aileen d. gianan m.d. 1 st year medical resident

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.


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


Autoimmune mechanisms

direct viral-induced myocyte damage, with associated release of intracellular proteins.


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


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


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


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


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.


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


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.


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


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


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


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 – 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 – 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

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aileen d. gianan m.d. 1 st year medical resident

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