fig. 1.7 JVP waveform.

The C wave reflects the tricuspid valve closure, which is not visible on examination. Two descents are present, an X descent (reflecting atrial relaxation) and a Y descent (reflecting ventricular filling).

Six cardinal symptoms should always be asked about during history-taking:

Chest pain, using the mnemonic ‘SOCRATES’ (Site, Onset, Character, Radiation, Associated factors, Timing, Exacerbating/relieving factors, Severity)

Shortness of breath (including orthopnoea and paroxysmal nocturnal dyspnoea)

Ankle swelling

Palpitations

Syncope or pre-syncope

Claudication

It is also important to ask about relevant risk factors and family history.

Cardiovascular investigations

Investigations are an essential part of the clinician’s arsenal, but must be used judiciously.

a.Blood tests

Cardiac biomarkers

Troponin is a component of skeletal and cardiac muscle which facilitates muscle contraction

Protein complex made up of three subunits troponin T (TnT), troponin I (Tnl) and troponin C (TnC)

TnT and TnI are highly sensitive and specific markers of myocardial injury

Creatine kinase (CK)

CK-MB isozyme is relatively cardiospecific, but the use of CK has largely been superseded by troponin

Rises and falls quickly (after 36 hours), and so may have a role in detecting reinfarction

Lipid panel (a fasting sample is not required)

Natriuretic peptides

b.Cardiac catheterisation

Involves passing catheters into the heart under radiographic guidance

May be diagnostic or therapeutic

Site of entry is identified, followed by administration of local anaesthetic; a guide wire is used to ensure correct placement of the catheter

Classically, the right radial (increasingly preferred) or right femoral arteries are used for arterial access in angiography

Haemodynamics may be measured during the process

Relatively safe procedure, with a mortality rate <0.1%

Complications

Contrast reaction, contrast induced nephropathy

Arrhythmias

Stroke

False aneurysm

Haemorrhage

Coronary artery dissection (which may require emergency coronary artery bypass grafting)

c.Cardiac magnetic resonance imaging (MRI)

Non-invasive imaging technique obtained by using controlled magnetic fields to alter hydrogen nuclei alignment

No radiation exposure, but expensive

Superior to echocardiography in visualising structure and function; not limited by body habitus (physique)

Valuable in assessing coronary artery disease, heart failure, cardiomyopathy and congenital heart disease

Contraindicated in patients with permanent pacemakers (unless MR-safe), implantable cardioverter defibrillators, jewellery and implants

d.Myocardial perfusion scanning

Form of nuclear stress testing

Observes passage of gadolinium contrast through the heart via T1-weighted sequencing

Contrast absorbed by myocardium; low signal indicates hypoperfusion

Assesses for the presence of coronary artery disease

Agents such as adenosine, dipyridamole and regadenoson are used as vasodilators in myocardial perfusion imaging stress tests

e.Echocardiography

Ultrasound allows the physician to visualise the heart and assess its function; may be in two or three dimensions

Transthoracic echocardiography (TTE) images the heart through the chest wall, but may yield poorer images in patients with a larger body habitus or with airway disease

Transoesophageal echocardiography (TOE) is an alternative, invasive method requiring sedation, which captures images via a probe placed down the oesophagus; TOE has a higher sensitivity and produces higher-quality images, while being particularly effective at imaging the posterior heart

Utilising echocardiography

Two-dimensional (2D) echocardiography

Three-dimensional (3D) echocardiography can be used to answer questions raised by 2D imaging (e.g. viewing valves from multiple angles)

Doppler echo

Allows for assessment of flow and severity of valvular heart disease

Stress echo

Echocardiography performed before and after exercise (or with dobutamine if exercise is not possible) to assess the myocardium

Myocardial wall motion is used as a surrogate marker for perfusion, because ultrasound cannot visualise blood flow in the arteries

Dobutamine, a positive inotrope and chronotrope, is used because it actively simulates exercise, but should not be used in patients with pacemakers or with left bundle branch block.

f.Electrocardiogram (ECG) – see Table 1.3.

g.Stress ECG

An ECG is recorded at rest and while the patient is exercising on a treadmill

The Bruce protocol is the most widely used protocol, and increases myocardial workload in stages

Traces are recorded up to 15 minutes after exercise has taken place

ST–T changes may indicate coronary artery disease, but the most reliable of these is horizontal or >1mm downsloping or ST segment depression

BP is also monitored during the test; a sustained decrease in BP may also suggest coronary artery disease

Sensitivity and specificity figures vary, but are estimated to be 78% and 70% respectively

NICE does not recommend the use of stress ECG testing, because of the relatively higher false positive and negative rate – but note that other guidelines (e.g. ESC) do still recommend it as a viable alternative

Fig. 1.8 Views of the heart and their corresponding leads.

Stress testing is contraindicated if patients have had a recent MI, have severe valvular disease or arrhythmias. The test should be stopped immediately if the patient experiences cardiac symptoms, light-headedness, arrhythmias, >1mm ST elevation or a >10mmHg fall in BP.

