Download Hypertrophic Cardiomyopathy

Universitatea Titu Maiorescu
Heart Wall
♥ Pericardum (outside) – visceral layer
of the serous pericardium.
♥ Myocardium (muscle) – cardiac
muscle layer forming the bulk of the
heart.
♥ Endocardium (within) – endothelial
layer of the inner myocardial surface.

The Heart Wall and Cardiac Muscle Tissue
The Anatomy of the Heart
Figure 12-4(a)
Pericardium
HEART
♥Membrane sac
♥Surrounds the heart
♥Protection
♥Anchors
♥Contains serous fluid
Pericarditis
inflammation of the pericardium
decreases serous fluid causing
painful adhesions interfering with
heart movements
Pericardium
Heart Anatomy
Chapter 18, Cardiovascular System
5
Figure 18.1
PERICARDIUM
CONFINES HEART TO THE
MEDIASTINUM
 ALLOWS SUFFICIENT
FREEDOM OF MOVEMENT.
 CONSISTS OF TWO
PARTS:THE FIBROUS AND
SEROUS.


EPICARDIUM: COMPOSED OF
MESOTHELIUM AND DELICATE
CONNECTIVE TISSUE (IMPARTS A
SLIPPERY TEXTURE TO THE OUTER
SURFACE OF THE HEART).

FIBROUS:THIN INELASTIC, DENSE
IRREGULAR CONNECTIVE TISSUE
---HELPS IN PROTECTION, ANCHORS HEART
TO MEDIASTINUM

SEROUS: THINNER, MORE DELICATE
DIVIDED INTO PARIETAL AND VISCERAL
Cardiac Muscle
♥Specialized muscle cells
♥Involuntary
♥Striated
♥Cushioned by endomysium
♥Joined by intercalated discs
♥Cardiac cell metabolism
♥Aeobic
♥Large mitochondria
♥Organic fuels: fatty acids & glucose
♥Fatigue resistance
CARDOIMIOPATHY
Definition
“A primary disorder of the heart
muscle that causes abnormal
myocardial performance and is not the
result of disease or dysfunction of
other cardiac structures … myocardial
infarction, systemic hypertension,
valvular stenosis or regurgitation”
12/98
medslides.com
11
Cardiomyopathies
Definition: diseases of heart muscle
 1980 WHO: unknown causes
– Not clinically relevant

1995 WHO: “diseases of the
myocardium associated with cardiac
dysfunction “
– pathophysiology
– each with multiple etiologies
Cardiomyopathies




Disorders of the heart muscle
Most cases idiopathic
Many due to ischemic heart disease and
hypertension.
Three categories:
– Dilated ( formerly, congestive)
– Hypertrophic
– Restrictive

Heart loses effectiveness as a pump
13
Cardiomyopathy
WHO Classification
anatomy & physiology of the LV
1.
2.
3.
4.
5.
Dilated
• Enlarged
• Systolic dysfunction
Hypertrophic
• Thickened
• Diastolic dysfunction
Restrictive
• Diastolic dysfunction
Arrhythmogenic RV dysplasia
• Fibrofatty replacement
Unclassified
• Fibroelastosis
• LV noncompaction
Circ 93:841, 1996
WHO Classification

Unknown cause
(primary)
–
–
–
–
12/98
Dilated
Hypertrophic
Restrictive
unclassified

Specific heart
muscle disease
(secondary)
–
–
–
–
–
–
Infective
Metabolic
Systemic disease
Heredofamilial
Sensitivity
Toxic
medslides.com
Br Heart J 1980;
44:672-673
15
Functional Classification

Dilatated (congestive, DCM, IDC)
– ventricular enlargement and syst
dysfunction

Hypertrophic (IHSS, HCM, HOCM)
– inappropriate myocardial hypertrophy
in the absence of HTN or aortic stenosis

Restrictive (infiltrative)
– abnormal filling and diastolic function
12/98
medslides.com
16
CM: Specific Etiologies








Ischemic
Valvular
Hypertensive
Inflammatory
Metabolic
Inherited
Toxic reactions
Peripartum
Ischemic: thinned, scarred tissue
Dilated cardiomyopathy
↓ C.O.; ↑ thrombi formation ; ↓ contractility, and
mitral valve incompetence, arrhythmias Tx:
relieve symptoms of heart failure, decrease
workload, and anticoagulants; transplants
18
Hypertrophic
Cardiomyopathy
C.O. is normal,↑ inflow resistance, and
mitral valve incompetence, arrhythmais
and sudden death.
19
Restrictive cardiomyopathy
Reduced diastolic compliance of the ventricle.
C.O. is normal or↓; ↑ formation of thrombi,
dilation of left atrium, and mitral valve
incompetence.
20
IDIOPATHIC DILATED CARDIOMYOPATHY
NEW INSIGHTS INTO
PATHOGENESIS AND TREATMENT
Dilated Cardiomyopathy
•Dilation and impaired contraction of ventricles:
•Reduced systolic function with or without heart failure
•Characterized by myocyte damage
•Multiple etiologies with similar resultant pathophysiology
•Majority of cases are idiopathic
•incidence of idiopathic dilated CM 5-8/100,000
•incidence likely higher due to mild, asymptomatic cases
•3X more prevalent among males and African-Americans
DCM: Etiology
Ischemic
Valvular
Hypertensive
Familial
Idiopathic
Inflammatory
Infectious
Viral – picornovirus, Cox B, CMV, HIV
Ricketsial - Lyme Disease
Parasitic - Chagas’ Disease, Toxoplasmosis
Non-infectious
Collagen Vascular Disease (SLE, RA)
Peripartum
Toxic
Alcohol, Anthracyclins (adriamycin), Cocaine
Metabolic
Endocrine –thyroid dz, pheochromocytoma, DM, acromegaly,
Nutritional
Thiamine, selenium, carnitine
Neuromuscular (Duchene’s Muscular Dystrophy--x-linked)
DCM: Infectious
Acute viral myocarditis
 Coxasackie B or echovirus
 Self-limited infection in young people
 Mechanism?:
– Myocyte cell death and fibrosis
– Immune mediated injury
– BUT:

No change with immunosuppressive drugs
DCM: toxic
Alcoholic cardiomyopathy
 Chronic use
 Reversible with abstinence
 Mechanism?:
– Myocyte cell death and fibrosis
– Directly inhibits:
mitochondrial oxidative phosphorylation
 Fatty acid oxidation

DCM: inherited
Familial cardiomyopathy
 30% of ‘idiopathic’
 Inheritance patterns
– Autosommal dom/rec, x-linked, mitochondrial

Associated phenotypes:
– Skeletal muscle abn, neurologic, auditory

Mechanism:
– Abnormalities in:


Energy production
Contractile force generation
– Specific genes coding for:

Myosin, actin, dystophin…
DCM: Peripartum
Diagnostic Criteria
 1 mo pre, 5 mos post
 Echo: LV dysfunction
– LVEF < 45%
– LVEDD > 2.7 cm/m2


Epidemiology/Etiology
1:4000 women
– JAMA 2000;283:1183

Proposed mechanisms:
– Inflammatory Cytokines:

TNFa, IL6, Fas/AP01
– JACC 2000 35(3):701.
PPCM: Prognosis

Death from CM: ’91-97
– 245 CM deaths in US, 0.88/100,000 live births,
70% peripartum
– Increased risk with:


Maternal age
AA 6.4x greater
– Whitehead SJ. ObGyn2003;102:1326.

