ST elevation myocardial infarction natural history and complications
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
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.
Complications
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
- A true left ventricular aneurysm is an outpouching formed by a stretched, thinned-out myocardial scar. Patients with transmural infarction and patients who do not receive reperfusion therapy are at increased risk. LV aneurysm may manifest acutely as low-output cardiogenic shock or chronically as heart failure or thromboembolism in the presence of mural thrombus. A large, diffuse point of maximal impulse and S3 gallops may be evident on physical examination. A chest radiograph may demonstrate a localized bulging segment in the cardiac silhouette. Dyskinetic or paradoxical motions of the aneurysmal segment may be detected by echocardiography or ventriculography. True aneurysm connects with the LV cavity by a wide neck and is less susceptible to rupture than a false aneurysm. ACE inhibitor and vasodilator are used in the mangement of chronic heart failure associated with ventricular aneurysm. Anticoagulant is indicated in the presence of mural thrombus. Sustained ventricular arrhythmia from an aneurysm may require defibrillator placement. Surgical resection may be considered in selected cases with refractory symptoms.
Pseudoaneurysm
- In contrast to the true aneurysm which contains viable myocardium in its wall, pseudoaneurysm lacks the myocardial elements and is formed by adherent pericardium and organized hematoma. Unlike true ventricular aneurysm, pseudoaneurysm communicates with the cavity of the left ventricle through a narrow neck and is more prone to rupture. Pseudoaneurysm may partially reduce stroke volume similar to a true aneurysm. Surgery is recommended for all patients regardless of symptoms or the size of pseudoaneurysm in light of a high risk for spontaneous rupture and sudden death.
Rupture of the papillary muscle
- Papillary muscle rupture is characterized by symptoms of acute severe mitral regurgitation and pulmonary edema and should be suspected in STEMI patients with a new soft holosystolic murmur at the apex. Posterior papillary muscle rupture, as occurs in inferior MI, is more common than anterior papillary muscle rupture which may be a complication of anterior or lateral MI. Posterior papillary muscle is considered more susceptible to ischemic rupture due to its singular blood supply from the posterior descending artery. In contradistinction to the posterior papillary muscle, the anterior papillary muscle receives a dual blood supply from the left anterior descending artery and the circumflex artery.[4] Urgent transthoracic echocardiography should be obtained to establish a definite diagnosis. Nitroglycerin or nitroprusside may be used to temporize the patient if systolic blood pressure is above 90 mm Hg. If the patient cannot tolerate vasodilator due to rapid hemodynamic deterioration, intra-aortic balloon counterpulsation should be instituted as a bridging therapy until emergency mitral valve replacement can be performed.
Rupture of the interventricular septum
- Patients with septal rupture frequently report chest pain, shortness of breath, and symptoms of low-output cardiogenic shock. Key physical findings include a harsh, loud holosystolic murmur best heard at the lower left sternal border, palpable thrill at the right precordium, S3 gallops, and accentuation of pulmonic component of the second heart sound. Color Doppler echocardiography is useful for determining the location and size of the defect and detecting left-to-right shunt and right ventricular overload. Septal rupture should be managed by temporary stabilization with intra-aortic balloon counterpulsation followed by intravenous vasodilator and early surgical closure.
Rupture of the LV free wall
- Free-wall rupture usually leads to hemopericardium and abrupt circulatory collapse. Clinical manifestations range from anginal, pleuritic, or pericardial chest discomfort to catastrophic symptoms of cardiogenic shock, cardiac tamponade, and sudden death. Echocardiography is useful for the diagnosis and emergency pericardiocentesis may be indicated for cardiac tamponade. Survival depends primarily on early recognition and prompt surgical repair.
| 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
Pericarditis
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)" |
Sources
- 2013 Revised ACCF/AHA Guidelines for the Management of ST-Elevation Myocardial Infarction [7]
References
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ GUSTO 1 trial
- ↑ 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
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