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CHAPTER9 Cardiology and vascular disease
Infectiveendocarditis
• New murmur + fever=endocarditis until proven otherwise.
Infective endocarditis occurs when there is infection of a heart valve (mitral
> aortic > tricuspid > pulmonary). The valve may be normal (50%— may
be associated with IV drug abuse), rheumatic, degenerative, congenitally
abnormal, or prosthetic. Uncommon but consequences may be disastrous
and often detected late.
Causes
• Common organisms Strep. viridans (35– 50%); Staph. aureus (20%)
• Non- bacterial causes SLE, malignancy
Presentation May be acute (acute heart failure) or subacute (course
worsening over days/ weeks). Symptoms/ signs:
• Infective Fever, weight d, night sweats, malaise, lethargy, clubbing,
splenomegaly, anaemia, mycotic aneurysms
• Heart murmurs ± heart failure
• Embolic Stroke, lung abscesses (right heart endocarditis)
• Vasculitic Microscopic haematuria, splinter haemorrhages, Osler’s nodes
(painful lesions on nger pulps), Janeway lesions (palmar macules),
Roth’s spots (retinal vasculitis), renal failure
High- risk patients Those with:
• Acquired valvular heart disease with stenosis or regurgitation
• Valve replacement
• Structural congenital heart disease, including surgically corrected or
palliated structural conditions, but excluding:isolated atrial septal defect,
fully repaired ventricular septal defect or fully repaired patent ductus
arteriosus, and closure devices that are endothelialized
• Hypertrophic cardiomyopathy
• Previous infective endocarditis
When to suspect infective endocarditis
suspicion and admit as an emergency for further investigation if:
• Febrile illness and murmur of new valvular regurgitation
• Febrile illness + pre- existing high- risk cardiac lesion and no clinically
obvious site of infection
• Febrile illness associated with any of:
• Predisposition and recent intervention with associated bacteraemia
(e.g. dental work or surgical procedure)
• Evidence of congestive cardiac failure
• New conduction disturbance
• Vascular or immunological phenomena, e.g. embolic event, Roth’s
spots, splinter haemorrhages, Janeway lesions, or Osler’s nodes
• New stroke
• Peripheral abscesses (renal, splenic, cerebral, vertebral) of
unknown cause
• Protracted history of sweats, weight d, anorexia or malaise, and at- risk
cardiac lesion
• New unexplained embolic event, e.g. CVA, limb ischaemia
G
Have a high index of
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INFECTIVEENDOCARDITIS
Investigations inprimary care ifnon- acutepresentation
• Blood Non- specic signs of infection, e.g. leucocytosis, i ESR/ CRP
• ECG 10% develop a conduction defect
• CXR
Management Admit as an emergency if suspected. Avoid starting anti-
biotics prior to admission as this might cause delay in diagnosis by rendering
the blood cultures sterile.
Hospital treatment Once conrmed, treatment is with prolonged IV
broad- spectrum antibiotics (≤2wk).
Prognosis 80% have major complications during admission, e.g. heart
failure. Valve replacement may be required— especially if endocarditis
is on a prosthetic valve. 16– 27% die— those with endocarditis aecting
a prosthetic valve have poorer prognosis. Other factors predicting poor
prognosis:
• Infecting organism— Staph aureus 30– 40% mortality; streptococci 10%
mortality
• i age
• Aortic valve involvement
• Associated heart failure
• CNS complications
• Co- morbidity, e.g. DM
Prevention of infective endocarditis Current guidance advises
against routine antibiotic prophylaxis because:
• There is no consistent association between having an interventional
procedure and development of infective endocarditis
• Regular toothbrushing presents a greater risk of infective endocarditis
than a single dental procedure because of repetitive exposure to
bacteraemia with oral ora
• Clinical eectiveness of antibiotic prophylaxis is not proven
• Antibiotic prophylaxis against infective endocarditis may lead to a
greater number of deaths through fatal anaphylaxis than a strategy of
no antibiotic prophylaxis, and is not cost- eective
Advise instead— about the:
• Importance of maintaining good oral health
• Symptoms that may indicate infective endocarditis and when to seek
expert advice
• The risks of undergoing invasive procedures, including non- medical
procedures such as body piercing or tattooing
0 Do not oer chlorhexidine mouthwash as prophylaxis against infective
endocarditis to people at risk undergoing dental procedures.
