Transcript Myopericarditis by Aileen Gianan 061109

MYOPERICARDITIS
Aileen D. Gianan M.D.
1st year Medical Resident
OBJECTIVES
 To present a case of young patient with a
chief complaint of chest pain
 To discuss the etiology, pathogenesis, and
management of myopericarditis
THE CASE
 B.B.
 22 year old male
 Filipino
 No known comorbidities
 Works as a call center agent
 From Bicutan, Paranaque
Chest pain
CHIEF COMPLAINT
HISTORY OF PRESENT ILLNESS
11 hours PTA
 substernal chest pain
pricking in character,
grade 5/10, nonradiating.
 Took NSAID which
8 hours PTA
temporarily relieved the
pain
HISTORY OF PRESENT ILLNESS
 4 hours PTA
 awaken by headache
 recurrence of chest
pain, crushing in
character, of
increasing severity,
8/10, non-radiating.
ER CONSULT
PAST MEDICAL HISTORY
 Non-hypertensive
 Non-diabetic
 Non-asthmatic
 No history of recent viral illness or URTI
 No PTB
FAMILY HISTORY
 No hypertension and cardiac disease
 No diabetes
 No asthma
SOCIAL HISTORY
 Smokes 2 sticks per day x 1 year
 Occasional alcoholic beverage drinker
 Denies illicit drug use
PHYSICAL EXAMINATION
 Conscious, coherent, not in cardiorespiratory distress
 BP 100/70 HR 90 RR 20 T 36.8C O2 sat 98% on RA
 Warm skin, no active skin lesions, no jaundice
 Anicteric sclerae, pinkish conjunctivae, no
tonsillopharyngeal discharge, no cervical LN, neck
veins not distended, no carotid bruit
 Symmetical chest expansion, no retractions, no point
tenderness, clear breath sounds
 Adynamic precordium, no point tenderness,
apex beat at 5th ICS LMCL, no murmurs,
distinct S1 and S2, no gallops
 Flat abdomen, normoactive bowel sounds, no
palpable mass, non-tender, no organomegaly
 Full and equal pulses, no cyanosis, no edema
IMPRESSION
 Acute Coronary Syndrome
 R/O Myocarditis
Chest pain
Acute Coronary Syndrome
Myocarditis
COURSE IN THE WARDS
 At the ER
 12L ECG
 CXR
 Normal
 2D Echo
 Triage Panel
 Electrolytes
 Na 141
 K 3.7
 CBC
 PT INR 0.94,
Activity 119.8%
 PTT 28.7 vs 26.6
COURSE IN THE WARDS
 At the ER
 Started on:
 Isosorbide dinitrate (Isoket drip)
 ASA 160 mg
 Diazepam 5mg
 Hooked to O2
 Streptokinase 1.5M units given  ICU admission
COURSE IN THE WARDS
 At the ICU
 Repeat 12L ECG
 Patient developed fever (T 38⁰C)
 Started on Enoxaparin 60mg SQ OD
 Urinalysis requested
 WBC 15/hpf, Epithelial cells 6/hpf, Bacteria 3/hpf
 Cefuroxime 750mg IV q8 started
 Patient started on the following meds:
ASA 80mg OD
Clopidogrel 75mg OD
Metoprolol 50mg ½ tab BID
Lactulose 30ml HS
Esomeprazole 40mg OD
Captopril 25mg ¼ tab TID
Rosuvastatin 10mg OD
COURSE IN THE WARDS
 Second Hospital Day
 Still with fever and chestpain
 Hematuria  Enoxaparin and Clopidogrel
discontinued
 CT of the chest requested
 CT Scan: Pleuroparechymal fibrosis, both lower lobes;
prominent paratracheal nodes; mildly enlarged spleen




Repeat 12L ECG
Repeat CBC
Repeat Cardiac enzymes
ESR requested
 ESR = 2.0 (Normal)
COURSE IN THE WARDS
 Second Hospital Day
 Spec 23:
Na 137
K 4.1
BUN 9
Crea 0.9
Cl 101
P 3.48
Ca 9.3
UA 8
SGPT 133H
SGOT 139 H
Chol 115.25
LDL 40.24
HDL 64.23
Trig 14.25
Alb 3.9
GGT 126
Alk P 181
Amy 59
CO2 31
COURSE IN THE WARDS
 Second Hospital Day
 Referred to ID service
 IMPRESSION:
 Fever etiology to be determined
 R/O 2 to SVI
 R/O 2 to SIRS from Acute MI
 Chestpain 2 to MI vs Myocarditis
 Leukocytosis 2 to MI vs myocarditis
 Blood CS and Monospot Test requested
 Monospot Test - Negative
 Cefuroxime continued
COURSE IN THE WARDS
 Third Hospital day
 still with fever
 no chest pain
 Isoket drip  NTG patch
 Fondaparinux 2.5mg SQ OD started
 Referred to interventional cardiologist
for coronary angiogram
COURSE IN THE WARDS
 Fourth Hospital Day
 Day 1 afebrile
 No Chest pain
 Coronary angiogram performed
 Impression: No obstructive coronary artery
disease. Dilated LV with mild global
hypokinesia with approximate EF of 45%
( systolic LV dysfunction).