Risk of recurrent pregnancy
– Retrospective survey : 44 women (16 vs 28)

Reduced EF, CHF 44% vs 21%, mortality 0 vs. 19%
– Elkyam U. NEJM.2001;344:1567.
– DSE:contractile reserve reduced in patients

7 women: change in Vcfc σES relationship
– Lampert MB. AJOG.1997.176.189.
Dilated Cardiomyopathy
MECHANISMS IN HEART FAILURE
Neurohormones
Ischemic injury
Cytokines
Myocardial disease
Oxidative stress
Genetics
Altered molecular expression
Ultrastructural changes
Myocyte hypertrophy
Myocyte contractile
dysfunction
Apoptosis
Fibroblast proliferation
Collagen deposition
Ventricular remodeling
Hemodynamic Derangement
Clinical Heart Failure
Arrhythmia
Pathophysiology
•Initial Compensation for impaired myocyte contractility:
•Frank-Starling mechanism
•Neurohumoral activation
• intravascular volume
•Eventual decompensation
•ventricular remodeling
•myocyte death/apoptosis
•valvular regurgitation
Clinical Findings
Biventricular Congestive Heart Failure
-Low forward Cardiac Output
-fatigue, lightheadedness, hypotension
-Pulmonary Congestion
-Dyspnea,
-orthopnea, & PND
-Systemic Congestion
-Edema
-Ascites
-Weight gain
Physical Exam
Decreased C.O.
Tachycardia
 BP and pulse pressure
cool extremities (vasoconstriction)
Pulsus Alternans (end-stage)
Pulmonary venous congestion:
rales
pleural effusions
Cardiac:
laterally displaced PMI
S3 (acutely)
mitral regurgitation murmur
Systemic congestion
 JVD
hepatosplenomegaly
ascites
peripheral edema
Diagnostic Studies
CXR -enlarged cardiac silhouette,
vascular redistribution interstitial edema,
pleural effusions
EKG –normal
tachycardia, atrial and ventricular
enlargement, LBBB, RBBB, Q-waves
Blood Tests
(ANA,RF, Fe2+, TFT’s,ferritin,)
Echocardiography
LV size, wall thickness function
valve dz, pressures
Cardiac Catheterization
hemodynamics
LVEF
angiography
Endomyocardial Biopsy
Echo in dilated CM
Criteria for NYHA Functional Classification
Class 1: No limitation of physical activity.
Ordinary physical activity w/o fatigue, palpitation, or dyspnea.
Class 2: Slight limitation of physical activity. Comfortable at rest, but
symptoms w/ ordinary physical activity
Class 3: Marked limitation of physical activity. Comfortable at rest, but less
than ordinary activity causes fatigue, palpitation, or dyspnea.
Class 4: Unable to carry out any physical activity without discomfort.
Symptoms include cardiac insufficiency at rest. If any physical
activity is undertaken, discomfort is increased.
J Cardiac Failure 1999;5:357-382
Aim of Treatment
•
Preload reduction
• Diuretics
• venodilators
•
Vasodilators
• ACEI
Inotropes
• Acutely
• Chronically
• mortality
•
Vasodilator Agents in Heart Failure
Drug
Mechanism
Action
Nitroglycerin Direct via nitric
and longoxide
acting nitrates*
Nitroprusside Direct via nitric
oxide
Hydralazine* Direct
Veno /
arterioloar
ACE
inhibitors#
Veno /
arterioloar
Reduced A-II
Incr. bradykinin
Use
Hemodynamic;
anti-ischemic;
long term
Arteriolar > Hemodynamic
venodilation
Arteriolar
?long term*
Long-term
*Hydralazine and a long-nitrate shown to reduce mortality long-term
# Other actions (aside from vasodilation) likely to be important
Dobutamine and Milrinone Effects
Electrical and Mechanical
Ventricular Dyssynchrony

Experimentally induced LBBB has effect on:
– expression of regional stress kinases
– calcium-handling proteins.


Expression of p38-MAPK (a stress kinase) is
elevated in the endocardium of the lateactivated region, whereas phospholamban is
decreased.
Sarcoplasmatic reticulum Ca2+-ATPase is
decreased in the region of early activation.
Deleterious Hemodynamic
Effects of LV Dyssynchrony

.
Diminished SV & CO due:
Atrioventricular

Intra-V

Inter-V


Cazeau, et al. PACE 2003; 26[Pt. II]: 137–143
Reduced diastolic filling
time1
Weakened contractility
2
Protracted MV
regurgitation 2
Post systolic regional
contraction 3
1. Grines CL, Circulation 1989;79: 845-853
2. Xiao HB, Br Heart J 1991;66: 443-447
3. Søgaard P, JACC 2002;40:723–730
CRT: Cardiac
Resynchronization Therapy
1. Improved hemodynamics
– Increased CO
– Reduced LV filling
pressures
– Reduced sympathetic
activity
– Increased systolic function
w/o MVO2
2. Reverse LV
remodeling/architecture
– Decreased LVES/ED
volumes
– Increased LVEF
– Circ ’02, JACC ’02, JACC
’02, NEJM’02
Hypertrophic Cardiomyopathy
Hypertrophic
Cardiomyopathy
Hypertrophic CM
 Most
common cause of death in young people.
 The
magnitude of left ventricular hypertrophy is
directly correlated to the risk of SCD.
 Young
pts with extreme hypertrophy and few or no
symptoms are at substantial long-term risk of SCD.
.
Spirito P. N Engl J Med. 1997;336:775-785.
Maron BJ. N Engl J Med. 2000;342:365-373.
Hypertrophic
Cardiomyopathy
Diastolic Dysfunction

