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Pathology
Lecture 25 Myocarditis, Cardiomyopathy & Hypertensive Heart Disease
1) To be familiar with the definition, clinical features, and etiologies of myocarditis.
Definition: inflammatory disease of heart characterized by myocyte damage and
inflammatory infiltrate.
Clinical features: arrhythmias, EKG changes (increased S-T, flat or inverted Twaves), heart failure, may have fever, fatigue, and dyspnea.
Etiologies:
1) infectious (particularly viral [coxsackie, influenza] but may be bacterial,
tuberculosis, fungal, parasitic [Chagas’ disease]).
2) Hypersensitivity, autoimmune, drug-induced.
3) Rejection of cardiac transplant.
4) Idiopathic (sarcoidosis, Fiedler’s, idiopathic giant cell myocarditis)
2) To know the gross and microscopic findings of the various forms of myocarditis.
Gross: may appear normal or dilated, often flabby.
Microscopic: mile fiber disintegration or necrosis with inflammatory response
(typically mononuclear in viral myocarditis, neutrophil ache in bacterial infections
and granulomatous in giant cell myocarditis).
3) To understand the concept of cardiomyopathy and to distinguish between
primary and secondary cardiomyopathies. Cardiomyopathy refers to diseases of
the heart muscle (myocardium) that are noninflammatory and not associated with
hypertension, congenital heart disease, valvular disease, or coronary artery disease. It
is usually characterized that otherwise unexplained ventricular dysfunction.
Primary cardiomyopathy: primary involvement is myocardial and of unknown
etiology. Note: Not all patients with myocarditis develop a cardiomyopathy.
Secondary cardiomyopathy: may be associated with another form of heart disease or
secondary to systemic disease.
4) To understand the mechanisms and pathologic features of dilated, hypertrophic
restrictive, and ARVD cardiomyopathies.
Cardiomyopathy
Dilated (most
common form)
Hypertrophic
Restrictive
Arrhythmogenic
Right Ventricular
Dysplasia (ARVD)
Mechanism
Cardiac insult from alcoholism, drugs or toxins,
pregnancy, thiamine deficiency, and chemotherapy
with Adriamycin (doxorubicin) - known toxicity.
Inherited as an autosomal dominant characteristic.
May result in left ventricular outflow obstruction,
placing the patient in danger of syncope in even
sudden-death.
Infiltrative processes within the myocardium resultant
stiffening of heart muscle, which interferes with
pumping action. Right and left-sided heart failure.
Ventricular arrhythmias, common cause of sudden
death in young adults. Familial forms occur, and a
genetic defect on chromosome 14 has been found.
Pathologic features
Dilation of both ventricles and
both right and left-sided heart
failure. Mural thrombi.
Gross: of ventricular wall
(asymmetric septal hypertrophy)
Micro: disoriented and tangled
myocardial fibers.
May result from endocardial
disease of myocardial processes
(amyloidosis).
Thinning and fibrosis of right
ventricle.
5) To distinguish between the nature of functional abnormalities of dilated,
hypertrophic, and restrictive cardiomyopathies.
Dilated - heart failure due to poor cardiac contractility, low ejection fraction.
Hypertrophic - decreased chamber size resulting in decreased preload.
Restrictive - decreased compliance resulting in decreased preload.
6) To know the basic abnormality occurring in amyloidosis and how it relates to
cardiac dysfunction. Amyloidosis results from abnormal folding of proteins, which
are deposited as fibrils in extracellular tissues and disrupt normal function. Cardiac
amyloidosis produces restrictive hemodynamics, but it can be asymptomatic or can be
manifested by dilation, arrhythmias, or features mimicking those of ischemic or
valvular disease owing to deposits in the interstitium, conduction system, vasculature,
and valves, respectively.
7) To be familiar with the definition of hypertension, its prevalence and risk
groups. Systemic hypertension is defined as persistent systolic pressure >140 mmHg
or diastolic pressure >90 mmHg. Prevalence in the US is 20-35% with increased risk
for blacks and women.
8) To know the criteria for defining hypertensive heart disease. 3 criteria include:
1) Cardiac enlargement, principally left ventricular hypertrophy.
2) Absence of other factors producing left ventricular hypertrophy.
3) History of hypertension (difficult to establish).
9) To understand the mechanisms involved in the pathogenesis of hypertensive
heart disease. The mechanisms involved in the pathogenesis of hypertensive heart
disease are as follows: vascular changes increase TPR impeding left ventricular
outflow, the heart responds by hypertrophy (left ventricle), the increasing size of
myofibers increases the diffusion distance for oxygen transport from blood, and this
results in relative hypoxia of myocardial cells. The hypertrophied myofibers appear
to lack normal contractility. Additionally, interstitial collagen increases thus altering
particular compliance. Atherosclerosis (accelerated in hypertension) of coronary
arteries can further decrease blood supply to the myocardium.
Gross: increased heart size and weight due to thickening of left ventricle wall.
Reduced left ventricular lumen size, may be accompanied by ventricular dilation.
Micro: increased fiber diameter, increased nuclear size ("boxcar" shaped).
10) To know the complications and causes of death associated with hypertension.
Most common cause of death in hypertension is congestive heart failure (40% of
cases). Other competitions include: coronary atherosclerosis, intracerebral
hemorrhage (strokes), arteriolar nephrosclerosis (which may lead to renal failure).
11) To be responsible for all information on handouts. Review handouts.
12) To be able to answer all questions in Directed Reading.