 Consider cardiomyopathy sec. to
Myopericarditis
COURSE IN THE WARDS
 Sixth Hospital day
 Day 3 afebrile
 No Chest pain
 Cefuroxime discontinued
 NTG patch, Rosuvastatin, Lactulose,
Diazepam, Fondaparinux discontinued
 Transferred out of the ICU
COURSE IN THE WARDS
 Seventh Hospital day
 Day 4 afebrile
 No Chest pain
 Blood CS: No growth after 5 days
 Repeat CBC
 BUN and Crea
 BUN 7.99
 Crea 0.8
COURSE IN THE WARDS
 Ninth Hospital day
 Repeat 12L ECG
 Repeat 2D Echo
 cleared for discharge
 Home medications:
 Metoprolol 50mg ½ tab BID
FINAL DIAGNOSIS
 Acute Myopericarditis
 s/p Coronary angiography
DISCUSSION
DEFINITION OF TERMS
 Pericarditis
 Inflammatory disease of the pericardium
 Myocarditis
 Inflammatory disease of the cardiac muscle
 Can be acute, subacute, or chronic
 May either be focal or diffuse involvement of the
myocardium
DEFINITION OF TERMS
 Myopericarditis
 primarily pericarditic syndrome with minor myocardial
involvement
 Perimyocarditis
 indicates a primarily myocarditic syndrome with minor
pericardial involvement.
However, these two terms are often used
interchangeably without regard to the
predominant type of cardiac involvement
ETIOLOGY and PATHOGENESIS
 Viral or Idiopathic myopericarditis – most
common cause
 Example: coxsackieviruses (especially Coxsackie B),
adenoviruses, cytomegalovirus, echovirus, influenza
virus, Epstein Barr virus, hepatitis C virus, and
parvovirus B19.
 Bacterial and non-viral infections – less common
 Auto-immune/Connective tissue disease
 Drug-induced – vaccine related; hypersensitivity
myopericarditis
• Viral-induced myocyte damage may lead to the
release of intracellular proteins that trigger
immunopathic responses in the presence of a
predisposing genetic background.
ETIOLOGY and PATHOGENESIS
 Autoimmune mechanisms
 the initial immune response limits the degree of
viremia early during infection and protects against
myopericarditis.
 If this response is insufficient, the virus may not be
eliminated and further myocyte injury may ensue.
 Idiopathic DCM:
 50%
 Occult infection
 Autoimmune process
ETIOLOGY and PATHOGENESIS
 Autoimmune mechanisms
 direct viral-induced myocyte damage, with associated
release of intracellular proteins.
ETIOLOGY and PATHOGENESIS
 Anti-alpha myosin antibodies
 In one study of 53 patients with clinical
myocarditis, 17 percent had anti-alpha myosin
antibodies, compared to only 4 percent of
patients with ischemic heart disease and 2 percent
of normal controls
ETIOLOGY and PATHOGENESIS
 Anti-beta-1 adrenoceptor antibodies
 detected in as many as 38 percent of patients with
an idiopathic DCM
 Removal of anti-beta-1 adrenoreceptor antibodies
by selective immunoadsorption has been
associated with clinical improvement in patients
with idiopathic DCM
ETIOLOGY and PATHOGENESIS
 Autoreactive T cells
 Cellular immunity also may be involved in the
development of a DCM.
