Myocardial Rupture Clinical Presentation

Updated: Nov 10, 2014
  • Author: Jamshid Shirani, MD; Chief Editor: Eric H Yang, MD  more...
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Presentation

History

Myocardial rupture after acute myocardial infarction (AMI) may occur from 1 day to 3 weeks after infarction. Most ruptures occur 3-5 days after infarction.

In most patients, myocardial rupture manifests as a catastrophic event (acute pulmonary edema, cardiogenic shock, or circulatory collapse) within days of a first, small, uncomplicated AMI. Older women, especially those with recurrent postinfarction angina, and patients with systemic hypertension more commonly experience myocardial rupture after AMI. [7]

Acute onset of shortness of breath, chest pain, shock, diaphoresis, unexplained emesis, cool and clammy skin, and syncope may herald the onset of ventricular septal rupture after AMI (see the image below).

Photograph of heart sectioned transversely at leve Photograph of heart sectioned transversely at level of middle left ventricle showing posterior ventricular septal defect at site of recent acute myocardial infarction.

Sudden death due to left ventricular (LV) free-wall rupture may be the first manifestation of coronary artery disease (CAD) in a small percentage of patients with AMI.

Immediate, early, or delayed acute pulmonary edema (associated with papillary muscle rupture), congestive heart failure (CHF; associated with ventricular septal rupture), and hypotension (associated with free-wall rupture) are the cardinal manifestations of myocardial rupture following blunt chest trauma. Concomitant rupture of the myocardium, pericardium, and diaphragm may result in the accumulation of blood in the abdominal cavity.

In patients with traumatic myocardial rupture, manifestations depend on the site, mode, and extent of cardiac injury. Sudden death occurs shortly after the injury in most patients with traumatic myocardial rupture and is due to pericardial tamponade or exsanguination. Cardiogenic or hypovolemic shock is the predominant manifestation of traumatic myocardial rupture in patients who reach a hospital. Patients with pericardial tamponade may present with dyspnea, chest pain, hypotension, cold peripheries, and mental status changes.

A small percentage of patients with significant penetrating cardiac trauma have few or no symptoms upon presentation to a hospital.

Pseudoaneurysms may manifest as cerebral or systemic embolic events or as sudden death (rupture). Hemoptysis may occur as a consequence of the formation of ventriculopulmonary fistulas. Approximately 10% of patients with a pseudoaneurysm are asymptomatic.

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Physical Examination

Of those patients who sustain cardiac trauma from stab wounds, 18-35% remain without clinical signs of myocardial injury.

Acute pulmonary edema from partial or complete papillary muscle rupture (see the image below) manifests as tachypnea, tachycardia, hypotension, respiratory distress, diffuse pulmonary rales, and signs of mitral regurgitation (MR).

Photograph of mitral valve and subvalvular apparat Photograph of mitral valve and subvalvular apparatus showing site of ischemic papillary muscle (PM) rupture (R).

The MR murmur may be absent or atypical (soft and not holosystolic) as a result of rapid equalization of pressures between the left ventricle and the left atrium. This equalization is due to the noncompliance of the acutely volume-overloaded left atrium (ie, the left atrial pressure increases sharply in response to sudden rise in volume). Sudden unexplained hypotension or pulmonary edema in patients experiencing their first inferior AMI should raise the possibility of papillary muscle rupture, even in the absence of a murmur.

Post-AMI pericarditis manifested as pleuritic chest pain and friction rub may be present in some patients before the onset of LV free-wall rupture and generally indicates transmural extension of the infarct (see the image below). Cardiogenic shock due to pericardial tamponade manifests as sudden onset of bradycardia, clear lung fields, distended neck veins, Kussmaul sign (ie, paradoxical inspiratory increase in jugular venous pressure), muffled heart sounds, and pulsus paradoxus (ie, an inspiratory drop in systolic blood pressure of more than 10 mm Hg).

Magnified photograph of transverse section of midd Magnified photograph of transverse section of middle left ventricle (LV) showing transmural lateral free-wall rupture (R).

Hypovolemic shock may occur due to direct communication with the thoracic or abdominal cavity through a pericardial tear. This manifests as hypotension, tachycardia, cool and clammy extremities, pallor, and diaphoresis.

In ventricular septal rupture, hypotension may be present. Patients may have acute pulmonary edema. A loud holosystolic murmur may be heard at the lower left sternal border or diffusely over the precordium and is often associated with a thrill. Ventricular arrhythmias may be present.

In pseudoaneurysm, a friction rub may be heard. Pseudoaneurysms frequently rupture, resulting in cardiogenic or hypovolemic shock. Some patients may have a systolic murmur due to the turbulent flow across the narrow neck of the pseudoaneurysm. Systemic embolism that originates from the pseudoaneurysm may result in various cerebrovascular or systemic ischemic symptoms. Arrhythmia may be present, especially ventricular tachycardia and fibrillation.

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