A 78-year-old woman comes to the emergency department due to a 3-day history of intermittent but progressive substernal chest pain. Medical history includes hypertension and hyperlipidemia, but the patient has had poor adherence with her medication and outpatient follow-up. She has a 30 pack-year smoking history. On admission, ECG reveals normal sinus rhythm with ST-segment elevation and pathologic Q waves in leads I, aVL, and V2 to V5. The patient refuses percutaneous coronary intervention and is treated medically. On the fifth day of hospitalization, she experiences severe dyspnea, sweating, and hypotension. Physical examination shows raised jugular venous pressure, no heart murmurs, and clear lungs. She rapidly loses consciousness and becomes pulseless, and the subsequent resuscitation attempt is ineffective. Which of the following most likely contributed to this patient's death?
Mechanical complications of acute myocardial infarction | ||
Complication | Time course | Clinical findings |
Papillary muscle rupture/dysfunction* | Acute or within 3-5 days |
|
Interventricular septum rupture | Acute or within 3-5 days |
|
Free wall rupture** | Within 5 days or up to 2 weeks |
|
Left ventricular aneurysm** | Up to several months |
|
*Usually due to right coronary artery occlusion. **Usually due to left anterior descending artery occlusion. MR = mitral regurgitation; RA = right atrium; RV = right ventricle. | ||
This patient was initially admitted with chest pain and ST-segment elevation in the anterolateral ECG leads, findings consistent with an ST-elevation myocardial infarction (MI) of the left ventricle. Several days later, her abrupt-onset dyspnea and hypotension were most likely due to left ventricular (LV) free wall rupture, a potential mechanical complication of transmural MI.
LV free wall rupture usually occurs within 5 days but can occur up to 2 weeks following MI. During this time, the infarcted myocardial wall is substantially weakened by coagulative necrosis, leukocyte infiltration, and enzymatic lysis of myocardial connective tissue and may be unable to withstand the shear stress generated by the high-pressure left ventricle. Delayed reperfusion (or absent reperfusion as in this patient), increases myocardial damage, further weakening the LV wall and increasing the risk of rupture.
With LV rupture, blood abruptly fills the pericardial space, resulting in hemopericardium and acute cardiac tamponade with rapidly increased intrapericardial pressure. At onset, patients may experience dyspnea, diaphoresis, and sometimes chest discomfort. Diastolic filling of the relatively low-pressure right-sided heart chambers is abruptly restricted (causing jugular venous distension), and blood flow through the pulmonary circulation to the left side of the heart drops precipitously (the lungs remain clear). Cardiac output profoundly decreases, resulting in hypotension and obstructive shock that rapidly leads to cardiac arrest.
(Choices B and D) Papillary muscle rupture, causing acute mitral regurgitation, and interventricular septum rupture, causing a ventricular septal defect, can occur acutely or within 5 days of MI. Both defects typically cause a new holosystolic murmur and lead to LV failure with pulmonary edema. Cardiogenic shock with hypotension commonly develops, but lung crackles would be expected on examination.
(Choice C) Ischemic reperfusion injury can occur when blood flow is abruptly restored to infarcted myocardium, and it may rarely lead to cardiac arrest (via precipitation of ventricular fibrillation or profound myocardial contractile dysfunction). However, it is extremely unlikely in this patient who received no reperfusion therapy.
(Choice E) LV aneurysm formation is typically a delayed mechanical complication of MI, occurring after several weeks or months. Patients typically develop gradually progressive heart failure or angina.
Educational objective:
Left ventricular free wall rupture is a mechanical complication that can occur within 5 days or up to 2 weeks following transmural (ST-elevation) myocardial infarction. Patients usually develop acute cardiac tamponade with hypotension and obstructive shock that rapidly leads to cardiac arrest.