1. Mechanical complications of MI usually involve rupture or tearing of infarcted tissue.
2. Occurs after the acute phase of myocardial infarction, so should be suspected in a patient with recent MI who rapidly becomes hemodynamically unstable or experiences new chest pain or murmur.
3. This can occur at various locations leading to slightly varying clinical pictures.
4. Is a true emergency. definitive treatment is usually surgical and should not be delayed.
5. Point of care ultrasound can be used to diagnose all of these in the ED and treatment in all cases is surgical.
6. The three main locations of rupture are the papillary muscles or chordae tendinae, interventricular septum, and free wall of the ventricles.

Interventricular septal rupture

• More common in anterior MI or in triple vessel CAD.
• Clinical findings:
• New holosystolic murmur as blood flows from left to right ventricle during systole.
• May be accompanied by palpable thrill at left sternal border.
• Increased chest pain and dyspnea as well.
• Echocardiogram (POCUS) demonstrating left to right shunt. Oxygenation increase of >10% between right atria and right ventricle is diagnostic (Tintinalli’s.)
• Treatment is surgical, if suspected cardiac surgery should be consulted immediately.

Rupture of papillary muscles

• Rupture of papillary muscles (which attach to chordae tendinae which are responsible for preventing atrio-ventricular valve prolapse during systole) is more common after inferior MI.
• Typically presents 3-5 days after infarction.
• Sudden onset dyspnea, increasing CHF, and new holosystolic murmur of mitral regurgitation.
• Posteromedial papillary muscle is most often ruptured as it is usually supplied by RCA.
• Doppler echo can be used to identify ruptured papilliae-chordae.
• Other causes of MVR should be ruled out.
• Treatment is surgical, if suspected cardiac surgery should be consulted immediately.

Rupture of septal free wall

• Occurs in 10% of MI fatalities.
• Usually occurs 1-5 days after infarction.
• Rupture of left septal freewall leads to cardiac tamponade. The mortality rate of which is >90%.
• Clinically this presents with sudden severe often tearing chest pain.
• Patients abruptly become hemodynamically unstable (hypotensive, tachycardic.)
• Beck’s triad may be present if tamponade is occurring (muffled heart sounds, distended neck veins, hypotension.)
• Diagnosis can be made with POCUS.
• Treatment is surgical, if suspected cardiac surgery should be consulted immediately.

Dressler’s syndrome

• A pericarditis like syndrome that occurs secondary to MI but can also happen after cardiac surgeries/invasive interventions or other forms of damage to the myocardium.
• Estimated by the namesake of the syndrome at 2-3% of patients. it is now much lower than this with reperfusion treatment of MI’s.
• Now it is more common in cases of transmural infarction.
• It is thought to be immune mediated as there is an increase in frequency during seasons of increased viral illness.
• In addition patients with Dressler’s syndrome have been found to have increased anti myocardial titres. It has been associated with Coxsackie B, Adenovirus and CMV.
• Infarcted tissue exposes damaged myocardial antigens, leading to antibody deposition in the pericardial space lungs and pleura.
• This in combination with the irritation of blood in the pericardium following infarction leads to inflammation that may precipitate pain.
• May present with or without pericardial or pleural effusion.
• Onset is usually 1-6 weeks after MI (or other cause of damage to Myocardium).
• Patients may present with chest pain similar to angina, fever and pleuropericarditis.
• Pain is similar to pericarditis: pleuritic, sharp, and positional (worse with lying down and improved with sitting up and leaning forward).
• Precordial friction rub may be auscultated in cases following RV or inferior infarction as they are closest to the anterior chest wall.
• Evaluation should be done with bedside ultrasound while formal ultrasound is awaited.
• These patients are at risk for tamponade, and care should be taken to examine for this in the emergency department.
• Where formal ultrasound is not accessible Chest X-ray can be utilized. In the case of pleural and pericardial effusions the costophrenic angles will be flattened and the cardiac silhouette enlarged.
• Chest X-ray should also be done to rule out pneumothorax, pneumonia, and may pleural show effusion if present.
• ECG may show ST elevation or T-wave inversion similar to pericarditis. As condition progresses electrical alternans (where the vector and amplitude become random beat to beat) or low voltage QRS segments may become notable if a pericardial effusion volume is large.
• Blood cultures should be collected to differentiate from infectious causes.
• Bloodwork should include CBC, Troponin, inflammatory markers such as ESR, or CRP. Leukocytosis and elevated inflammatory markers are common. Elevated anti-heart antibodies may be elevated. Ideally, pericardial fluid should be sent for count, differential, cultures, Gram stain, cytology, total protein, and triglyceride levels.

Dressler’s syndrome

• Mainstay of treatment is anti-inflammatories. Aspirin or ibuprofen are most commonly used.
• There is a logical preference for aspirin as virtually all post-MI patients will be on dual anti-platelet therapy, one of which will likely be aspirin.
• If using aspirin a common regime is 750-1000mg q6-8hours gradually tapering over 4 weeks by decreasing the daily total by 650-800 each week. (ie. week 1: 750-1000mg q6-8, week 2: 500-750mg q6-8, week 3: 250-500, week 4 250mg q6-8h.)
• A common regime for ibuprofen is 600-800 q 6-8h, decreasing by 400-800mg of the daily dose each week.
• Consider co-prescribing a GI protective agent in combination with either of these agents to decrease GI side effects.
• If refractory to NSAIDs colchicine or steroids can be considered as well. Dosing regimes for pericarditis can be used in that case.

1. Leib, A. D., Foris, L. A., Nguyen, T., Karam, ;, & Affiliations, K. (2021). Dressler Syndrome Continuing Education Activity. https://www.ncbi.nlm.nih.gov/books/NBK441988/?report=printable

   
   

2. Stapczynski, J. S., Ma, J., Cline, D., Cydulka, R., & Meckler, G. (2011). Tintinalli’s Emergency Medicine (J. Tintinalli, Ed.; 7th ed.). McGraw-Hill.

   
   

3. Damluji, A., van Diepen, S., Katz, J., Menon, V., Tamis-Holland, J., Bakitas, M., Cohen, M., Balsam, L., & Chikwe, J. (2021). Mechanical Complications of Acute Myocardial Infarction: A Scientific Statement From the American Heart Association. Circulation, 144(2).

   
   

4. Farkas, J. (2021, November 24). Post MI complications. Internet Book of Critical Care.