40-50% of pts w/
CHF have nml LVEF
– Vasan JACC ’99
– Grossman Circ ‘00

Prevalence:
– increases with age
– higher in women


Etiology: HTN & LVH
Diagnosis:
– MV& PV Doppler
– TDI, Color m-mode
Echo Doppler Parameters
Zile MR. Circ;105:1387
Hypertrophic Cardiomyopathy
Left ventricular hypertrophy not due to pressure overload
Hypertrpohy is variable in both severity and location:
-asymmetric septal hypertrophy
-symmetric (non-obstructive)
-apical hypertrophy
Vigorous systolic function, but impaired diastolic function
impaired relaxation of ventricles
elevated diastolic pressures
prevalence as high as 1/500 in general population
mortality in selected populations 4-6% (institutional)
probably more favorable (1%)
Etiology
Familial in ~ 55% of cases with autosomal dominant transmission
Mutations in one of 4 genes encoding proteins of cardiac sarcomere
account for majority of familial cases
-MHC
cardiac troponin T
myosin binding protein C
-tropomyosin
Remainder are
spontaneous
mutations.
Hypertrophic Cardiomyopathy
Hypertrophic Cardiomyopathy
Hypertrophic
cardiomyopathy
Apical Hypertrophic
Cardiomopathy
Pathophysiology
HCM with outflow obstruction
Dynamic LVOT obstruction (may not be present at rest)
SAM (systolic anterior motion of mitral valve)
LVOT Obstruction  LVOT gradient
 wall stress  MVO2  ischemia/angina
 LVOT gradient:  HR (DFP), preload (LVEDV),
 afterload(BP).
 LVOT gradient:  BP (Afterload),  LVEDV(preload)
Symptoms of dyspnea and angina more related to diastolic
dysfunction than to outflow tract obstruction
Syncope: LVOT obstruction (failure to increase CO during exercise
or after vasodilatory stress) or arrhythmia.
Physical Exam
Bisferiens pulse (“spike and dome”)
S4 gallop
Crescendo/Descrescendo systolic ejection murmur
HOCM vs. Valvular AS
Valsalva (preload,  afterload)
Squatting ( preload,  afterload)
Standing (preload,  afterload)
Intensity of murmur
HOCM
AS






Holosystolic apical blowing murmur of mitral regurgitation
Diagnostic Studies

EKG
– NSR
– LVH
– septal Q waves

2D-Echocardiography
– LVH; septum >1.4x free wall
– LVOT gradient by Doppler
– Systolic anterior motion of
the mitral valeregurgitation

Cardiac Catheterization
– LVOT gradient and pullback
– provocative maneuvers
– Brockenbrough phen
HCM-ASH using contrast
Treatment
For symptomatic benefit
-blockers
 mvO2
 gradient (exercise)
arrythmias
Calcium Channel blockers
Anti-arrhythmics
afib
amiodorone
Disopyramide
AICD for sudden death
antibiotic prophylaxis for endocarditis
No therapy has been shown to improve mortality
HCM: Surgical Treatment
For severe symptoms with large outflow gradient (>50mmHg)
Does not prevent Sudden Cardiac Death
Myomyectomy
removal of small portion of upper IV septum
+/- mitral valve replacement
5 year symptomatic benefit in ~ 70% of patients
Dual Camber (DDD pacemaker) pacing
decreases LVOT gradient (by~25%)
randomized trials have shown little longterm benefit
possible favorable morphologic changes
ETOH septal ablation
AICD to prevent sudden death
Prognosis
Sudden Death
2-4%/year in adults
4-6% in children/adolescents
AICD for:
survivors of SCD with Vfib
episodes of Sustained VT
pts with family hx of SCD in young family members
High risk mutation (TnT, Arg403Gln)
Predictors of adverse prognosis:
early age of diagnosis
familial form with SCD in 1st degree relative
history of syncope
ischemia
presence of ventricular arrhythmias on Holter (EPS)
EPS
Amiodorone (low dose)
Prophylactic AICD?
HCM vs Athletes Heart

Endurance training:
– Physiologic increase in LV mass


Wall thickness and cavity size
Early HCM vs Athlete’s heart
– DEFINITION: Symmetric, <13mm
– 947 elite athletes: 16 thickness=13-16mm

15 rowers, EDD=55-63 c/w 728 athletes/22 other

NEJM1991;324:295
– 286 cyclists: 25 thickness 13-15

50% increased EDD w/ 12% reduced LVEF

JACC 2004;44:144.
Restrictive Cardiomyopathy

..
Restrictive Cardiomyopathy
Characterized by:
• impaired ventricular filling due to an abnormally stiff (rigid) ventricle
•normal systolic function (early on in disease)
•intraventricular pressure rises precipitously with small increases in volume
restriction
Pressure
normal
Volume
Causes : infiltration of myocardium by abnormal substance
fibrosis or scarring of endocardium
Amyloid infiltrative CM
Amyloidosis
Primary Amyloidosis
immunoglobulin light chains -- multiple myeloma
Secondary Amyloidosis
deposition of protein other than immunoglobulin
senile
familial
chronic inflammatory process
restriction caused by replacement of normal myocardial contractile
elements by infiltrative interstitial deposits
Amyloidosis
Amyloid Cardiomyopathy
Sarcoidosis
.
Sarcoidosis


Multisystem disorder of unknown
etiology that most commonly affects
the lungs, but can also affect other
organs.
Beethoven is thought to have been the
first person described with this
condition.
Erythema Nodosum
Lupus Pernio
Systems affected by Sarcoidosis
Signs and symptoms
Neurologic Cranial nerve palsy, seizures, basal granulomatous
meningitis, hypothalamic or pituitary lesions,
5%
hydrocephalus, peripheral neuropathy, psychiatric
Ocular
Uveitis, chorioretinitis, keratoconjunctivitis,
glaucoma, cataracts, blindness, Heerfordt
20%
syndrome
Pulmonary Asymptomatic or dyspnea, nonproductive cough,
wheezing, radiographic findings from hilar
90%
adenopathy to fibrosis
Renal
Hypercalcemia, hypercalciuria, renal insufficiency
Clinical Presentation




Most patients have the pulmonary
manifestations, most commonly
presenting with incidental findings on
CXR.
Interstitial disease
Symptoms include dry cough,
dyspnea, and chest discomfort
Unpredictable course
4 Stages of Pulmonary
Sarcoidosis
I
Bilateral hilar lymphadenopathy
and paratracheal adenopathy
55-90%
remission
II
Mediastinal adenopathy with
pulmonary parenchymal
involvements
Pulmonary parenchymal without
adenopathy
40-70%
III
IV
Pulmonary fibrosis with
honeycombing
10-20%
0-5%
Stages
Treatment




