Inflammatory cardiac diseases

Dr. Mohammad Badawi

Medical resident
• Acute pericarditis

• Myocarditis

• Endocarditis
Anatomy of the heart
 The pericardium
• Pericardium is a fibroelastic sac
• visceral and parietal layers separated by a
(potential) space, the pericardial cavity.
• This space contains about 10-50 ml of fluids.
• Works as barrier that protects the heart .
• Facilitate cardiac movement by decreasing
friction.
 Pericardial diseases
• Acute and recurrent pericarditis
• Pericardial effusion without major
hemodynamic compromise
• Cardiac tamponade
• Constrictive pericarditis
 Acute pericarditis
• Inflammation of the pericardial sac.
• Acute pericarditis is the most common
disorder involving the pericardium.
• 5 percent of patients admitted to the
Emergency Department for nonacute
myocardial infarction chest pain.
• Isolated or 2ry to underlying disease.
 Etiology
• Infectious :Viral, Bacterial, fungal (purulent) ,
Others (Rickettsia, Chlamydia, Borrelia,
Mycoplasma, Treponema, Ureaplasma,
Nocardia, Tropheryma)
IATROGENIC :
• Radiation
• Post cardiac injury syndrome
• Post-myocardial infarction
• Post-pericardiotomy
• Post-traumatic (including iatrogenic)
• Drugs and toxins
• Metabolic (uremia, dialytic, myxedema,
ovarian hyperstimulation syndrome)
• Malignancy (especially lung and breast cancer,
Hodgkin lymphoma, and mesothelioma)
• Collagen vascular disease RA, SLE
• Idiopathic
 Clinical presentation
• Chest pain.
• Pericardial friction rub.
• Electrocardiogram (ECG) changes.
• Pericardial effusion
 symptoms
Chest pain :
• Gradual in onset.
• sharp and pleuritic.
• improved by sitting up and leaning forward.
• increases with lying supine.
• not related to exertion.
• continuous.
• Other associated symptoms depends on the
underlying cause .
 Pericardial friction rub
• highly specific for acute pericarditis.
• generated by friction between the two inflamed layers of the
pericardium.
• consists of three phases :atrial systole , ventricular systole, and in
the rapid filling phase of early ventricular diastole.
• Triphasic , biphasic , monophasic.
• Scratchy
• best heard with the diaphragm of the stethoscope. loudest over
the left sternal border.
• The intensity increases with the patient leaning forward or resting
on elbows and knees.
• It usually varies with time an position , need to repeat auscultation
to detect it.
 Ecg findigs
• It typically evolves in 4 stages
• Typical findings are present in 60% of cases.
•
 Stage 1
• first hours to days,
• is characterized by diffuse ST elevation
(typically concave up) with reciprocal ST
depression in leads aVR and V1.
• elevation of the PR segment in lead aVR and
depression of the PR segment in other limb
leads and in the left chest leads.
 Stage 2
• in the first week.
• characterized by normalization of the ST and
PR segments.
 Stage 3
• Diffuse T inversion.
• After normalization of ST segment.
 Stage 4
• Normalization of the changes
• If normalization doesn’t happen this indicates
chronic pericarditis
• It takes up to a month
• Treatment can fasten the progression of
changes.
 How to differentiate from MI??
morphology
• The ST segment elevation rarely exceeds 5
mm.
• concave
• in a STEMI patient the st segment is convex
(dome-shaped) ST elevation , and may be
more than 5 mm in height.
 How to differentiate from MI??
distribution
• ST segment elevations in STEMI are
characteristically limited to anatomical
groupings of leads that correspond to the
localized vascular area of the infarct.
• in pericarditis the ST changes are more
generalized and typically are present in most
leads.
• In acute pericarditis st elevation in I , II is more
than that in lead III.
 How to differentiate from MI??
Reciprocal changes
• Acute STEMI is often associated with
reciprocal ST segment changes, which are not
seen with pericarditis except in leads aVR and
V1.
 How to differentiate from MI??
Concurrent ST and T wave changes
• ST segment elevation and T wave inversions
do not generally occur simultaneously in
pericarditis, while they commonly coexist in
acute STEMI.
 How to differentiate from MI??
Hyperacute T waves
• Peaked T waves (>10mm high in precordial
leads, >5 mm high in limb leads), can be seen
in STEMI but are not typical of pericarditis.
 How to differentiate from MI??
Q waves
• Pathologic Q waves, which may occur with
extensive injury in STEMI, are generally not
seen in pericarditis.
 How to differentiate from MI??
PR segment
• PR segment elevation in aVR with PR
depression in other leads frequently seen in
acute pericarditis but rarely seen in acute
STEMI.
 How to differentiate from MI??
QT prolongation
• Prolongation of the QT interval with regional T
wave inversion , favors the diagnosis of
myocardial ischemia over pericarditis alone.
 Echocardiogram
• Usually shows pericardial effusion.
• If negative doesn't r/o pericarditis.
 Other investigations
• CXR is normal .
• Cardiac markers may present in up to 30% of
cases. Especially in case of myopericarditis.
