1/4/01 - Angelfire
1/501 Felix Morales
10:00 am Richard Guerrero
Pathology
Dr. Graham
Cardiomyopathy
Scribe Note: Dr. Graham began the lecture by saying that there is some material like vasculitis will not be covered in detail in her lectures. She is certain that whatever she can’t cover that classes like Intro to Internal Medicine will pick up things that she can’t. As far as testable material for her lectures she said to concentrate on her class notes.
She also began class by completing some information from the previous day:
Marantic Endocarditis (Fig. 13-20, p. 576)
1. It involves a hypercoaguable state under such conditions like tumors, sepsis, and burns.
2. It can involve in any valve, if a cardiac catheter is in placed it will involve the right side.
3. There is usually fibrin-based, small, nondestructive vegetations that are not invasive or destructive of the valve.
4. Usually associated with terminal disease.
Libman-Sacks (SLE) Endocarditis
1. Closely associated with marantic endocarditis except that the vegetations are more destructive of the valve.
a. valvulitis with fibrinoid necrosis
2. Rare endocarditis that involves patients with systemic lupus erythematosis.
3. It’s an antiphospholipid syndrome with hypercoaguability.
4. Visually difficult to distinguish from marantic endocarditis, but be able to distinguish by the clinical syndromes associated with each.
Artificial Valve Complications (Fig. 13-22, p. 578)
1. Usually involves infections associated with the rings and sutures. They have to be replaced in 5 to 10 years.
2. Complications include:
a. thromboemboli
b. infective endocarditis, vegetations and structural deterioration of the bioprostheses
c. Hemolysis (blood shear)
d. Fibrous overgrowth
Carcinoid Heart Disease (Fig. 13-21, p.577)
1. A carcinoid is a low-grade malignant glandular tumor that arises from the GI tract in the small intestines.
2. Episodes involve skin flushing and GI symptoms.
3. It involves endocardial thickening of the right heart (not with elastic fibers) in a 1/3 of the cases.
a. Right-sided valves affected i.e. pulmonic stenosis, tricuspid leaflets become rigid with right-sided heart failure.
4. Seratonin and bradykinin from liver limits left-sided involvement and inactivates the lungs
5. Liver metastasis or venous drainage bypassing the liver needed for effect
6. Left-sided endocardial plaques
a. High blood pressure levels needed for start
b. Lung or ovary carcinoids
c. Involves a right to left shunt
d. Seratonin analog meds produce a similar pattern
i. ergotamine for migraine
ii. fenfluramine and phentermine appetite suppressants
Cardiomyopathy (Fig. 13-23, p. 579)
A. Dilated Cardiomyopathy (Fig. 13-24, p. 581)
1. Most start out in the left heart but affects all four chambers of the heart.
2. Present at any age and is the most common cardiomypoathy.
3. End stage of the dilated heart that results in death by congestive heart failure in seven years.
4. Systolic dysfunction involves hypocontraction of the dilated heart.
5. Causes: Coxsackie B myocarditis, other viral myocarditis, alcohol, thiamine deficiency (beriberi), iron overload (oxygen radical damage), and peripartum.
6. Familial in 20-30% of the cases many are idiopathic.
7. Four chamber dilatation, 2-3 times (600-800 grams) the normal size, hypertrophy, small scars, patchy scars, and myocardium may be thin, normal, or thick.
8. Normal arteries or not enough damage to the arteries to cause any problems.
9. Mural thrombi are common and are usually found in the all the chambers.
10. Right ventricular dysplasia infiltrated by fat seen in young people who die of sudden death.
B. Hypertrophic Cardiomyopathy (Fig. 13-25, p. 582)
1. Diastolic defect of compliance and filing leads to hypercontraction.
2. Usually an inherited disease.
3. Primarily notable for a massive hypertrophy of the left ventricle, this leads to the enlargement of the left atrium.
4. Distinct histologic pattern: myocardial fiber disarray, extreme hypertrophy of fibers, and increased myocardial fibrosis.
5. Myocardial hypertrophy without dilatation.
6. Small banana shaped chamber with asymmetrical hypertrophy, the septum may be thicker than the ventricle.
7. Hypertrophy of the ventricle and the septal bump will lead to subaortic compression leading to an outflow obstruction (Idiopathic Hypertrophic Subaortic Stenosis (IHSS)). Flow from the aortic outflow is closed off during systole. Periodic outflow obstruction occurs in about 1/3 of the patients.
8. Familial autosomal dominant with variable expression in about 50% of the cases. This can be attributed to B-myosin heavy chain and troponin defects.
9. The patient presents with dyspnea and angina (b/c of the aortic stenosis).
10. Mural thrombi, atrial fibrillation, infective endocarditis, and embolization can occur because of the dilatation of the left atrium.
Restrictive Cardiomyopathy
1. The ventricle is not thickened but can not dilate due to something in the myocardium that is preventing dilatation (amyloid, sarcoid). The left atrium will enlarge.
2. Rare and often idiopathic, causes can be:
a. amyloidosis: isolated heart or systemic
b. sarcodosis: diffuse multi-system non-caseating granulomatous disease
c. radiation fibrosis: due to radiation of the mediastinum
3. Differential diagnosis: constrictive pericarditis (prevents diastolic filling), hypertrophic cardiomyopathy
Other (Fig. 13-26, p. 585)
1. Endomyocardial fibrosis involves both ventricles; it generally occurs in African and tropical areas to young children. Proliferation of fibrous tissue thickens the ventricles. May result in mural thrombi.
2. Loeffler’s endomyocarditis is similar, but not just tropical, also involves eosinophilia and leukemia.
3. Endocardial fibroelastosis occurs in young children ( ................
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