Aetiology of myocarditis
- Viruses: Coxsackievirus A and B, ECHO, influenza, HIV, CMV
- Chlamydiae: C. psittaci, Rickettsia
- Bacterial: Corynebacterial diptheriae (toxin mediated), Neisseria meningococcus, Borrelia (Lyme disease - rash, athritis, neurological - rhythm disturbance)
- Fungi: Candida
- Protozoa: Trypanosoma cruzi (Chagas disease - South America, 50% of some populations affected by Chagas disease), toxoplasmosis
- Helminths: trichinosis
Immune mediated: post-viral, post-streptococcal (RF), SLE, drug hypersensitivity, transplant rejection.
Unkown: Sarcoidosis, giant cell myocarditis.
Macroscopic features of myocarditis
Variable, thrombi may be present.
Microscopic features of myocarditis
Interstitial inflammatory infiltarte and focal necrosis of myocaytes adjacent to inflammatory cells, most commonly lymphocytes.
Hypersensitivity: lymphocytic, eosinophils and macrophage infiltrates, principally perivascular.
Changas: paarasites (trypanosomes) seen on myofibrils with accompanied acute inflammatory cell infiltrate
Clinical features of myocarditis
- Regurgitation secondary to heart dilatation
- Occasionally sudden death
- Precordial discomfort and mever
- May mimic AMI
- Years later - dilatedcardiomyopathy
Causes of pericarditis
Pericardial inflammation cna be acute or chronic, usually secondary to infectious, immune mediated or miscellaneous agents.
Classification of pericaditis
- Fibrinous and serofibrinous
- Non-infectious inflaations - RF, SLE, renal failure (ureaemia).
- Soemtimes inflammation in adjacent pleura/cavities may stimulate sterile effusion, post-viral or as part of myocarditis.
- Serous fluid with scant inflammatory cells is seen in the pericardial cavity.
- Fribrous adhesions between the pericardial saca nd pericardium rarely occur.
Fibrinous and serofibrinous pericarditis
Most common types, serous fluid + fibrinous exudate.
Commonly: AMI, post infarction - Dressler syndrome, autoimmune, uraemia, radiation, RF, SLE, trauma, post cardiac surgery.
Macroscopic features of fibrinous and serofibrinous pericarditis
Dry granular roughening, increased inflamamtory process in serofibrinous with thicker fluid containing leukocytes and erythrocytes and fibri-pericardial friction rub.
Purulent or sppurative pericarditis
Presence of infective organisms that may reach the space by:
- Direct extension
- Seeding form the blood
- Post surgery
- Via lymphatics
RF - immunosuppression.
Pus in the pericardial sac.
Acute inflammatory cell infiltrate, may extend into the mediastinum, with organisation a sequelae - constrictive pericarditis.
Blood plus serous/fibrinous/suppurative and is most commonly seen in malignant neoplastic involvement - may see malignant cellson cytology of a pericardial tap.
Pericardial sac is obliterated with adherence of the external aspect of the parietal layer to surrounding structures ie heart pulling on parietal pericardium and surrounding structures (diaphragm, ribs etc). Increased work load for the heart.
Heart encased in a dense fibrous (up to 0.5-1cm thick) fibrocalcific scar that limits diastolic expansion and restricts cardiac output resembling restrictive cardiomyopathy. Quiet heart sounds secondary to scar tissue.
Normally only 30-50mL of clear straw coloured fluid in the pericardial sac. Effusions can contain blood or inflammatory cells. Large pericardial effusions cause a globular enlargement of the heart on CXR. Large effusions that restrict cardiac filing are a medial emergency known as cardiac tamponade.