Myocardial Disease Flashcards
Dilated Cardiomyopathy causes
Caused by myocarditis
-Coxsackie virus B
EtOH and metabolites are toxic to myocardium
Thiamine deficiency can cause DCM
Doxorubicin (chemo agent)
Gene mutations causing dilated cardiomyopathy
Mitochondrial genes
dystrophin genes
Genes encoding enzymes involved in beta oxidation of FAs
DCM clinical
Slowly progressive CHF
50% die within 2 yrs
25% survive longer than 5 years
Death due to progressive cardiac failure or arrhythmia
Hypertrophic Cardiomyopathy
Massive myocardial hypertrophy
Abnormal diastolic filling
In 1/3of cases: intermittent LV outflow obstruction
Hypercontracting
- systolic function is preserved
- primarily a diastolic disorder
HCM morphology
Massive myocardial hypertrophy without ventricular dilation
Classic: asymmetrical septal hypertrophy
Usually most prominent in subaortic area
Endocardial thickening of LV outflow tract and thickening of ant mitral leaflet
HCM microscopic morphology
Myocyte hypertrophy
Haphazard disarray of bundles of myocytes
Interstitial and replacement fibrosis
HCM pathogenesis
Mutations in genes that encode sarcomeric proteins
Autosomal dominant with variable expression
HCM clinical
Reduced chamber size
Poor compliance, reduced SV due to:
- impaired diastolic filling of LV
- massively hypertrophied LV
Exertion also dyspnea due to decreased CO and increased pulmonary venous pressure
Harsh systolic ejection murmur due to ventricular outflow obstruction
Angina pain
SUDDEN DEATH IN ATHLETES
Myocarditis
Inflammatory process plays a primary role in development of myocardial injury
Coxsackie viruses A and B
Trypanosoma Cruzi
Myocarditis morphology
Heart normal or dilated
Lesions diffuse or patchy
Ventricular myocardium is flabby
Mural thrombi may be present in any chamber
Myocarditis microscopic
Interstitial infiltrate and injury (lymphocytes)
Hypersensitivity myocarditis
Perivascular infiltrate- lymphocytes, macrophages and eosinophils
Giant Cell myocarditis
Giant cells are present
Poor prognosis
Pericardial effusion
Fluid in pericardium
Hemopericardium
Blood in pericardium
Purulent pericarditis
Pus in pericardium
Globular enlargement
Due to slow accumulation of fluid and is < 500 ml
Cardiac Tamponade
Due to a large chronic effusion (> 500ml) or accumulate rapidly
Restricts cardiac filling
Serous pericarditis
Non infectious inflammation
- rheumatic fever
- systemic lupus erythematosus
- scleroderma
- tumors
- uremia
Serous pericarditis morphology
Neutrophils, lymphocytes, and histiocytes on epicardial and pericardial surfaces
Acute pericarditis morphology
Fibrinous: surface is dry with a fine granular roughening
Serofibrinous: thick yellow to bloody fluid and fibrin
FIBRINOUS DEVELOPS A LOUD PERICARDIAL FRICTION RUB
Purulent pericarditis clinical
Active phase is similar to fibrinous along with signs of systemic infection- spiking temps, chills, fever
Hemorrhagic pericarditis
TB or malignant neoplasm ( most common)
bacterial infections
Bleeding diathesis
Cardiac surgery
Healed pericarditis
Healing causes adhesive mediastinopericarditis
Pericardial sac in obliterated
Heart adheres to surrounding structures
- systolic retraction of the rib cage and diaphragm
- pulsus paradoxus
- hypertrophy and dilation of heart
Constrictive Pericarditis
Encased in dense fibrous or fibrocalcific scar
- limits diastolic expansion
- restricts CO