When considering stress testing, a general rule of thumb should be to consider exercise treadmill tests if the patient has few comorbidities, and pharmacological testing if the patient has underlying ECG abnormalities or is unable to exercise. Vasodilator agents (such as dipyridamole and adenosine) should be used with caution in patients with a history of bronchospasm or carotid stenosis and dobutamine should not be used in patients with a history of ventricular arrhythmia.

Cardiac pharmacology

ACE inhibitors are used in the treatment of hypertension and heart failure; the most notable side effects are a dry cough and angioedema, which may be avoided by switching or stopping the medication. ACE inhibitors should be prescribed with caution in patients with hyponatraemia, hyperkalaemia or renal dysfunction, and are contraindicated in pregnancy.

Angiotensin receptor blockers (ARBs) mimic the effects of ACE inhibitors and antagonise the ATII receptor. Likewise, similar considerations and contraindications should be considered when prescribing ARBs. These are good alternatives in patients who develop ACE inhibitor associated cough.

Beta blockers exert their effect by antagonising the action of epinephrine and norepinephrine at beta adrenergic receptors. They are prescribed to treat heart failure, arrhythmias and coronary artery disease, and should be used with caution in asthmatics.

Calcium channel blockers (CCBs) are generally divided into two main classes – non-rate-limiting (dihydropyridines, e.g. amlodipine, nifedipine) and rate-limiting (non-dihydropyridines, e.g. verapamil, diltiazem).

Antiplatelet agents prevent thrombus formation and are indicated in the prevention and treatment of cardiovascular events. Aspirin inhibits cyclo-oxygenase (COX) to prevent the production of thromboxane A2. P2Y-12 inhibitors (such as clopidogrel, prasugrel and ticagrelor) antagonise the ADP receptor and prevent platelet aggregation.

Anticoagulants interfere with prothrombotic mediators in the coagulation cascade. Warfarin inhibits the synthesis of Vitamin K dependent clotting factors (II, VII, IX and X). Novel oral anticoagulants (NOACs), such as apixaban, dabigatran and rivaroxaban, are used increasingly as they do not require therapeutic monitoring. However, these medications have no direct antidote, except for dabigatran. The FDA approved idarucizumab as an antidote in 2015.

Nitrates are vasodilators that are used in the treatment of angina. Common (usually short-lived) side effects include headaches and flushing. Tolerance is a common complication of nitrate administration.

Diuretics are used to treat oedema and heart failure by increasing urinary sodium excretion and urine output. Hypotension and hyponatraemia are potential side effects in all classes. Thiazide diuretics (e.g. bendroflumethiazide) and loop diuretics (e.g. furosemide) can also cause hypokalaemia, hyperuricaemia and gout. Ototoxicity is specific to loop diuretics. Potassium-sparing diuretics (e.g. spironolactone) can cause hyperkalaemia.

Lipid-lowering agents are exemplified by the statins, which work by inhibiting HMG CoA reductase, thereby reducing synthesis of cholesterol in the liver. (This occurs mostly at night, which is why most statins should be taken at night.) Well-known side effects include myositis and abnormal liver enzyme profiles. Note that deranged LFTs are far more common than myopathy. Rhabdomyolysis is a very rare complication. Other lipid-lowering agents include ezetimibe (which inhibits intestinal absorption of cholesterol), fibrates (which may increase the risk of developing rhabdomyolysis if co-prescribed with a statin) and bile acid sequestrants. However, it should be borne in mind that, unlike statins, these medications do not lower mortality.

Digoxin inhibits the sodium-potassium pump and is a negative chronotrope and positive inotrope. Patients on digoxin should be monitored for complications (see Section 1.14.1).

Atherosclerosis

Atherosclerotic cardiovascular disease is the number one worldwide cause of death and disability. It is a complex process, affecting principally medium- to large-sized arteries. It normally results in luminal stenosis which may be progressive over time. Pathologically, there is focal accumulation within the intimal layer of the arterial wall of cells, lipids, fibrous tissue and complex proteoglycans, eventually leading to the formation of an atherosclerotic plaque. As they advance, these plaques also accumulate calcium, giving rise to the colloquial term ‘hardening of the arteries’.

Smoking is by far the greatest cause of preventable mortality and has been implicated as a risk factor in the development of numerous disease processes. NICE encourages practitioners to discuss smoking cessation with patients when appropriate, advising practitioners as follows:

Attempt to offer therapy when patients feel ready to quit

Options include nicotine replacement therapy (NRT), varenicline or bupropion, but none of these should be prescribed together (apart from various subtypes of NRT)

Bupropion is contraindicated in patients with seizures or eating disorders

Varenicline is contraindicated in patients with mood disorders (a helpful way to remember this is the phrase ‘Varenicline makes your mood decline’).

For most patients, establishing a target stop date is key to smoking cessation.