Further information
British Society for Antimicrobial Chemotherapy (2015) Guidelines for the
diagnosis and antibiotic treatment of endocarditis in adults. M www.bsacarc.com/ #details/ 218
NICE (2008, updated 2016)Prophylaxis against infective endocarditis. M
www.nice.org.uk/ guidance/ CG64
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CHAPTER9 Cardiology and vascular disease
Rheumatic fever, myocarditis, and
pericarditis
Rheumatic fever There has been a dramatic d in incidence of rheum-
atic fever in industrialized countries since 1950s, but recently numbers of
cases have i. Rheumatic fever is still an endemic disease in developing countries. Peak incidence:age 5– 15y.
Cause Rheumatic fever is due to an abnormal immunological response to
portance lies in the permanent damage caused to heart valves in some of
those aected and subsequent risk of endocarditis.
Diagnosis Can be made if Revised Jones criteria are met (Table 9.7).
Management If suspected refer for specialist care. Specialist management
includes evaluation of heart lesions with Echo, bed rest, penicillin, and
symptom control (e.g. analgesia, sedatives for chorea). Anti- inammatory
agents such as corticosteroids and aspirin may be used to try to d complications of carditis but their use is controversial.
Prognosis
• 60% develop chronic rheumatic heart disease (70% mitral valve; 40%
aortic; 10% tricuspid; 2% pulmonary). Likelihood correlates with severity
of initial disease
• Recurrence may occur after further streptococcal infection or be
precipitated by pregnancy or combined hormonal contraception
Table9.7 Revised Jones criteria fordiagnosis ofrheumatic fever
Requirements for diagnosis of rheumatic fever
Evidence of previous streptococcal infection (scarlet fever, +ve throat swab and/
Major criteria Minor criteria
Carditis (45–70%)—arrhythmia, new
murmur, pericardial rub, heart failure,
conduction defects
Migratory polyarthritis (‘itting’—75%) red,
tender joints
Sydenham’s chorea (St Vitus’ dance—10%)
Subcutaneous nodules (2–20%)
Erythema marginatum (2–10%)
Source:data from Gewitz MH etal. Revision of the Jones Criteria for the Diagnosis of Acute
Rheumatic Fever in the Era of Doppler Echocardiograph y:A Scientic Statement from the
American Heart Association. Circulation, 131(20), 1806– 181, Copyright © 2015 American Heart
Association, Inc.
or i ASO titre >200u/mL)
1 major + 2 minor criteria
and
2 major criteria
or
Prolonged P–R interval on ECG (but
not if carditis is one of the major
criteria)
Arthralgia (but not if arthritis is one
of the major criteria)
Fever
i ESR or i CRP
History of rheumatic heart disease or
rheumatic fever
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RHEUMATIC FEVER, MYOCARDITIS, AND PERICARDITIS
Secondary prevention Penicillin 250mg bd po or sulfadiazine 1g od (500mg
od for patients <30kg) for ≤5y to prevent recurrence. Duration of prophylaxis is dependent on whether there was carditis in the initial attack (no
carditis— continued for 5y; if cardiac involvement— continued until age 25y
or longer).
Acute myocarditis Inammation of the myocardium. May present in a
similar way to MI or with palpitations. Causes:viral infection, e.g. Coxsackie
virus; diphtheria; rheumatic fever; drugs.
Management Admit for specialist cardiologist care. Treatment is supportive.
Some recover spontaneously— others progress to intractable heart failure
requiring transplantation.
