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{{ST elevation myocardial infarction}}
{{ST elevation myocardial infarction}}
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==Overview==
==Overview==
The natural progression of ST elevation myocardial infarction depends on epicardial artery patency and the risk for early vessel reocclusion. Without treatment, ST elevation myocardial infarction can prove deadly.


==[[ST elevation myocardial infarction complications|Complications]]==
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.


==[[ST elevation myocardial infarction prognosis|Prognosis]]==
==Complications==
 
===Ischemic Complications===
 
[[Reinfarction]] or reocclusion of the infarct-related artery is associated with a doubling of [[mortality]].<ref name="pmid12849652">{{cite journal| author=Gibson CM, Karha J, Murphy SA, James D, Morrow DA, Cannon CP et al.| title=Early and long-term clinical outcomes associated with reinfarction following fibrinolytic administration in the Thrombolysis in Myocardial Infarction trials. | journal=J Am Coll Cardiol | year= 2003 | volume= 42 | issue= 1 | pages= 7-16 | pmid=12849652 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12849652  }} </ref> 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.<ref name="pmid21482968">{{cite journal| author=Dangas GD, Caixeta A, Mehran R, Parise H, Lansky AJ, Cristea E et al.| title=Frequency and predictors of stent thrombosis after percutaneous coronary intervention in acute myocardial infarction. | journal=Circulation | year= 2011 | volume= 123 | issue= 16 | pages= 1745-56 | pmid=21482968 | doi=10.1161/CIRCULATIONAHA.110.981688 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21482968  }} </ref><ref name="ClemmensenHof2014">{{cite journal|last1=Clemmensen|first1=Peter|last2=Hof|first2=Arnoud van't|last3=Deliargyris|first3=Efthymios N.|last4=Coste|first4=Pierre|last5=ten Berg|first5=Jurrien|last6=Cavallini|first6=Claudio|last7=Hamon|first7=Martial|last8=Dudek|first8=Dariusz|last9=Zeymer|first9=Uwe|last10=Tabone|first10=Xavier|last11=Clayton|first11=Tim|last12=Bernstein|first12=Debra|last13=Prats|first13=Jayne|title=PREDICTORS ASSOCIATED WITH ACUTE STENT THROMBOSIS AFTER PRIMARY PCI: THE EUROMAX TRIAL|journal=Journal of the American College of Cardiology|volume=63|issue=12|year=2014|pages=A27|issn=07351097|doi=10.1016/S0735-1097(14)60027-9}}</ref> 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]], [[ventricular septal rupture|septal rupture]], and [[Myocardial rupture|free-wall rupture]] which portend a dismal prognosis and may be differentiated on the basis of [[physical examination|physical]] and [[echocardiography|echocardiographic]] findings or [[hemodynamic|hemodynamic profiles]]. Other mechanical sequelae include true or false [[ventricular aneurysm]], [[Left ventricular outflow tract obstruction|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 [[MI|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 [[PMI|point of maximal impulse]] and [[S3|S<sub>3</sub> 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 [[pseudoaneurysm|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 [[implantable cardioverter defibrillator|defibrillator]] placement. Surgical resection may be considered in selected cases with refractory symptoms.
 
====[[Left ventricular aneurysm|Pseudoaneurysm]]====
:* In contrast to the [[Left ventricular aneurysm|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]].
 
====[[Papillary muscle rupture|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 MI|anterior]] or [[lateral MI]]. Posterior papillary muscle is considered more susceptible to [[ischemia|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]].<ref name="pmid7882478">{{cite journal| author=Voci P, Bilotta F, Caretta Q, Mercanti C, Marino B| title=Papillary muscle perfusion pattern. A hypothesis for ischemic papillary muscle dysfunction. | journal=Circulation | year= 1995 | volume= 91 | issue= 6 | pages= 1714-8 | pmid=7882478 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7882478 }}</ref> Urgent [[transthoracic echocardiography]] should be obtained to establish a definite diagnosis. [[Nitroglycerin]] or [[nitroprusside]] may be used to temporize the patient if [[SBP|systolic blood pressure]] is above 90 mm Hg. If the patient cannot tolerate [[vasodilator]] due to rapid hemodynamic deterioration, [[intra-aortic balloon pump|intra-aortic balloon counterpulsation]] should be instituted as a bridging therapy until emergency [[mitral valve replacement]] can be performed.
 
====[[Rupture of the ventricular septum|Rupture of the interventricular septum]]====
:* Patients with [[Rupture of the ventricular septum|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|S<sub>3</sub> gallops]], and accentuation of pulmonic component of the second [[heart sound]]. [[Doppler echocardiography|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 pump|intra-aortic balloon counterpulsation]] followed by [[intravenous]] [[vasodilator]] and early surgical closure.
 
====[[Myocardial rupture|Rupture of the LV free wall]]====
:* [[Free wall rupture|Free-wall rupture]] usually leads to [[hemopericardium]] and abrupt [[collapse|circulatory collapse]]. Clinical manifestations range from [[angina|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.
 