1.1 Stable angina

Ischaemic heart disease refers to a group of conditions that result from an imbalance between myocardial oxygen supply and demand, leading to tissue hypoxia. This discrepancy is most commonly caused by atherosclerotic disease, although possible non-atherosclerotic causes, such as coronary artery anomalies (younger individuals) and systemic vasculitides (older individuals), should also be kept in mind. Ischaemic heart disease can be categorised as either stable angina or acute coronary syndrome.

Definition: stable angina generally occurs due to a fixed narrowing of the coronary arteries, resulting in symptoms typically associated with exertion, emotion, eating and cold weather. The onset of symptoms is predictable and resolves once the stimulus is removed (e.g. resting after exertion).

Epidemiology:

Men affected almost twice as much as women; South Asians more likely to be affected

Modifiable risk factors include diabetes mellitus, hypertension, hyperlipidaemia, smoking and obesity

The term ‘angina’ is a commonly used form of ‘angina pectoris’, which is derived from the Latin words angere and pectus which, taken together, mean ‘to strangle the chest’. As one might imagine, angina is typically described by patients as ‘pressure’ or a ‘crushing sensation’ retrosternally. If the pain is ‘stabbing’, positional or sharp, the underlying pathological process is less likely to be ischaemic in nature.

Aetiology/pathophysiology:

Coronary artery narrowing by an atherosclerotic plaque reduces blood flow and oxygen delivery to the myocardium

The atheroma also causes endothelial dysfunction, reducing vasodilator release (e.g. nitric oxide and prostacyclin)

The demand for increased myocardial oxygen supply (e.g. by walking uphill) is unable to be met due to the stenotic lesion, resulting in myocardial ischaemia

Ischaemia causes acidosis, decreased ATP production and release of lactate and other chemokines, which stimulate nerve cells in myocytes, producing the sensation of pain

Clinical features

NICE guideline: Chest pain of recent onset (NICE 2010, CG95)

Key features:

Central chest pain (in reality, stable angina is rarely described as frank ‘pain’; rather, the nature of the discomfort may be heaviness, pressure or squeezing)

Precipitated by exertion

Relieved by rest or nitrates, usually within 5 minutes

NICE considers a patient with all three features to have typical angina, a patient with two features to have atypical angina, and a patient with one or none of these features to have non-anginal pain.

Investigations

Investigations should be undertaken in the following order.

Stepwise plan:

1 Obtain an electrocardiogram (ECG)

2 Arrange blood tests

FBC, U&Es, LFTs (required for statin therapy), glucose, cholesterol, HDL, LDL and triglycerides

3 Stratify patients according to clinical risk

Determining probability (NICE 2010, CG95)

When a person has stable angina, NICE recommends stratifying the probability of coronary artery disease (CAD). Gender (being male), increasing age, typicality of chest pain and associated risk factors (diabetes, smoking, hyperlipidaemia) point to a higher likelihood of CAD.

Likelihood of CAD: shown in Table 1.4 below.

Cardiovascular disease refers to a collection of diseases, which include:

Coronary heart disease (e.g. angina pectoris/myocardial infarction)

Cerebrovascular disease (e.g. TIA/stroke)

Peripheral artery disease (e.g. intermittent claudication)

Risk calculators, such as QRISK3 or Framingham, are useful for doctors to predict a patient’s risk of developing a CVD within a 10-year period. However, these risk assessment tools are not recommended for use with patients who are type 1 diabetics or those with pre-existing cardiovascular disease.

Exercise stress testing is no longer recommended by NICE because it is only moderately specific. However, this does not mean that there is little place for stress testing in general. It is still used in many centres, and the European Society of Cardiology (ESC) guidelines still support its use. Stress ECG testing represents a cost-effective alternative to various imaging modalities, and is suitable for evaluating the majority of patients. Stress myocardial perfusion or stress echocardiography (using agents such as dobutamine, which mimic cardiac stress) are more specific investigations than the stress ECG and can be used in patients with contraindications to stress ECG testing, or where ECGs may not be viable (e.g. if the patient has a pacemaker or bundle branch block). Exercise capacity in itself is measured in metabolic equivalents, or METs, which is a strong indicator of prospective mortality. An increase of 1 MET (defined as 3.5ml O2/kg/min) is said to confer a greater than 10% increase in survival.

Management

Stepwise management of stable angina (NICE 2011, CG126)

Ensure that the patient has up-to-date information about their condition. Aspirin and statins should be prescribed for patients with angina.

1 Optimise diet and lifestyle, prescribe aspirin and a statin

2 Institute pharmacological therapy

Glyceryl trinitrate (GTN) should be used as and when necessary, repeating a second time after 5 minutes if the pain persists; call an ambulance if the pain persists 5 minutes after a second dose

First line: beta blocker or calcium channel blocker (rate-limiting, e.g. verapamil)

Increase the dose of monotherapy if still symptomatic

Second line: beta blocker and calcium channel blocker combination therapy (use a non-rate-limiting agent, e.g. nifedipine)

Third line: if either drug is contraindicated, alternative agents may be tried (ivabradine, nicorandil or ranolazine – of these, ranolazine has the best, albeit limited, evidence); the side effects of ivabradine include visual disturbances, particularly bright spots and luminous phenomena

