454
U N I T 5
Circulatory Function
heart and extends through the myocardium to involve
more of the transmural thickness of the ischemic zone.
Myocardial cells that undergo necrosis are gradu-
ally replaced with scar tissue. An acute inflammatory
response develops in the area of necrosis approximately
2 to 3 days after infarction.
6
Thereafter, macrophages
begin phagocytizing the damaged necrotic tissue; the
infarcted area is gradually replaced with an ingrowth
of highly vascularized granulation tissue, which in turn
becomes less vascular and more fibrous in composition.
At approximately 3 to 7 days, the center of the infarcted
area remains soft and yellow; therefore, if rupture of the
ventricle, interventricular septum, or valve structures
occurs, it will usually happen at this time. Replacement
of the necrotic myocardial tissue usually is complete by
the 7th week. Importantly, areas of the myocardium
that have been replaced with scar tissue lack the ability
to contract and initiate or conduct action potentials.
The stages of recovery from MI are closely related
to the size of the infarct. Fibrous scar tissue lacks the
contractile, elastic, and conductive properties of normal
myocardial cells; the residual effects and the complica-
tions of the MI are determined essentially by the extent
and location of the injury. Among the numerous com-
plications of MI are life-threatening arrhythmias, peri-
carditis, stroke, thromboemboli, and mechanical defects
(e.g., mitral valve regurgitation, ventricular septal rup-
ture, left ventricular wall rupture, and left ventricular
aneurysm). Depending on its severity, MI has the poten-
tial for compromising cardiac contractility resulting in
cardiogenic shock or heart failure (see Chapter 20).
These serious complications are discussed later.
Pericarditis tends to occur in patients with large
infarcts, a lower ejection fraction, and a higher occur-
rence of heart failure. It may appear as early as the 2nd
or 3rd day postinfarction or up to several weeks later.
12
Pericarditis that occurs weeks to months after MI or
Dessler syndrome is thought to be mediated by autoim-
mune mechanisms. In contrast to the pain associated
with MI, the pain with pericarditis is sharp and stabbing,
and this pain increases with inspiration. The pain may
be relieved by positional changes. Because of reperfusion
therapy, this complication has been greatly reduced.
Mechanical defects result from changes that occur
in the necrotic and subsequently inflamed myocardium
and include rupture of the ventricular septum, papillary
muscle, or free ventricular wall (Fig. 19-9).
6,12
Partial
or complete rupture of a papillary muscle is a rare
but often fatal complication of transmural myocardial
infarction. It is detected by the presence of a new systolic
murmur and clinical deterioration, often with pulmo-
nary edema. Ventricular septal rupture occurs less fre-
quently than in the past because of reperfusion therapy.
Previously thought to require surgical intervention only
in symptomatic patients, surgical repair is now recom-
mended for all patients with ventricular septal rupture.
Complete rupture of the free wall of the infarcted ventri-
cle occurs in up to 10% of patients and usually results in
immediate death.
12
It usually occurs 3 to 7 days postin-
farction, usually involves the anterior wall, and is more
frequent in older women.
6
A more common mechanical
postinfarction complication is mitral valve regurgita-
tion, which results from early ischemic dysfunction of
the papillary muscle and underlying myocardium.
A left ventricular aneurysm is a sharply delineated
area of scar tissue that bulges paradoxically during sys-
tole
6,12
(Fig. 19-10). This section of the myocardium
does not contract with the rest of the ventricle during
systole. Instead, it diminishes the pumping efficiency of
the heart and increases the work of the left ventricle,
predisposing the patient to heart failure. Ischemia in the
surrounding area predisposes the patient to develop-
ment of arrhythmias, and stasis of blood in the aneu-
rysm can lead to thrombus formation. Surgical resection
may be performed to prevent these complications when
other treatment measures fail.
12
Chronic Ischemic Heart Disease
Myocardial ischemia is defined as the inability of the
coronary arteries to supply blood to meet the metabolic
demands of the heart. Most often limitations in coro-
nary blood flow are the result of atherosclerosis, but
vasospasm may serve as an initiating or contributing
factor.
20,21
Coronary artery disease is divided into three
FIGURE 19-9.
Acute mechanical complications of myocardial infarction.
(A)
Papillary muscle
rupture.
(B)
Interventricular septum rupture.
(C)
Rupture of the free wall of the left ventricle with
pseudoaneurysm formation. LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.
A
B
LV
RV
RA
LA
Pericardium
LV
RV
C
Thrombus
Pseudoaneurysm
Transmural infarct
with rupture