Pericarditis Sharp, constant sternal pain relieved by sitting forwards. May
radiate to left shoulder ± arm or into the abdomen. Worse lying on the left
side and on inspiration, swallowing and coughing. Apericardial rub may be
present at the left sternal edge on auscultation. Causes:
• Infection, e.g. Coxsackie virus, TB
• Malignancy
• Uraemia
• MI (Dressler syndrome E p. 231)
Investigations ECG— concave (saddle- shaped) ST elevation in all leads.
Management Refer to cardiology; treat the cause (if possible); symptomatic
treatment with NSAID for pain; steroids in resistant cases.
Complications
• Pericardial eusion Fluid in the pericardial sac. Presentation:heart failure,
cardiac tamponade (inability of the heart to dilate in diastole resulting
in tachycardia, d BP, i JVP). CXR— large, globular heart. Echo is
diagnostic. Management:admit for urgent cardiology assessment
• Constrictive pericarditis Pericardium becomes brosed and non-
expansile. Most common cause is TB. Presentation:right heart failure,
hepatosplenomegaly, ascites, d BP, i JVP. Management:refer to
cardiologist for conrmation of diagnosis. Treatment involves surgical
release of the pericardium
• Trauma
• Radiotherapy
• Connective tissue disease
• Hypothyroidism
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CHAPTER9 Cardiology and vascular disease
Cardiomyopathy and hearttransplant
Cardiomyopathy is primary disease of the heart muscle. Although some
cardiomyopathies are ‘unclassied’ most fall into the following 4 groups:
Dilated (congestive) cardiomyopathy Prevalence 835/ 100,000.
♂ > ♀. Dilation of left ± right ventricle and d contractility. Usually presents
with heart failure; may also present with arrhythmia, syncope, peripheral
embolism, or abnormalities on ECG/ Echo. ECG:non- specic S- T abnormalities; CXR:cardiac enlargement and pulmonary venous hypertension.
Echo is diagnostic. Causes:
• Idiopathic (50%)
• Familial (20%)
• Cardiovascular— IHD, i BP,
congenital heart disease, rheumatic
heart disease
• Alcohol
• Infection (Coxsackie virus)
• Endocrine disease— myxoedema,
thyrotoxicosis, acromegaly
Management Advise patients to stop drinking alcohol as alcohol may make
cardiomyopathy worse. Specialist management is needed in all cases and
involves:
• Treatment of heart failure and arrhythmias (may require cardiac
resynchronization and/ or implantable cardiac debrillator device)
• Most patients require long- term anticoagulation
• Surgery— cardiomyoplasty or heart transplantation
Mortality 40% in 2y (sudden death, cardiogenic shock).
Hypertrophic cardiomyopathy Autosomal dominant inheritance,
although 50% are sporadic. In its most common form causes asymmetrical
septal hypertrophy ± aortic outow obstruction (hypertrophic obstructive
cardiomyopathy or HOCM).
Presentation Most cases are diagnosed in childhood (<14y) through Echo
screening of asymptomatic patients with a FH. Symptoms/ signs:
• Palpitations— associated with arrhythmias— 5% have AF
• Breathlessness on exertion
• Chest pain— may be angina or atypical pain
• Murmur— due to outow obstruction and/ or mitral valve dysfunction
• Faints/ collapses
Investigations
• ECG— LVH and ischaemic changes, e.g. T- wave inversion
• CXR— normal until disease is in its late stages
• Echo— diagnostic. Refer if suspicious symptoms or family history
Management and prognosis Ongoing specialist care is essential to provide
symptomatic treatment, e.g. β- blockers for chest pain, amiodarone for arrhythmia (digoxin is contraindicated). Implantable cardiac debrillators improve prognosis for those at high risk of sudden death. Surgical options
include septal ablation and myotomy/ myectomy to debulk the septum and
relieve obstruction.
• Cardiotoxic drugs
• Pregnancy
• Connective tissue disease (SLE,
PAN, systemic sclerosis)
• Sarcoidosis
• Amyloidosis
• Haemochromatosis
• Malignancy
• Muscular dystrophy
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CARDIOMYOPATHY AND HEARTTRANSPLANT
Mortality Sudden death is unrelated to severity of symptoms.
