Myocardial Rupture Clinical Presentation

Myocardial rupture after 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 following AMI.^[2]

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 following AMI. See the image below.

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

Immediate, early, or delayed acute pulmonary edema (papillary muscle rupture), congestive heart failure (ventricular septal rupture), and hypotension (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 sudden death (rupture). Hemoptysis may occur due to the formation of ventriculopulmonary fistulas. Approximately 10% of patients with pseudoaneurysm are asymptomatic.

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

Papillary muscle rupture (partial or complete)

See the image below.

Acute pulmonary edema manifests as tachypnea, tachycardia, hypotension, respiratory distress, diffuse pulmonary rales, and signs of MR.

The MR murmur may be absent or atypical (soft and not holosystolic) due to rapid equalization of pressures between the left ventricle and 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 and/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.

Left ventricle free-wall rupture

Post-AMI pericarditis manifested as pleuritic chest pain and friction rub may be present in some patients prior to onset of rupture and generally indicates transmural extension of the infarct, as shown 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 >10 mm Hg). See the image below.

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.

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.

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.

Acute myocardial infarction

Risk factors for myocardial rupture following AMI include a relatively small first AMI, female sex, age older than 60 years, hypertension, use of nonsteroidal anti-inflammatory drugs (NSAIDs) or steroids during the acute phase of AMI (interference with the healing process), late thrombolysis (>11 h), postinfarct angina and elevated peak serum C-reactive protein.

Protective factors include LV hypertrophy, history of previous infarcts, congestive heart failure, history of chronic ischemic heart disease, early use of beta-blockers after AMI, and successful (and timely) primary percutaneous coronary intervention.

Trauma

Trauma may be blunt or penetrating.

Trauma also may be iatrogenic in nature, resulting from (1) diagnostic catheterization, including transseptal puncture and endomyocardial biopsy; (2) balloon valvuloplasty; (3) pericardiocentesis; (4) placement of temporary or permanent pacing catheters; and (5) cardiac surgery, especially mitral valve replacement.

Infection

Rupture of a myocardial abscess or AMI secondary to coronary embolism of the vegetative material may occur in patients with infective endocarditis.

Other infections may include tuberculosis, echinococcal cysts, and myocarditis.

Aortic dissection

Aortic dissection is also a cause.

Malignancy

Primary cardiac tumors may be present. Patients may have secondary or metastatic tumors of the heart. Patients may have lymphoma or acute myeloblastic leukemia.

Sarcoidosis

Sarcoidosis has been noted.