Myocardial rupture |
Classification and external resources |
ICD-10 |
I23.3-I23.5, S26.8 |
DiseasesDB |
8569 |
eMedicine |
med/1571 |
MeSH |
D006341 |
Myocardial rupture (or heart rupture) is a laceration or tearing of the walls of the ventricles or atria of the heart, of the interatrial or interventricular septum, of the papillary muscles or chordae tendineae or of one of the valves of the heart. It is most commonly seen as a serious sequela of an acute myocardial infarction (heart attack).
It can also be caused by trauma.[1]
Contents
- 1 Etiology
- 2 Incidence
- 3 Classification
- 4 Signs and symptoms
- 5 Diagnosis
- 6 Treatment
- 7 Prognosis
- 8 References
Etiology
The most common cause of myocardial rupture is a recent myocardial infarction, with the rupture typically occurring three to five days after infarction.[2] Other causes of rupture include cardiac trauma, endocarditis (infection of the heart),[3][4] cardiac tumors, infiltrative diseases of the heart,[3] and aortic dissection.[citation needed]
Risk factors for rupture after an acute myocardial infarction include female gender,[5][6] advanced age of the individual,[5][6] and a low body mass index.[5] Other presenting signs associated with myocardial rupture include a pericardial friction rub, sluggish flow in the coronary artery after it is opened i.e. revascularized with an angioplasty, the left anterior descending artery being often the cause of the acute MI,[5][6][7] and delay of revascularization greater than 2 hours.[6]
Incidence
The incidence of myocardial rupture has decreased in the era of urgent revascularization and aggressive pharmacological therapy for the treatment of an acute myocardial infarction. However, the decrease in the incidence of myocardial rupture is not uniform; there is a slight increase in the incidence of rupture if thrombolytic agents are used to abort a myocardial infarction.[8] On the other hand, if primary percutaneous coronary intervention is performed to abort the infarction, the incidence of rupture is significantly lowered.[6] The incidence of myocardial rupture if PCI is performed in the setting of an acute myocardial infarction is about 1 percent.[5]
Classification
Myocardial ruptures can be classified as one of three types.
- Type I myocardial rupture is an abrupt slit-like tear that generally occurs within 24 hours of an acute myocardial infarction.
- Type II is an erosion of the infarcted myocardium, which is suggestive of a slow tear of the dead myocardium. Type II ruptures typically occur more than 24 hours after the infarction occurred.
- Type III ruptures are characterized by early aneurysm formation and subsequent rupture of the aneurysm.[9]
Another method for classifying myocardial ruptures is by the anatomical portion of the heart that has ruptured. By far the most dramatic is rupture of the free wall of the left or right ventricles, as this is associated with immediate hemodynamic collapse and death secondary to acute pericardial tamponade. Rupture of the interventricular septum will cause a ventricular septal defect. Rupture of a papillary muscle will cause acute mitral regurgitation.
Signs and symptoms
Symptoms of myocardial rupture are recurrent or persistent chest pain, syncope, and distension of jugular vein.
Diagnosis
Due to the acute hemodynamic deterioration associated with myocardial rupture, the diagnosis is generally made based on physical examination, changes in the vital signs, and clinical suspicion. The diagnosis can be confirmed with echocardiography.
Treatment
The treatment for myocardial rupture is supportive in the immediate setting and surgical correction of the rupture, if feasible.[citation needed] A certain small percentage of individuals do not seek medical attention in the acute setting and survive to see the physician days or weeks later. In this setting, it may be reasonable to treat the rupture medically and delay or avoid surgery completely, depending on the individual's comorbid medical issues.
Prognosis
The prognosis of myocardial rupture is dependent on a number of factors, including which portion of the myocardium is involved in the rupture. In one case series, if myocardial rupture involved the free wall of the left ventricle, the mortality rate was 100.0%.[5] Even if the individual survives the initial hemodynamic sequelae of the rupture, the 30 day mortality is still significantly higher than if rupture did not occur.[5]
References
- ^ Nan YY, Lu MS, Liu KS, et al. (September 2009). "Blunt traumatic cardiac rupture: therapeutic options and outcomes". Injury 40 (9): 938–45. doi:10.1016/j.injury.2009.05.016. PMID 19540491.
- ^ Figueras J, Alcalde O, Barrabes JA, Serra V, Alguersuari J, Cortadellas J, et al. Changes in Hospital Mortality Rates in 425 Patients with Acute ST-Elevation Myocardial Infarction and Cardiac Rupure Over a 30-Year Period. Circulation. 2008;118:2783–9.
- ^ a b Lin TH, Su HM, Voon WC, Lai HM, Yen HW, Lai WT, Sheu SH. (2006). "Association between hypertension and primary mitral chordae tendinae rupture.". Am J Hypertens 19 (1): 75–9. doi:10.1016/j.amjhyper.2005.06.020. PMID 16461195.
- ^ de Diego C, Marcos-Alberca P, Pai RK. (2006). "Giant periprosthetic vegetation associated with pseudoaneurysmal-like rupture." (PDF). Eur Heart J 27 (8): 912. doi:10.1093/eurheartj/ehi540. PMID 16569654.
- ^ a b c d e f g Yip HK, Wu CJ, Chang HW, Wang CP, Cheng CI, Chua S, Chen MC. (2003). "Cardiac rupture complicating acute myocardial infarction in the direct percutaneous coronary intervention reperfusion era." (PDF). Chest 124 (2): 565–71. doi:10.1378/chest.124.2.565. PMID 12907544.