{| style="border: 2px solid #DCDCDC; font-size: 90%;"
|+ ''Features of mechanical complications in ST elevation MI''<ref name="pmid12409546">{{cite journal| author=Birnbaum Y, Fishbein MC, Blanche C, Siegel RJ| title=Ventricular septal rupture after acute myocardial infarction. | journal=N Engl J Med | year= 2002 | volume= 347 | issue= 18 | pages= 1426-32 | pmid=12409546 | doi=10.1056/NEJMra020228 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12409546  }} </ref>
| align="center" style="background: #DCDCDC; width: 13%;" rowspan=2 | '''Feature'''
| align="center" style="background: #DCDCDC;" colspan=3 | '''Mechanical Complication of ST Elevation Myocardial Infarction'''
|-
| style="padding: 0 5px; background: #DCDCDC; width: 29%;" align=center | '''Papillary Muscle Rupture'''
| style="padding: 0 5px; background: #DCDCDC; width: 29%;" align=center | '''Ventricular Septal Rupture'''
| style="padding: 0 5px; background: #DCDCDC; width: 29%;" align=center | '''Free-Wall Rupture'''
|-
| style="padding: 0 5px; background: #DCDCDC;" align=left valign=top | '''Physical Findings'''
| style="padding: 0 5px; background: #F5F5F5;" align=left valign=top | Soft pansystolic murmur best audible at the apex with radiation to the axilla, ⊖ precordial thrill, variable signs of RV overload
| style="padding: 0 5px; background: #F5F5F5;" align=left valign=top | Harsh pansystolic murmur best audible at the lower left sternal border with radiation to the right parastenal area, ⊕ precordial thrill, S<sub>3</sub>, accentuated second heart sound
| style="padding: 0 5px; background: #F5F5F5;" align=left valign=top | Diminished heart sounds, pericardial rub, to-and-fro murmur, jugular venous distention, pulsus paradoxus
|-
| style="padding: 0 5px; background: #DCDCDC;" align=left valign=top | '''Echocardiographic Findings'''
| style="padding: 0 5px; background: #F5F5F5;" align=left valign=top | Hypercontractile LV, torn papillary muscle or chordae tendineae, flail leaflet, severe mitral regurgitation
| style="padding: 0 5px; background: #F5F5F5;" align=left valign=top | Left-to-right shunt at the ventricular level, pattern of RV overload
| style="padding: 0 5px; background: #F5F5F5;" align=left valign=top | 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
|-
| style="padding: 0 5px; background: #DCDCDC;" align=left valign=top | '''Hemodynamic Profiles'''
| style="padding: 0 5px; background: #F5F5F5;" align=left valign=top | No oxygen saturation gradient from the RA to RV, large V waves in pulmonary artery and capillary wedge tracings, high pulmonary-capillary wedge pressure
| style="padding: 0 5px; background: #F5F5F5;" align=left valign=top | Step-up in oxygen saturation between the RA and RV (or PA), large V waves
| style="padding: 0 5px; background: #F5F5F5;" align=left valign=top | 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 <ref>GUSTO 1 trial</ref>.  New onset atrial fibrillation is likely a marker for left atrial distension due to impaired left ventricular compliance.
 
* [[Atrial flutter]]
* [[Postinfarction conduction abnormalities]]
 
===Arrhythmic Complications===
 
* [[Sudden cardiac death]]
 
===Embolic Complications===
 
* [[Stroke]]
* [[DVT]]
 
===Pericarditis===
 
* [[Post myocardial infarction pericarditis]]
* [[Dressler's syndrome]]
 
==2013 Revised ACCF/AHA Guidelines for the Management of ST-Elevation Myocardial Infarction (DO NOT EDIT)<ref name="pmid23247303">{{cite journal |author=O'Gara PT, Kushner FG, Ascheim DD, ''et al.'' |title=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 |journal=Circulation |volume= |issue= |pages= |year=2012 |month=December |pmid=23247303 |doi=10.1161/CIR.0b013e3182742c84|url=}}</ref>==
 
===Assessment of Left Ventricular Function (DO NOT EDIT)<ref name="pmid23247303">{{cite journal |author=O'Gara PT, Kushner FG, Ascheim DD, ''et al.'' |title=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 |journal=Circulation |volume= |issue= |pages= |year=2012 |month=December |pmid=23247303 |doi=10.1161/CIR.0b013e3182742c84|url=}}</ref>===
 
{|class="wikitable" style="width: 80%"
|-
| colspan="1" style="text-align:center; background:LightGreen"|[[ACC AHA guidelines classification scheme#Classification of Recommendations|Class I]]
|-
| bgcolor="LightGreen"|<nowiki>"</nowiki>'''1.''' [[LV]] [[ejection fraction]] should be measured in all patients with [[STEMI]]. ''([[ACC AHA guidelines classification scheme#Level of Evidence|Level of Evidence: C]])''<nowiki>"</nowiki>
|}
 
==Sources==
* 2013 Revised ACCF/AHA Guidelines for the Management of ST-Elevation Myocardial Infarction <ref name="pmid23247303">{{cite journal |author=O'Gara PT, Kushner FG, Ascheim DD, ''et al.'' |title=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 |journal=Circulation |volume= |issue= |pages= |year=2012 |month=December |pmid=23247303 |doi=10.1161/CIR.0b013e3182742c84|url=}}</ref>


==References==
==References==
{{reflist|2}}
{{reflist|2}}
{{WH}}
{{WS}}


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[[Category:Cardiology]]
[[Category:Ischemic heart diseases]]
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Latest revision as of 00:17, 30 July 2020

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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

Pseudoaneurysm

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

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

  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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