Myocardial Rupture 

  • Author: Jamshid Shirani, MD; Chief Editor: Eric H Yang, MD   more...
 
Updated: Dec 2, 2011
 

Background

Myocardial rupture occurs in the setting of acute myocardial infarction (AMI), blunt and penetrating cardiac trauma (see image below), primary cardiac infection, primary and secondary cardiac tumors, infiltrative diseases of the heart, and aortic dissection. The clinical presentation of myocardial rupture depends on the mechanism and site of injury and the hemodynamic effects of the rupture. Mortality rates are extremely high unless early diagnosis and surgical intervention are provided rapidly.

See the image below.

Photograph of the heart of a 43-year-old man demonPhotograph of the heart of a 43-year-old man demonstrating the site of a stab wound over the left ventricular lateral free wall (shown as a vertical tear).
Next

Pathophysiology

AMI is the most common etiology of myocardial rupture. Ischemic myocardial rupture may involve the left ventricular (LV) and right ventricular (RV) free walls, ventricular septum, and LV papillary muscle, in decreasing order of frequency. Myocardial rupture rarely involves the left or right atrial walls.

The consequences of myocardial rupture in the setting of AMI can include pericardial tamponade, ventricular septal defect (VSD) with left-to-right shunt, acute mitral regurgitation (MR), or formation of a pseudoaneurysm. In most instances, the catastrophic clinical presentation occurs within 3-5 days of a rather small AMI. Both hemodynamic factors (increased intracavitary pressure) and regional myocardial structural weakness (myocyte necrosis, collagen matrix resolution, intense inflammation) are important contributory factors to myocardial rupture in the setting of AMI.

In rare instances, patients have been reported to simultaneously experience LV free wall rupture and ventricular septal or papillary muscle rupture (double rupture) following AMI. In the case of a papillary muscle rupture, the posteromedial papillary muscle is twice as likely to rupture as is the anterolateral papillary muscle. This likelihood is because the anteromedial papillary muscle is more often supplied by 2 arterial systems (left anterior descending and left circumflex coronary arteries), whereas the posteromedial papillary muscle is frequently supplied by only one coronary artery (usually the right) system. Rupture of both papillary muscles following AMI has been reported.

In some patients who survive LV free wall rupture following AMI, the rupture can be sealed by the epicardium (visceral pericardium) or by a hematoma on the epicardial surface of the heart. This entity has been referred to as LV diverticulum or contained myocardial rupture and represents a subacute pathologic condition between free rupture into the pericardial cavity and formation of a pseudoaneurysm. A pseudoaneurysm is formed if the area of rupture is contained locally by the adjacent parietal pericardium and represents the chronic stage of LV free wall rupture. The most common etiology of LV pseudoaneurysm is AMI. (LV pseudoaneurysm is twice as common with inferior, rather than anterior, AMI.) LV pseudoaneurysms may develop following surgery, especially following mitral valve replacement.

Blunt cardiac trauma, most commonly in the setting of an automobile accident, may cause myocardial rupture as a result of cardiac compression between the sternum and the spine, direct impact (sternal trauma), or from deceleration injury. It may result in rupture of the papillary muscles, cardiac free wall, or the ventricular septum. The cardiac chambers involved are, in decreasing order of frequency, the right ventricle, left ventricle, right atrium, and left atrium.

However, among those who reach the hospital alive, the right atrium is the most commonly involved chamber. In up to 30% of cases, the rupture involves more than one chamber. Delayed myocardial rupture has been reported as a result of cardiac contusion. Acute mitral or tricuspid regurgitation, VSD, or pericardial tamponade may result from myocardial rupture secondary to blunt cardiac trauma.

Penetrating myocardial injury occurs most commonly as a result of stab or gunshot wounds, as shown below. Unlike blunt trauma, penetrating cardiac injury always involves the pericardium. Consequently, ventricular free-wall rupture in this setting may result in either pericardial tamponade (if the pericardial wound is obliterated) or intrathoracic hemorrhage. While pericardial tamponade is more common with stab wounds, gunshot wounds more frequently are associated with hypovolemic shock. The cardiac chambers involved are, in decreasing order of frequency, the right ventricle, left ventricle, right atrium, and left atrium. See the image below.

Photograph of the heart of a 43-year-old man demonPhotograph of the heart of a 43-year-old man demonstrating the site of a stab wound over the left ventricular lateral free wall (shown as a vertical tear).

