Pericarditis and Myocarditis
High risk
Causes
Assessment
T >38.5, subacute onset, immunosupp, recent trauma, anticoagulation, myopericarditis, large pericardial effusion
Idiopathic: 25%
Viral: enterovirus (coxsackie, echovirus), adenovirus, mumps, EBV, VZV, hep B, flu, HIV
Bacterial: Staph aureus, pneumococci, beta-haemolytic strep, strep pneumonia, legionella, salmonella, psittacosis,
military TB / direct pul spread
Ca: 25%; occurs in 10% Ca patients; adults (lung, breast, lymphoma, leukaemia, melanoma); children (Hodgkins,
lymphosarcoma, leukaemia); results in tamponade in 50-85%
MI: transmural; within 1-5/7
Auto-immune: RA (most common autoimmune cause), SLE, Dressler’s syndrome (up to 6/52 post-MI, MOST
COMMON CAUSE), sarcoidosis
Drugs: hydralazine, procainamide
Other: Serum sickness, trauma, irradiation, cardiac surgery (v common), severe uraemia (tamponade common)
Sx: CP (relieved sitting forward; absent in 50% (esp if chronic / Ca); low grade fever; dysphagia; SOB; weakness;
syncope
OE: pericardial rub (high pitched, best with diaphragm over L sternal border; may be triphasic or biphasic; incr on
inspiration / sitting forward / with heart beat; transient – may last only 30mins; decr as pericardial effusion
increases); pericardial effusion
Ix
ECG: abnormal in 90%; may be normal if uraemic / RA; Changes usually diffuse but may be localized; DD = early
repolarization (usually only V1-3), MI (usually regional); widespread Q waves not seen in pericarditis
Phase 1 – hrs to days: widespread non-regional concave STE in I, II, V5-6 (not in aVR, V1, II, III, aVF)
Present in initial ECG in 66%; in 95% with incr trop; in 60% without incr trop
PR depression in 80% (most common in II; can occur in all leads except aVR, V1)
ST depression and PR elevation in aVR and V1
No distinct J point; slightly short QTc
Knuckle sign in PR segment of aVR
Phase 2 – days:
ST segments normalize
PR depression in 60%
Small T waves
Phase 3 – days to wks: TWI in leads that prev had STE
Low voltages; sinus tachy
Phase 4 – 1-3 months: Normalisation; some T wave changes may be permanent
Mng
CXR: pneumonia / pleural effusions if bacterial; underlying cause
Straightening of L heart border; globular heart (if >200ml effusion and slow onset); pericardial
calcification in 50% chronic; pericardial fat lines on lateral (high spec for pericardial effusion)
Echo: pericardial effusion in 40%; pericardial thickening; localized wall motion abnormalties in 7%
Trop I: incr in 50% at presentation; incr in most with WMA; myocarditis in significantly incr
Other bloods: FBC; ESR and CRP (used to track trt)
Pericardial aspiration: MC+S, AFB staining, ANF, RF
Supportive; NSAIDs (not aspirin); relieve tamponade if needed
Bacterial: broad spectrum ABx, pericardial aspiration, HDU/ICU
Myocarditis
Uraeamic: dialysis
Autoimmune: immunosupp
Dressler’s: steroids
More common in children and young adults; common cause of sudden death in previously well
Causes: viral and autoimmune as above, bacterial (Q fever, N meningitidis, M pneumoniae, C diptheriae,
chlamydia, C burnetti, beta haem strep), parasitic (Chagas disease most common cause worldwide, toxoplasma),
drugs (doxorubicin, ETOH, cloazpine, radiation)
Sx: non-specific; weakness, SOB, CP, fever, dizziness, palpitations, recent flu-like illness
OE: incr HR out of proportion to fever, incr RR, hepatomegaly, fever, creps, normal/high BP but poor perfusion,
maybe rapid deterioration, LVF uncommon
Ix: incr HR, low ECG voltages in 80%, ST/T changes, conduction disturbances, long QTc, may be normal early;
cardiomegaly, pleural effusions; global decr contractility on echo, decr EF, V dilation; incr cardiac markers; incr ESR
in autoimmune; myocardial biopsy (50-70% sens)
Mng: supportive; CCF trt; bed rest; inotropes, diuretics, vasoD, ACEi, trt arrhythmia; mechanical support if
hypoperfusion despite meds (ECMO, V assist devices); steroids / immunosupp if autoimmune
Prognosis: most deaths in 3-4/7; >95% survivial if last >72hrs; often progresses to dilated CM; no competitive sport
for 6/12
Causes of acute pericarditis: In western countries most cases of
acute pericarditis in immunocompetent patients are due to viral infection
or are idiopathic. Typically the illness follows a brief and benign course
after empiric treatment with anti-inflammatory drugs. Other causes
need to be considered in high risk patients. These include tuberculosis,
bacterial infections, neoplasms, uremia, connective tissue / autoimmune
disorders, drugs, trauma and myocardial infarction.
