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Myocardial rupture
Classification and external resources
ICD-10 I23.3-I23.5
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 sequelae of an acute myocardial infarction (heart attack).



The most common cause of myocardial rupture is a recent myocardial infarction, with the rupture typically occurring three to five days after infarction. Other causes of rupture include cardiac trauma, endocarditis (infection of the heart),[1][2] cardiac tumors, infiltrative diseases of the heart,[1] and aortic dissection.

Risk factors for rupture after an acute myocardial infarction include female gender,[3][4] advanced age of the individual,[3][4] and a low body mass index.[3] Other presenting signs associated with myocardial rupture include a pericardial friction rub, sluggish flow in the coronary artery after it is opened, the left anterior descending artery being the cause of the acute MI,[3][4][5] and delay of revascularization greater than 2 hours.[4]


The incidence of myocardial rupture has decreased in the era of urgent revascularization and aggressive pharmacological therapy for the treatment of an acute myocardial rupture. 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.[6] On the other hand, if primary percutaneous coronary intervention is performed to abort the infarction, the incidence of rupture is significantly lowered.[4] The incidence of myocardial rupture if PCI is performed in the setting of an acute myocardial infarction is about 1 percent.[3]


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.[7]

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 veins.


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.


The treatment for myocardial rupture is supportive in the immediate setting and surgical correction of the rupture, if feasible. 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.


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%.[3] 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.[3]


  1. ^ 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.  
  2. ^ 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.  
  3. ^ 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.  
  4. ^ 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.  
  5. ^ 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.  
  6. ^ 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.  
  7. ^ Becker AE, van Mantgem JP. (1975). "Cardiac tamponade. A study of 50 hearts.". Eur J Cardiol 3 (4): 349–58. PMID 1193118.  


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