462
U N I T 5
Circulatory Function
Paroxysmal atrial tachycardia and atrial fibrillation
develop in 30% to 40% of persons with symptomatic
mitral stenosis.
38
Together, fibrillation and distention of
the atria predispose the person to mural thrombus for-
mation. The risk of arterial embolization, particularly
stroke, is significantly increased in persons with atrial
fibrillation.
Mitral Valve Regurgitation.
Mitral valve regurgita-
tion is characterized by incomplete closure of the mitral
valve, with the left ventricular stroke volume being
divided between the forward stroke volume that moves
blood into the aorta and the regurgitant stroke volume
that moves it back into the left atrium during systole
(see Fig. 19-15). Mitral valve regurgitation can result
from many processes that result in a rigid and thickened
valve that does not open or close completely, such as IE
or RHD. It can also result from rupture of the chordae
tendineae or papillary muscles due to an MI, papillary
muscle dysfunction, or stretching of the valve struc-
tures due to dilation of the left ventricle or valve orifice.
Mitral valve prolapse is a common cause of mitral valve
regurgitation in lean, thin women.
The hemodynamic changes associated with chronic
mitral valve regurgitation occur gradually, allowing
the left atrium to undergo compensatory responses. An
increase in left ventricular end-diastolic volume permits
an increase in total stroke volume, with restoration of
forward flow into the aorta. Augmented preload and
reduced or normal afterload (provided by unloading
the left ventricle into the left atrium) facilitate left ven-
tricular ejection. At the same time, a gradual increase in
left atrial size allows for accommodation of the regurgi-
tant volume at a lower filling pressure. A characteristic
feature of mitral valve regurgitation is an enlarged or
hypertrophied left ventricle, a hyperdynamic left ven-
tricular impulse, and a pansystolic (throughout systole)
heart murmur. Mitral regurgitation, like mitral stenosis,
predisposes to atrial fibrillation.
The increased volume work associated with mitral
regurgitation is relatively well tolerated, and many per-
sons with the disorder remain asymptomatic for many
years, developing symptoms between 6 and 10 years
after diagnosis. The severity of regurgitation reflects the
degree of left ventricular enlargement and may correlate
with murmur intensity
39
and typically correlates with
the patients’ symptoms.
38
As the disorder progresses,
left ventricular function becomes impaired, the forward
(aortic) stroke volume decreases, and the left atrial pres-
sure increases, with the subsequent development of
pulmonary congestion. It is usually recommended that
valve surgery be performed before the onset of these
symptoms.
Mitral Valve Prolapse.
Sometimes referred to as floppy
mitral valve syndrome, mitral valve prolapse occurs in
1% to 2.5% of the general population.
37
The disorder is
seen more frequently in thin women, and there may be a
familial basis. Familial mitral valve prolapse is transmit-
ted as an autosomal dominant trait, and several chro-
mosomal loci have been identified. Although the exact
cause of the disorder usually is unknown, it has been
associated with Marfan syndrome, osteogenesis imper-
fecta, and other connective tissue disorders, and with
cardiac, hematologic, neuroendocrine, metabolic, and
psychological disorders.
Pathologic findings in persons with mitral valve pro-
lapse include a myxedematous (mucinous) degenera-
tion of mitral valve leaflets that causes them to become
enlarged and floppy so that they prolapse or balloon
back into the left atrium during systole
37
(Fig. 19-16).
Secondary fibrotic changes reflect the stresses and injury
that these ballooning movements impose on the valve.
Certain forms of mitral valve prolapse may arise from
disorders of the myocardium that place undue stress on
the mitral valve because of abnormal movement of the
ventricular wall or papillary muscle. Mitral valve pro-
lapse may or may not cause mitral regurgitation.
Most people with mitral valve prolapse are asymp-
tomatic and the disorder is discovered during a routine
physical examination. A minority of people have symp-
toms such as chest pain, dyspnea, fatigue, anxiety, pal-
pitations, and light-headedness. Unlike angina, the chest
pain often is prolonged, ill defined, and not associated
with exercise or exertion. The pain has been attributed
to ischemia resulting from traction of the prolapsing
valve leaflets. Palpitations, arrhythmias, and anxiety
may result from abnormal autonomic nervous system
function that commonly accompanies the disorder. Rare
cases of sudden death have been reported for persons
with mitral valve prolapse, mainly those with a family
history of similar occurrences.
The disorder is characterized by a spectrum of aus-
cultatory findings, ranging from a silent form to one or
more midsystolic clicks followed by a late systolic or
pansystolic murmur heard best at the apex. The clicks
are caused by the sudden tensing of the mitral valve
FIGURE 19-16.
Mitral valve prolapse. A view of the mitral
valve from the left atrium shows redundant and deformed
leaflets that billow into the left atrial cavity. (From Saffitz JE.
The heart. In: Rubin E, Strayer DS, eds. Rubin’s Pathology:
Clinicopathologic Foundations of Medicine. 6th ed.
Philadelphia, PA: Wolters Kluwer Health | Lippincott Williams &
Wilkins; 2012:518.)