Restrictive cardiomyopathy R are. Sti ventricle limits lling. Presents
with heart failure. Echo is diagnostic. Causes:amyloid, sarcoidosis, haemochromatosis. Management: Specialist management is required. Treatment
is symptomatic.
Arrhythmogenic right ventricular cardiomyopathy Rare gen-
etic condition of progressive inltration of the right ventricular myocardium
with bro- fatty tissue. Often asymptomatic until presents with cardiac arrest. Refer any patients with a suspicious family history.
Family history ofsudden death Refer 1st- degree relatives of vic-
tims of sudden cardiac death who died aged <45y to cardiology. Antenatal
screening for familial cardiomyopathy and LQTS syndrome is possible if familial mutation is known. If FH HOCM and no genetic test:
• Children under <10y— screen with ECG and Echo every 3– 5y
• Children aged 10– 16y— screen every 6– 12mo if there is a family history
of HOCM— disease is likely to become apparent at this age
• Young people aged 16– 20y— screen annually
• >20y— screen every 5y if FH late- onset hypertrophic cardiomyopathy
0 Screening intervals are not established for other cardiomyopathies but
should be adapted to the pattern of disease within that particular family.
Heart transplantation Considered in patients with estimated 1y
survival <50%.
Indications/ contraindications Table 9.8.
Assessment Each eligible patient is assessed for psychosocial factors and
physical factors (e.g. renal failure, obesity, age, peripheral vascular disease)
which aect prognosis before a decision whether to place the patient on
the transplant list is made.
Postoperatively Patients require lifelong immunosuppression— usually with
ciclosporin. Follow- up is undertaken in specialist clinics.
Prognosis 1 in 4 patients die on the transplant list; 60% receive a transplant in
<2y. Perioperative mortality is <10%; 1y survival 92%; 5y survival 75%; 10y
survival 60%. Patients have accelerated graft atherosclerosis. Complications
of immunosuppression include i risk of infection and cancer.
Table9.8 Indications and contraindications forheart transplant
Indications Contraindications
All patients must have end stage
heart disease. Causes:
• IHD (50%)
• Cardiomyopathy (40%)
• Valvular and congenital heart
defects (5%)
Systemic disease likely to aect life expectancy
(e.g. malignancy)
Active infection (HIV, hepatitis B or C)
Signicant pulmonary vascular disease.
Continued excess alcohol consumption
Signicant cerebral/systemic vascular disease
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Patient information and support
British Heart Foundation F 0300 330 3311 M www.bhf.org.uk
Cardiomyopathy Association F 0800 018 1024 M www.cardiomyopathy.org
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CHAPTER9 Cardiology and vascular disease
Valvedisease
Heart murmurs E p. 206
• All patients with newly detected valve disease, except those with mitral valve prolapse or aortic sclerosis, require cardiology referral.
• Admit If suspected endocarditis
• Refer urgently/ admit If symptomatic valve disease or if valve disease
underlies the presenting condition, e.g. heart failure caused by aortic
stenosis, AF caused by mitral valve disease
Mitral stenosis Usually due to rheumatic fever.
Presentation
• Symptoms Breathlessness, palpitations, fatigue. May result in pulmonary
hypertension which presents with right heart failure, haemoptysis and/
or recurrent bronchitis
• Signs Peripheral cyanosis (‘malar ush’ on cheeks), left parasternal heave,
tapping apex beat, AF, rumbling mid- diastolic murmur at the apex
Management Conrm with Echo. Refer to cardiology. Treatment is medical
(treatment of AF, heart failure and anticoagulation) ± surgical (valvotomy,
balloon valvoplasty, valve replacement).
