Viral Infections in which cardiovascular manifestations dominate Flashcards

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1
Q

What is the definition and etiology of myocarditis?

A

• Definition: inflammation of the heart muscle. • Etiology: – Predominantly viral in North America and Europe. – Other infectious causes include bacterial and parasitic infection. – Noninfectious causes include inflammatory disorders and toxin-mediated events.

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2
Q

What are common viruses that have been shown to cause myocarditis?

A

– Enteroviruses (particularly Coxsackie B) – Adenovirus Cytomegalovirus – Epstein-Barr Virus – Parvovirus B19

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3
Q

what are less common viruses that can cause myocarditis?

A

– Arboviruses including Dengue virus – Herpes simplex virus – Measles virus – Respiratory syncytial virus – Rubella virus – Varicella-zoster virus – Influenza – Mumps – Polio – HIV – Hepatitis A virus – Hepatitis C virus

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4
Q

When does myocarditis spike? who is most at risk?

A

– In US- peak enterovirus activity in summer and fall. – Young children are most susceptible.

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5
Q

What is the pathophysiology of myocarditis?

A

• Direct myocyte invasion by infecting agent. • Development of CD4 and CD8 T-lymphocyte response. • Circulating antiheart antibody involvement described against contractile, structural, and mitochondrial proteins. • Exercise, pregnancy, malnutrition, cold exposure, and immunosuppression can lead to more severe enteroviral disease. • Presence of Coxsackie-Adenovirus receptor on cardiac myocytes.

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6
Q

explain the pathology seen in myocarditis? what can also help for diagnosing myocarditis?

A

• Dallas Criteria: – Active Myocarditis- Inflammatory cellular infiltrate with myocyte necrosis – Borderline Myocarditis- Inflammatory infiltrate without myocyte necrosis – No Myocarditis – Inflammatory infiltrates classified as either lymphocytic, eosinophilic, or granulomatous with differing levels of inflammation. – These criteria lack sensitivity. • Immunohistochemical stains can help with diagnosis by further classifying inflammatory infiltrate. – Myocarditis defined as “ immunohistochemical evidence of mononuclear infiltrates with more than 14 cells/mm squared on endomyocardial biopsy in addition to enhanced expression of HLA class II molecules” (Long, et al. Principles and Practice of Pediatric Infectious Disease, 5th edition.)

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7
Q

What are the clinical manifestations of myocarditis?

A

• Viral prodrome: myalgias, fevers, chest pain, dyspnea, tachypnea, gastroenteritis. • Abrupt onset of hemodynamic collapse. • Range of Cardiac Signs/Symptoms: Asymptomatic with EKG changes to cardiogenic shock.

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8
Q

What are the symptoms of viral myocarditis?

A

• Symptoms – Fatigue/irritability – Dyspnea – Palpitation – Chest pain – Syncope – +/- Fever

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9
Q

What are the signs of viral myocarditis?

A

– Pericardial rub – Sinus tachycardia – Atrial or ventricular arrhythmias – Conduction disturbances – Cardiomegaly – Right or left S3 or S4 gallop sounds – Congestive heart failure – Decreased peripheral pulses – Tachypnea – Hepatomegaly

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10
Q

What are other cardiac problems that can manifest and look like myocarditis?

A

• Other cardiac diseases can present in similar manner or concurrently. • Endocarditis- primary valvular disease, positive blood cultures, echo with vegetations. • Pericarditis-precordial chest pain, pericardial fluid, no arrhythmia. • Myocardial infarction can also be confused with myocarditis.

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11
Q

Explain the diagnosis of myocarditis?

A

• If clinically suspect: – CXRay – EKG – Echocardiogram – Labs • Nonspecific: elevations in ESR, CRP, serum transaminases, brain natriuretic protein, CK-MB, cardiospeciifc troponin elevation (in pediatrics). – MRI • Fuctional, morphologic, and tissue abnormalities can be visualized. – Endomyocardial biopsy

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12
Q

EKG findings of myocarditis?

A

• ST-segment elevations in two contiguous leads • T-wave inversions • ST-segment depressions • Q waves • Low-voltage complexes in standard and precordial leads • Other: tachycardia, arrhythmias, conduction disturbances. • Most changes resolve within 1-2 months.

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13
Q

Echocardiography findings with myocarditis?

A

• Heart wall motion abnormalities secondary to inflammation and edema of myocardium. • Valvular regurgitation • Left ventricular dilatation • Biventricular dysfunction seen in severe disease. • Useful to follow over time.

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14
Q

What is the Gold standard to diagnose myocarditis?

A

Endomyocardial Biopsy • Gold standard. – Has remained gold standard but has limited sensitivity and specificity. Must way risks vs benefits. Limited indications for using this as diagnostic tool. Useful if done earlier in course of illness.

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15
Q

How do you find the causative agent in myocarditis?