Haemorrhagic pericarditis involves blood mixed with a fibrinous or
supperative effusion, and is most commonly caused by tuberculosis or
direct neoplastic invasion. This condition can also occur in severe
bacterial infections or in patients with bleeding diathesis. It is common
after cardiac surgery.
Serous pericarditis is characteristically produced by non-infectious
inflammatory diseases such as rheumatic fever, SLE, scleroderma,
tumours, and uremia. Uremic pericarditis has a prevalence of 6-10% of
patients with acute or chronic renal failure with cardiac ultrasonography
revealing a pericardial effusion in at least 50% of cases.
Caseous pericarditis is a rare type of pericarditis that is tuberculous in
origin until proven otherwise. Infrequently fungal infections evoke a
similar reaction.
Fibrinous pericarditis occurs in inflammatory pericarditis with
fibrinogen leaking out of blood vessels and being converted to fibrin
which forms a fibrinous exudate. Fibrinous and serofibrinous are the 2
most frequent types of pericarditis. Common causes include post MI,
uremia, chest radiation, rheumatic fever, SLE, and trauma. A fibrinous
reaction also follows routine cardiac surgery.
Purulent or Suppurative pericarditis: Caused by invasion of the
pericardial space by microbes resulting in an exudate that ranges from
a thin cloudy fluid to frank pus up to 400 to 500 mL in volume. Complete
resolution is infrequent, and organization by scarring is the usual
outcome. The intense inflammatory response and the subsequent
scarring frequently produce constrictive pericarditis
Constrictive pericarditis; is the result of scarring and consequent loss
of the normal elasticity of the pericardial sac resulting in impaired
normal diastolic filling. The top 3 causes of constrictive pericarditis in
descending order are idiopathic (presumably viral), cardiothoracic
surgery and radiotherapy. All the other causes of pericarditis can also
result in restrictive pericarditis. Tuberculous and bacterial pericarditis,
while rare, are closely associated with constrictive pericarditis. The
incidence of constrictive pericarditis post acute idiopathic/viral was 0.76
cases per 1000 person-years, but 31.7 cases for 1000 person-years for
acute tuberculous pericarditis and 52.7 cases per 1000 person-years for
purulent pericarditis.
Causes of acute pericarditis: In western countries most cases of
acute pericarditis in immunocompetent patients are due to viral infection
or are idiopathic. Typically the illness follows a brief and benign course
after empiric treatment with anti-inflammatory drugs. Other causes need
to be considered in high risk patients. These include tuberculosis,
bacterial infections, neoplasms, uremia, connective tissue / autoimmune
disorders, drugs, trauma and myocardial infarction
Myocardial infarction: Pericardial disease, manifested as pericarditis
and/or effusion, is a common event following acute myocardial
infarction. Both types of pericardial disease are related to infarct size
and are less common in the era of revascularization. Acute pericarditis
post MI occurred in 6.7% of patients receiving thrombolysis in the
GISSI-1 and GISSI-2 trials. Later immunologically mediated pericarditis
known as Dressler’s syndrome has become uncommon following the
advent of reperfusion treatments.
Trauma causing pericarditis may be blunt or sharp and may be
iatrogenic in origin including all cardiac invasive diagnostic and
therapeutic procedures, and rarely following cardiopulmonary
resuscitation.
Drugs and toxins: There is a long list of drugs that may cause
pericardial disease. Procainamide, hydralazine, isoniazid and
phenytoin can induce a lupus like syndrome. Penicillins may cause a
hypersensitivity pericarditis with eosinophillia. Doxorubicin and
danorubicin are more often associated with cardiomyopathy, but may
cause pericardiopathy, as may other chemotherapy agents.
Bacterial: While any bacterial infection may involve the pericardium,
the most notable include staphylococcus, pneumococcus,
streptococcus (rheumatic pancarditis), haemophilus, and M.
tuberculosis.
Systemic lupus erythematous (SLE) and rheumatoid arthritis are the
most common rhematic diseases to involve the pericardium. In SLE the
pericardium is involved in almost one half of patients. Pericardial
effusion, when present, is usually clinically silent.