Complications of Acute Myocardial Infarction

Complications of acute M.I. occur in a time-dependent manner, and can be

directly related to the anatomy of the coronary artery blood supply.
Complications may occur due to ischemic or injured tissue and therefore may
begin within 20 minutes of the onset of M.I., when myocardial tissue injury
begins. These complications include arrhythmias and heart block (due to injured
or ischemic conduction system tissue), and hypotension and congestive heart
failure (due to ischemic or injured muscle tissue, resulting in abnormal filling
{"diastolic dysfunction"} or abnormal emptying {"systolic dysfunction"}).
Several days later, complications of M.I. can ensue due to "yellow softening" of
the myocardial tissue, resulting in one of several "mechanical complications" of
M.I., which are discussed below. In addition, inflammation surrounding the
injured myocardial tissue can lead to post-infarction pericarditis (i.e.
inflammation of the lining around the heart).
To better understand the possible complications following M.I., we need to begin
with a review of the anatomy of the coronary artery blood supply to the heart.
For a review of the coronary blood supply, please refer to the textbook, pages 6
through 8, and refer to the diagram below.

Arrhythmias / Heart block:

Almost any cardiac arrhythmia may occur in the setting of acute MI.
Arrhythmias will be discussed more extensively in the EKG lecture.

Briefly, the LAD supplies most of the conduction system below the A-V node
(the His-Purkinje system), while the RCA supplies most of the conduction
system at and above the A-V node (including the S-A node and the A-V nodes
themselves).
Any type of infarct can lead to an abnormal conduction interface (where normal
tissue is adjacent to injured tissue), which may lead to re-entry rhythms
including ventricular tachycardia and atrial flutter. Likewise, any infarct can lead
to impaired LV filling, leading to acute atrial enlargement, leading to atrial
arrhythmias including atrial fibrillation.
Hypotension:

Hypotension may occur in various settings following acute MI. These include:
1) Hypovolemia
2) Excessive vasodilatation from nitrate therapy
3) Decreased left ventricular filling, secondary to right ventricular infarction
4) Marked reduction in cardiac output due to extensive infarction or to a
mechanical complication of MI as described below.
It is important to distinguish between the various causes of hypotension in the
setting of acute MI because they are treated quite differently.
One of the ways that M.I.s can be categorized includes the use of hemodynamic
monitoring (Swan-Ganz catheter) to construct Frank-Starling relationships for
post-MI patients.

Mechanical Complications after MI

Some of the potentially correctable mechanical complications of MI are described
below, and their peak incidence is usually between 3 and 7 days following MI,
when the myocardial tissue is softest, and most vulnerable to rupture.
Acute mitral regurgitation:
Acute MR may occur abruptly from rupture of a left ventricular papillary muscle
resulting in a flail mitral leaflet, usually the posterior leaflet. This results in an
abrupt decrease in forward cardiac output, leading to congestive heart failure
and often to cardiogenic shock.
This occurs more commonly in the setting of inferior MI, since the RCA and
circumflex arteries supply the postero-medial head of the papillary muscle,
which is more prone to rupture than the antero-lateral head.

Ventricular septal rupture:

Acute ventricular septal rupture can occur usually several days following the
acute infarction, due to softening of the necrotic portion of the septum. This can
occur in both inferoposterior and in anterior myocardial infarction. A loud
systolic ejection murmur usually occurs and results in an acute left-to-right shunt

with congestive heart failure and usually cardiogenic shock.

Diagnosis is made by detection of a new systolic ejection murmur, often
associated with a precordial thrill. Diagnostic right heart catheterization (SwanGanz catheter) will demonstrate an oxygen saturation "step-up" between the
right atrium and the right ventricle of at least 5%, as exemplified below:
Left ventricular free wall rupture:
Rupture of the left ventricular free wall is analogous to ventricular septal defect
but occurs in the free wall of the left ventricle, usually resulting in abrupt
cardiogenic shock due to "cardiac tamponade" (see chapter 14, pp 233-236).
Rarely a "pseudoaneurysm" of the left ventricle occurs if there is incomplete
rupture of the free wall and this may be undetected clinically until abrupt
deterioration occurs.

Other complications after MI

Left ventricular aneurysm formation:
Left ventricular apical aneurysm formation usually occurs following anteroapical myocardial infarction, after LAD occlusion. This weakening of the apical
wall results in an outpouching or "dyskinesis" of the apex of the heart during
systole.
The resultant stasis of blood in the dyskinetic segment of the apex may result in
thrombus formation and systemic embolization. The reduced left ventricular
ejection fraction may lead to congestive heart failure and predispose to
ventricular arrhythmias.
Treatment for apical aneurysm formation includes anti-coagulation to prevent
embolization, and afterload reduction to reduce LV wall tension.
Right ventricular infarction:
Right ventricular infarction occurs almost exclusively in the setting of right
coronary artery occlusion. Hallmarks include elevation of the jugular venous
pressure in the absence of pulmonary congestion. Hypotension often occurs in
the absence of an elevated pulmonary capillary wedge pressure. Elevation of the
ST segments may be present in the right precordial EKG leads.

Treatment includes fluid administration to augment LV filling (since the right

ventricle assumes the role of a passive conduit), and to improve LV stroke
volume.
Pericarditis:
Post infarction pericarditis usually begins several days after the infarct, due to an
inflammatory exudate in the pericardium. Pericarditis pain is distinguishable
from infarct pain because of its pleuritic nature, radiation to the left trapezius
ridge, and the associated low-grade fever and pericardial friction rub.
Treatment for post-MI pericarditis includes non-steroidal anti-inflammatory
medication, to reduce the pain and inflammation in the sensitive pericardial
tissue.

Cardiogenic shock

Cardiogenic shock results when there is a marked reduction in forward cardiac

output leading to hypotension, decreased organ perfusion, and at the same time
elevated left ventricular filling pressures leading to congestive heart failure. This
can be due to either massive left ventricular infarction or can be the result of one
of the mechanical complications described above.
The first step in management is to exclude potentially correctable causes of
cardiogenic shock, such as RV infarction (treated with fluid infusions) or
mechanical complications which may require surgical repair.
Once these possibilities are excluded, if the patient presents early into the course
of MI, acute intervention with PTCA or CABG can be considered, to try to limit
infarct size and improve prognosis by emergently re-canalizing or bypassing the
infarct-related artery.
If the patient presents late in the course of infarct (i.e. greater than 12 hours after
pain onset), management includes supportive measures: i.e. optimizing fluid
status via Frank-Starling curves, infusing inotropic agents, and, occasionally,
using an intra-aortic balloon pump to mechanically augment diastolic coronary
perfusion pressure and reduce afterload.tion of a new systolic murmur, and by
the documentation of giant "V-waves" on the pulmonary capillary wedge tracing.

Diagnosis may also be made via transthoracic or transesophageal

echocardiography, by visualization of the "flail" posterior mitral valve leaflet.