This document provides an overview and management of pericarditis and myocarditis. It begins with a case presentation of a 21-year-old male student presenting with fever, chills, and muscle pain. It then defines pericarditis and myocarditis, discusses their diagnosis, clinical presentation, staging, complications, treatment, and prognosis. Diagnostic tests like electrocardiography, echocardiography, viral genomes, and cardiac magnetic resonance imaging are covered. Complications like dilated cardiomyopathy are also summarized.

1. Presented by: Farah El Soheil
Presented to: Dr. Diana Malaeb
1

2. Lebanese International University
School of Pharmacy
Advanced Pharmacy Practice Experience
Fall 2019 2020
Cardiac Inflammatory Diseases
Pericarditis & Myocarditis:
Overview & Management
Dec 4, 2019

3. Outline
i. Case presentation
ii. Definitions
iii. Diagnosis
iv. Clinical presentation
v. Staging
vi. Complications
vii. Treatment
viii. List of Avoidance
ix. Follow up & prognosis
x. References
3

4. Case Presentation
 JZ is 21 year old student who presented to the winter park
ED with a history of fever, chills, general malaise, diaphoresis
and muscle pain for several days.
 3 weeks prior to admission in Ohio where he resides he
developed a URI and he was prescribed Zithromax. he then
relocated to Oriando where he attended full sail university
because he still didn’t feel good. he was prescribed levaquin
however he didn’t feel any better and he developed petechial
rash and swelling in his lower extremities where he was
admitted to the ER and diagnosed with lobar pneumonia.
 The day following admission he developed hypotension and
tachycardia.
 Social history: never smoker, he doesn’t drink alcohol or
abuse drugs
4

5. Physical Examination
 T: 37.1 P: 127 R: 21 BP:
80/51
 H&N: JVD +ve
 Pulmonary: diminished breath sounds in right
basal lung, no rhonchi or wheezing
 Cardiac: decreased S1 normal S2, murmur
 GIT: soft & tender abdomen, BS present
 Extremities without cyanosis or clubbing
 Skin: petechial rash
5

6. Imaging
 CXR:
 Cardiomegaly
 RUL and RML consolidation
 Right upper pleural effusion
 ECG:
 Sinus tachycardia
6

7. Labs
 WBC 18.2
 N 86 (H)
 L 3(L)
 M 6
 E 0
 rbc 5.3
 HB 16
 HCT 46
 MCV 85
 PLT 90 (L)
 INR 2.39 (H)
 pt 26.2 (H)
7

8. Chemistry
 Na 121 (L)
 K 5.7 H
 Cl 86 L
 CO2 22 L
 ALT 1919
 AST 547
 BUN 42 H
 SCr 1.49 H
 Ca 8.3 L
 ANA -ve
 CK 270 MB 10.8
 ABG 7.47
8

9. Anatomy
9

10. Definitions
Endocarditis inflammation of the lining of the heart (endocardium) can
occur in areas other than the valves, including outflow tracts, septi, and
the mural endocardium
Myocarditis is an inflammatory infiltrate of the myocardium with cerosis &/
or degeneration of the adjacent cardiac myocytes not typical of the
ischemic damage associated with CAD
Pericarditis is inflammation of the lining around the heart - the
pericardium, generally with a fluid collection between the pericardium and
the heart
Acute myocarditis and acute pericarditis are not always associated
10
Myocarditis. (5, February). Retrieved from https://www.ahajournals.org/doi/full/10.1161/circresaha.115.306573

11. Dallas Criteria
• Myocarditis (+/- fibrosis) : unequivocal
inflammatory cells and myocardial cell damage
• Borderline myocarditis: few inflammatory cells
but no definite myocardial damage
• No myocarditis
Primary
Biopsy
• Ongoing persistent myocarditis
• Resolving myocarditis
• Resolved myocarditis
Subsequent
biopsy
11
Molecular Pathobiology of Myocarditis. (n.d.). Retrieved from
https://www.sciencedirect.com/science/article/pii/B9780124052062000089

12. Descriptors of Inflammatory
Infiltrates
 Distribution:
 Focal
 Multifocal
 Diffuse
 Extent:
 Mild
 Moderate
 Severe
 Type:
 Lymphocytic
 Eosinophyllic ( Drug induced HSN)
 Penicillin
 Cephalosporins
 Tetracyclines
 Phenytoin
 Diuretics
 Sulfonamides
12
Molecular Pathobiology of Myocarditis. (n.d.). Retrieved from
https://www.sciencedirect.com/science/article/pii/B9780124052062000089