• Markers of inflamation.
• Others according to the suspected diagnosis.
 Myopericarditis
• Elevation of cardiac biomarkers
• Detection of focal kinetic changes of
echocardiogram.
• Similar st changes
• Patient must be admitted to the hospital.
Complications of acute pericarditis
• Most patients recovers completely without
complications .(it’s mostly idiopathic)
• Chronic and recurrent pericarditis
• Constrictive pericarditis.
• Cardiac tamponade
• Both complications happens in < 1% of idiopathic
pericarditis
• Usually happens if 2ry pericarditis ( malignancy ,
TB , collagen vascular disease….etc )
 Treatment
• Depends on the etiology
• However most cases are idiopathic ( viral ?).
• If other findings suggest 2ry causes we look
for the cause and managed accordingly.
• In most cases we assume that patient has
idiopathic pericarditis.
• Medical treatment ……anti-inflammatory
drugs.
• Surgical treatment ( large pericardial effusion,
a hemodynamically significant pericardial
effusion, a suspicion of a bacterial or
neoplastic etiology, or evidence of constrictive
pericarditis ) : pericardial drainage and/or
pericardiotomy.
• According to the cause.
 Inpatient vs outpatient management
• Fever (>38ºC [100.4ºF]) and leukocytosis
• Evidence suggesting cardiac tamponade
• A large pericardial effusion (ie, an echo-free space of more
than 20 mm)
• Immunosuppressed state
• A history of oral anticoagulant therapy
• Acute trauma
• Failure to respond within seven days to NSAID therapy
• Elevated cardiac troponin, which suggests myopericarditis
• If no risk factors present patient can be treated safely as
outpatient.
 Outpatient treatment
• Activity restriction
• NSAID for 2 weeks : reliefs pain and decreases
inflammation.
• Most patients will respond within a week
• If no improvement within a week patient
should be evaluated for causes other than
idiopathic.
•
• Use of anticoagulation may increase the risk
of bleeding into pericardium and leads to
tamponade.
• Asa and plavix are not associated with
increased risk of bleeding.
 Colchicine
• Used if symptoms fail to respond to NSAIDs
• Recurrent pericarditis
• Can be used after cardiac surgery to prevent
postpericardiotomy symptoms.
 steroids
• Patients with symptoms refractory to standard
therapy (NSAIDs and colchicine)
• Acute pericarditis due to connective tissue
disease
• Autoreactive (immune-mediated) pericarditis
• Uremic pericarditis.
• We should r/o infective cause like TB ,
bacterial but not viral
MYOCARDITIS
• inflammatory disease of cardiac muscle.
• acute, subacute, or chronic.
• focal or diffuse involvement of the
myocardium.
 Etiology
• Infectious vs non infectious
 Clinical manifistation
• Heart failure
• fatigue and decreased exercise capacity are the
initial manifestations.
• if rapid in evolution and diffuse can result in
acute myocardial failure and cardiogenic shock.
• right ventricular failure : increased jugular
venous pressure, hepatomegaly, and peripheral
edema.
• left ventricular :dyspnea, orthopnea, pulmonary
rales, and, in severe cases, acute pulmonary
edema.
• Chest pain is not significant unless
myopericarditis.
• Sudden cardiac death : usually due to
arrythmias , 22% of unexplained death in
patients <30 year old.
• Arrythmia
 Clinicopathological classification
• Fulminant myocarditis — Fulminant myocarditis presents with acute heart
failure up to 2 weeks after a distinct viral prodrome. Patients have severe
cardiovascular compromise and may require mechanical circulatory
support.
• Acute myocarditis — Acute myocarditis presents with a less distinct onset
of illness. Patients present with established ventricular dysfunction and
may progress to dilated cardiomyopathy.
• Chronic active myocarditis — Chronic active myocarditis also presents
with a less distinct onset of illness. Affected patients often have clinical
and histologic relapses and develop ventricular dysfunction associated
with chronic inflammatory changes, and mild to moderate fibrosis on
histologic study.
• Chronic persistent myocarditis — Chronic persistent myocarditis, which
also presents with a less distinct onset of illness, is characterized by a
persistent histologic infiltrate, often with foci of myocyte necrosis but
without ventricular dysfunction, despite other cardiovascular symptoms
such as chest pain or palpitation.
 Invistigations
• Cardiac enzymes ….positive in up to 60%
• Ecg ………(if no pericardial involvement )non
specific changes , may mimic acute MI.
• CXR ……signs of heart failure (increased
cardiothoracic ratio , pulmonary congestion)
• Echocardigram …..usually global hypokinsia.
• Cardiac MRI ….detects myocardial edema and
myocyte injury.
 Prognosis
• Depends on the underlying cause , presenting
symptoms , and the degree of ECG changes.
• Myocarditis due to viral infection ….50%
• Giant cell myocarditis ……very high mortality
• Presence of q waves , high grade heart block ,
arrythmias were associated with poorer
prognosis.
 Treatment
• underlying cause.