3 Instituting lipid modification therapy (NI CE 20 14, CG181)

Measure a full lipid profile, including total cholesterol, HDL, LDL, triglycerides and liver function tests

Ratio of total cholesterol to HDL cholesterol is the best predictor of CVD risk, while LDL cholesterol helps guide goals of lipid therapy

Offer atorvastatin 20mg for primary prevention if estimated 10-year cardiovascular risk using QRISK3 is >10% (note that this is still controversial in some centres)

Offer atorvastatin 80mg for secondary prevention in patients with pre-existing CVD

LFTs should be measured within 3 months of starting treatment and at 12 months; statins are safe to start as long as liver transaminase results are less than 3 times the upper limit of normal

Coronary artery bypass grafting is recommended in:

Significant left main disease

Three vessel disease

Two vessel disease in diabetics

Metabolic syndrome is characterised by having three of any of the following five criteria:

Hyperinsulinaemia (elevated fasting plasma glucose)

Decreased HDL (as opposed to LDL levels, which are not required in making the diagnosis)

Central obesity

Hypertriglyceridaemia

Hypertension (>130/85)

This syndrome confers a threefold increase in the risk of cardioembolic events.

Adult Treatment Panel (ATP III) Guidelines

The ATP III Guidelines are also a useful accessory when evaluating lipid-lowering therapy in ischaemic heart disease. Patients are stratified according to their 10-year risk, with >20% risk being a coronary heart disease equivalent; ≤20% conferring moderate risk; and patients with 0–1 risk factor (or a lower than 10% 10-year risk score by default) being regarded as low risk. Target LDL levels are thus recommended, using a fasting lipid panel:

CHD equivalent (>20%) – target LDL <100mg/dl (<70 in very high-risk patients)

Moderate risk (≤20%) – target LDL <130mg/dl

Zero to one risk factors (low risk) – target LDL <160mg/dl

1.2 Acute coronary syndrome

Definition: the term acute coronary syndrome (ACS) refers to a group of conditions that result from a sudden and unpredictable disruption in coronary blood flow. ACS exists on a continuum, from myocardial ischaemia (unstable angina) to the development of myocardial infarction and necrosis (NSTEMI or STEMI; see Fig. 1.9). Clinically, these conditions are classified according to changes in the electrocardiogram and biochemical markers of myocardial necrosis.

Fig. 1.9 Acute coronary syndrome.

Epidemiology:

ACS accounts for approximately 30% of all deaths worldwide

While there is a male preponderance, the condition may be underdiagnosed in women

The GRACE registry suggests that up to 30% of patients with ACS present with STEMI

Aetiology/pathophysiology:

Atherosclerosis is the most common cause

Risk factors (see Table 1.5)

ACS usually results from atherosclerotic plaque rupture, promoting thrombus formation which imposes varying degrees of luminal impingement, precipitating an acute coronary event

If the resultant thrombus occludes the vessel completely, myocardial infarction (characterised by ST elevation on ECG) will most often develop

In the absence of total thrombotic occlusion, an NSTEMI or unstable angina may commonly develop, and ECG changes (such as ST segment depression and/or T wave inversion) may occur

Clinical features:

Chest pain in ACS is classically acute, central, crushing and retrosternal in nature, with or without radiation to the jaw, neck or arm

Other symptoms include shortness of breath, sweating, nausea and vomiting

Variant (or Prinzmetal) angina may present similarly to acute coronary syndrome, but the underlying pathophysiological process is usually attributed to coronary artery vasospasm. The gold standard for diagnosis is coronary angiography with a provocative agent, such as ergonovine, to induce an attack. The condition is treated with calcium channel blockers or nitrates. Note that the use of aspirin or beta blockers may worsen vasospasm.

ACS may present atypically in some patients, particularly those with autonomic dysfunction (diabetics and the elderly). They may have a silent MI (with no chest pain) or they may present with delirium, hypotension or epigastric pain.

Immediate investigations (see Fig. 1.10)

Fig. 1.10 Approach to ACS.

1 Obtain ECGs

Should be recorded 15–30 minutes apart, looking for dynamic changes, and compared with older ECGs if possible

2 Arrange chest X-ray

Assess cardiomediastinal contours (e.g. the presence of cardiomegaly, mediastinal widening in aortic dissection), lung fields (e.g. signs of heart failure) and exclude non-cardiac causes of chest pain (e.g. pneumothorax, pneumonia)

3 Arrange blood tests

Troponin T or I (serial, 6h apart, looking for a peak in the measured values), FBC, U&Es, LFTs

With the advent of high-sensitivity troponin assays, very low levels of troponin can be detected. While these newer assays improve diagnostic sensitivity, they are likely to affect clinical specificity. This is primarily because troponin can be elevated in several other conditions: acute heart failure, myocarditis, pericarditis, pulmonary embolism, renal failure and sepsis.

