Carditis

• ·       Endocarditis – inflammation of the endocardium

  ·       Myocarditis – inflammation of the heart muscle

  ·       Pericarditis – inflammation of the pericardium
• Pathologic process of pericarditis:

  1.     Acute (purulent) bacterial pericarditis

  2.     Viral (idiopathic) pericarditis- It is called idiopathic because viruses are not routinely cultured in our locality.

  3.     Chronic (constrictive) pericarditis - Fibrous tissue, Most commonly caused by Mycobacterium tuberculosis
• Viruses are primarily the main cause of pericarditis.

  
  

  · Viruses

  → Enteroviruses (i.e. Coxsackieviruses A and B and Echovirus) - Most common

  → Herpes viruses

  → Adenoviruses

  → Influenza viruses

  → HIV

  → Mumps virus
• Other causes of pericarditis

  ·       Bacteria (gram positive - most common)

  →    Staphylococcus aureus

  →    Streptococcus pneumoniae

  →    Other streptococci

  ·       Mycobacterium tuberculosis - Causes chronic constrictive pericarditis, common in our locality

  ·       Fungi - Candida, Most common
• Clinical Manifestations of Pericarditis [Freak PK JEDA]

  1. Friction Rub
  2. Pulsus paradoxus
  3. Kussmaul's sign
  4. Jugular venous distention and abnormal jugular venous pulsations
  5. Ewart's sign
  6. Decreased or muffled heart sounds
  7. Abnormal electrocardiographs
• Friction rub is heard as a leathery or scratchy three-component or two-component sound. Clinical diagnosis of acute pericarditis
• Pulsus paradoxisus →    Drop in peak systolic blood pressure of more than 20 mmHg on inspiration.

  →Associated with cardiac tamponade.
• Cardiac Tamponade is an accumulated fluid in the pericardial sac that restricts the heart leading to heart compression which will reduce the heart contractility
• Kussmaul’s sign*

  →    Paradoxical increase in venous distention and pressure during inspiration.

  →    Associated with cardiac tamponade.
• Ewart’s sign*

  →    Area of dullness to percussion at the tip of the left scapula

  →    Very important to do PE. Especially to patients with a high risk of pericarditis.
• Decreased or muffled heart sounds

  →    More common when large amounts of fluid are in the pericardium
• Abnormal electrocardiographs (i.e. ECG or EKG)

  →    Quite similar to patients with an acute myocardial infarction or in someone with normal-variant repolarization abnormality

  →    In a patient with pericarditis, ST segment is elevated in all leads

  →    ST-segment elevation shows upward concavity (“smiling face”)

  →    PR interval is depressed
• These manifestations are associated with cardiac tamponade.

  • Friction Rub
  • Pulsus paradoxus
  • Kussmaul's sign
  • Jugular venous distention and abnormal jugular venous pulsation
• How does infection in pericardium spread?

  →    Blood stream (hematogenous)

  ○      When you have bacteremia

  →    Direct extension from a lung pathology.

  →    Direct inoculation during surgery, invasive medical procedures, or trauma.

  →    Stimulation of an inflammatory reaction resulting in the accumulation of serous (i.e. viral pericarditis) or purulent exudate (i.e. purulent pericarditis) which may in turn causes cardiac tamponade and circulatory failure
• Difference between viral, purulent, and tuberculous pericarditis.

  Viral Pericarditis - Mild inflammatory reaction

  Purulent Pericarditis - Strong, rapidly progressing purulent immune reaction

  Tuberculous Pericarditis - Commonly caused by M. tuberculosis
• Difference between viral, purulent, and tuberculous pericarditis.

  Viral Pericarditis - Associated with focal damage to the adjacent myocardium (myocarditis)

  Purulent Pericarditis - PMNs in the purulent material

  Tuberculous Pericarditis - Large pericardial effusion (>300 ml); predominance of mononuclear cells or even lymphocytes
• Difference between viral, purulent, and tuberculous pericarditis.