 Overexpression of activated helper and cytotoxic
T cells was associated with the presence of
coxsackie B virus, which may have been the
trigger for a superantigen-mediated immune
response
ETIOLOGY and PATHOGENESIS
 Role of cytokines
 In the postviral setting, cytokines regulate lymphocyte
function in a positive and negative manner and exert a
marked influence on the activities of many other cell
types engaged in tissue repair and restoration of
homeostasis
ETIOLOGY and PATHOGENESIS
 A three-phase model to characterize the stages of the
progression of acute viral infection to DCM has been
proposed
 First phase: viral infection with acute cellular damage.
 Second phase: autoimmune reaction

Third phase: fibrosis replaces areas of cellular inflammation. The
ventricle remodels under hemodynamic neurohumoral stresses.
ETIOLOGY and PATHOGENESIS
 Drug-induced
 Hypersensitivity myopericarditis
 characterized by acute rash, fever, peripheral eosinophilia
 Initiated by medication: sulfonamide, methyldopa,
hydrochlorothiazide, furosemide, ampicillin, tetracycline,
aminophylline, phenytoin, benzodiazepines, and tricyclic
antidepressants).
 does not always develop early in the course of drug use
ETIOLOGY and PATHOGENESIS
 Drug-induced
 Vaccinia-Associated Myopericarditis
 within 30 days after smallpox vaccination in the
absence of evidence of another likely cause
 Estimated incidence range from 0.01 to 3 percent
CLINICAL MANIFESTATIONS
 reflects the degree of myopericardial
involvement, which may be focal or diffuse,
affecting one or more cardiac chambers
 Many cases are subclinical.
 In other patients, cardiac symptoms and signs
are overshadowed by systemic manifestations of
infection or inflammation, such as fever,
myalgias, and gastrointestinal symptom
CLINICAL MANIFESTATIONS
 positional or pleuritic chest pain with or
without fatigue
 decreased exercise capacity, or palpitations.
 Chest pain - occasionally difficult to distinguish
from ischemic pain, because signs of
myocardial involvement can simulate an acute
coronary syndrome as reported in acute
myocarditis.
PHYSICAL EXAMINATION
 Myocarditis or Pericarditis
 Signs of fluid overload like distended neck veins,
edema, etc
 S3 and occasionally S4 gallops.
 If the right or left ventricular dilatation is severe,
auscultation may reveal murmurs of functional mitral
or tricuspid insufficiency
 Pericardial Friction Rub or effusion
PHYSICAL EXAMINATION
 Pericardial friction rub
 highly specific for acute pericarditis but this finding is
not universal and is not well-documented.
 said to be generated by friction of the two inflamed
layers of the pericardium
 have a superficial scratchy or squeaking sound best
heard with the diaphragm of the stethoscope
 usually best heard over the left sternal border
LABORATORY EXAMS
 Routine labs show signs of inflammation
 CBC  would show leukocytosis
 ESR  elevated
 CRP  positive
 Cardiac enzymes
 Cardiac enzyme elevations reflect myocardial
necrosis
 Noted to be elevated in patients with
myopericarditis
ANCILLARY PROCEDURES
 Electrocardiogram
 A typical pattern of ECG evolution commonly
occurs in both myopericarditis and acute
pericarditis.
 Includes diffuse ST elevation and PR depression,
followed by normalization of ST and PR segments,
and then diffuse T wave inversions.
 The ECG differential diagnosis of both
myopericarditis and acute pericarditis includes
acute coronary syndrome and early repolarization
ANCILLARY PROCEDURES
 Electrocardiogram
 In acute pericarditis evolves through four stages:
 Stage 1
 first hours to days: diffuse ST elevation (typically concave up) with
reciprocal ST depression in leads aVR and V1.
 Stage 2
 normalization of the ST and PR segments.
 Stage 3
 development of diffuse T wave inversions, generally after the ST
segments have become isoelectric. However, this stage is not seen
in some patients.
 Stage 4
 ECG may become normal or the T wave inversions may persist
indefinitely ("chronic" pericarditis)
ANCILLARY PROCEDURES
 Electrocardiogram
 In a series of 274 with acute pericarditis, 40 had
myopericarditis as defined by serum troponin I
elevation. The following findings occurred significantly
more often in the patients with myopericarditis:
 Atypical ECG changes characterized by localized ST-elevation
(inferolateral or anterolateral) and T-wave inversion before STsegment normalization (42 versus 21 percent)
 Cardiac arrhythmias (65 versus 17 percent) including
supraventricular or ventricular ectopic beats, as well as
nonsustained ventricular tachycardia.