13. Types
 Acute infective, toxic or autoimmune inflammation of
the heart
 Reversible toxic myocarditis occurs in diphtheria and
sometimes in infective endocarditis when autoimmune
mechanisms may also contribute
 Persistent viral infection of the myocardium was first
demonstrated a decade ago
 Slow growing organisms such as chlamydia and
trypanosomal infection in Chagas' disease are causes
of chronic myocarditis
 Non-infective causes in sarcoidosis and the collagen
vascular diseases need to be sought
13

14. Prevalence
 The prevalence of acute myocarditis is unknown
because most cases are not recognized on
account of non-specific or no symptoms (but
sudden death may occur)
 Myocarditis may develop as a complication of an
upper respiratory or gastrointestinal infection with
general constitutional symptoms, particularly fever
and skeletal myalgia, malaise, and anorexia
 Myocarditis may not develop for several days or
weeks after the symptoms and after a return to
normal work and leisure activity
14

15. Etiology of Myocarditis
 Infectious
 Viral
 In western countries enteroviruses, especially coxsackie B 1–6 serotypes, are the most frequent
( 1st world)
 The recent identification of a common coxsackie virus B and adenovirus receptor (CD55 or k
accelerated receptor on monocytes) has explained why these very different virus types both
cause myocarditis
 Others: HIV, CMV, parvovirus B19
 Protozoan
 Tryponema cruzi: chagas disease
 Primary cause in South America
 Bacterial
 Burellia burgdorferi : chronic lyme disease
 Noninfectious
 Idiopathic: viral
 Rhematic fever: streptoccemia
 Autoimmune diseases: SLE, scleroderma, sarcoidosis, IBD, kawasaki, chrug strauss
 Cardiotoxins: doxorubicin, CO poison, cocaine and abused alcohol
 Heavy metals: copper, iron, lead
15

16. Etiology of Pericarditis
16
Autoimmune
• SLE,
RA,
sclerode
rma,
Sjögren
syndrom
e,
vasculiti
s
• Autoinfla
mmatory
diseases
(FMF
and TNF
associat
ed
periodic
syndrom
e
Postcardiacinjurysyndromes
• Immune-
mediated
after
cardiac
trauma in
predisposed
individuals
• Other -
Granulomat
osis with
polyangiitis
(Wegener's)
,
polyarteritis
nodosa,
sarcoidosis,
IBD
(Crohn's,
ulcerative
colitis),giant
cell arteritis,
Behçet
syndrome,
rheumatic
fever
Neoplasm
• Metastatic
- Lung or
breast
cancer,
Hodgkin's
disease,
leukemia,
melanoma
• Primary –
Rhabdomy
osar coma,
teratoma,
fibroma,
lipoma,
leiomyoma
, angioma
• Paraneopl
astic
Cardiac
• Early
infarction
pericarditis
• Late
postcardia
c injury
syndrome
(Dressler's
syndrome),
also seen
in other
settings
(eg, post-
myocardial
infarction
and post-
cardiac
surgery)
• Myocarditi
s
• Dissecting
aortic
aneurysm
Metabolic
• Hypothy
roidism -
Primarily
pericardi
al
effusion
• Uremia
• Ovarian
hypersti
mulation
syndrom
e

17. Staging
17

18. Staging
18
Insults:
Virus
Autoimmune
Allergen
Toxin
Others
Inflammation
Myocyte death
Swelling
Inflammatory markers
Interferon gamma, natural killer cells,
and nitric oxide
Viral nucleic acid
Metabolic changes
MyocardialDamag
eMyocardial
edema
Loss of function
Arrythmia
Recovery
Healing
Normal function
Myocardial
Damage
Myocardial fibrosis
Loss of function
Acute Abnormalities Chronic Changes