Observation
Initiating corticosteroid therapy when
appropriate
Monitoring response to therapy
Discontinuing corticosteroids when
clinically or physiologically indicated.
Endomyocardial Fibrosis
Endemic in parts of Africa, India, South and Central America, Asia
15-25% of cardiac deaths in equatorial Africa
hypereosinophilic syndrome (Loffler’s endocarditis)
Thickening of basal inferior wall
endocardial deposition of thrombus
apical obliteration
mitral regurgitation
80-90% die within 1-2 years
Clinical Findings
Right > Left heart failure
Dyspnea
Orthopnea/PND
Peripheral edema
Ascites/Hepatomegaly
Fatigue/ exercise tolerance
Clinically mimics constrictive Pericarditis
Diagnostic Studies
2D-Echo/Dopplermitral in-flow velocity
rapid early diastolic filling
Catheterization –
diastolic pressure equilibration
restrictive vs constrictive
hemodynamics
Endomyocardial biopsydefinite Dx of restrictive pathology
Treatment
Treat underlying cause
r/o constriction which is treatable (restriction poor prognosis)
amyloid (melphalan/prednisone/colchicine)
Endomyocardial Fibrosis (steroids, cytotoxic drugs, MVR)
Hemochromatosis (chelation, phlebotomy)
Sarcoidosis (steroids)
Diuretics
For congestive symptoms, but  LV/RV filling   CO
Digoxin (avoid in amyloidosis)
Antiarrhythmics for afib
amiodorone
Pacemaker for conduction system disease
Anticoagulation for thrombus (esp in atrial appendages)
Arrhythmogenic RV
Dysplasia

..
Arrhythmogenic RV Dysplasia

Myocardium of RV free wall replaced:
– Fibrofatty tissue
– Regional wall motion/function is reduced

Ventricular arrhythmias
– SCD in young
MRI: RV Dysplasia
LV Noncompaction
Diagnostic Criteria
 Prominent trabeculations, deep recesses in LV
apex
 Thin compact epicardium, thickened endocardium

Stollberger C, JASE ‘04
Other phenotypic findings
Prognosis and Treatment
 Increased risk of CHF, VT/SCD, thrombosis



Oechslin EN, JACC ‘00
Hereditary risk
– Screening of offspring

Pregnancy: case report
Echo: LV Noncompaction
Myocarditis
,
CAUSATION


A large variety of infections, systemic
diseases, drugs, and toxins have been
associated with the development of
this disease
Viruses, bacteria, protozoa, and even
worms have been implicated as
infectious agents.
Pathophysiology

Several mechanisms of myocardial damage
(1) Direct injury of myocytes by the
infectious agent
(2) Myocyte injury caused by a toxin such
as that
from Corynebacterium diphtheriae
(3) Myocyte injury as a result of infectioninduced immune reaction or
autoimmunity.
Pathophysiology

Triphasic disease process
Phase I: Viral Infection and
Replication
Phase 2: Autoimmunity and injury
Phase 3: Dilated Cardiomyopathy
Phase I: Viral Infection and
Replication


Coxsackievirus B3 causes an infectious
phase, which lasts 7-10 days, and is
characterized by active viral replication
During this phase initial myocyte injury
takes place, causing the release of
antigenic intracellular components
such as myosin into the bloodstream
Phase 2: Autoimmunity and
injury


The local release of cytokines, such as
interleukin-1, interleukin-2, interleukin-6,
tumor necrosis factor (TNF), and nitric oxide
may play a role in determining the T-cell
reaction and the subsequent degree of
autoimmune perpetuation
These cytokines may also cause reversible
depression of myocardial contractility
without causing cell death.
Phase 2: Autoimmunity and
injury



Immune-mediated by CD8
lymphocytes and autoantibodies
against various myocyte components
Antigenic mimicry, the cross reactivity
of antibodies to both virus and
myocardial proteins
Myocyte injury may be a direct result
of CD8 lymphocyte infiltration
Phase 3: Dilated
Cardiomyopathy




Viruses may also directly cause myocyte apoptosis.
During the autoimmune phase, cytokine activate
the matrix metalloproteinases, such as gelatinase,
collagenases, and elastases.
In later stages of immune activation, cytokines play
a leading role in adverse remodeling and
progressive heart failure.
Cardiomyopathy developed despite the absence of
viral
proliferation but was correlated with elevated
levels of
cytokines such as TNF.
Clinical Findings

Symptoms and Signs
- Patients(59%) frequently present days to weeks
after an acute febrile illness, particularly a flu-like
syndrome
- Myocarditis is most commonly asymptomatic, with
no evidence of left ventricular dysfunction
- fever, malaise, fatigue, arthralgias, myalgias, and
skin rash.
-Cardiac symptoms may result from systolic or
diastolic left ventricular dysfunction or from
tachyarrhythmias or bradyarrhythmias (dyspnea,
fatigue, decreased exercise tolerance, palpitations )
Clinical Findings

Symptoms and Signs
- Chest discomfort(35%) is a common
symptom
and is typically pericardial in nature
- Myocarditis may present as sudden death,
as a
result of malignant ventricular arrhythmias
or
complete heart block
-Systemic and pulmonary thromboemboli
have also been noted.
Clinical Findings

Physical Examination
-Tachycardia, hypotension, fever and tachycardia
may be disproportionate to the degree of fever
-Bradycardia is seen rarely, and a narrow pulse
pressure is occasionally detected
-Murmurs of mitral or tricuspid regurgitation are
common , S3 and S4 gallops may also be heard.
-Distended neck veins, pulmonary rales, wheezes,
gallops, and peripheral edema may be detected
Diagnostic Studies

Electrocardiography
-The most common abnormality is
sinus tachycardia.
- may show ventricular arrhythmias or
heart block, or it may mimic the
findings in acute myocardial infarction
or pericarditis.
-Relations between these clinical and
laboratory findings
Diagnostic Studies

Chest radiograph
-Mild to moderate cardiomegaly from
dilatation of the left or right ventricular
cavity
-The cardiac silhouette may also be globular
when a pericardial effusion is present
- Venous congestion and pulmonary edema
may be seen in more severe cases
Diagnostic Studies

Echocardiography
-myocardial contractility , chamber sizes ,
valvular function
-Left ventricular systolic dysfunction,
regional wall motion abnormalities , global
hypokinesis
- LV may be normal in size or minimally
enlarged
-Mitral or tricuspid regurgitation
-Mural thrombi in 15% of cases
Diagnostic Studies