Myocardial abscesses accompanying infective endocarditis may rupture transmurally, resulting in VSD or pericardial tamponade (pyohemopericardium). Such abscesses are observed most commonly in the setting of Staphylococcus aureus endocarditis involving prosthetic valves in the aortic position. Rarely, myocardial necrosis due to acute myocarditis, tuberculosis, or sarcoidosis may result in myocardial rupture.

Myocardial rupture is rarely caused by primary (hemangiopericytoma, angiosarcoma, lymphoma) or secondary (metastatic) cardiac tumors. Lymphomas and acute myeloblastic leukemia also have been associated with myocardial rupture.

Previous
Next

Epidemiology

Frequency

United States

Myocardial rupture complicates up to 10% of AMIs. Approximately 6-10% of penetrating chest wounds and 15-75% of blunt chest traumas are associated with cardiac injury. Myocardial rupture occurs in 10-15% of fatal motor vehicle accidents. Incidence of cardiac rupture following blunt trauma is 0.5-2% among hospital trauma admissions.

Mortality/Morbidity

Myocardial rupture is responsible for nearly 15% of all in-hospital deaths among patients with AMI. It is the second most common cause, after pump failure, of in-hospital mortality among patients with AMI.

The overall mortality rate from myocardial rupture following blunt trauma is 76-93%. However, among those who reach the hospital alive, the mortality rate is 29-50%. Mortality from myocardial rupture resulting from penetrating trauma ranges from 62-89% in the field to 2-83% after reaching a hospital. The latter largely depends on the type of injury, rapidity of the transfer to a hospital, and patients' vital signs and condition upon arrival.

Following myocardial rupture as a result of penetrating cardiac trauma, hospital mortality is higher in those presenting with hypovolemia rather than pericardial tamponade (22% vs 8%). In-hospital mortality is lowest for patients with RV rupture.

Sex

Myocardial rupture after AMI is reported more commonly in women than in men (1.4:1).

Traumatic myocardial rupture is more common in males (up to 85% in some series) than in females.

Age

Myocardial rupture after AMI is more common in patients aged 60 years or older.

Traumatic myocardial rupture is observed more commonly in those aged 15-63 years (mean, 34 y).[1]

Previous
 
 
Contributor Information and Disclosures
Author

Jamshid Shirani, MD  Director of Cardiology Fellowship Program, Director of Echocardiography Laboratory, St Luke's Hospital and Health Network

Jamshid Shirani, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Cardiology, American College of Physicians, American Federation for Medical Research, American Heart Association, American Society of Echocardiography, and Association of Subspecialty Professors

Disclosure: Nothing to disclose.

Coauthor(s)

Jamshid Alaeddini, MD, FACC  Clinical Cardiac Electrophysiologist, Inland Cardiology Associates

Jamshid Alaeddini, MD, FACC is a member of the following medical societies: American College of Cardiology and American Heart Association

Disclosure: Boston Scientific Honoraria Speaking and teaching; Medtronic Honoraria Speaking and teaching; St. Jude Honoraria Speaking and teaching; Reliant Honoraria Speaking and teaching

Alessandra Brofferio, MD  Fellow, Department of Cardiovascular Medicine, Geisinger Medical Center

Disclosure: Nothing to disclose.

Specialty Editor Board

Eric Vanderbush, MD, FACC  Chief, Department of Internal Medicine, Division of Cardiology, Harlem Hospital Center; Clinical Assistant Professor of Cardiology, Columbia University College of Physicians and Surgeons

Eric Vanderbush, MD, FACC is a member of the following medical societies: American College of Cardiology and American Heart Association

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Marschall S Runge, MD, PhD  Charles and Anne Sanders Distinguished Professor of Medicine, Chairman, Department of Medicine, Vice Dean for Clinical Affairs, University of North Carolina at Chapel Hill School of Medicine

Marschall S Runge, MD, PhD is a member of the following medical societies: American Association for the Advancement of Science, American College of Cardiology, American College of Physicians-American Society of Internal Medicine, American Federation for Clinical Research, American Federation for Medical Research, American Heart Association, American Physiological Society, American Society for Clinical Investigation, American Society for Investigative Pathology, Association of American Physicians, Association of Professors of Cardiology, Association of Professors of Medicine, Southern Society for Clinical Investigation, and Texas Medical Association

Disclosure: Pfizer Honoraria Speaking and teaching; Merck Honoraria Speaking and teaching; Orthoclinica Diagnostica Consulting fee Consulting

Amer Suleman, MD  Private Practice

Amer Suleman, MD is a member of the following medical societies: American College of Physicians, American Heart Association, American Institute of Stress, American Society of Hypertension, Federation of American Societies for Experimental Biology, Royal Society of Medicine, and Society of Cardiac Angiography and Interventions

Disclosure: Nothing to disclose.