19. Clinical Presentation
 Most patients are asymptomatic
 In symptomatic patients, the cardiac presentation is
 Acute heart failure (HF)
 A syndrome mimicking acute myocardial infarction or a tachyarrhythmia,
including
 Sudden death
 High-grade heart block may occur
 Pericarditis : If the epicardium is involved, pericarditis may be associated
with
 Pleuritic chest pain: Typically sharp and pleuritic, improved by sitting up and
leaning forward
 Radiation of chest pain to the trapezius ridge has also been considered to be fairly
specific for pericarditis
 Pericardial effusion: Pericardial friction rub –A superficial scratchy or squeaking
sound best heard with the diaphragm of the stethoscope over the left sternal
border
 Infectious etiology: signs and symptoms of systemic infection such as fever
and leukocytosis. Viral etiologies in particular may be preceded by "flu-like"
respiratory or gastrointestinal symptoms
19

20. ACS like syndrome:
• 5-10% of patients presumed to
be ACS
• 30% viral prodrome
• Injury/ inflammatory
signals rapidly decline
Specific:
• ACS like
• Sudden cardiac death
• Fulminant heart failure
• Dilated cardiomyopathy
Sudden cardiac death:
• Young male athletes
• 13 % of patients rescucitated
Non Specific:
• unusual symptoms (multisystem
disorders like SLE and odd labs
• myocarditis plus
Fulminant Myocarditis:
• Fever, rapid onset cardiogenic
shock
• Injury/ inflammatory signals
• Supportive care
• Good prognosis if supported
Clinical Presentation
20

21. Fever (>38ºC
[100.4ºF])
Cardiac tamponade
(eg, hemodynamic
compromise)
Pericardial effusion
(ie, an end-diastolic
echo-free space of
more than 20 mm)
Immunosuppression
A history of therapy
with vitamin K
antagonists or
NOACs
Acute trauma
Failure of 1st line
treatment
Elevated cardiac
troponin
The Need for Hospitalization
21

22. Physical Examination & Labs
 Tachycardia, soft S1 sounds, S3 or S4 gallop
 Lymphadenopathy (sarcoidosis)
 Rash (hypersensitivity)
 Polyarthritis, subcutaneous nodules, or erythema
marginatum (acute rheumatic fever)
 Levels of cardiac biomarkers, including CK-MB,
troponin I, and troponin T, are elevated in a
minority of cases (indicating myocardial damage)
 The serum concentration of troponin I is increased
more frequently than that of CK-MB fractions in
patients with acute myocarditis
22

23. Electrocardiography & Echocardiography
 Electrocardiography may show
 Nonspecific ST-T wave changes
 ST elevation mimicking acute myocardial infarction
 Typically concave up
 AV block
 Depression of the PR segment
 Echocardiography
 Rule out other causes of heart failure, such as
valvular, congenital, or amyloid heart disease
 Classic findings include global hypokinesis with or
without pericardial effusion
23

24. MI Versus Acute Pericarditis
24
ECG features Findings in acute pericarditis Findings in acute MI
ST segment elevation morphology
•ST segment elevation begins at J point,
rarely exceeds 5 mm, normal concavity
•ST segment elevation begins at J point,
often exceeds 5 mm in height, abnormal
concavity (convex or "dome-shaped")
ST segment elevation distribution
•Widespread ST segment elevation in
most/all leads
•Typically most prominent in inferolateral
leads
•Anatomical groupings of leads show ST
segment elevation, which corresponds to
vascular territory of infarction
Reciprocal ST segment changes •Usually not seen
•ST segment depressions usually seen
in reciprocal leads
Concurrent ST elevation and T wave
inversion
•Unusual unless concomitant myocarditis •Common
PR segment changes
•PR elevation in aVR and PR depression
in most/all other leads
•Rare
•Other ECG findingsHyperacute T waves
•Q waves
•QT prolongation
•Rare; if seen, due to fusion of elevated
ST segment and T wave
•Not usually new from acute pericarditis
•Unusual
•Commonly seen at onset of acute
infarction/ischemia
•Seen late in course of MI due to
transmural injury
•Can be seen

25. Viral Genomes
 The presence of viral genomes in heart tissue
from patients with acute myocarditis may
predict adverse events
 The absence of viral genomes in patients with
chronic myocarditis may identify a subset of
patients who will respond to a short course of
immunosuppression
25

26. Routine Diagnostic Tests:
 Low specificity for myocarditis
 ECG, echo, blood troponin, CRP, CBC
 Specialist diagnostic tests
 biopsy: evidence of inflammation + cell type(L/E)
 very invasive and low sensitivity
 The class I indications for EMB:
 New-onset heart failure (<2 weeks) associated with a normal or dilated
left ventricle with hemodynamic compromise
 New-onset heart failure of 2 weeks to 3 months' duration with a dilated
left ventricle, ventricular arrhythmia, or high degree atrioventricular
blockade
 Conditions that fail to respond to treatment in 1 to 2 weeks.
 CMR: non invasive: assess myocardial function + detect site of
inflammation
 Nuclear imaging
26