Posterior STEMIs are usually characterised by horizontal ST depression, tall R waves and upright T waves (all changes in leads V1–3). The left circumflex or right coronary artery is often implicated. Posterior STEMI is confirmed by placing leads V7–9 (V7 posterior axillary line, V8 at tip of left scapula and V9 left paraspinal region – all leads at same horizontal plane as V6).

Guidelines: Third Universal Definition of Myocardial Infarction (2012)

The joint ESC/ACCF/AHA/WHF task force published the following recommendations for the diagnosis of acute MI in 2012.

A rise and/or fall of cardiac biomarkers (troponin) with at least one value above the 99th percentile of the upper reference limit (URL) in conjunction with evidence of myocardial ischaemia, with at least one of the following:

Symptoms of ischaemia

ECG changes indicative of new ischaemia (ST–T changes or new LBBB)

Development of pathological Q waves in the ECG

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

Identification of an intracoronary thrombus by angiography

Classification of myocardial infarction

Stepwise management of acute coronary syndrome

The aim of management is to instigate antiplatelet therapy expeditiously, to re-perfuse the myocardium in STEMI, and to prevent the progression of unstable angina and NSTEMI. The approach to management can be divided into three steps: initial management, advanced management and post-acute management.

1 Initial management for ALL patients (MONAC)

Continuous cardiac monitoring

Ideally move to a controlled environment (e.g. Coronary Care Unit)

Administer (or check) aspirin 300mg, plus another antiplatelet agent (e.g. clopidogrel, prasugrel, ticagrelor); antiplatelet agents lower mortality

Oxygen: indicated only if SpO2 <94%; the evidence indicates that oxygen may have a vasoconstrictive effect on the coronary arteries and should be avoided if the patient is not hypoxic

GTN: may be given via the sublingual or buccal route – if minimal to no response, an IV infusion may be considered; note that GTN should be avoided if systolic BP <90mmHg

IV morphine for pain: (e.g. 2.5mg boluses, 5 minutes apart), with up-titration if clinically indicated; may also be used for pulmonary oedema, shortness of breath or anxiety

IV metoclopramide: ischaemia and morphine are both emetogenic

Tight glucose control: glucose should be monitored regularly

2 Advanced management

After immediate management, further therapy depends on the type of ACS, STEMI or NSTEMI/UA and the clinical condition of the patient.

a.STEMI

1.Establish diagnosis of STEMI

2.Primary percutaneous coronary intervention (PPCI)

This is the gold standard reperfusion strategy in STEMI

Features of STEMI on ECG:

ST elevation of ≥1mm in at least 2 adjacent limb leads or ≥2mm in 2 contiguous precordial leads OR

New onset of LBBB (this is less specific for STEMI)

Indicated if symptom onset occurs within 12 hours

Procedure should be performed within 90–120 minutes of diagnosis

Bivalirudin (direct thrombin inhibitor), in combination with aspirin and clopidogrel, is recommended for patients with STEMI undergoing PPCI (although practice may vary between centres)

LMWH or unfractionated heparin are the anticoagulants of choice in patients undergoing PPCI who have been treated with prasugrel or ticagrelor

NICE recommends against the routine use of glycoprotein IIb/IIIa inhibitors before planned PPCI

3.Thrombolysis in STEMI

Should only be performed if patients are unable to receive PPCI within 90–120 minutes of diagnosis, or where PPCI is contraindicated

ECG should be performed 90 minutes after thrombolysis

Look for 50% reduction in ST elevation

If inadequate response, consider rescue PCI within 6 hours of thrombolysis

b. NSTEMI/UA

1.Establish the diagnosis

NSTEMI: positive troponin ± ischaemic changes on ECG (e.g. ST depression, T wave inversion)

UA: negative troponin ± ischaemic changes on ECG

2.Assess risk of future adverse cardiovascular events:

NICE recommends the GRACE score to predict 6-month mortality

If low risk (predicted 6-month mortality <3%):

Offer patients anticoagulation (fondaparinux 2.5mg SC is recommended for 8 days or until discharge) without early angiography and proceed to post-acute management

If intermediate (3–6%) or high risk (>6%):

Consider IV glycoprotein IIb/IIIa inhibitors and anticoagulation (bivalirudin or unfractionated heparin recommended)

Arrange coronary angiography within 96 hours of admission and consider PCI

3 Post-acute management

Antiplatelet agents

Aspirin 75mg lifelong following ACS

P2-Y12 inhibitors: (clopidogrel, ticagrelor, prasugrel) for 12 months

Statin therapy lowers mortality; NICE recommends atorvastatin 80mg

Beta blockers lower mortality and provide symptomatic relief

Nitrates,regular (if required), and PRN (for all patients)

ACE inhibitors lower mortality, and prevent ventricular remodelling and subsequent heart failure

Structured cardiac rehabilitation and lifestyle modification

Driving limitations:

If angioplasty – 1 week

No angioplasty – 4 weeks

Sexual intercourse:

Generally best avoided for at least 1 week after an uncomplicated MI

Patients who are able to carry out physical activity may be advised to resume sexual activity on a case-by-case basis

Air travel:

Avoid for 2 months

Complications of acute coronary syndrome

This can be memorised using the popular mnemonic ‘Sudden Death on PRAED Street’.

