C h a p t e r 1 9
Disorders of Cardiac Function
457
Endocardial and Valvular
Disorders
The endocardium, which lines the heart and covers the
heart valves, is continuous with the tunica intima of the
blood vessels entering and leaving the heart. It is com-
posed of an inner endothelium, consisting of endothe-
lial cells and subendothelial connective tissue; a middle
layer of connective tissue and smooth muscle cells; and
a deeper layer of loose connective tissue, called the sub-
endocardial layer, which is continuous with the con-
nective tissue of the myocardium. The subendocardium
contains small blood vessels, nerves, and Purkinje fibers
from the cardiac conduction system.
Disorders of the Endocardium
Among the disorders that affect the endocardium are
infective endocarditis, rheumatic fever, and valvular
heart disorders.
Infective Endocarditis
Infective endocarditis (IE) is a serious and potentially
life-threatening infection of the inner surface of the heart
including the cardiac valves. Although rare in most con-
temporary population surveys (annual incidence 3 to
7 per 100,000 persons),
24,25
IE is associated with sig-
nificant mortality.
26
Infective endocarditis is character-
ized by colonization or invasion of the valves and the
mural endocardium by a microbial agent, leading to
vegetations and destruction of underlying cardiac tis-
sues.
6
Although other microorganisms, such as fungi,
can cause endocarditis, the vast majority of cases are
caused by bacteria.
Infective endocarditis is commonly classified into
acute or subacute–chronic forms, depending on the
onset, etiology, and severity of the disease.
27
The onset of
acute IE is usually rapid and occurs in patients with pre-
viously normal cardiac valves who are healthy and per-
haps have a history of intravenous drug abuse, whereas
subacute-chronic IE evolves over months, usually in per-
sons who have underlying heart valve abnormalities.
28
Etiology and Pathogenesis.
Two factors contribute
to the development of IE: a portal of entry by which the
organism gains access to the circulatory system and a
damaged endocardial surface. The portal of entry into
the bloodstream may be an obvious infection, a dental
or surgical procedure that causes transient bacteremia,
intravenous injection of a contaminated substance
directly into the blood, or an occult source such as the
oral cavity, gut, or a subcutaneous injury.
6
Although
infective endocarditis can develop in individuals with
normal heart valves, persons with structural abnor-
malities of the values, such as mitral valve prolapse
or congenital heart disease, are at significantly higher
risk. Host factors such as neutropenia, immunodefi-
ciency, malignancy, therapeutic immunosuppression,
diabetes, and alcohol or intravenous drug use are pre-
disposing factors.
6
Infections may also be associated
with cardiovascular prostheses and devices, such as
pacemakers, defibrillators, and left ventricular assist
devices.
Staphylococcal infections are the leading cause of
IE, with streptococci and enterococci as the other two
most common infectious agents. Other bacterial agents
include the so-called HACEK group (
Haemophilus
species,
Actinobacillus actinomycetemcomitans, Cardio
bacterium hominis, Eikenella corrodens,
and
Kingella
kingae
), all commensals in the oral cavity.
6,27
Less com-
monly, gram-negative bacteria and fungi are involved.
The causative agents differ somewhat in high-risk
groups. For example,
Staphylococcus aureus
is the major
offender in intravenous drug users, whereas prosthetic
heart valve infective endocarditis tends to be caused by
coagulase-negative staphylococci (e.g.,
Staphylococcus
epidermidis).
6
In both acute and subacute–chronic forms of IE, fria-
ble, bulky, and potentially destructive vegetative lesions
form on the heart valves (Fig. 19-12). The aortic and
mitral valves are the most common sites of infection,
although the right heart may also be involved, par-
ticularly in intravenous drug abusers. The vegetative
lesions consist of a collection of infectious organisms
and cellular debris enmeshed in the fibrin strands of
clotted blood. The lesions may be singular or multiple,
may grow as large as several centimeters, and usually
are found loosely attached to the free edges of the valve
surface.
6
The infectious loci continuously release bac-
teria into the bloodstream and are a source of persis-
tent bacteremia, sometimes contributing to pericarditis.
Serum biomarkers, which are useful tools
for predicting the extent and progress of MI,
represent intracellular contents of necrotic cells
that have diffused into the blood.
■■
Unstable angina/NSTEMI is an accelerated
form of angina that is caused by subtotal or
intermittent coronary occlusion.
■■
Acute STEMI, also known as heart attack, refers
to the ischemic death of myocardial tissue
associated with obstructed blood flow in the
coronary arteries, potentially fatal arrhythmias,
and other adverse cardiac events.
■■
The chronic ischemic heart diseases include
chronic stable angina, variant (vasospastic)
angina, and silent myocardial ischemia.
Chronic stable angina is associated with a fixed
atherosclerotic obstruction and pain that is
precipitated by increased work demands on the
heart and relieved by rest. Variant angina results
from spasms of the coronary arteries or other
dysfunctions. Silent myocardial ischemia occurs
without symptoms.