Mitral regurgitation (incompetence) Causes:
• Congenital
• Rheumatic fever
• Mitral valve
prolapse
Presentation
• Symptoms Dyspnoea, fatigue
• Signs Displaced apex (l left axilla), pansystolic murmur at the apex
radiating to axilla, AF, left ventricular failure
Management Conrm with Echo. Refer to cardiology. Treatment is medical (treatment of AF, heart failure and anticoagulation) ± surgical (valve
replacement).
Mitral valve prolapse Prevalence 71 in 20.
Presentation
• Symptoms Usually none. Rarely atypical chest pain, palpitations,
syncope, postural hypotension, emboli
• Signs Late systolic murmur over apex
Management Conrm with Echo. If syncope or palpitations refer to
cardiology— a rare complication is ventricular arrhythmia.
Aortic sclerosis Thickening and stiening of the aortic valve not asso-
ciated with outow obstruction that occurs with age. Clinically an ejection
systolic murmur is present but no other symptoms or signs. CXR may show
a calcied valve. No treatment is required.
• Ventricular
dilatation
• Endocarditis
• Cardiomyopathy
• Ruptured papillary
muscle/ chordae
tendineae following MI
• RA
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VALVEDISEASE
Aortic stenosis Causes:
• Congenital
• Rheumatic fever
Presentation
• Symptoms Angina, breathlessness, syncope or ‘funny turns’, dizziness,
sudden death
• Signs Small- volume pulse, low pulse pressure (dierence between
systolic and diastolic BP), ejection systolic murmur loudest in the aortic
area which radiates to carotids and apex
Management Echo is diagnostic and gives an estimate of the gradient across
the valve and thus severity of the condition. Refer to cardiology. Surgery
(valve replacement or transcutaneous valvoplasty) is considered for those
with syncope or if systolic gradient across the valve is >50mmHg. Avoid
treatment with ACE inhibitors.
• Bicuspid valve
• Degenerative calcication
• Hypertrophic
cardiomyopathy
Aortic regurgitation Causes:
• Congenital, e.g. VSD
• Bicuspid aortic valve
• Rheumatic fever
Presentation
• Symptoms Dyspnoea, palpitations (extrasystoles)
• Signs Prominent pulse (‘water- hammer’), wide pulse pressure, visible
neck pulsation (Corrigan’s sign), head nodding in time with pulse (De
Musset’s sign), visible capillary pulsations (e.g. in nail bed— Quincke’s
sign), displaced apex beat, high- pitched early diastolic murmur (easily
missed)
Management Conrm with Echo. Refer to cardiology for consideration of
surgery.
• Aortic dissection
• Endocarditis
• Cardiomyopathy
• Syphilis
• Marfan’s or Ehlers–
Danlos syndrome
Right heart valve disease Echo is diagnostic. Always requires spe-
cialist management.
• Tricuspid stenosis Mitral valve disease coexists. Cause:rheumatic fever.
Murmur:early diastolic (left sternal edge in inspiration). Treatment is
with diuretics ± surgery (valvotomy or replacement)
• Tricuspid regurgitation Causes:RV enlargement, endocarditis (IV drug
misusers), carcinoid, rheumatic fever, congenital. Presents with oedema,
breathlessness, pulsatile hepatomegaly (± jaundice), ascites, pansystolic
murmur loudest at left sternal edge. Treatment is with diuretics,
vasodilators, ± surgery (valve replacement or annuloplasty)
• Pulmonary stenosis Causes:congenital (Fallot’s tetralogy), rheumatic,
carcinoid. Murmur:ejection systolic murmur (loudest to left of upper
sternum, radiating to left shoulder). ECG:RVH. CXR:dilated pulmonary
artery. Treatment (if needed) is with pulmonary valvotomy
• Pulmonary regurgitation Due to pulmonary hypertension (E p. 236).
Murmur:decrescendo early diastolic murmur at left sternal edge
251
• Women planning pregnancy who have known valve disease require
review for specialist advice.
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CHAPTER9 Cardiology and vascular disease
Other structural abnormalities
oftheheart
Coarctation of the aorta Localized narrowing of the descending
aorta usually distal to the origin of the left subclavian artery.