Sudden Death

Pump failure or Pericarditis

Rupture (e.g. of LV free wall, septum or papillary muscle)

Aneurysm or Arrhythmia

Embolism

Dressler syndrome

Complications of myocardial infarction

Careful monitoring of patients post MI is essential because of the risk of complications. These include:

Recurrent MI or re-occlusion

Should be suspected with recurrent or new chest pain post MI; may have new ECG changes

CK-MB may be useful in detecting re-infarction, as troponin levels take 14 days to normalise

Rare complication, requires angiography and potential revascularisation to treat

In-stent thrombosis incidence is reduced by appropriate adherence to antiplatelet therapy

Acute pulmonary oedema (see Chapter 12)

Common complication

Cardiogenic shock

Arrhythmia:

Ventricular tachycardia and ventricular fibrillation may result in sudden death in up to one-fifth of patients

Bradycardia and heart block are more commonly associated with an inferior wall MI; heart block associated with inferior MIs is usually self-limiting but should be monitored closely

Bradycardia and heart block in the setting of an anterior wall MI are associated with a poorer prognosis, and pacing should be considered

Killip class may be used to help evaluate congestive heart failure in MI. Patients with a higher Killip class have a higher 30-day mortality.

Class I: no clinical signs of heart failure

Class II: presence of crackles, elevated JVP or third heart sound

Class III: acute pulmonary oedema

Class IV: cardiogenic shock

Ventricular septal rupture:

Uncommon, often occurs within a week of MI

Associated with anterior MI

Septal rupture may be associated with the sudden onset of shock and pulmonary oedema

Development of a new systolic murmur best heard at the lower left sternal border

Echocardiography is first line (transoesophageal is superior to transthoracic, but this depends on the stability of the patient); alternatively, catheterisation demonstrates characteristic stepping up in oxygen saturation in right ventricle

Requires surgical closure

Ventricular free wall rupture:

Leads to pericardial tamponade and imminent death if left untreated

Urgent pericardiocentesis and surgery are essential

LV aneurysm typically develops after 4–5 weeks, presenting with LV failure, VT and systemic emboli. ECG shows persistent ST elevation. Treat with anticoagulation and/or excision.

Papillary muscle rupture:

Associated with acute mitral regurgitation and inferior infarctions in particular; life-threatening complication

Holding treatments include reducing afterload (e.g. treating with sodium nitroprusside), inotropes, diuretics, ventilation, followed by urgent surgical repair/replacement

Right ventricular failure:

Associated with inferior wall MI

Suspect if clear lung fields, elevated JVP and systemic hypotension

Fluid boluses that augment RV preload are required (e.g. 250ml 0.9% NaCl over 10 minutes)

Avoid prescribing nitrates and diuretics

Nitrates and diuretics reduce preload, which will worsen the condition of right ventricular failure, as filling of the right side of the heart is already impaired.

Mural thrombus

Cholesterol embolus

May affect various organs, e.g. renal failure if kidneys are affected

Classically presents with gangrene of the extremities, particularly the toes, if emboli lodge in the lower limbs

Suspect if the patient develops distal ischaemia, renal failure or hypertension

Pericarditis

Common complication, particularly in the first few days, following transmural infarcts

May be clinically silent or the patient may experience pleuritic chest pain that classically improves on sitting up

There may be a pericardial rub and evidence of a pericardial effusion on chest X-ray or echocardiography

Late pericardial inflammation is termed Dressler syndrome. This is an autoimmune condition that presents 2–6 weeks post MI with recurrent pericarditis, fever and effusions. Often associated with large pericardial and pleural effusions, the former predisposing to cardiac tamponade. Treatment is with aspirin, colchicine or steroids. NSAIDs may also be used, but the evidence, while not particularly clear, does suggest that they may in some way interfere with myocardial healing.

1.3 Heart failure

Definition: heart failure refers to the inability of the heart to produce a cardiac output sufficient to meet the body’s metabolic demands.

Epidemiology:

Incidence and prevalence increase with age

Affects 1–2% of the population in the western world

Aetiology:

The most common causes of heart failure are ischaemic heart disease, valvular heart disease, cardiomyopathy and hypertension

Other causes include infiltrative disease, toxins, infections (e.g. Chagas disease) and drugs

Pathophysiology: the pathophysiological process that takes place in heart failure involves a complex interplay of many factors. As cardiac output begins to decline, compensatory mechanisms (both mechanical and neurohumoral in nature) are activated in an attempt to sustain adequate tissue perfusion. These may initially be beneficial, but will lead to worsening heart failure over time as their ability to compensate declines.

