MYOPERICARDITIS

1. Aileen D. Gianan M.D. 1st year Medical Resident MYOPERICARDITIS

2. OBJECTIVES • To present a case of young patient with a chief complaint of chest pain • To discuss the etiology, pathogenesis, and management of myopericarditis

3. THE CASE

4. B.B. • 22 year old male • Filipino • No known comorbidities • Works as a call center agent • From Bicutan, Paranaque

5. Chest pain CHIEF COMPLAINT

6. 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

7. 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

8. PAST MEDICAL HISTORY • Non-hypertensive • Non-diabetic • Non-asthmatic • No history of recent viral illness or URTI • No PTB

9. FAMILY HISTORY • No hypertension and cardiac disease • No diabetes • No asthma

10. SOCIAL HISTORY • Smokes 2 sticks per day x 1 year • Occasional alcoholic beverage drinker • Denies illicit drug use

11. 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

12. 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

13. IMPRESSION • Acute Coronary Syndrome • R/O Myocarditis

14. Chest pain Acute Coronary Syndrome Myocarditis

15. 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

16. 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

17. 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

18. Patient started on the following meds: ASA 80mg OD Esomeprazole 40mg OD Clopidogrel 75mg OD Captopril 25mg ¼ tab TID Metoprolol 50mg ½ tab BID Rosuvastatin 10mg OD Lactulose 30ml HS

19. 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)

20. COURSE IN THE WARDS • Second Hospital Day • Spec 23: Na 137 Chol 115.25 K 4.1 LDL 40.24 BUN 9 HDL 64.23 Crea 0.9 Trig 14.25 Cl 101 Alb 3.9 P 3.48 GGT 126 Ca 9.3 Alk P 181 UA 8 Amy 59 SGPT 133H CO2 31 SGOT 139 H

21. 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

22. 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

23. 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

24. 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

25. 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

26. COURSE IN THE WARDS • Ninth Hospital day • Repeat 12L ECG • Repeat 2D Echo • cleared for discharge • Home medications: • Metoprolol 50mg ½ tab BID

27. FINAL DIAGNOSIS • Acute Myopericarditis • s/p Coronary angiography

28. DISCUSSION

29. 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

30. 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

31. 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

32. Viral-induced myocyte damage may lead to the release of intracellular proteins that trigger immunopathic responses in the presence of a predisposing genetic background.

33. 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.

34. Idiopathic DCM: • 50% • Occult infection • Autoimmune process

35. ETIOLOGY and PATHOGENESIS • Autoimmune mechanisms • direct viral-induced myocyte damage, with associated release of intracellular proteins.

36. 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

37. 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

38. 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

39. 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

40. 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.

41. 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

42. 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

43. 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

44. 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.

45. 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

46. 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

47. 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

48. 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

49. 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)

50. 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.