-helpful in demonstrating abnormalities of
diastolic filling that mimic restrictive
cardiomyopathy and indistinguishing
ventricular dilatation from pericardial
effusion
-monitor the course of the illness and to
evaluate therapy
Radionuclide ventriculography
-provides accurate estimates of chamber
volumes, as well as left and right ventricular
ejection fractions
Diagnostic Studies

Myocardial imaging
-Gallium-67 imaging
-> active inflammation of the myocardium
and pericardium
-Indium-111 monoclonal antimyosin
antibody imaging
-> detecting myocyte injury in patients
-Contrast media-enhanced MRI
->detecting myocardial inflammation
Diagnostic Studies

Cardiac catheterization
-elevated left ventricular end-diastolic
pressure, a depressed cardiac output,
and increased ventricular volumes
-Coronary angiogram typically
demonstrates normal coronary
arteries.
Diagnostic Studies

Endomyocardial biopsy
- gold standard for the diagnosis of
myocarditis
-Dallas criteria
(an inflammatory infiltrate of the
myocardium +injury to the adjacent
myocytes)
-borderline myocarditis is made when the
infiltrate is not accompanied by myocyte
injury
Normal Myocardium
Borderline Myocarditis
Active Myocarditis
Others test



elevated erythrocyte sedimentation
rate (ESR) , mild to moderate
leukocytosis
CPK-MB , Cardiac troponin-I
Other laboratory analyses that may
be useful include a Mono-spot test,
Epstein-Barr virus titers, hepatitis
serology, and urine and serum for
cytomegalovirus (CMV).
Triphasic disease process.
Endocarditis
.
Contents of Lecture



Endocarditis
– Definitions
– Epidemiology
– Pathogenesis
– Clinical Presentations
– Diagnosis
– Complications/Mortality
Septic thrombophlebitis
Mycotic aneurysm
Endocarditis: Definition



Infective Endocarditis: a microbial
infection of the endocardial surface of
the heart
Common site: heart valve, but may
occur at septal defect, on chordae
tendinae or in the mural endocardium
Classification:
– acute or subacute-chronic on temporal
basis, severity of presentation and
progression
– By organism
– Native valve or prosthetic valve
ENDOCARDITIS
Characteristic pathological lesion: vegetation,
composed of platelets, fibrin, microorganisms
and inflammatory cells.
Pathogenesis



Altered valve surface
– Animal experiments suggest that IE is almost
impossible to establish unless the valve surface is
damaged
Deposition of platelets and fibrin – nonbacterial
thrombotic vegetation (NBTE)
Bacteraemia – attaches to platelet-fibrin deposits
– Covered by more fibrin
– Protected from neutrophils
– Division of bacteria
– Mature vegetation
Pathogenesis

Haemodynamic Factors
– Bacterial colonisation more likely to occur
around lesions with high degrees of
tubulence

eg. small VSD, valvular stenosis
– Large surface areas, low flow and low
turbulence are less likely to cause IE

eg large VSD,
Pathogenesis

Bacteraemia
– Transient bacteraemia occurs when a heavily
colonised mucosal surface is traumatised







Dental extraction
Periodontal surgery
Tooth brushing
Tonsillectomy
Operations involving the respiratory, GI or GU tract
mucosa
Oesophageal dilatation
Biliary tract surgery
Site of Infection


Aortic valve more common than mitral
Aortic:
– Vegetation usually on ventricular aspect,
all 3 cusps usually affected
– Perforation or dysfunction of valve
– Root abscess

Mitral:
– Dysfunction by rupture of chordae
tendinae
EPIDEMIOLOGY




Changing over the
past decade due
to:
Increased
longevity
New predisposing
factors
Nosocomial
infections



In U.S and Western
Europe incidence of
community –acquired
endocarditis is 1.7-6.2
cases per 100,000
person-years.
M:F ratio 1.7:1
Mean age now 47-69
(30-40 previously)
EPIDEMIOLOGY


Incidence in IVDA group is estimated
at 2000 per 100,000 person-years,
even higher if there is known valvular
heart disease
Increased longevitiy leads to more
degenerative valvular disease,
placement of prosthetic valves and
increased exposure to nosocomial
bacteremia
PROSTHETIC VALVES




7-25% of cases of infective endocarditis
The rates of infection are the same at 5 years
for both mechanical and bioprostheses, but
higher for mechanical in first 3 months
Culmulative risk: 3.1% at 12 months and 5.7%
at 60 months post surgery
Onset:
– within 2 months of surgery early and usually
hospital acquired
– 12 months post surgery late onset and
usually community acquired
Nosocomial Infective
Endocarditis



7-29% of alll cases seen in tertiary referral
hospitals
At least half linked to intravascular devices
Other sources GU and GIT procedures or
surgical-wound infection
Aetiological Agents
1.
Streptococci
–
Viridans streptococci/α-haemolytic streptococci
S. mitis, S. sanguis, S. oralis
S. bovis

–

2.
Associated with colonic carcinoma
Enterococci



E. faecalis, E. faecium
Associated with GU/GI tract procedures
Approx. 10% of patients with enterococcal
bacteraemia develop endocarditis
Aetiological Agents
3. Staphylococci

Staphylococcci have surpassed
viridans streptococci as the most common
cause of infective endocarditis
– S. aureus


Native valves
acute endocarditis
– Coagulase-negative staphylococci

Prosthetic valve endocarditis
Aetiological Agents
4. Gram-negative rods
–
HACEK group


–
Uncommon
Pseudomonas aeruginosa

–
Fastidious oropharyngeal GNBs
E. coli, Klebsiella etc

–
Haemophilus aphrophilus, Actinobacillus
actinomycetemcomitans, Cardiobacterium hominis,
Eikenella corrodens, Kingella kingae.
IVDA
Neisseria gonorrhoae

Rare since introduction of penicillin
Aetiological Agents
5.
Others
– Fungi

–
–
–
–
Candida species, Aspergillus species
Q fever
Chlamydia
Bartonella
Legionella
Clinical Manifestations






Fever, most common symptom, sign
(but may be absent)
Anorexia, weight-loss, malaise, night
sweats
Heart murmur
Petechiae on the skin, conjunctivae,
oral mucosa
Splenomegaly
Right-sided endocarditis is not
associated with peripheral
emboli/phenomena but pulmonary
findings predominate
Oslers’ nodes
Tender, s/c
nodules
Janeway lesions
Nontender
erythematous,
haemorrhagic,
or pustular
lesions often
on palms or
soles.
Prosthetic valvePresentation