• Treatment of heart failure in general

 Treating the underlying cause
• Antiviral treatment (ribavirin and interferon
alfa ) only if started early…….limited to acute
fulminant myocarditis , institutional outbreaks
, laboratory related infections.
• Myocarditis due giant cell myocrditi …..no
specific treatment.
• Myocarditis related SLE , sarcoidosis ,
eosinophilic myocarditis …….glucocorticoids .
• Treatment of heasrt failure in general
• Treatment of arrythmias
Endocarditis
• Infective vs non infective
• Non infective endocarditis (sterile , lymban
sacs endocarditis) : usually related to
autoimmune disease SLE , RA
 Infective endocarditis
• Bacterial or fungal infection of endocardium
• Native valve , prosthetic valve , endocardial
surface , implanted prosthetic device .
• Results from bacteremia and adherence of the
causing agent to an endocardial lesion usually
valvular.
• Staphylococcus is the most common cause in
native , prosthetic valves.
• It used to be streptococcal infection.
• Mortality rate of 20%
 Risk factors
• Valvular heart disease with stenosis or
regurgitation.
• Valve replacement.
• Previous IE.
• Hypertrophic cardiomyopathy.
• recreational drug abuse and invasive vascular
procedures.
• Structural congenital heart disease, including
surgically corrected or palliated structural
conditions, but excluding:
– Isolated atrial septal defect.
– Fully repaired ventricular septal defect.
– Fully repaired patent ductus arteriosus.
– Closure devices that are judged to be
endothelialised.
 Most common site
• Mitral valve.
• Aortic valve.
• Combined mitral and aortic valve.
• Tricuspid valve.
• Pulmonary valve - rare.
 Causing agents
Staphylococcus aureus:

• The most common cause of IE overall (acute and subacute);

• most common with prosthetic valves,
• acute IE and subacute IE
• related to intravenous drug abuse.
• High mortality rate.