27. Diagnostic Criteria
Acute pericarditis (at least two criteria of four should be present)*:
1. Typical chest pain
2. Pericardial friction rub
3. Suggestive ECG changes (typically widespread ST segment elevation)
4. New or worsening pericardial effusion
27

28. Complications
 Dilated cardiomyopathy (DCM)
 There are several mechanisms that explain the
pathology:
 Direct viral damage
 Humoral or cellular immune responses to
persistent viral infection
28

29. Direct Injury
The initial change is
myocyte damage in the
absence of a cellular
immune response
After entry into the cell
through the CAR receptor,
the viral genome is
translated into structural
capsid proteins and
proteases that cleave the
viral polyprotein
Viral protease 2A can also
cleave certain host
proteins
Protease 2A cleaves
dystrophin, leading to
disruption of the
dystrophin-glycoprotein
complex that is essential
for normal cardiac function
Disruption of the
dystrophin-glycoprotein
complex is also present in
hereditary
cardiomyopathies that are
related to a dystrophin
mutation
29

30. Persistent viral infection
 The initial immune response plays a protective
role against the development of coxsackie B
myocarditis
 Enteroviral & coxsackie B RNA was present in
acute myocarditis and persisted during the chronic
phase of cardiomyopathy
 Indirect support for a pathogenetic role of
persistent viral infection was provided in a report
cited above of 172 consecutive patients with viral
infection of the myocardium by PCR
 The LVEF increased in the one-third of patients
who had spontaneous clearance of the viral
genome
30

31. Treatment of
Myocarditis
31

32. Antivirals
 Viral infection is the most common identified cause of
lymphocytic myocarditis
 The efficacy of antiviral therapy for myocarditis is uncertain
 Routine antiviral therapy is not recommended to treat
myocarditis
 Antiviral therapy with ribavirin or interferon alfa reduces the
severity of myocardial lesions and mortality in experimental
murine myocarditis due to Coxsackievirus
 This beneficial effect is seen only if therapy is started prior to
inoculation or soon thereafter
 The applicability of these findings to humans is therefore
uncertain, since patients with viral myocarditis are usually not
seen in the earlier stages
32

33. Immunosuppression
 Preliminary studies suggest that immunosuppressive therapy
may be beneficial in selected patients with chronic
myocarditis but immunosuppressive therapy has not proven
to be effective in acute lymphocytic myocarditis of unspecified
etiology
 Further study is needed to
 Identify an effective regimen for chronic myocarditis
 Determine if the absence of viral genomes on EMB identifies
patients who are more likely to improve with immunosuppressive
therapy
 Glucocorticoid therapy doesn’t reduce mortality or improve
functional status in patients with viral myocarditis, though
improvement in left ventricular ejection fraction (LVEF)
 There’s a clinical benefit from combination
immunosuppressive therapy with glucocorticoids,
azathioprine, or cyclosporine
33

34. IVIG
 IVIG has antiviral and immunomodulatory
effects, suggesting that it may play a role in
the treatment of viral myocarditis
 There are insufficient data from
methodologically strong studies to recommend
routine IVIG therapy in patients with acute
myocarditis
34

35. Treatment of
Pericarditis
35

36. Initial Combination Treatment
For initial combination treatment of most patients:
Aspirin¶ 650 to 1000 mg orally three times
daily
One to two weeks
Weekly decrease once patient is
symptom-free and CRP has
normalized
OR
Ibuprofen¶ 600 to 800 mg orally three times
dailyΔ One to two weeks
Weekly decrease once patient is
symptom-free and CRP has
normalized
OR
Indomethacin¶
25 to 50 mg orally three times daily One to two weeks
Weekly decrease once patient is
symptom-free and CRP has
normalized
PLUS
Colchicineפ
0.5 to 0.6 mg orally two times daily
Three months (acute)
Six months or longer (recurrent)
Usually not tapered¥
36