Often indolent illness with low grade
fever or acute toxic illness
Locally invasive : new murmurs and
congestive cardiac failure
If prosthetic valve in situ and
unexplained fever suspect endocarditis
Nosocomial Endocarditis




May present acutely without signs of
endocarditis
Suggested by: Bacteremia persisting
for days before treatment or for 72
hours or more after the removal of an
infected catheter and initiation of
treatment (esp in those with abnormal
or prosthetic valves)
Risk if prosthetic valve and
bacteremia: 11%
Risk if prosthetic valve and
candidaemia: 16%
Investigations
1.
2.
Blood culture
Echo
– TTE
– TOE
3.
4.
5.
FBC/ESR/CRP
Rheumatoid Factor
MSU
Duke Criteria
 Definite
: 2 major criteria
: 1 major and 3 minor criteria
: 5 minor criteria
: pathology/histology findings
 Possible : 1 major and 1 minor criteria
: 3 minor criteria
 Rejected : firm alternate diagnosis
: resolution of manifestations of IE with
4 days antimicrobial therapy or less
Echocardiography


Trans Thoracic Echocardiograpy (TTE)
– rapid, non-invasive – excellent specificity
(98%) but poor sensitivity
– obesity, chronic obstructive pulmonary
disease and chest wall deformities
Transesophageal Echo (TOE)
– more invasive, sensitivity up to 95%, useful
for prosthetic valves and to evaluate
myocardial invasion
– Negative predictive valve of 92%
– TOE more cost effective in those with S.
aureus catheter-associated bacteremia and
bacteremia/fever and recent IVDA
Culture Negative
Endocarditis





5-7% of patients with endocarditis will have
sterile blood cultures
1 Year study from France
– 44 of 88 cases of CNE, negative cultures
were associated with prior administration
of antibiotics
Fasidious or non-culturable organism
Non-infective endocarditis
Withhold empirical therapy until cultures
drawn
COMPLICATIONS OF
ENDOCARDITIS

Cardiac :
– congestive cardiac failure-valvular damage,
more common with aortic valve
endocarditis, infection beyond valve→ CCF,
higher mortality, need for surgery, A-V,
fascicular or bundle branch block,
pericarditis, tamponade or fistulae

Systemic emboli
– Risk depends on valve (mitral>aortic), size
of vegetation, (high risk if >10 mm)
– 20-40% of patients with endocarditis,
– risk decreases once appropriate
antimicrobial therapy started.


Prolonged Fever: usually fever associated
with endocarditis resolves in 2-3 days after
commencing appropriate antimicrobial
therapy with less virulent organisms and 90%
by the end ot the second week
Recurrent fever:
–
–
–
–
infection beyond the valve
focal metastatic disease
drug hypersentivity
nosocomial infection or others e.g. Pulmonary
embolus
Therapy

Antimicrobial therapy
– Use a bactericidal regimen
– Use a recommended regimen for the organism
isolated

E.g. American Heart Association JAMA 1995; 274:
1706-13., British Society for Antimicrobial
Chemotherapy
– Repeat blood cultures until blood is
demonstrated to be sterile

Surgery
– Get cardiothoracic teams involved early
Therapy

Streptococci/Enterococci
–
–
–
–

Determine MIC of Penicillin
Penicillin +/- aminoglycoside
Ceftriaxone alone
Vancomycin +/- aminoglycoside
HACEK group
– Cefotaxime/ceftriaxone
Therapy

Staphylococci
– Native valve
 Flucloxacillin +/- aminoglycoside
 Vancomycin +/- aminoglycoside/
rifampicin
– Prosthetic valve
 Flucloxacillin + aminoglycoside +
rifampicin
 Vancomycin + aminoglycoside +
rifampicin
Surgical Therapy

Indications:
– Congestive cardiac failure
– perivalvular invasive disease
– uncontrolled infection despite maximal
antimicrobial therapy

Pseudomonas aeruginosa, Brucella species,
Coxiella burnetti, Candida and fungi
– Presence of prosthetic valve endocarditis
unless late infection
– Large vegetation
– Major embolus
– Heart block
Surgical Therapy

The hemodynamic status at the
time determines principally
operative mortality
MORTALITY





Depends on ORGANISM
Presence of complications
Preexisting conditions
Development of perivalvular or
myocardial abscess
Use of combined antimicrobial and
surgical therapy
MORTALITY

Viridans Streptococci and S. bovis : 416%





Enterococci:15-25%
S. aureus: 25-47%
Q fever: 5-37% (17% in Ireland)
P. aeruginosa, fungi,
Enterobacteriaceae > 50%
Overall mortality 20-25% and for
right-sided endocarditis in IVDA is
10%
Prevention