Chief Editor

Eric H Yang, MD  Associate Professor of Medicine, Director of Interventional Cardiology Fellowship Program, Henry Ford Hospital

Eric H Yang, MD is a member of the following medical societies: Alpha Omega Alpha

Disclosure: Nothing to disclose.

References
  1. Javaid MM, Grigoriou A, Katsianos D, Kon SP. NEPHROTIC AND ANTI-PHOSPHOLIPID SYNDROMES: MULTISYSTEM CONDITIONS ASSOCIATED WITH ACUTE MYOCARDIAL INFARCTION IN YOUNG PATIENTS. J Ren Care. Sep 14 2011;[Medline].

  2. Suzuki M, Enomoto D, Seike F, Fujita S, Honda K. Clinical Features of Early Myocardial Rupture of Acute Myocardial Infarction. Angiology. Nov 8 2011;[Medline].

  3. Rajendra H. Mehta, MD, MS; Joshua D. Grab, MS; Sean M. O'Brien, PhD; Donald D. Glower, MD;Constance K. Haan, et al. Clinical characteristics and in-hospital outcomes of patients with cardiogenic shock undergoing coronary artery bypass surgery: insights from the Society of Thoracic Surgeons National Cardiac Database. Circulation. 2/2008;117:876-885. [Medline]. [Full Text].

  4. Barnard SP, Kitching PA, Kulatilake EN. Right ventricle rupture after coronary surgery. Cardiovas Surg. Dec 1994;2 (6):723-24. [Medline].

  5. Birnbaum Y, Chamoun AJ, Anzuini A, et al. Ventricular free wall rupture following acute myocardial infarction. Coron Artery Dis. Sep 2003;14(6):463-70. [Medline].

  6. Birnbaum Y, Fishbein MC, Blanche C, Siegel RJ. Ventricular septal rupture after acute myocardial infarction. N Engl J Med. Oct 31 2002;347(18):1426-32. [Medline].

  7. Brodie BR, Stuckey TD, Hansen CJ, et al. Timing and mechanism of death determined clinically after primary angioplasty for acute myocardial infarction. Am J Cardiol. Jun 15 1997;79(12):1586-91. [Medline].

  8. Frances C, Romero A, Grady D. left ventricular pseudoaneurysm. J Am Col Cardiol. Sep 1998;32 (3):557-61. [Medline].

  9. Geist M, Gilon D, Gotsman MS, Hasin Y. Cardiac rupture during coronary angioplasty. Eur Heart J. Jul 1993;14(7):1002-3. [Medline].

  10. Hayashi T, Hirano Y, Takai H, et al. Usefulness of ST-segment elevation in the inferior leads in predicting ventricular septal rupture in patients with anterior wall acute myocardial infarction. Am J Cardiol. Oct 15 2005;96(8):1037-41. [Medline].

  11. Helmy TA, Nicholson WJ, Lick S, Uretsky BF. Contained myocardial rupture: a variant linking complete and incomplete rupture. Heart. Feb 2005;91(2):e13. [Medline].

  12. Honan MB, Harrell FE Jr, Reimer KA, et al. Cardiac rupture, mortality and the timing of thrombolytic therapy: a meta-analysis. J Am Coll Cardiol. Aug 1990;16(2):359-67. [Medline].

  13. Laws HL. The broken heart. Am Surg. Jun 1998;64 (6):485-92. [Medline].

  14. March KL, Sawada SG, Tarver RD, et al. Current concepts of left ventricular pseudoaneurysm: pathophysiology, therapy, and diagnostic imaging methods. Clin Cardiol. Sep 1989;12(9):531-40. [Medline].

  15. May AK, Patterson MA, Rue LW 3rd, et al. Combined blunt cardiac and pericardial rupture: review of the literature and report of a new diagnostic algorithm. Am Surg. Jun 1999;65(6):568-74. [Medline].

  16. Minami H, Mukohara N, Obo H, et al. Papillary muscle rupture following acute myocardial infarction. Jpn J Thorac Cardiovasc Surg. Aug 2004;52(8):367-71. [Medline].

