myopericarditis
DESCRIPTION
Aileen D. Gianan M.D. 1 st year Medical Resident. MYOPERICARDITIS. 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 - PowerPoint PPT PresentationTRANSCRIPT
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
B.B. 22 year old male Filipino No known comorbidities Works as a call center
agent From Bicutan, Paranaque
Chest pain
HISTORY OF PRESENT ILLNESS
11 hours PTA
8 hours PTA
substernal chest pain pricking in character, grade 5/10, non-radiating.
Took NSAID which 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 141K 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 Esomeprazole 40mg
ODClopidogrel 75mg OD Captopril 25mg ¼ tab
TIDMetoprolol 50mg ½ tab BID Rosuvastatin 10mg
ODLactulose 30ml HS
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 Chol 115.25K 4.1 LDL 40.24BUN 9 HDL 64.23Crea 0.9 Trig 14.25Cl 101 Alb 3.9P 3.48 GGT 126Ca 9.3 Alk P 181UA 8 Amy 59SGPT 133H CO2 31SGOT 139 H
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
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 ST-segment 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 kinase-MB 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
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
Platelet Count
270,000 253,000 311,000
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)
Dimension
Value Dimension
Value
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 0.7-1.2)
%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 0.7-1.2)
%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