Mechanical compensatory mechanisms include Frank–Starling forces (stretch on myocardial fibres increases subsequent stroke volume)

Neurohumoral compensatory mechanisms include increased sympathetic nervous system stimulation and activation of the renin–angiotensin–aldosterone system

Classification of heart failure

Heart failure can be classified as follows:

New York Heart Association (NYHA)

classification of the extent of heart failure

Clinical features

Dyspnoea

Orthopnoea and paroxysmal nocturnal dyspnoea

Other symptoms include a nocturnal cough, chest discomfort, peripheral oedema and fatigue

Note that individual symptoms may differ based on the aetiological cause of the heart failure and the duration of onset

The presence of two major, or one major and two minor, criteria in the Framingham criteria may also be used to help suggest the diagnosis of heart failure

Examination findings:

Signs of right heart failure: elevated JVP, hepatomegaly, ascites, significant peripheral oedema

Signs of left heart failure: displaced apex beat, S3, pulmonary congestion

Note that in clinical practice both types of heart failure often occur simultaneously, which is termed congestive cardiac failure.

Investigations

Investigations should be undertaken in the following order.

Stepwise plan:

1 Arrange blood tests

FBC, U&Es, LFTs, TFTs, lipid levels and glucose

2 Assess B-type natriuretic peptide (BNP)

This is released in response to myocardial stretch:

If levels of BNP ≥100pg/ml, investigate further and arrange for specialist referral within 6 weeks

If levels of BNP ≥400pg/ml, refer for specialist referral and echocardiography within 2 weeks

3 Obtain chest X-ray

Characteristic ‘ABCDE’ features (see Fig. 1.11)

Fig. 1.11 Classic ‘ABCDE’ findings on a CXR in a patient with heart failure.

4 Arrange for echocardiogram

Key investigation in suspected heart failure

Enables assessment of ventricular function, wall motion abnormalities and valvular or structural abnormalities

5 Obtain ECG

Useful in evaluating potential causes

6 Arrange other investigations

May include angiography, CT scanning and cardiac MRI

BNP levels above 400pg/ml are associated with a poor prognosis. BNP levels decrease once treatment is initiated. A higher BNP level correlates with higher mortality, and a BNP level below 100pg/ml has a very high (approximately 95%) negative predictive value in excluding heart failure. NICE, SIGN and the ESC guidelines all recommend the use of BNP in the assessment of heart failure.

Management of heart failure (NICE CKS, 2015)

General principles: the aim of management is to ensure treatment of all underlying pathology, encourage lifestyle changes (including treating sleep apnoea, which has been linked to poorer outcomes), manage symptoms and prevent episodes of acute decompensation as far as possible. Weighing the patient daily may also help provide an assessment of fluid status.

Stepwise management of heart failure

1 Lifestyle modification

Smoking cessation

Adequate fluid and salt restriction (<3g salt/day)

Restrict alcohol, optimise diet and exercise

2 Diuretics

Loop diuretics prescribed first line (e.g. furosemide)

Symptomatic relief of fluid overload

Does not reduce mortality

Introduce one drug at a time; once the person is stable on the first drug, add the second drug

3 ACE inhibitors

Improve morbidity and mortality

Improve ventricular function

Switch to an angiotensin receptor blocker (ARB) if cough (common side effect) not tolerated

4 Beta blockers

Improve morbidity and mortality

Bisoprolol, carvedilol and nebivolol are recommended in the treatment of heart failure

Titrate dose slowly and incrementally, preferably every 2 weeks if dosage requires adjustment

NICE recommends using clinical judgment when deciding which drug to start first.

For example, the preferred initial treatment might be:

– a beta blocker, if the person has angina

– an ACE inhibitor, if the person has diabetes

– a diuretic and ACE inhibitor, if the person still has signs of fluid overload.

Note that beta blockers are still the first-line choice for rate control when managing heart failure with accompanying atrial fibrillation. Digoxin is used as an alternative.

5 Mineralocorticoid receptor antagonists (MRAs)

Improve mortality

MRA therapy is used early in post-STEMI patients who have evidence of heart failure

Added to treatment regimen if still symptomatic despite use of ACE inhibitors, beta blockers and loop diuretics

Eplerenone is more expensive, but has fewer endocrine side effects compared to spironolactone

6 Ivabradine

Note that ivabradine is not recommended for use if AF is present

Indicated if patient’s symptoms fail to improve on triple therapy with beta blockers, ACE inhibitors and aldosterone antagonists, or if beta blockers are contraindicated in the first instance

7 Hydralazine plus nitrate

Improves mortality

Recommended for patients whose symptoms are still not controlled, and this treatment is particularly recommended for Afro-Caribbean patients

8 Device therapy and surgical management

Cardiac resynchronisation therapy pacemaker (CRT-P)

Improves mortality

Indicated in severe heart failure with LVEF <35% and broad QRS complexes on ECG

Implantable cardioverter defibrillator

Indications include previous ventricular fibrillation/ventricular tachycardia and a reduced ejection fraction

Can be integrated with CRT devices (CRT-D)

Left ventricular assist device (LVAD)

Used as a bridge to transplantation or recovery

Cardiac transplantation

Rarely undertaken, utilised in particular for young patients with refractory end-stage disease

One of the newest agents to emerge in the past few years is the combination tablet valsartan/sacubitril. Two major trials, PARADIGM-HF and PARAMOUNT, were instrumental in establishing that combination therapy with valsartan/sacubitril improves mortality and is far more effective in reducing frequency of admissions than enalapril therapy alone. This was seen in both HFrEF and HFpEF. Sacubitril, the newer agent, is an angiotensin receptor neprilysin inhibitor (ARNI), which exerts its effects by causing increased peptide degradation and promoting natriuresis.

