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I. Classification
A. Dilated
B. Restricted
C. Hypertrophic
II. Dilated Cardiomyopathy
A. Clinical Presentation
1. Signs of cardiomegaly
2. LV/RV heave
3. S3 common
4. Occasional mitral or tricuspid regurgitation
5. Jugular venous distention
6. Pulmonary rales/ peripheral edema
7. Occasional arrhythmia
8. Fatigue, exertional dyspnea, orthopnea
B. Etiology
1. End stage hypertrophic disease
2. Multi-infarct or ischemic disease
3. Toxins
4. Infections (myocarditis)
5. Endocrinopathy (DM, Thyroid)
6. Connective tissue disease
7. Muscular Dystrophy
8. Post partum
C. Physiology
1. Reduced ventricular ejection fraction
2. High end-diastolic filling volume/pressure
3. Reduced cardiac output
4. High pulmonary capillary wedge pressure
D. Natural History
1. Prognosis dependent on degree of LV dysfunction
2. Without ischemia, 3 yr. mortality about 30%
3. With ischemia, prognosis twice as poor
4. 60% with myocarditis resolve completely
5. Onset may be acute or chronic dependent on etiology
E. Evaluation
1. Measure ejection fraction with echo or nuclear
2. Measure LV wall motion and chamber size: echo
3. ECG for signs of ischemia or arrhythmia
4. Functional capacity (NYHA 1-4)
5. Laboratory screen: electrolytes, thyroid, glucose
6. Screen for ischemia where appropriate: stress and/or cath
7. Thorough and detailed history
8. Myocardial biopsy where indicated
9. Arrhythmia evaluation: SAECG, etc.
F. Therapy
1. Salt and water restriction
2. Preload reduction
3. Afterload reduction
4. Inotrope
5. Anti-arrhythmic as indicated
6. Transplant or other assist device
III. Restrictive Cardiomyopathy
A. Clinical Presentation
1. Symptoms similar to Dilated Cardiomyopathy
2. S4 more common than S3
3. Resting tachycardia
4. Valvular dysfunction less common
5. No evidence of LV dilation
B. Etiology
1. Infiltrative disease (sarcoid, amyloid, hemochromatosis)
2. Tuberculosis
3. Diabetes Mellitus
4. Fibroelastosis
C. Physiology
1. Normal systolic contractility
IV. Reduction in diastolic relaxation and filling capacity
V. High resting LV end diastolic filling pressure
VI. High pulmonary wedge pressure, especially with exercise
A. Natural History
1. Three year mortality about 20%
2. Patients live longer, but are harder to treat than dilated
B. Evaluation
1. Diagnosis of exclusion: CHF in presence of normal systolic function
2. Echocardiogram to demonstrate LV size and function
3. Functional capacity (NYHA 1-4)
4. Laboratory screen: glucose, ferritin
5. PPD
6. Myocardial biopsy when indicated
C. Therapy
1. Judicious preload reduction
2. Afterload reduction not generally indicated
3. Inotrope of little value
4. Direct therapy to underlying disease
5. Beta blocker/calcium blocker may aid in relaxation
VII. Hypertrophic Cardiomyopathy
A. Clinical Presentation
1. Sudden death
2. Palpitations/ arrhythmias
3. Chest pain
4. Dizziness/ syncope
5. Bifid carotid upstroke
6. Basilar systolic murmur, worse on standing
7. Resting tachycardia frequent
B. Pathophysiology
1. Genetic inheritance: autosomal dominant
2. Myositis in disarray
3. May hypertrophy asymmetrically, obstructing outflow
4. Outlet obstruction pulls anterior mitral leaflet out of position, causing
5. LV filling volumes reduced due to diastolic stiffness
6. High pulmonary capillary wedge pressure
7. Pulmonary hypertension
8. Normal LV systolic contractility
C. Evaluation
1. 2D echocardiography essential
2. Physical exam characteristic
3. Family history revealing
4. ECG may show ST-T changes
D. Therapy
1. Avoid vigorous physical activity
2. Avoid preload and afterload reducing agents
3. Myomectomy
4. Septal ablation with catheters
5. Beta blocker/Calcium blocker or disopyramide aid in slowing heart
rate and relaxation
6. Maintain sinus rhythm
7. Electronic pacing