Inflamatory Heart Disease
Inflamatory Heart Disease
Inflamatory Heart Disease
• 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.