A

• Isolation directly from myocardial tissue • Isolation from other body sites/fluids • Serology • PCR • Epidemiologic clues

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16
Q

how do you manage myocarditis?

A

• Supportive therapy – Medications used: vasodilator therapy, diuretics, ACE inhibitors, Beta-Blockers – Treatment of arrythmias, bedrest. – Extreme cases: ventricular assist devices, ECMO.

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17
Q

what are some drugs we can give for the following viral etiologies? Influenza, CMV, VZV/HSV, Adenovirus, Parainfluenza, Enterovirus

A

– Influenza-Neuraminidase Inhibitors – CMV-Ganciclovir – VZV/HSV-Acyclovir – Adenovirus-Cidofovir – Parainfluenza/RSV -IV Ribavarin – Enterovirus-Pleconaril was used but now not available.

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18
Q

what are some complications of myocarditis? prevention?

A

• Complications: CHF, Arrythmias, Cardiac Rupture, Death, Dilated Cardiomyopathy. • Prevention: Hand hygiene, respiratory hygiene, sanitary food/water

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19
Q

What is pericarditis? Can be which types? Range of disease manifestations?

A

• Definition: inflammation of the pericardium and proximal portion of great vessels. • Acute , subacute, or chronic. • Infectious and noninfectious causes. • Range of disease manifestations ranges from asymptomatic to severe.

20
Q

Infectious and non-infectious etiologies of pericarditis?

A

• Infectious – Purulent- Bacterial – Benign- Viral or Hypersensitivity, Postinfectious, or Postpericardiotomy syndromes. – Granulomatous- M. tuberculosis, fungal. • Noninfectious: cardiac injury, radiation, uremia, neoplasia, collagen vascular disease, IBD, drugs.

21
Q

what viruses can cause viral pericarditis?

A

• Enterovirus • Adenovirus • Influenza • HSV • CMV • EBV • Mumps • LCM • VZV • HIV • Hepatitis B and C • Parvovirus B19

22
Q

when does viral pericarditis peak? More common in?

A

• Late summer and fall. • Follows peak season of common viral agents. • More common in adults.

23
Q

What is the pathogenesis of pericarditis?

A

• Inflammation-fibrin, PMLs and mononuclear cells, fluid accumulates in pericardial space. Leads to restricted cardiac filling. • Myocarditis is often present concurrently in people with pericarditis secondary to enteroviruses.

24
Q

Clinical manifestations of pericarditis?

A

• Precordial chest pain – Pain can be focal over trapezius and scapula or diffuse or radiate down arm or referred. – Worse when lying down. • Fever • Activity Intolerance • Malaise • Rash • Prodromal URI

25
Q

What does the Physical exam of pericarditis reveal?

A

• Muffled heart sounds • Pericardial friction rub – Heard during deep inspiration or knee-chest – High-pitched, creaking sound, usually heard throughout cardiac cycle • Tamponade: tachycardia, peripheral vasoconstriction, reduced arterial pressure, pulsus parodoxus. • Kussmaul sign-rise or lack of fall of jugular venous pressure with inspiration • Beck triad-decreased BP, muffled heart sounds, elevated jugular venous pressure.

26
Q

Tools used to make the diagnosis of pericarditis?

A

• Hx, PE, Imaging. • EKG • Echo • CXRay • Pericardial Fluid Analysis

27
Q

EKG findings of pericarditis?

A

• ST segment elevations without reciprocal ST depression except in leads V1 and aVR • Return to baseline after a few days • Then, Flattening/inversion of T-waves • Low-volatge QRS

28
Q

ECHO importance in pericarditis?

A

• Most important to diagnose pericarditis and delineate severity. • M-mode best to assess pericardial fluid. • 2D used to guide drainage.

29
Q

What will the chest x-ray and CT/MRI show for pericarditis?

A

• CXRay- Enlarged heart • CT/MRI to delineate masses as cause

30
Q

What will a pericardial fluid analysis look for in the fluid?

A

• Gram Stain • AFB • Fungal Stain • Culture for bacteria, viruses, mycobacteria, and fungi • Blood cultures/cxs from other contiguous foci

31
Q

How to diagnose the virus in pericarditis?

A

• Culture • Rapid antigen tests • Serology • Molecular genetics • PCR • Viral recovery from fluid rare • *** Virus isolated from other sites can be considered likely cause.

32
Q

What are the criteria for diagnosing pericarditis?

A

• TWO OF THE FOLLOWING – Pericardial friction rub – Pericardial effusion on 2D echo – Non-ischemic chest pain – EKG evidence of PR depression or ST deviation

33
Q

What is the treatment for pericarditis?

A

• Supportive for small effusion of viral cause. • If large or tamponade or bacterial or fungal origin- removal of fluid. • Antimicrobial therapy for purulent pericarditis, fungal, M. TB.

34
Q

Complications of pericarditis?

A

• Constrictive Pericarditis • Recurrent disease.

35
Q

What is cytomegalovirus? Transmission? incubation?