- ^ a b c d e Moreno R, Lopez-Sendon J, Garcia E, Perez de Isla L, Lopez de Sa E, Ortega A, Moreno M, Rubio R, Soriano J, Abeytua M, Garcia-Fernandez MA. (2002). "Primary angioplasty reduces the risk of left ventricular free wall rupture compared with thrombolysis in patients with acute myocardial infarction.". J Am Coll Cardiol 39 (4): 598–603. doi:10.1016/S0735-1097(01)01796-X. PMID 11849857.
- ^ Sugiura T, Nagahama Y, Nakamura S, Kudo Y, Yamasaki F, Iwasaka T. (2003). "Left ventricular free wall rupture after reperfusion therapy for acute myocardial infarction.". Am J Cardiol 92 (3): 282–4. doi:10.1016/S0002-9149(03)00625-8. PMID 12888132.
- ^ Becker RC, Gore JM, Lambrew C, Weaver WD, Rubison RM, French WJ, Tiefenbrunn AJ, Bowlby LJ, Rogers WJ. (1996). "A composite view of cardiac rupture in the United States National Registry of Myocardial Infarction.". J Am Coll Cardiol 27 (6): 1321–6. doi:10.1016/0735-1097(96)00008-3. PMID 8626938.
- ^ Becker AE, van Mantgem JP. (1975). "Cardiac tamponade. A study of 50 hearts.". Eur J Cardiol 3 (4): 349–58. PMID 1193118.
- Cardiovascular disease: heart disease
- Circulatory system pathology
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Ischaemic |
Coronary disease
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- Coronary artery disease (CAD)
- Coronary artery aneurysm
- Coronary artery dissection
- Coronary thrombosis
- Coronary vasospasm
- Myocardial bridge
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Active ischemia
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- Angina pectoris
- Prinzmetal's angina
- Stable angina
- Acute coronary syndrome
- Myocardial infarction
- Unstable angina
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Sequelae
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- hours
- Hibernating myocardium
- Myocardial stunning
- days
- weeks
- Aneurysm of heart / Ventricular aneurysm
- Dressler's syndrome
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Layers |
Pericardium
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- Pericarditis
- Acute
- Chronic / Constrictive
- Pericardial effusion
- Cardiac tamponade
- Hemopericardium
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Myocardium
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- Myocarditis
- Cardiomyopathy: Dilated (Alcoholic), Hypertrophic, and Restrictive
- Loeffler endocarditis
- Cardiac amyloidosis
- Endocardial fibroelastosis
- Arrhythmogenic right ventricular dysplasia
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Endocardium /
valves
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Endocarditis
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- infective endocarditis
- Subacute bacterial endocarditis
- non-infective endocarditis
- Libman–Sacks endocarditis
- Nonbacterial thrombotic endocarditis
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Valves
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- mitral
- regurgitation
- prolapse
- stenosis
- aortic
- tricuspid
- pulmonary
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Conduction /
arrhythmia |
Bradycardia
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- Sinus bradycardia
- Sick sinus syndrome
- Heart block: Sinoatrial
- AV
- Intraventricular
- Bundle branch block
- Right
- Left
- Left anterior fascicle
- Left posterior fascicle
- Bifascicular
- Trifascicular
- Adams–Stokes syndrome
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Tachycardia
(paroxysmal and sinus)
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Supraventricular
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- Atrial
- Junctional
- AV nodal reentrant
- Junctional ectopic
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Ventricular
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- Accelerated idioventricular rhythm
- Catecholaminergic polymorphic
- Torsades de pointes
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Premature contraction
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Pre-excitation syndrome
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- Lown–Ganong–Levine
- Wolff–Parkinson–White
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Flutter / fibrillation
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- Atrial flutter
- Ventricular flutter
- Atrial fibrillation
- Ventricular fibrillation
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Pacemaker
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- Ectopic pacemaker / Ectopic beat
- Multifocal atrial tachycardia
- Pacemaker syndrome
- Parasystole
- Wandering pacemaker
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Long QT syndrome
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- Andersen–Tawil
- Jervell and Lange-Nielsen
- Romano–Ward
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Cardiac arrest
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- Sudden cardiac death
- Asystole
- Pulseless electrical activity
- Sinoatrial arrest
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Other / ungrouped
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- hexaxial reference system
- Right axis deviation
- Left axis deviation
- QT
- T
- ST
- Osborn wave
- ST elevation
- ST depression
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Cardiomegaly |
- Ventricular hypertrophy
- Left
- Right / Cor pulmonale
- Atrial enlargement
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Other |
- Cardiac fibrosis
- Heart failure
- Diastolic heart failure
- Cardiac asthma
- Rheumatic fever
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noco/cong/tumr, sysi/epon, injr
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proc, drug (C1A/1B/1C/1D), blte
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Chest trauma, excluding fractures (S20–S29, 860–862)
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Cardiac and
circulatory system injuries |
- vascular: Traumatic aortic rupture
- heart: Myocardial contusion/Commotio cordis
- Cardiac tamponade
- Hemopericardium
- Myocardial rupture
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Lung and
lower respiratory tract injuries |
- Pneumothorax
- Hemothorax
- Hemopneumothorax
- Pulmonary contusion
- Pulmonary laceration
- Tracheobronchial injury
- Diaphragmatic rupture
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anat (a:h/u/t/a/l,v:h/u/t/a/l)/phys/devp/cell/prot
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noco/syva/cong/lyvd/tumr, sysi/epon, injr
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proc, drug (C2s+n/3/4/5/7/8/9)
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noco/cong/tumr, sysi/epon, injr
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proc, drug (C1A/1B/1C/1D), blte
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anat (n, x, l, c)/phys/devp
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noco (c, p)/cong/tumr, sysi/epon, injr
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proc, drug (R1/2/3/5/6/7)
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