Myopericarditis vs STEMI
 Distribution of ST elevation is different.
 ST segment elevations in STEMI are localized
 In myopericarditis, ST-T changes are more diffuse
 ST segment elevation and T wave inversions do not
generally occur simultaneously in myopericarditis,
although they commonly do so in acute STEMI
ANCILLARY PROCEDURES
 Chest X-Ray
 typically normal in patients with myopericarditis
with minimal or small pericardial effusion and
normal ventricular function.
 An enlarged cardiac silhouette may be detected in
patients with substantial pericardial effusion or
significant left ventricular dysfunction
ANCILLARY PROCEDURES
 Coronary Angiogram
 Excludes Acute Coronary Syndrome
 Usually normal in myopericarditis
DIAGNOSIS
 Acute pericarditis is diagnosed by the presence
of two or more of the following features:
 chest pain
 pericardial friction rub
 ECG changes (diffuse ST segment elevation or PR
depression)
 pericardial effusion
 When acute pericarditis is present,
myopericarditis has been diagnosed by the
detection of one or both of the following in the
absence of evidence of another cause
 Elevation in serum cardiac biomarkers, such as cardiac
troponin I or T (cTnI or cTnT) and/or creatine kinaseMB fraction (CK-MB)
 New or presumed new focal or global left ventricular
systolic dysfunction on imaging studies
Treatment
 Limited data are available to guide treatment
of myopericarditis.
 Myopericarditis is generally managed as
acute pericarditis when ventricular function is
preserved and there are no significant
ventricular arrhythmias
Treatment
 Nonsteroidal antiinflammatory drugs (NSAIDs)
 mainstay of therapy for acute pericarditis
 In animal models of myocardial inflammation, NSAIDs
are not beneficial and may even enhance the
myocarditic process and increase mortality.
Treatment
 Antiviral therapy
 Antiviral therapy with ribavirin or interferon alfa
reduces the severity of myocardial lesions and
mortality in experimental murine myocarditis due to
Coxsackievirus B3.
 The applicability of these findings to humans is
therefore uncertain, since patients with viral
myocarditis are usually not seen in the earlier stages.
Treatment
 Immunosuppressive therapy
 In acute pericarditis, the 2004 ESC guidelines
recommend use of high doses of glucocorticoids (eg,
prednisone 1 mg/kg/day) when indicated with rapid
tapering to reduce the risk of systemic side effects. In
patients with a co-existing pericardial effusion,
intrapericardial steroids is an option that limits
systemic toxicity
Non-specific Therapy Regimen
 Avoidance of exercise
 Electrocardiographic monitoring
natural history and therapy of myocarditis, Cooper et al..., Aug 2008
Non-specific Therapy Regimen
 Anticoagulation
 Thromboembolic complications can occur when
HF is severe or protracted
 Warfarin is recommended to patients with atrial
fibrillation and to stable patients in sinus rhythm
who fulfill the following criteria:
 Symptomatic HF with an LVEF below 20.
 Minimal risk factors for hemorrhage.
 A stable hemodynamic profile without evidence of
liver synthetic dysfunction
natural history and therapy in adults...Cooper et al...Aug 2008
Prognosis
 Limited data are available on the
natural history of myopericarditis.
 The prognosis for idiopathic and viral
cases of myopericarditis is generally
good, particularly when clinical
manifestations are predominantly
pericardial.
Title:
 Subjects: 234 patients with viral or idiopathic
acute pericarditis
: 40 patients with myopericarditis
 Results:
 the frequency of complications (including
recurrences, cardiac tamponade and constriction)
was similar in both groups.
 At 12 months, echocardiography,
electrocardiography, and treadmill testing were
normal in 39 of the 40 myopericarditis cases.
 When substantial myocardial involvement is
present (ie, perimyocarditis), the prognosis
depends upon the nature and extent of
myocardial disease.
Summary and Recommendations
( by:
 Evaluation
 The evaluation of patients with suspected
myopericarditis should include the following:
 History and physical examination
 Hospitalization is generally recommended for the
diagnosis and monitoring of myocardial involvement.