  Viral Pericarditis - Direct cellular damage by the virus Destruction of viral-infected cells

  Purulent Pericarditis - Tissue damage due to toxin and enzyme production by the bacteria and rapidly progressing cardiac tamponade

  Tuberculous Pericarditis - Fusion of parietal and visceral pericardium (Causing constriction)
• Difference between viral, purulent, and tuberculous pericarditis

  Viral pericarditis - Self-limiting; rarely fatal*; only type that does not progress to constrictive pericarditis

  Purulent pericarditis - Extensive fibrosis; progress to chronic constrictive pericarditis

  Tuberculous pericarditis - Constrictive pericarditis (caused by TB’s characterisitic scarring); circulatory failure
• Substernal pain - most common complaint of pericarditis patient
• Diagnosis of Pericarditis

  ·       Chest radiographs

  Flask-shaped, enlarged cardiac silhouette

  ·       Echocardiography

  →    Initial test of choice for pericarditis.

  →    Detect pericardial thickening and pericardial fluid accumulation

  Electrocardiograph (ECG)
• A.    TREATMENT (ACUTE IDIOPATHIC PERICARDITIS)

  ·       Bed rest

  ·       Anti-inflammatory (aspirin 2-4 g/day)

  ·       Nonsteroidal anti-inflammatory drugs (NSAIDs)

  ·       Ibuprofen (600-800 mg TID)

  ·       Indomethacin (25-50 mg TID)

  ·       Colchicine (0.5 mg qd <70 kg and 0.5 mg BID > 70 kg) x 3 months

  · Glucocorticoids (prednisone 1 mg/kg per day) for 2 to 3 days
• A.    TREATMENT (PURULENT PERICARDITIS)

  ·       Surgical drainage

  →    Main management

  →    Drain the focus

  →    Goal is to evacuate the pericardial sac of purulent material

  ·       Systemic antibiotics

  →    Depends on what organism you are thinking about based on etiology

  →    Most common are gram positive bacteria

  o   S. aureus

  o   S. pneumoniae

  →    Usually the medication of choice for gram positive is oxacillin.

  →    There is no methicillin and nafcillin in the Philippines.

  →    When there is methicillin-resistant bacteria, you give vancomycin
• A.    TREATMENT (CHRONIC PERICARDITIS)

  ·       Same regimen with TB treatment.

  ·       Isoniazid, ethambutol, rifampin, and pyrazinamide

  ·       Glucocorticoids

  ·       Pericardiotomy (since it is constrictive)

  →    Surgical management

  →    Pericardial resection pre-op

  o   Sodium restriction

  o   Diuretics
• MYOCARDITIS

  ·       Inflammation of the myocardium

  ·       Most often attributable to infective agents

  ·       Characterized by myocyte (muscle) necrosis
• ETIOLOGY OF MYOCARDITIS

  ·       Infection

  →    Virus (among all the infectious agents, viral cause is the one that can push the condition into fulminant myocarditis)

  1.     Enteroviruses (coxsackieviruses B)

  2.     Herpes viruses

  3.     Mumps viruses

  4.     HIV
• ETIOLOGY OF MYOCARDITIS

  →    Bacterial

  1.     Legionella

  2.     Chlamydia

  3.     Borrelia burgdorferi (Lyme disease)

  →    Fungal

  1.     Commonly infects the immunocompromised patients

  2.     Aspergillus

  3.     Candida

  4.     Cryptococcus

  →    Parasitic

  1.     Trypanosoma cruzi (Chagas disease)

  2.     Trichinella spiralis

  ·       Toxic exposure (e.g. zidovudine, hypersensitivity to penicillin)

  ·       Autoimmune reactions (e.g. SLE)

  ·       Others (e.g. sarcoidosis, giant cell myocarditis)
• PATHOGENESIS OF MYOCARDITIS

  ·       Direct Invasion

  →    Respiratory and GI tract entry; infect specific receptors (coxsackie-adenovirus receptors in the heart - AV node and intercalated disks)

  ○      Viral infection and replication can cause myocardial injury and lysis.

