Myocardial rupture
Myocardial rupture is a laceration of the ventricles or atria of the heart, of the interatrial or interventricular septum, or of the papillary muscles. It is most commonly seen as a serious sequela of an acute myocardial infarction.
It can also be caused by trauma.
Signs and symptoms
Symptoms of myocardial rupture are recurrent or persistent chest pain, syncope, and distension of jugular vein. Sudden death caused by a myocardial rupture is sometimes preceded by no symptoms.Causes
The most common cause of myocardial rupture is a recent myocardial infarction, with the rupture typically occurring three to five days after infarction. Other causes of rupture include cardiac trauma, endocarditis, cardiac tumors, infiltrative diseases of the heart, and aortic dissection.Risk factors for rupture after an acute myocardial infarction include female gender, advanced age of the individual, first ischemic event, and a low body mass index. Other presenting signs associated with myocardial rupture include a pericardial friction rub, sluggish flow in the coronary artery after it is opened i.e. revascularized with an angioplasty, the left anterior descending artery being often the cause of the acute MI, and delay of revascularization greater than 2 hours.
Diagnosis
Due to the acute hemodynamic deterioration associated with myocardial rupture, the diagnosis is generally made based on physical examination, changes in the vital signs, and clinical suspicion. The diagnosis can be confirmed with echocardiography. The diagnosis is ultimately made at autopsy.Classification
Myocardial ruptures can be classified as one of three types.- Type I myocardial rupture is an abrupt, slit-like tear that generally occurs within 24 hours of an acute myocardial infarction.
- Type II is an erosion of the infarcted myocardium, which is suggestive of a slow tear of the dead myocardium. Type II ruptures typically occur more than 24 hours after the infarction occurred.
- Type III ruptures are characterized by early aneurysm formation and subsequent rupture of the aneurysm.
The rupture will most often occur near the edge of the necrotic myocardium where it abuts healthy myocardium where the inflammatory response is at its greatest. Further, the rupture will occur in an area of greatest shear stress. Within the left ventricle, these areas are adjacent to both anterior and posterior papillary muscles.
Left ventricular free wall rupture almost always results in hemopericardium and pericardial tamponade. An accumulation of as little as 75 ml of blood, acquired acutely in a patient without pre-existing pericardial effusion, is sufficient to produce tamponade.