ST elevation myocardial infarction natural history and complications

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ST Elevation Myocardial Infarction Microchapters


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Pathophysiology of Vessel Occlusion
Pathophysiology of Reperfusion
Gross Pathology


Differentiating ST elevation myocardial infarction from other Diseases

Epidemiology and Demographics

Risk Factors


Natural History and Complications

Risk Stratification and Prognosis



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Pre-Hospital Care

Initial Care

Beta Blockers
The coronary care unit
The step down unit
STEMI and Out-of-Hospital Cardiac Arrest
Pharmacologic Reperfusion
Reperfusion Therapy (Overview of Fibrinolysis and Primary PCI)
Reperfusion at a Non–PCI-Capable Hospital:Recommendations
Mechanical Reperfusion
The importance of reducing Door-to-Balloon times
Primary PCI
Adjunctive and Rescue PCI
Rescue PCI
Facilitated PCI
Adjunctive PCI
Management of Patients Who Were Not Reperfused
Assessing Success of Reperfusion
Antithrombin Therapy
Antithrombin therapy
Unfractionated heparin
Low Molecular Weight Heparinoid Therapy
Direct Thrombin Inhibitor Therapy
Factor Xa Inhibition
DVT prophylaxis
Long term anticoagulation
Antiplatelet Agents
Thienopyridine Therapy
Glycoprotein IIbIIIa Inhibition
Other Initial Therapy
Inhibition of the Renin-Angiotensin-Aldosterone System
Magnesium Therapy
Glucose Control
Calcium Channel Blocker Therapy
Lipid Management

Pre-Discharge Care

Recommendations for Perioperative Management–Timing of Elective Noncardiac Surgery in Patients Treated With PCI and DAPT

Post Hospitalization Plan of Care

Long-Term Medical Therapy and Secondary Prevention

Inhibition of the Renin-Angiotensin-Aldosterone System
Cardiac Rehabilitation
Pacemaker Implantation
Long Term Anticoagulation
Implantable Cardioverter Defibrillator
ICD implantation within 40 days of myocardial infarction
ICD within 90 days of revascularization

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]


Without treatment, ST elevation myocardial infarction can prove fatal. Complications of ST elevation MI are divided into the following categories: ischemic, mechanical, arrythmic, embolic, and pericarditis. The prognosis for patients with myocardial infarction varies greatly depending upon simple demographic variables like age, infarct artery location, the presence of signs and symptoms of heart failure on presentation, the symptom to door time, and comorbidities that are present. Several risk stratification tools have been developed to predict a patient's mortality. Most of these risk scores are based upon clinical data obtained at the time of admission rather than at the time of discharge.


Ischemic Complications

Reinfarction or reocclusion of the infarct-related artery is associated with a doubling of mortality.[1] Unfortunately, it is difficult to predict who will reinfarct following fibrinolytic therapy. Among patients undergoing primary PCI, bivalirudin monotherapy has been associated with stent thrombosis in the HORIZONS-AMI and EUROMAX trials.[2][3] Aggressive antiplatelet and antithrombotic therapy minimizes the risk of reinfarction.

Mechanical Complications

A new murmur in patients with ST elevation myocardial infarction should raise an immediate concern of mechanical complicaitons such as papillary muscle rupture, septal rupture, and free-wall rupture which portend a dismal prognosis and may be differentiated on the basis of physical and echocardiographic findings or hemodynamic profiles. Other mechanical sequelae include true or false ventricular aneurysm, dynamic left ventricular outflow tract obstruction, cardiogenic shock, and heart failure.