1.4 Hypertension

Definition: blood pressure is a continuous variable, with a skewed normal distribution (bell-shaped curve) that varies with race, sex and age. The definition of hypertension is therefore arbitrary, although the higher the diastolic and/or systolic blood pressure, the greater the risk of cardiovascular disease, stroke and renal disease. Evidence shows that this increased risk begins with any blood pressure over 120mmHg systolic. Hypertension is therefore usually defined as a BP that increases the risk of cardiovascular morbidity and mortality, the treatment of which results in more benefit than harm.

Epidemiology:

Affects around one-third of patients aged 45–54

Affects approximately 70% of patients aged 75 and over

Aetiology/pathophysiology:

95% of cases are classified as essential –i.e. having no underlying discernible cause

The remaining 5% are classified as secondary and may be due to:

Renal disease (e.g. diabetic nephropathy, glomerulonephritis, polycystic kidneys, renovascular disease)

Endocrine disease (e.g. Conn syndrome, phaeochromocytoma)

Others: pre-eclampsia, coarctation of the aorta

Clinical features:

Hypertension is usually asymptomatic

Symptoms observed may be related to an underlying secondary cause (e.g. headaches, palpitations and sweating in phaeochromocytoma)

Essential hypertension is a multifactorial environmental and genetic condition. There is a greater prevalence of hypertension in first-degree relatives with hypertension, and a high concordance in identical twins. The exact pathophysiology, however, remains undefined.

Guidelines: Defining hypertension (NICE 2011, CG127)

Stage 1 hypertension

Clinic blood pressure (CBP) = 140/90mmHg or higher and

Ambulatory blood pressure monitoring (ABPM) average or home blood pressure monitoring (HBPM) average = 135/85mmHg or higher

Stage 2 hypertension

Clinic blood pressure = 160/100mmHg or higher and

ABPM/HBPM average = 150/95mmHg or higher

Severe hypertension

Clinic systolic BP ≥180mmHg OR

Clinic diastolic BP ≥110mmHg

Investigations (NICE 2011, CG127)

Investigations should be undertaken in the following order.

Stepwise plan:

1 Take blood pressure at clinic

Measure ABPM or HBPM if clinic reading is ≥140/90

2 Arrange for ABPM or HBPM readings

ABPM: at least 2 readings per hour every waking hour, with an average of 14 readings required for diagnosis

HPBM: BP measured twice a day, with each entry being the average of 2 readings taken at least 1 minute apart with the patient sitting down

3 Additional investigations

U&Es, creatinine, eGFR and assessment of renal function

Renal ultrasound

Echocardiogram

ECG

Fasting blood glucose and lipid profile

Additional investigations if a secondary cause is suspected

Complications of hypertension

Hypertension predisposes patients to:

Acute coronary syndrome

Stroke (ischaemic or haemorrhagic)

Chronic kidney disease (note that chronic kidney disease may itself cause hypertension)

Hypertensive retinopathy

Aortic dissection/aneurysm

Management

General principles: treatment should be initiated for patients with stage 1 hypertension, under the age of 80, with end organ damage, cardiovascular or renal disease or diabetes. All patients with stage 2 hypertension should be offered treatment. Encourage patients to modify specific lifestyle factors, such as preventing obesity, stopping smoking, and adopting a low salt diet.

Treatment targets

Under 80 years: CBP <140/90mmHg

Over 80 years: CBP <150/90mmHg

Diabetics: CBP <130/80mmHg

Stepwise management of hypertension (see Fig. 1.12)

Fig. 1.12 Stepwise management of hypertension.

1 ACE inhibitors or calcium channel blockers

Below 55 years of age, offer ACE inhibitor or ARB if intolerant

If above 55 years of age, or of Afro-Caribbean origin, offer calcium channel blocker

Newer agents, such as direct renin inhibitors (e.g. aliskiren) block the conversion of angiotensinogen to angiotensin I. At present, they are recommended if patients are unable to take other anti-hypertensive agents.

Some patients may present with a hypertensive emergency (accelerated or malignant hypertension) or hypertensive urgency, all of which encompass a severely elevated BP (usually systolic BP >220mmHg or diastolic BP >120mmHg) but are differentiated by the degree of end organ damage.

With hypertensive urgency, there is no end organ damage. Accelerated hypertension presents with evidence of hypertensive retinopathy, no worse than grade 3 (e.g. flame haemorrhages, soft exudates) and without papilloedema. The definition of malignant hypertension requires papilloedema.

End organ damage is not necessarily limited to hypertensive retinopathy. Encephalopathy (headache, visual disturbances, altered consciousness, seizures), myocardial ischaemia (angina, LV failure) or renal failure are also common presentations in a