  →    Nonspecific (innate) host response to infection.

  →    Secondary acquired (adaptive) immune response addressed against viral proteins.

  ○      Disruption of normal cellular responses

  ○      Production of cardiotoxic substance

  ○      Stimulation of chronic inflammation
• CLINICAL MANIFESTATIONS OF MYOCARDITIS

  ·       Can range from asymptomatic to flu-like illness with chest pain

  ·       Arrythmias, or signs of right and left sided congestive heart failure.

  ·       Acute decompensation of heart failure (e.g., tachycardia, gallop, mitral regurgitation, and edema)

  ·       Pericardial friction rub

  →    Concomitant pericarditis

  →    Accumulated slight fluid in the pericardium
• DIAGNOSIS OF MYOCARDITIS

  ·       Blood tests

  ·       ECGs

  ·       Chest radiograph

  ·       Echocardiography

  ·       Contrast MRI
• DIAGNOSIS OF MYOCARDITIS

  ·       Blood tests

  →    Leukocytosis (if bacterial)

  →    Elevated cardiac troponin I, creatine kinase MB

  ○      These are also elevated in acute myocardial infarction

  →    Elevated ESR and acute phase reactants (CRP, complement, alpha 2 macroglobulin)

  ○      Inflammatory markers
• DIAGNOSIS OF MYOCARDITIS

  ·       ECGs

  →    Nonspecific

  →    Does not give much information

  →    ST and T wave changes, ventricular or atrial arrhythmias, and conduction defects

  ·       Chest radiograph

  →    Pulmonary edema

  →    Cardiac dilatation
• DIAGNOSIS OF MYOCARDITIS

  ·       Echocardiography

  →    If there’s left ventricular failure, the ejection fraction is low

  ·       Contrast MRI

  →    Helpful imaging

  ·       Endomyocardial biopsy

  →    Definitive diagnosis

  →    However, this is only indicated when a new presentation of heart failure is accompanied by conduction blocks or ventricular tachyarrythmias.
• Key Dallas criteria of myocarditis: lymphocytic infiltrate with evidence of myocyte necrosis and are negative in 80-90% of patients with clinical myocarditis
• TREATMENT OF MYOCARDITIS

  ·       Viral myocarditis

  →    Bed rest

  →    Contraindications are steroids and NSAIDs (there is no role for them in viral myocarditis)

  ·       Bacterial, fungal, and parasitic myocarditis

  →    Treat the causative agent
• ·       Vegetation

  →    Prototypic lesion of infective endocarditis (IE)

  →    Mass of platelets, fibrin, microorganisms, and scant inflammatory cells
• Types of Endocarditis

  • Infective Endarteritis
  • Acute Endocarditis
  • Subacute Endocarditis
• INFECTIVE ENDARTERITIS

  ·       Involving arteriovenous shunts, arterio-arterial shunts (PDA) or coarctation of the aorta

  →    Involves the big vessels
• ACUTE ENDOCARDITIS

  ·       Febrile illness

  ·       Rapidly damages the cardiac structure

  ·       Seeds extracardiac sites

  ·       Can have embolism
• SUBACUTE ENDOCARDITIS

  ·       Indolent course

  ·       Rarely metastasizes

  ·       Gradually progressive
• PREDISPOSING CONDITIONS TO ENDOCARDITIS

  ·       Predisposing conditions:

  →    Chronic rheumatic heart disease (still a common predisposition in developing countries)

  →    Illicit IV drug use

  →    Degenerative valve disease

  →    Intracardiac devices

  ·       Elderly

  ·       Valve replacement

  ·       Cardiovascular implantable electronic devices (CIEDs)

  →    You ask the patient, “have you ever had a heart surgery?”