• Coagulase-negative S. aureus: causes subacute disease

similar to Streptococcus viridans. Accounts for 30% of IE
associated with prosthetic valves.
• Streptococci:
– S. viridans: 50-60% of subacute IE cases.
– Group D streptococci: usually subacute and the third
most common cause of IE.
– Streptococcus intermedius: acute and subacute
infection. Causes 15% of all cases of IE.
– Group A, C and G streptococci: acute IE is similar to
that with S. aureus. High mortality (up to 70%).
– Group B streptococci: acute disease, high mortality
often requiring valve replacement. Occurs in
pregnancy and the elderly particularly.
• Pseudomonas aeruginosa: usually acute IE and
requires surgery for cure.
• HACEK organisms (Haemophilus
spp.,Aggregatibacter actinomycetemcomitans,
Cardiobacterium spp., Eikenella corrodens,
Kingella kingae): usually subacute disease and
about 5% of all IE.
• Fungi: cause subacute disease.
• Enterococci.
 Clinical presentation
• The clinical presentation is very variable.
• It may present as an acute, rapidly progressive
infection
• subacute or chronic disease, with nonspecific
symptoms - eg, fatigue, low-grade fever, flu-like
illness, polymyalgia-like symptoms, loss of
appetite, back pain, pleuritic pain, abdominal
symptoms and weight loss.
• May present with congestive cardiac failure
• So you have to suspect IE in high risk patients.
 Physical exam
• Fever.
• Heart murmurs: 85% have murmur.
• The most common murmur is aortic
regurgitation.
• Petechiae:
• Conjunctivae.
• Hands and feet (dorsum).
• Chest and abdominal wall.
• Oral mucosae and soft palate.
 Immunologic phenomena
• Splinter hemorrhages :nonblanching, linear
reddish-brown lesions found under the nail
bed
• Roth’s spot :exudative, edematous
hemorrhagic lesions of the retina.
• Arthritis
• Glomerulonephritis
•
 Embolic phenomena
• Focal neurological deficit stroke
• Renal and splenic infarcts
• In right sided infective endocarditis ….pulmonary
embolism
• Osler’s nodes :painful, violaceous nodules found
in the pulp of fingers and toes
• Janeway's lesions: irregular painless
erythematous macules on the thenar and
hypothenar eminence (usually with acute IE and
S. aureus).
• Infective endocarditis is suspected :
• in a patient who has known valvular
lesion(e.g rheumatic valvular disease)
• Presents with symptoms of infection (fever ,
genralized weakness …etc
• Symptoms of heart failure
• Presence of changing murmur.
• A protracted history of sweats, weight loss,
anorexia or malaise and an at-risk cardiac lesion.
• Any new unexplained embolic event (eg, cerebral
or limb ischaemia).
• Unexplained, persistently positive blood cultures.
• Intravascular catheter-related bloodstream
infection with persistently positive blood cultures
72 hours after catheter removal.
• Vascular or immunological phenomena: embolic
event, Roth's spots, splinter haemorrhages,
Janeway's lesions, Osler's nodes.
 investigations
• Nonspecific signs of infection - eg, elevated
CRP or ESR, leukocytosis, anaemia and
microscopic haematuria.
• CXR: as part of the initial assessment.
• ECG is useful to detect the 10% of patients
who will develop conduction defects.
 Blood cx
• Should be taken prior to starting treatment.
• Meticulous aseptic technique is required.
• three sets of blood cultures should be taken from
peripheral sites with at least six hours between
them prior to commencing antimicrobial therapy.
• In patients with suspected IE and severe sepsis or
septic shock at the time of presentation, two sets
of blood cultures should be taken at different
times within one hour prior to commencement of
empirical therapy.
• Bacteraemia is continuous in IE rather than
intermittent, so positive results from only one
set out of several blood cultures should be
regarded with caution.
• Once a microbiological diagnosis has been
made, routine repeat blood cultures are not
recommended
• Blood cultures should be repeated if a patient
is still febrile after seven days of treatment.
 Echocardiography
• must be performed as soon as possible (ideally
within 24 hours) in all patients with suspected IE.
• Transthoracic echocardiography (TTE) is the initial
investigation of choice.
• In cases with an initially negative
TTE/transoesophageal echocardiography (TOE)
examination, repeat TTE/TOE should be
performed 7-10 days later if the clinical suspicion
of IE remains high.
• TEE will show vegetations.
 Modified duke’s criteria
major criteria
• Positive blood culture for IE: typical micro-organism
consistent with IE from two separate blood cultures.
• Evidence of endocardial involvement:
– Positive echocardiogram for IE:

• Oscillating intracardiac mass on valve or supporting structures, in

the path of regurgitant jets, or on implanted material in the
absence of an alternative anatomical explanation; or
• Abscess; or
• New partial dehiscence of prosthetic valve); or
• New valvular regurgitation (worsening or changing of pre-existing
murmur not sufficient).
 Modified duke’s criteria
minor criteria
• Predisposition: predisposing heart condition or intravenous
drug use.
• Fever: temperature >38°C.
• Vascular phenomena: major arterial emboli, septic
pulmonary infarcts, mycotic aneurysm, intracranial
haemorrhage, conjunctival haemorrhages and Janeway's
lesions.
• Immunological phenomena: glomerulonephritis, Osler's
nodes, Roth's spots and rheumatoid factor.
• Microbiological phenomena: positive blood culture but
does not meet a major criterion as noted above or
serological evidence of active infection with organism
consistent with IE.
• PCR: broad-range PCR of 16S (polymerase
chain reaction using broad-range primers
targeting the bacterial DNA that codes for the
16S ribosomal subunit).
• Echocardiographic findings consistent with IE
but do not meet a major criterion as noted
above.
• Definitive diagnosis requires:
• 2 major criteria
• 1 major and 3 minor
• 5 minor
 complications
• Myocardial infarction, pericarditis, cardiac
arrhythmias.
• Heart valve insufficiency.
• Congestive heart failure.
• Aortic root or myocardial abscesses.
• Arterial emboli, infarctions, mycotic
aneurysms.
• Arthritis, myositis.
• Glomerulonephritis, acute kidney injury.
• Stroke syndromes.
• Mesenteric or splenic abscess or infarction.
 Prognosis
• 30% mortality rate
• the prognosis varies markedly according to a
variety of factors.
• Predictors of poor outcone include:
• Patient characteristics: older age, prosthetic valve
IE, diabetes
• Clinical complications of IE: heart failure, renal
failure, greater than moderate area of ischaemic
stroke, brain haemorrhage, septic shock.
• Micro-organism: S. aureus, fungi, non-HACEK
Gram-negative bacilli.
• Echocardiogram findings: peri-annular
complications, severe left-sided valve
regurgitation, low left ventricular ejection
fraction, pulmonary hypertension, large
vegetations, severe prosthetic valve
dysfunction, premature mitral valve closure
and other signs of elevated diastolic pressures.
• Have a high index of suspesion.
• Use IV antibiotics
• Tretment duration 4-6 weeks.
 Initial empirical therapy while
awaiting culture results
• Native valve endocarditis (NVE) - indolent
presentation: amoxicillin AND (optional) gentamicin.
• NVE, severe sepsis (no risk factors for
Enterobacteriaceae, Pseudomonas spp.): vancomycin
AND gentamicin.
• NVE, severe sepsis AND risk factors for multiresistant
Enterobacteriaceae, Pseudomonas spp: vancomycin
AND meropenem.
• Prosthetic valve endocarditis (PVE): pending blood
cultures or with negative blood cultures: vancomycin
AND gentamicin AND rifampicin.
 Indications for surgery
• Heart failure
Aortic or mitral IE with:
• Severe acute regurgitation or valve obstruction causing
refractory pulmonary oedema/shock (emergency).
• Fistula into a cardiac chamber or pericardium causing
refractory pulmonary oedema/shock (emergency).
• Severe acute regurgitation or valve obstruction and
persisting heart failure or echocardiographic signs of
poor haemodynamic tolerance (urgent).
• Severe regurgitation and no heart failure (elective).
• Uncontrolled infection
• Locally uncontrolled infection including
abscess, false aneurysm, enlarging vegetation
(urgent).
• Persisting fever and positive blood culture for
at least ten days after commencing
appropriate antimicrobial therapy (urgent).
• Infection caused by fungi or multiresistant
micro-organisms (urgent/elective).
• Prevention of embolism
• Aortic or mitral IE with large vegetations (>10
mm) resulting in one or more embolic episodes
despite appropriate antibiotic therapy (urgent).
• Aortic or mitral IE with large vegetations (>10
mm) and other predictors of complicated course
like heart failure, persistent infection or abscess
(urgent).
• Isolated very large vegetations >15 mm (urgent).
Thank you