Antimicrobial prophylaxis is given to at risk
patients when bacteraemia-inducing
procedures are performed
Look up and follow guidelines
– American Heart Association. Circulation 1997;
96: 358-366
– British Society for Antimicrobial Chemotherapy.
Journal of Antimicrobial Chemotherapy 1993;
31: 347-438
– BNF
Pericarditis
Pericardial Anatomy
Visceral – transparent
Parietal – translucent
Transverse sinus – curved probe
Pericardium
HEART
♥Membrane sac
♥Surrounds the heart
♥Protection
♥Anchors
♥Contains serous fluid
Pericarditis
inflammation of the pericardium
decreases serous fluid causing
painful adhesions interfering with
heart movements
Pericardium
Pericardium: Anatomy
Pericardial Layers:
• Visceral layer
• Parietal layer
• Fibrous pericardium
Function of the
Pericardium
1. Stabilization of the heart within the thoracic cavity by virtue of its ligamentous
attachments -- limiting the heart’s motion.
2. Protection of the heart from mechanical trauma and infection from adjoining
structures.
3. The pericardial fluid functions as a lubricant and decreases friction of cardiac
surface during systole and diastole.
4. Prevention of excessive dilation of heart especially during sudden rise in intracardiac volume (e.g. acute aortic or mitral regurgitation).
Etiologies
of
Pericarditis
I. INFECTIVE
1. VIRAL - Coxsackie A and B, Influenza, adenovirus, HIV, etc.
2. BACTERIAL - Staphylococcus, pneumococcus, tuberculosis, etc.
3. FUNGAL - Candida
4. PARASITIC - Amoeba, candida, etc.
II. AUTOIMMUNE DISORDERS
1. Systemic lupus erythematosus (SLE)
2. Drug-Induced lupus (e.g. Hydralazine, Procainamide)
3. Rheumatoid Arthritis
4. Post Cardiac Injury Syndromes i.e. postmyocardial Infarction
(Dressler's)
Syndrome, postcardiotomy syndrome, etc.
III. NEOPLASM
1. Primary mesothelioma
2. Secondary, metastatic
3. Direct extension from adjoining tumor
IV. RADIATION PERICARDITIS
V. RENAL FAILURE (uremia)
VI. TRAUMATIC CARDIAC INJURY
1. Penetrating - stab wound, bullet wound
2. Blunt non-penetrating - automobile steering wheel accident
VII. IDIOPATHIC
Pericardial Effusion
Normal 15-50 ml of fluid
ETIOLOGY
1. Inflammation from infection, immunologic process.
2. Trauma causing bleeding in pericardial space.
3. Noninfectious conditions such as:
a. increase in pulmonary hydrostatic pressure e.g. congestive
heart failure.
b. increase in capillary permeability e.g. hypothyroidism
c. decrease in plasma oncotic pressure e.g. cirrhosis.
4. Decreased drainage of pericardial fluid due to obstruction of thoracic duct as a
result of malignancy or damage during surgery.
• Effusion may be serous, serofibrinous, suppurative, chylous, or hemorrhagic
depending on the etiology.
• Viral effusions are usually serous or serofibrinous
• Malignant effusions are usually hemorrhagic.
Pathophysiology
Pericardium relatively stiff
Symptoms of cardiac compression dependant on:
1. Volume of fluid
2. Rate of fluid accumulation
3. Compliance characteristics of the pericardium
A. Sudden increase of small
amount of fluid (e.g.
trauma)
B. Slow accumulation of
large amount of fluid (e.g.
CHF)
Pathogenesis
1) Vasodilation:
 transudation of fluid
2) Increased vascular permeability
 leakage of protein
3) Leukocyte exudation
neutrophils and mononuclear cells
Pathology
depends on underlying cause and severity of inflammation
serous pericarditis
serofibrinous pericarditis
suppurative (purulent) pericarditis
hemorrhagic pericarditis
Clinical Features of Acute
Pericarditis
Idiopathic/viral
* Pleuritic Chest pain
* Fever
* Pericardial Friction Rub
3 component:
a) atrial or pre-systolic component
b) ventricular systolic component (loudest)
c) ventricular diastolic component
* EKG: diffuse ST elevation
PR segment depression
Clinical features
Small effusions do not produce hemodynamic abnormalities.
Large effusions, in addition to causing hemodynamic compromise, may lead
to compression of adjoining structures and produce symptoms of:
dysphagia (compression of esophagus)
hoarseness (recurrent laryngeal nerve compression)
hiccups (diaphragmatic stimulation)
dyspnea (pleural inflammation/effusion)
Physical Findings
Physical Findings:
 Muffled heart sounds
 Paradoxically reduced intensity of rub
 Ewart's sign:
Compression of lung leading to an area of
consolidation in the left infrascapular
region (atalectasis, detected as dullness
to percussion and bronchial breathing)
EKG findings in
Pericarditis
Diagnostic Tests
Echocardiogram: Pericardial effusion
N.B.: absence does not rule out pericarditis
N.B.: Pericarditis is a clinical diagnosis, not an Echo diagnosis!
Blood tests: PPD, RF, ANA
Viral titers
Search for malignancy
Pericardiocentesis:
low diagnostic yield
done therapeutically
Diagnostic studies
CXR: “water bottle” shaped heart
EKG:
 low voltage
 “electrical alternans”
Echocardiogram
Tamponade -- Diagnosis
EKG: low voltage, sinus tachycardia,
electrical alternans
Echocardiography
pericardial effusion
(r/o other etiologies in dif dx)
RA and RV diastolic collapse
Cardiac Tamponade
Fluid under high pressure compresses the cardiac chambers:
acute: trauma, LV rupture – may not be very large
gradual: large effusion, due to any etiology of acute pericarditis
Tamponade-- Clinical
Features
Symptoms:
Acute: (trauma, LV rupture)
profound hypotension
confusion/agitation
Slow/Progressive large effusion (weeks)
Fatigue (CO)
Dyspnea
JVD
Signs:
Tachycardia
Hypotension
rales/edema/ascites
muffled heart sounds
pulsus paradoxus
Jugular venous
pressure waves

Normal JVP contours
(1) A-wave
 1) results from ATRIAL contraction
 2) Timing - PRESYSTOLIC
 3) Peak of the a-wave near S1
(2) V-wave
1) results from PASSIVE filling of the right atrium while the
tricuspid valve is closed during ventricular systole (Remember
the V-wave is a "V"ILLING WAVE)
2) Large V-waves on the left side of the heart may be seen with
mitral regurgitation, atrial septal defect, ventricular septal defect.
The v-wave in the jugular venous pulse reflects right atrial events.
To see the v-wave on the left side of the heart Swan-Ganz
monitoring is needed
3) timing - peaks just after S2
(3) X-descent
1) results from ATRIAL RELAXATION
2) timing - occurs during ventricular systole, at the same time
as the carotid pulse occurs
(4) Y-descent
1) results from a FALL in right atrial pressure associated with
opening of the tricuspid valve
2) timing - occurs during ventricular diastole
(5) Generalizations
1) the A-wave in a normal individual is always larger than the Vwave
2) the X-descent is MORE PROMINENT than the Y-descent
Pulsus Paradoxus
Intrapericardial pressure (IPP) tracks intrathoracic
pressure.
Inspiration:
negative intrathoracic pressure is transmitted to the
pericardial space
 IPP
 blood return to the right ventricle
 jugular venous and right atrial pressures
 right ventricular volume  interventricular septum
shifts towards the left ventricle
 left ventricular volume
 LV stroke volume
  blood pressure (<10mmHg is normal) during
inspiration
Pulsus Paradoxus
Exaggeration of normal physiology
> 10 mm Hg drop in BP
with inspiration
CardiacTamponade -Pathophysiology
Accumulation of fluid under high pressure:
compresses cardiac chambers & impairs
diastolic filling of both ventricles
 SV
venous pressures
 CO
systemic
Hypotension/shock
Reflex tachycardia
JVD
hepatomegaly
ascites
peripheral edema
pulmonary congestion
rales
Treatment
Pain relief
analgesics and anti-inflammatory
ASA/NSAID’s
Steroids for recurring pericarditis
Antibiotics/drainage for purulent pericarditis
Dialysis for uremic pericarditis
Neoplastic: XRT, chemotherapy
Tamponade -- Treatment
Pericardiocentesis
Pericardial Window
Balloon Pericardiotomy
Pre-pericardiocentisis
Post-pericardiocentesis
Constrictive Pericarditis
Late complication of pericardial disease
Fibrous scar formation
Fusion of pericardial layers
Calcification further stiffens pericardium
Etiologies:
any cause of pericarditis
idiopathic
post-surgery
tuberculosis
radiation
neoplasm
Pathophysiology
Rigid, scarred pericardium encircles heart:
Systolic contraction normal
Inhibits diastolic filling of both ventricles
 SV
venous pressures
 CO
systemic
Hypotension/shock
Reflex tachycardia
JVD
hepatomegaly
ascites
peripheral edema
pulmonary congestion
rales
Physical exam
HR, BP
ascites, edema, hepatomegaly
early diastolic “knock”
after S2
sudden cessation of ventricular diastolic filling imposed
by rigid pericardial sac
Kussmaul’s sign
Kussmaul’s Sign
inspiration: intrathoracic pressure,  venous return to thorax
intrathoracic pressure not transmitted though to RV
 no pulsus paradoxus!
no inspiratory augmentation of RV filling (rigid pericardium)
intrathoracic systemic veins become distended
JVP rises with inspiration (normally falls)
Diagnosis
CXR:
calcified cardiac silhouette
EKG:
non-specific
CT or MRI: pericardial thickening
Cardiac Catheterization
Elevated and equalized diastolic pressures (RA=RVEDP=PAD=PCW)
Prominent y descent:
rapid atrial emptying
“dip and plateau”:
rapid ventricular filling
then abrupt cessation of blood
flow due to rigid pericardium
Constriction vs.
Restriction
Similar presentation and physiology, important to differentiate as
constriction is treatable by pericardiectomy
Majority of diseases causing restriction are not treatable
Constrictive Pericarditis
Tachycardia, low voltage
Equalized diastolic pressures
Thickened pericardium
Thickened pericardium
RV=LV,dip & plateau
Kussmaul’s
Constriction vs. Tamponade
Summary