  17. Molajo AO, McWilliam L, Ward C, Rahman A. Cardiac lymphoma: an unusual case of myocardial perforation--clinical, echocardiographic, haemodynamic and pathological features. Eur Heart J. May 1987;8(5):549-52. [Medline].

  18. Neiman J, Hui WK. Posteromedial papillary muscle rupture as a result of right coronary artery occlusion after blunt chest injury. Am Heart J. Jun 1992;123 (6):1694-9. [Medline].

  19. Nishiyama K, Okino S, Andou J, et al. Coronary angioplasty reduces free wall rupture and improves mortality and morbidity of acute myocardial infarction. J Invasive Cardiol. Oct 2004;16(10):554-8. [Medline].

  20. Ohri SK, Nihoyannopoulos P, Taylor KM, Keogh BE. Angiosarcoma of the heart causing cardiac rupture: a rare cause of hemopericardium. Ann Thorac Surg. Feb 1993;55(2):525-8. [Medline].

  21. Okino S, Nishiyama K, Ando K, Nobuyoshi M. Thrombolysis increases the risk of free wall rupture in patients with acute myocardial infarction undergoing percutaneous coronary intervention. J Interv Cardiol. Jun 2005;18(3):167-72. [Medline].

  22. Perchinsky MJ, Long WB, Hill JG. Blunt cardiac rupture. The Emanuel trauma center experience. Arch Surg. Aug 1995;130 (8):852-6. [Medline].

  23. Shirani J, Berezowski K, Roberts WC. Out-of-hospital sudden death from left ventricular free wall rupture during acute myocardial infarction as the first and only manifestation of atherosclerotic coronary artery disease. Am J Cardiol. Jan 1994;73(1):88-92. [Medline].

  24. Smedira NG, Zikri M, Thomas JD, et al. Blunt traumatic rupture of a mitral papillary muscle head. Ann Thorac Surg. May 1996;61(5):1526-8. [Medline].

  25. Symbas PN. Traumatic heart disease. Curr Probl Cardiol. Aug 1991;16(8):537-82. [Medline].

  26. Topol EJ. Acute coronary syndromes. New York, NY: Marcel Dekker; 1998:. 269-325.

  27. Ueda S, Ikeda U, Yamamoto K, et al. C-reactive protein as a predictor of cardiac rupture after acute myocardial infarction. Am Heart J. May 1996;131(5):857-60. [Medline].

  28. Vargas-Barron J, Molina-Carrion M, Romero-Cardenas A, et al. Risk factors, echocardiographic patterns, and outcomes in patients with acute ventricular septal rupture during myocardial infarction. Am J Cardiol. May 15 2005;95(10):1153-8. [Medline].

  29. Wehrens XH, Doevendans PA. Cardiac rupture complicating myocardial infarction. Int J Cardiol. Jun 2004;95(2-3):285-92. [Medline].

  30. Weinstein L, Brusch JL. Infective endocarditis. London, UK: Oxford University Press; 1996:. 176-7.

  31. Yip HK, Fang CY, Tsai KT, et al. The potential impact of primary percutaneous coronary intervention on ventricular septal rupture complicating acute myocardial infarction. Chest. May 2004;125(5):1622-8. [Medline].

  32. Zidar N, Jeruc J, Balazic J, Stajer D. Neutrophils in human myocardial infarction with rupture of the free wall. Cardiovasc Pathol. Sep-Oct 2005;14(5):247-50. [Medline].

Previous
Next
 
Photograph of the heart of a 43-year-old man demonstrating the site of a stab wound over the left ventricular lateral free wall (shown as a vertical tear).
Photograph of a heart sectioned transversely at the mid left ventricular level showing a posterior ventricular septal defect at the site of a recent acute myocardial infarction.
Photograph of the mitral valve and subvalvular apparatus showing the site of an ischemic papillary muscle (PM) rupture (R).
Magnified photograph of a transverse section of the mid left ventricle (LV) showing a transmural lateral free-wall rupture (R).
Chest radiograph in posteroanterior projection showing a large pseudoaneurysm manifesting as a bulge in the left cardiac border.
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2012 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.

DISCLAIMER: The content of this Website is not influenced by sponsors. The site is designed primarily for use by qualified physicians and other medical professionals. The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The information provided here is for educational and informational purposes only. In no way should it be considered as offering medical advice. Please check with a physician if you suspect you are ill.