37. Initial Combination Therapy Following
MI
For initial combination therapy of patients following myocardial infarction:
Aspirin¶ 650 to 1000 mg orally
three times daily
One to two weeks
Weekly decrease once
patient is symptom-free
and CRP has normalized
PLUS
Colchicineפ 0.5 to 0.6 mg orally two
times daily
Three months (acute)
Six months or longer
(recurrent)
Usually not tapered¥
37

38. Treatment of Refractory
Pericarditis
For refractory cases or patients with a contraindication to NSAID therapy:
Prednisone 0.2 to 0.5 mg/kg/day
Two weeks (acute)
Two to four weeks
(recurrent)
Gradual tapering over
three months; refer to
UpToDate topic review
of treatment of acute
pericarditis, section on
glucocorticoids
PLUS
Colchicineפ 0.5 to 0.6 mg orally two
times daily
Three months Usually not tapered¥
38

39. NSAIDS
 Function to both reduce inflammation and
relieve pain in most patients
 Oral NSAIDs
 Ibuprofen
 Aspirin
 Ketorolac
 Parenteral NSAID is also effective
 Some patients may require ibuprofen every six hours (four
times daily), in which case the dose should not exceed 600
mg every six hours
 Indomethacin is associated with more side effects, and it is
usually considered for recurrences
39

40. NSAIDS Duration
 Duration of treatment is based upon
 The resolution of symptoms, which usually
occurs in two weeks or less, with tapering
once the patient is symptom-free for at least
24 hours
 The resolution of symptoms and normalization
of C-reactive protein (CRP)
 CRP is assessed at presentation and then weekly,
using the anti-inflammatory dose of NSAIDs until
complete resolution of symptoms (for at least 24
hours) and normalization of CRP, at which point
tapering begins
40

41. Glucocorticoids
 Glucocorticoids should be used for initial
treatment of acute pericarditis only in
 Patients with contraindications to NSAIDs
 Systemic inflammatory diseases
 Pregnancy
 Renal failure
 Should be used at the lowest effective dose
41

42. Glucocorticoids
 Moderate initial dosing (eg, 0.2 to 0.5
mg/kg/day of prednisone) followed by a slow
taper rather than high doses with a rapid taper
 Rapid tapering of systemic glucocorticoids
increases the risk of treatment failure and
recurrence
 Use of lower doses (eg, prednisone 0.2 to 0.5
mg/kg/day) may be equally efficacious and
safer than higher doses
42

43. Colchicine Uses
 The duration of colchicine therapy for recurrent or
refractory pericarditis is at least six months
 Colchicine is generally efficacious for pericarditis
caused by systemic inflammatory diseases and post-
cardiac injury syndromes
 For patients with diagnosed bacterial pericarditis,
colchicine has not been proven efficacious and, on the
contrary, may theoretically impair the clearance of the
infectious agent
 Additionally, colchicine is also not proven to be
efficacious in malignancy-related pericarditis and
pericardial effusion
 When used as an adjunct to NSAID therapy, reduces
symptoms, decreases the rate of recurrent
pericarditis, and is generally well tolerated
43

44. Colchicine Uses
 In the ICAP trial, colchicine added to standard
anti-inflammatory therapy significantly reduced the
risk of recurrence (17 versus 38 percent with anti-
inflammatory therapy alone; relative risk reduction
0.56, 95% CI 0.30-0.72) & significantly better
rates of remission and fewer hospitalizations
compared with anti-inflammatory treatment alone
 No serious adverse events were observed
 Reduced risk of recurrent pericarditis at 18
months in patients being treated for acute (hazard
ratio [HR] 0.40, 95% CI 0.27-0.61) or recurrent
(HR 0.37, 95% CI 0.24-0.58) pericarditis
44

45. Colchicine dosing
 Colchicine may be given with or without a loading
dose. When a loading dose is chosen, the loading
dose is typically 0.5 to 1 mg (or 0.6 to 1.2 mg)
twice daily on day 1, depending upon the patient’s
body weight.
 The daily maintenance dose of colchicine is
weight-based:
 ●Patients weighing ≥70 kg should receive 0.5 to
0.6 mg twice daily
 ●Patients weighing <70 kg should receive 0.5 to
0.6 mg once daily
45