TAMPONADE
Low cardiac output state
JVD present
NO Kussmaul’s sign
Equalized diastolic
pressures
RA: blunted y descent
Decreased heart sounds






CONSTRICTION
Low cardiac output state
JVD present
Kussmaul’s sign
Equalized diastolic
pressures
RA: rapid y descent
Pericardial “knock”
Constriction vs. Tamponade
Summary



TAMPONADE
Pulsus paradoxus:
Present
Echo/MRI:
Normal systolic function
Large effusion
RA & RV compression
Treatment:
Pericardiocentesis



CONSTRICTION
Pulsus paradoxus:
Absent
Echo/MRI:
Normal systolic function
No effusion
Pericardial thickening
Treatment:
Pericardial stripping
Calcified Pericardium
Pericardial calcifications
CT
Pericardial calcification
on echo


Normal
pericardium is
highly reflective
Bright pericardial
echo cannot alone
diagnose
constrictive
pericarditis
Acute Pericarditis/
ECG conference
,
Pericardium

Visceral / serous
– Direct contact with epicardium (ST elev)
– single layer mesothelial cells

Parietal / fibrous
– mesothelial and fibrous layer

Etiology – Acute Pericarditis
Infectious
– Viral : Coxsackie, Echo, EBV, Influenza, HIV
– Bacterial: TB, staph, hemophillus, pneumococcal, salmonella
– Fungal/other: histo/blasto/coccidio, rickettsia

Rheumatologic
– SLE, Sarcoid, RA, Dermatomyositis, Ankylosing Spondylitis, Scleroderma,
PAN

Neoplastic
– Primary: angiosarcoma, mesothelioma
– Metastatic: breast, lung, lymphoma, melanoma, leukemia

Immunologic
– Celiac sprue, Inflammatory Bowel Disease

Drug
– Hydralizine, Procainamide

Other
– MI, Dressler’s, Post Pericardiotomy, Chest Trauma, Aortic dissection
– Uremic, Post Radiation
– IDIOPATHIC
Acute Pericarditis –
Clinical

History
– preceding viral illness, etc

Symptoms
– Chest pain

Signs
– Friction Rub

ECG
– early: PR / ST changes
– late: isoelectric ST/ T inv
History


Often preceding viral illness 1-2wk
prior
Chest Pain
– Sudden, sharp,pleuritic, constant
– worse supine/ L lat decub, relief sitting
up
– radiation: back, trapezius ridge
– symptoms usually resolve by 2 weeks,
ECG abnormalities may persist for months
Auscultory – Rub(s)

Endopericardial (classic)
–
–
–

Pleuropericardial
–
–

“exopericardial”, extension into adjacent structures
marked resp variation, musical quality
Conus
–
–

“triphasic”: atrial sys, ventricular sys, early diastole
may only hear 2 phase (afib or tachycardia) or 1
loudest LSB, raised extremities/increased venous return
dilation of pulm conus in hyperactive heart
PE, thyroid storm, acute beriberi
Pneumohydropericardium
– air/gas overlying pcard fluid
– metallic tinkle (small amt) ; churning/splashing “mill-wheel
sound” (lg)
ECG


PR depression
ST elevation
– concave up, ST/T V6 >.25, no reciprocal

DDx:
–
–
–
–
–
Acute MI
Early Repolarization
Myocarditis
Aneurysm
other: Brugada, BBB
ECG
Acute Pericarditis Stages

Stage I
– first few days  2 weeks
– ST elev, PR depression
– up to 50% of pt with sxs/rub do NOT have/evolve stage
I1

Stage II
– last days  weeks
– ST returns to baseline, flat T

Stage III
– after 2-3 weeks, lasts several weeks
– T wave inversion

1
Stage IV
– lasts up to several months
– gradual resolution of T wave changes
Spodick DH, Pericardial Disease. Braunwauld 6th
Acute PCARD – Stage III
19 y/o Female after 1 wk in hospital with Acute Pericarditis
Treatment

NSAIDS/ASA
– ASA 650 q3-4hr
– Ibuprofen 300-600 q 6-8 hrs x 1-4days


Avoid Indocin, reduces CBF
Steroids
– if no response after 48hr NSAID
– use concurrent NSAID

Colchicine
– .6 q12 chronic +/- NSAID
– useful in recurrent pericarditis
– symptom free period 3.1 +/- 3mos vs 43 +/- 35mos
(p<.00001)
in largest multicenter trial to date1
– Anecdotal evidence of benefit in Acute PCARD, effusion
1Adler
Y, et al. Circulation, 1998 June 2
Complications


Pericardial Effusion/Tamponade
Constrictive Pericarditis
– can be “transient” – 10% may have
transient sxs within 1st month, resolves
by 3 months

Recurrent Pericarditis (20-25%)
– Rx – NSAIDS/Colchicine +/- steroids
Universitatea Titu Maiorescu