Presentation Heart failure, i BP, murmur heard incidentally (ejection sys-
tolic murmur over the left side of the chest radiating to the back), lack of
femoral pulses or radio- femoral delay. Rarely presentation is with a complication, e.g. subarachnoid haemorrhage or endocarditis. CXR— prominent
left ventricle. ECG— Left ventricular hypertrophy.
Management Refer to cardiology— surgery to remove the narrowed portion of the aorta is usually indicated.
Atrial septal defect (ASD) A hole connects the 2 atria. Holes high in
the septum (ostium secundum) are most common (2 in 1000 live births);
holes lower in the septum (ostium primum) are associated with AV valve
abnormalities. Blood ows from L l R through the shunt and the right heart
takes the burden.
Presentation
• Ostium secundum defects Symptoms are rare in infancy and uncommon
in childhood. If detected in these groups, presents as a murmur
(systolic— loudest in the 2nd left interspace) found incidentally, with
breathlessness or tiredness on exertion or recurrent chest infections.
Presentation is usually in the 3rd or 4th decade with heart failure,
pulmonary hypertension, and/ or atrial arrhythmias
• Ostium primum defects Heart failure commonly develops in infancy/
childhood ± severe pulmonary hypertension. In addition to the ASD
murmur, there may be a pansystolic murmur signifying mitral or tricuspid
valve regurgitation
Investigation
• CXR Cardiomegaly with a prominent right atrium ± pulmonary artery ±
pulmonary plethora
• ECG Right axis deviation (ostium secundum defect) or left axis deviation
(ostium primum defect), RVH ± RBBB
• Echo Diagnostic
Management Refer to cardiology. Cardiac surgery to close the defect is
usually indicated.
Ventricular septal defect (VSD) A hole connects the 2 ventricles.
Blood ows initially from L l R through the hole. May be congenital (2 in
1000 live births) or acquired (usually septal rupture post MI).
Acquired VSD Suspect if new pansystolic murmur ± heart failure develop
after MI. Investigate as for congenital VSD. Refer to cardiology (speed of referral will depend on state of the patient) for advice on further management.
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OTHER STRUCTURAL ABNORMALITIES OFTHEHEART
CongenitalVSD
• Small VSD (‘maladie de Roger’) Normally asymptomatic. Athrill may
be palpable at lower left sternal border; harsh pansystolic murmur—
small holes give loud murmurs. CXR and ECG are normal. Diagnosis is
conrmed on Echo. Refer to cardiology
• Moderate VSD Symptoms usually appear in infancy— breathlessness
on feeding/ crying, failure to thrive, recurrent chest infections. As the
child gets older symptoms improve (relative size of the defect d). On
examination, there may be cardiomegaly, a thrill palpable at the left
sternal edge, and a pansystolic murmur. CXR shows cardiomegaly
± prominent pulmonary arteries ± pulmonary plethora. Diagnosis is
conrmed on Echo. Refer to cardiology
• Large VSD Presents with heart failure at 73mo of age though there may
be symptoms of breathlessness on feeding/ crying prior to then. On
examination, the baby is obviously unwell— underweight, breathless,
pulmonary oedema ± cyanosis, large heart, thrill over left sternal edge
± parasternal heave, murmur— often not pansystolic due to high right
ventricular pressures. Admit to paediatrics— medical treatment ±
surgery is always needed
Marfan’s syndrome Autosomal dominant connective tissue disease
causing abnormalities of brillin (a glycoprotein in elastic bres). Features
include:
• Arachnodactyly (long spidery ngers)
• High- arched palate
• Arm span > height
• Lens dislocation ± unstable iris
• Aortic dilatation (β- blockers appear to slow this)
• Aortic incompetence may occur, e.g. in pregnancy
• Aortic dissection may cause sudden death— Echo screening may be
helpful for aected individuals
If suspected refer to cardiology ± genetics. There is currently no antenatal
screening test available.
Other congenital heart disease E p. 858
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