46. Colchicine Side Effects
 Most commonly gastrointestinal (eg, diarrhea,
nausea, vomiting), are uncommon at low doses
(0.5 to 1.2 mg per day), even when given
continuously over years
 Less common (<1 percent) side effects include
bone marrow suppression, hepatotoxicity, and
myotoxicity
 Chronic renal insufficiency leading to increased
colchicine levels appears to be the major risk
factor for side effects and other possible negative
interactions. In addition, colchicine has drug
interactions and altered metabolism in certain
46

47. Colchicine Contraindications
 Elevated levels of
 Aminotransferases
 Creatinine
 Troponin
 Liver diseases
 Myopathy
 Blood dyscrasias
 Inflammatory bowel disease
 Pregnant or lactating women
 Bacterial or neoplastic pericarditis
47

48. Response
 At follow-up, aspirin resistance is associated with
significant increases in the rates of recurrent
pericarditis and constrictive pericarditis
 Response to treatment includes
 Improvement/resolution of symptoms within one to
two weeks of initiation of therapy
 Normalization of C-reactive protein level
 Absence of:
 Fever
 Pleuritic chest pain
 A new pericardial effusion
 worsening of general illness
48

49. GI Protection
 NSAIDs can lead to gastrointestinal toxicity (ie, gastritis, ulcers,
etc) particularly when used:
 In high doses
 For prolonged periods of time
 Patient related factors:
 History of peptic ulcer disease
 Age greater than 65 years
 Concurrent use of aspirin, corticosteroids, or anticoagulants
 Patients considered at risk of gastrointestinal toxicity related to
NSAID treatment should be treated with NSAIDs for the shortest
interval possible and receive concomitant gastroprotective therapy
while taking NSAIDs
 Proton pump inhibitors (eg, omeprazole, pantoprazole) are
generally preferred for prevention of gastrointestinal toxicity due to
their efficacy and favorable safety profile
49

50. Hemorragic Risk
 Concomitant use of heparin and anticoagulant therapies is often
perceived as a possible risk factor for the development of a
worsening or hemorrhagic pericardial effusion that may result in
cardiac tamponade
 The available evidence does not support this
 An analysis of 453 consecutive cases of acute pericarditis did not
show a higher risk of hemorrhagic effusion in patients on
antithrombotics [9].
 A study of 274 patients with acute pericarditis or myopericarditis, the
use of heparin or other anticoagulants was not associated with an
increased risk of cardiac tamponade (odds ratio [OR] 1.1, 95% CI
0.3-3.5)
 CTCS have less bleeding risk however the potential benefits of
reduced risk of bleeding should be weighed against potential side
effects and a higher rate of recurrent pericarditis associated with
glucocorticoids
50

51. List of Avoidance in Myocarditis
 Strenous sports:
 Recommendation of three to six months abstinence from competitive
sports after myocarditis
 Before clearance, patients should be assessed with a symptom-limited
exercise test, Holter monitor, and echocardiogram
 Heavy alcohol consumption:
 Alcohol restriction to at most one alcoholic drink per day (14 to 15 g
alcohol), since heavy alcohol intake may enhance the severity of the
myocarditis
 NSAIDS
 Nonsteroidal antiinflammatory drugs are not effective
 To the contrary, they may actually enhance the myocarditic process and
increase mortality
 In addition, nonsteroidal antiinflammatory drugs should be avoided in
patients with HF generally, given the risk of HF exacerbation and
possible risk of increase mortality
51

52. Follow up
 All patients with myocarditis should be followed,
initially at intervals of one to three months
 The examiner should be alert to persistent or recurring
S3 and S4 gallops
 Echocardiography should be used for monitoring the
size of the cardiac chambers, valve function, and the
left ventricular ejection fraction
 If the echocardiogram does not provide the necessary
information, cardiovascular magnetic resonance,
nuclear testing, or cardiac computed tomography are
alternatives, depending upon availability
 Cardiac function is assessed at one and six months
and then yearly or as indicated by symptoms
52

53. Prognosis
 The prognosis for patients with acute myocarditis
varies and depends on clinical presentation, ejection
fraction (EF), and pulmonary artery pressure
 Several case reports and studies suggest that patients
with fulminant myocarditis and hemodynamic
compromise at presentation have better outcomes
than those with acute nonfulminant myocarditis
 The group of patients with fulminant myocarditis and
acute myocarditis had higher pulse rates, lower blood
pressure levels, higher C-reactive protein levels,
higher cardiac biomarker levels, wider QRS
complexes, and decreased LVEFs on admission
compared with the nonfulminant group
53