 Cardiac biomarkers, ECG, echocardiography, and chest
x-ray should be obtained in all patients.
Summary and Recommendations
 Treatment
 In the absence of significant ventricular dysfunction,
management of myopericarditis is similar to that for
acute pericarditis.
 Prognosis
 the clinical evolution of myopericarditis with
predominant pericardial involvement is generally
benign with normalization of clinical findings in the
majority of cases
THANK YOU
COMPLETE BLOOD COUNT
1-06-09
1-07-09
1-11-09
Hgb
15.7
14.7
16.7
Hct
46.6
44.3
49
WBC
7,830
21,870
8,590
Seg
56
86
57
Lym
30
2
24
270,000
253,000
311,000
Platelet
Count
Cardiac Enzymes
1-06-09 x
1-07-09 x
Trop I
15.10
CPK
1,283
726
CKMB
59.6
44.8
Myoglobin
155
BNP
9.7
12L ECG 1-06-09 1400H
12L ECG 1-06-09 1800H
12L ECG 1-07-09
12L ECG 1-13-09
Jan 6 2D Echo - Plax
Jan 6 2D Echo – Short Axis Mitral
Jan 6 2D Echo – 2 Chamber
Jan 6 2D Echo – 4 Chamber
Jan 6 2D Echo – PLAX Color
Jan 6 2D Echo – 4 Chamber Color
Jan 6 2D Echo – Short Axis Color
Jan 12 2D Echo – PLAX
Jan 12 2D Echo – Short Axis Mitral
Jan 12 2D Echo – 2 Chamber
Jan 12 2D Echo – 4 Chamber
Jan 12 2D Echo – PLAX Color
Jan 12 2D Echo – 4 Chamber Color
Jan 12 2D Echo – Short Axis Color
2D Echo 1-6-09 x
 Normal LV Dimension with
normal wall thickness with
normal wall motion and
contractility. EF 61%. Normal
LAD. Normal RA and RV
dimension. Normal main
pulmonary artery diameter.
Aortic root and visible
proximal ascending aorta
(2.5cm). Prolapse of the
anterior mitral valve leaflet.
Normal MV, AV, TV, PV. No
pericardial effusion. MR trace,
TR trace. Normal LV diastolic
function indices (IVRT 83msec)
Dimensio Value
n
Dimensio Value
n
LVID (ed)
4.9 (NV
3.2 – 5)
Aorta
(ed)
2.7 (NV
2.6-3.6)
LVID (es)
3.3
LA (es)
3.2 (NV
1.2-3.5)
LV Vol (ed)
113
RVID (ed)
2.5 (NV 3)
LV Vol (es)
44
IVST (ed)
1 (NV 0.71.2)
%FS
33 (NV
28-37)
IVST (es)
1.5 (NV
0.8-2.0)
LV %EF
61 (NV
53-80%)
PLWT (ed)
1.1 (NV
1.7-1.2)
PLWT (es)
1.2 (NV
1.3-2)
EPSS
0.5 (NV
0.2-1.0)
2D Echo 1-13-09 x
 Normal LV Dimension
with normal wall
thickness with normal
wall motion and
contractility. EF 60%.
Normal LAD. Normal
RA, RV, main
pulmonary artery,
aortic root, proximal
ascending aorta and
arch dimension.
Normal MV, AV, TV, PV.
TR trace. PAP 39mmHg
(mild pulmonary
hypertension)
Dimension Value
Dimension Value
LVID (ed)
4.8 (NV
3.2 – 5)
Aorta
(ed)
2.2 (NV
2.6-3.6)
LVID (es)
3.3
LA (es)
3.2 (NV
1.2-3.5)
LV Vol (ed)
109
RVID (ed)
2.8 (NV 3)
LV Vol (es)
44
IVST (ed)
1 (NV 0.71.2)
%FS
31 (NV
28-37)
IVST (es)
1.4 (NV
0.8-2.0)
LV %EF
60 (NV
53-80%)
PLWT (ed)
1.2 (NV
1.7-1.2)
Cardiac
Output
4.3 (NV
2.2 – 6.7)
PLWT (es)
1.4 (NV
1.3-2)
EPSS
0.7 (NV
0.2-1.0)
CORONARY ANGIOGRAM