146 Part IV / Mechanical Complications
Results
There are several series of acute papillary muscle rupture in the literature, with oper-
ative mortalities ranging from 17% to 40% (33,39,40). Nishimura et al. (12) reported
the Mayo Clinic experience on the surgical treatment of seven consecutive patients
with postinfarction papillary muscle rupture. Five of the patients presented with cardio-
genic shock and pulmonary edema, whereas two patients had just pulmonary edema.
They all underwent “early” mitral valve replacement within 4 d of presentation. All of
the patients survived the perioperative period. The authors concluded by recommend-
ing early surgical intervention in patients suffering a postinfarction papillary muscle
rupture with acute mitral regurgitation.
VENTRICULAR FREE WALL RUPTURE
Rupture of the left ventricle free wall after myocardial infarction was first described
by William Harvey in 1647 (41). The first successful repair of a ventricular free wall
rupture was performed by Cobbs and Hatcher in 1968 (42). Postinfarction left ventric-
ular free wall rupture accounts for up to 24% of fatal myocardial infarctions (43). Most
of these patients die before making it to emergency surgery.
Anatomy
Batts and colleagues (44) reported 100 consecutive autopsied cases of postinfarction
rupture of the left ventricular free wall at the Mayo Clinic. All of the recent myocardial
infarctions were transmural. One-half of the ruptures were classified as simple,
through-and-through ruptures, whereas the other half were complex with a serpiginous
route through the myocardium. Sixty-six of the ruptures occurred in the middle third of
the ventricle rather than the apical or basal third. The rupture was most often in the lat-
eral left ventricular wall (44%) as opposed to the anterior or inferior walls.
Critical coronary artery atherosclerotic lesions were noted in 98 of the 100 cases.
Eighty-three of the patients had two or more vessel disease. Coronary artery thrombo-
sis was present in 73 patients. This involved the left anterior descending artery in 23,
left circumflex artery in 22, right coronary artery in 27, and left main artery in 1.
Pathophysiology
Clinically, ruptures can be classified as early (acute) or secondary (subacute) (45).
The early acute rupture, or “blowout,” typically occurs immediately after the chest
pain. This type of rupture quickly leads to cardiogenic shock and death from pericar-
dial tamponade. These patients deteriorate rapidly prior to any surgical intervention.
Secondary or subacute ruptures are usually observed within the first 5 d after the
myocardial infarction (45). This type of rupture starts out as a small left ventricular tear
that may not be actively bleeding (5). Patients with subacute free wall ruptures can sur-
vive for days (46). However, the nonbleeding small tear may progress to a larger tear,
resulting in pericardial tamponade. It is these subacute ruptures that potentially provide
the surgeon with a small window of opportunity for surgical intervention.
Preoperative Strategy
Once the diagnosis of postinfarction left ventricular free wall rupture has been estab-
lished by echocardiography, no time is wasted in transferring the patient to the operat-
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