Left ventricular aneurysm


Rupture of the papillary muscle

Rupture of the interventricular septum

Rupture of the LV free wall

Features of mechanical complications in ST elevation MI[5]
Feature Mechanical Complication of ST Elevation Myocardial Infarction
Papillary Muscle Rupture Ventricular Septal Rupture Free-Wall Rupture
Physical Findings Soft pansystolic murmur best audible at the apex with radiation to the axilla, ⊖ precordial thrill, variable signs of RV overload Harsh pansystolic murmur best audible at the lower left sternal border with radiation to the right parastenal area, ⊕ precordial thrill, S3, accentuated second heart sound Diminished heart sounds, pericardial rub, to-and-fro murmur, jugular venous distention, pulsus paradoxus
Echocardiographic Findings Hypercontractile LV, torn papillary muscle or chordae tendineae, flail leaflet, severe mitral regurgitation Left-to-right shunt at the ventricular level, pattern of RV overload Layered high-acoustic echoes within the pericardium, pericardial effusion, RA and RV diastolic collapse, dilated inferior vena cava, marked respiratory variations in mitral and tricuspid inflow
Hemodynamic Profiles No oxygen saturation gradient from the RA to RV, large V waves in pulmonary artery and capillary wedge tracings, high pulmonary-capillary wedge pressure Step-up in oxygen saturation between the RA and RV (or PA), large V waves Equalization of diastolic pressures among the cardiac chambers

Conduction Abnormalities

Atrial Fibrillation

New onset atrial fibrillation in the setting of STEMI is associated with a very poor prognosis [6]. New onset atrial fibrillation is likely a marker for left atrial distension due to impaired left ventricular compliance.

Arrhythmic Complications

Embolic Complications


2013 Revised ACCF/AHA Guidelines for the Management of ST-Elevation Myocardial Infarction (DO NOT EDIT)[7]

Assessment of Left Ventricular Function (DO NOT EDIT)[7]

Class I
"1. LV ejection fraction should be measured in all patients with STEMI. (Level of Evidence: C)"


  • 2013 Revised ACCF/AHA Guidelines for the Management of ST-Elevation Myocardial Infarction [7]


  1. Gibson CM, Karha J, Murphy SA, James D, Morrow DA, Cannon CP; et al. (2003). "Early and long-term clinical outcomes associated with reinfarction following fibrinolytic administration in the Thrombolysis in Myocardial Infarction trials". J Am Coll Cardiol. 42 (1): 7–16. PMID 12849652.
  2. Dangas GD, Caixeta A, Mehran R, Parise H, Lansky AJ, Cristea E; et al. (2011). "Frequency and predictors of stent thrombosis after percutaneous coronary intervention in acute myocardial infarction". Circulation. 123 (16): 1745–56. doi:10.1161/CIRCULATIONAHA.110.981688. PMID 21482968.
  3. Clemmensen, Peter; Hof, Arnoud van't; Deliargyris, Efthymios N.; Coste, Pierre; ten Berg, Jurrien; Cavallini, Claudio; Hamon, Martial; Dudek, Dariusz; Zeymer, Uwe; Tabone, Xavier; Clayton, Tim; Bernstein, Debra; Prats, Jayne (2014). "PREDICTORS ASSOCIATED WITH ACUTE STENT THROMBOSIS AFTER PRIMARY PCI: THE EUROMAX TRIAL". Journal of the American College of Cardiology. 63 (12): A27. doi:10.1016/S0735-1097(14)60027-9. ISSN 0735-1097.
  4. Voci P, Bilotta F, Caretta Q, Mercanti C, Marino B (1995). "Papillary muscle perfusion pattern. A hypothesis for ischemic papillary muscle dysfunction". Circulation. 91 (6): 1714–8. PMID 7882478.
  5. Birnbaum Y, Fishbein MC, Blanche C, Siegel RJ (2002). "Ventricular septal rupture after acute myocardial infarction". N Engl J Med. 347 (18): 1426–32. doi:10.1056/NEJMra020228. PMID 12409546.
  6. GUSTO 1 trial
  7. 7.0 7.1 7.2 O'Gara PT, Kushner FG, Ascheim DD; et al. (2012). "2013 ACCF/AHA Guideline for the Management of ST-Elevation Myocardial Infarction: Executive Summary: A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines". Circulation. doi:10.1161/CIR.0b013e3182742c84. PMID 23247303. Unknown parameter |month= ignored (help)

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