A

• Microbiology: – DNA virus – Member of the Beta-Herpesvirus group • General Epidemiology: – Species specific – Ubiquitous – No seasonal pattern. – Persists in latent form, can reactivate, and a person can be reinfected with other strains of CMV. • Transmission: – Horizontal from person-person contact through secretions (e.g. salivary, urine, seminal, and cervical fluids). – Vertical from mother-child in utero, during passage through infected genital tract, and after birth through ingestion of CMV+ milk. – Transfusions of blood, platelets, and WBCs. – Organ transplantation. • Incubation: – Unknown for horizontal transmission. – 3-12 weeks post blood transfusion. – 1-4 months after tissue transplant.

36
Q

Clinical manifestations of CMV?

A

• Most Common: asymptomatic infections. • Teens/Adults: Heterophile-negative mononucleosis-like syndrome with prolonged fever and hepatitis. • Immunocompromised hosts: pneumonia, colitis, retinitis. • Congenital Infection.

37
Q

Congenital CMV leads to?

A

10% with clinical manifestations at birth: – IUGR – Jaundice – Purpura – HSM – Microcephaly – Intracerebral calcifications – Retinitis • As child grows: developmental delays and sensorineural hearing loss. – Congenital CMV is most common nongenetic cause of SNHL in US. – May be present at birth, found years later, or deteriorate.

38
Q

Diagnosis of CMV?

A

• Cell culture from body fluids/tissues. – Recovery from target organ suggests infection. – Isolation from urine, stool, respiratory secretions, or CSF suggests congenital infection in first 2-4 weeks of life. • Serology – Immunofluorescent assays, IHA, LA, and EIA. – Fourfold increase in antibody titer in paired specimens. – Strongly positive IgM helpful in early infancy but less useful later. • PCR • pp65 antigen detection in white blood cells in immunocompromised hosts.

39
Q

Treatment of CMV?

A

• Ganciclovir/valganciclovir: – Approved for: • Induction and maintenance tx of CMV retinitis. • Prevention of infection in transplant recipients. – Also used to treat: • Infections at other sites and immunosuppressed adults with CMV antigenemia/viremia. • Congenitally infected symptomatic infants. • SCT recipients with pneumonia benefit from ganciclovir and IGIV. • Other drugs used for CMV: • Foscarnet • Cidofovir (not studied in children).

40
Q

What is the isolation for CMV? Immunoprophylaxis? Prevention of transmission by blood transfusion? Prevention of Milk transmission?

A

• Isolation: Standard • Immunoprophylaxis: CMV IGIV for prophylaxis of dz in seronegative transplant recipients. • Prevention of Transmission by Blood Transfusion: CMV Ab-negative donors, freezing RBCs in glycerol, removal of buffy coat, filtration to remove WBCs. • Prevention of Milk Transmission: Pasteurization or freezing.

41
Q

Epstein Barr virus microbiology? General epidemiology?

A

• Microbiology: – Gammaherpesvirus/DNA virus. • General Epidemiology: – Approx. 90% of US adults have been infected. – Close contact needed for transmission. – Transmission: saliva, blood transfusion, transplant. – Prolonged secretion, latency, intrafamilial spread common. – Incubation pd for mono: 30-50 days.

42
Q

Clinical manifestations of Epstein Barr?

A

• Infectious Mononucleosis: – Fever – Exudative Pharyngitis – LN – HSM – Atypical Lymphocytosis – Rash-more common in pts txd with ampicillin. – CNS complications: aseptic meningitis, encephalitis, myelitis, optic neuritis, CNP, transverse myelitis, GBS. – Heme complications: splenic rupture, low plts, agranulocytosis, hemolytic anemia, and HLH. – Infrequent: pneumonia, orchitis, and myocarditis.

43
Q

what are the epstein barr associated lymphoproliferative disorders?

A

• B or T-lymphocyte lymphomas • X-linked lymphoproliferative syndrome • Post-transplant lymphoproliferative disorders • Burkitt Lymphoma • Nasopharyngeal carcinoma

44
Q

What is the diagnosis of epstein barr?

A

• Heterophil Ab – Primarily IgM response – Appears during first 2 wks of illness and gone by 6 months. – Not reliable in kids<4yrs • Atypical Lymphocytosis -seen in 2nd week of illness and nonspecific. • Serology-See below. • Isolation of Virus- not routine. • PCR.

45
Q

Treatment of Epstein Barr?

A
  • Mono: – Avoid contact sports. – No ampicillin or amoxicillin. – Steroids: • Impending airway obstruction • Massive splenomegaly • Myocarditis • Hemolytic anemia
  • HLH (also cytotoxic agents and immunomodulators).
  • Post-transplant lymphoproliferative d/o: decreasing immunosuppressive tx.
  • Acyclovir, ganciclovir, valacyclovir sometimes used with actively replicating EBV with or w/o IGIV.